Escolar Documentos
Profissional Documentos
Cultura Documentos
Surface infections
Trachoma........................................ 247
Tetanus........................................... 248
Leprosy........................................... 252
6.
281
284
STD........................................................................265
Yaws...................................................................... 269
AIDS...................................................................... 271
...........
..........
.................................
285
Obesity...................................................................316
Blindness................................................................319
Accidents and Injuries........................................... 323
...........
..........
..................................
329
...........
..........
..................................
349
...........
..........
..........
..........
383
...........
..........
..................................
438
...........
..........
..................................
488
...........
..........
..................................
519
...........
..........
..................................
595
5.DISASTER MANAGEMENT
............
..........
..................................
600
6.OCCUPATIONAL HEALTH
............
..........
..................................
606
............
..........
..........
..........
622
8.MENTAL HEALTH
............
..........
..................................
632
..........
..........
..........
638
19.
............
..........
...........
..........
653
............
..........
..................................
666
............
..........
..........
..........
685
2.INTERNATIONAL HEALTH
............
..........
..........
..........
704
............
..........
..........
..........
712
20.
INDEX
I-------------------------------------------------------------------------------------- ------------
-------------------------------------------------------------------------------------- 1
^fl
JL
2 MANANDMEDICINE:TOWARDSHEALTHFORALL
back to the Vedic times, about 5000 BC. During this period,
medical history was associated with mythological figures, sages
and seers. Dhanvantari, the Hindu god of medicine is said to have
been born as a result of the churning of the oceans during a 'tug of
war' between gods and demons. According to some authorities, the
medical knowledge in the Atharvaveda (one of the four Vedas)
gradually developed into the science of Ayurveda.
In ancient India, the celebrated authorities in Ayurvedic
medicine were Atreya, Charaka, Susruta and Vaghbhatt. Atreya
(about 800 BC) is acknowledged as the first great Indian physician
and teacher. He lived in the ancient university of Takshashila,
about 20 miles west of modern Rawalpindi (5). Ayurveda
witnessed tremendous growth and development during the
Buddhist times. King Ashoka (226 BC) and the other Buddhist
kings patronised Ayurveda as State medicine and established
schools of medicine and public hospitals. Charaka (200 AD), the
most popular name in Ayurvedic medicine, was a court physician
to the Buddhist king, Kaniska. Based on the teachings of Atreya,
Charaka compiled his famous treatise on medicine, the "Charaka
Samhita". Charaka mentions some 500 drugs. The Indian snakeroot
(rauwolfia) was employed for centuries by the Indian physicians,
before reserpine was extracted from the root and found
spectacularly effective in the treatment of hypertension.
Among the many distinguished names in Hindu medicine, that
of Susruta, the "father of Indian surgery" stands out in prominence.
He compiled the surgical knowledge of his time in his classic
"Susruta Samhita". It is believed that this classic was compiled
between 800 BC and 400 AD. Though this work is mainly devoted
to surgery, it also includes medicine, pathology, anatomy,
midwifery, ophthalmology, hygiene and bedside manners. The
early Indians set fractures, performed amputations, excised
tumours, repaired hernias and excelled in cataract operations and
plastic surgery (6). It is stated that the British physicians learned
the art of rhinoplasty from Indian surgeons in the days of East
India Company (7). However, during Buddhist times, Indian
surgery suffered a setback because of the doctrine of ahimsa (nonviolence).
Of significance in Ayurveda is the "tridosha theory of disease".
The doshas or humors are: vata (wind), pitta (gall) and kapha
(mucus). Disease was explained as a disturbance in the equilibrium
of the three humors; when these were in perfect balance and
harmony, a person is said to be healthy (8). This theory of disease
is strikingly similar to the "theory of four humors" in Greek
medicine. Medical historians admit that there was free exchange of
thought and experience between the Hindu, Arab, Persian, Greek
and Jewish scholars. The Samhitas of Charaka and Susruta were
translated into Persian and Arabic about 800 AD.
Hygiene was given an important place in ancient Indian
medicine. The laws of Manu were a code of personal hygiene.
Archaeological excavations at Mohenjo-daro and Harappa in the
Indus valley uncovered cities of over two thousand years old which
revealed rather advanced knowledge of sanitation, water supply
and engineering. The golden age of Indian medicine was between
800 BC and 600 AD. During the Moghul period and subsequent
years, Ayurveda declined due to lack of State support.
Medical historians admit that Indian medicine has played in
Asia the same role as the Greek medicine in the west, for it has
spread in Indochina, Indonesia, Tibet, Central Asia, and as far as
Japan, exactly as the Greek medicine has done in Europe and Arab
countries (7).
Mention must be made of the other indigenous systems of
medicine namely Unani-Tibb and Homoeopathy, which are not of
Indian origin. The Unani-Tibb system of medicine, whose
Chinese medicine
Chinese medicine claims to be the world's first organized body
of medical knowledge dating back to 2700 BC (11). It is based on
two principles - the yang and the yin. The yang is believed to be an
active masculine principle and the yin a negative feminine
principle. The balance of these two opposing forces meant good
health. Hygiene, dietetics, hydro-therapy, massage, drugs were all
used by the Chinese physicians.
The Chinese were early pioneers of immunization. They
practised variolation to prevent smallpox. To a Chinese, "the great
doctor is one who treats not someone who is already ill but
someone not yet ill". The Chinese have great faith in their
traditional medicine, which is fully integrated with modern
medicine. The Chinese system of "bare-foot doctors" and
acupuncture have attracted worldwide attention in recent years
(12).
Egyptian medicine
Egypt had one of the oldest civilizations about 2000 BC. A lot
is known about ancient Egypt because they invented picture
writing and recorded their doings on papyrus. In Egyptian times,
the art of medicine was mingled with religion. Egyptian physicians
were co-equals of priests, trained in schools within the temples.
They often helped priests care for the sick who were brought to the
temples for treatment. There were no practical demonstrations in
anatomy, for Egyptian religion enjoined strict preservation of the
human body. Egyptian medicine reached its peak in the days of
Imhotep (2800 BC) who was famous as a statesman, architect,
builder of the step pyramid at Saqqarah and physician. The
Egyptians worshipped many gods. Imhotep was considered both a
doctor and divinity. Specialization prevailed in Egyptian times.
There were eye doctors, head doctors and tooth doctors. All these
doctors were officials paid by the State. Homer speaking of the
doctors of the ancient world considered the Egyptians to be the
"the best of all" (13).
Egyptian medicine was far from primitive. They believed that
disease was due to absorption from the intestine of harmful
substances which gave rise to putrefaction of blood and formation
of pus. They believed that the pulse was "the speech of the heart".
Diseases were treated with cathartics, enema, blood-letting and a
wide range of drugs. The best known medical manuscripts
belonging to the Egyptian times are the Edwin Smith papyrus
(3000-2500 BC), and the Ebers papyrus (1150 BC). The Edwin
Smith papyrus, the oldest treatise on surgery, accurately describes
partial paralysis following cerebral lesions in skull fractures. The
Ebers papyrus which was found with a mummy on the banks of the
Nile, is a unique record of some 800 prescriptions based on some
700 drugs. Castor oil, tannic acid,
were laid in all the countries of the western world. After the First
World War, there were three particular newcomers to the public
health scene - Yugoslavia, Turkey and Russia (19). These three
countries in 1920 presented the typical picture of the
underdeveloped world. Today they are quite advanced in public
health.
While public health made rapid strides in the western world, its
progress has been slow in the developing countries such as India
where the main health problems continue to be those faced by the
western world 100 years ago. The establishment of the WHO
providing a Health Charter for all people provided a great fillip to
the public health movement in these countries.
Germ theory of disease
For long, man was groping in darkness about the causation of
disease. Several theories were advanced from time to time to
explain disease causation such as the supernatural theory of
disease, the theory of humors by Greeks and Indians, the theory of
contagion, the miasmatic theory which attributed disease to
noxious air and vapours, the theory of spontaneous generation, etc.
The breakthrough came in 1860, when the French bacteriologist
ILouis Pasteur (1822-1895) demonstrated the presence of bacteria
in air. He disproved the theory of "spontaneous generation". In
1873, Pasteur advanced the "germ theory of diseasjPTJln 1877,
Robert Koch (1843-1910) showed that anthrax was caused by a
bacteria. The discoveries of Pasteur and Koch confirmed the germ
theory of disease. It was the golden age of bacteriology. Microbe
after microbe was discovered in quick succession - gonococcus in
1847; typhoid bacillus, pneumococcus in 1880; tubercle bacillus in
1882; cholera vibrio in 1883; diphtheria bacillus in 1884, and so
on. These discoveries and a host of others at the turn of the century
marked a turning point in our aetiological concepts. All attention
was focussed on microbes and their role in disease causation. The
germ theory of disease came to the forefront, supplanting the
earlier theories of disease causation. Medicine finally shed the rags
of dogma and superstition and put on the robes of scientific
knowledge.
Birth of preventive medicine
Preventive medicine really dates back to the 18th century. It
developed as a branch of medicine distinct from public health.
Curiously, it came into existence even before the causative agents
of disease were known. James Lind (1716-1794), a naval surgeon
advocated the intake ofjr,esh fruit and vegetables for the prevention
of scurvy in 1753(Edward Jenner (1749-1823) of Great Britain, a
pupil of JohnHunter, discovered vaccination against smallpox in
1796~Jhese two discoveries marked the beginning of a new era, the
era of disease prevention by specific measures.
Preventive medicine got a firm foundation only after the
discovery of causative agents of disease and the establishment of
the germ theory of disease. The latter part of the 19th century was
marked by such discoveries ]nt>reventive medicine as [Pasteur's
anti-rabies treatment (1883^|cholera vaccine (1892), jcTTphtheria
antitoxin (1894), anti-typhoid vaccine (1898), antiseptics and
disinfectants (1827-1912), etc. A further advance was the
elucidation of the modes of disease transmission. For example, in
1896, Bruce, a British Army surgeon, demonstrated that the African
sleeping sickness was transmitted by tsetse fly. In 1898ij?oss
demonstrated that malaria was transmitted by the AnopfieTes*""^
In 1900, Walter Reed and his colleagues jdemonstralea that yellow
fever was transmitted by the Aedes irnpsquito. With the knowledge
derived from bacteriology, it became possible to control disease by
specific measures such as blocking the channels of transmission,
e.g., quarantine, water purification, pasteurization of milk,
protection of foods, proper disposal of sewage, destruction of
insects and disinfection. The
care, but it has escalated the cost of medical care and placec
specialist medical care beyond the means of an average citizen
without outside aid or charity. It has infringed upon the basic tenets
of socialism (i.e., the greatest good of the greatest number and
paved the way to varying degrees of social control ove: medicine.
Specialization has also contributed to the decline o general practice
and the isolation of medical practitioners at the periphery of the
medical care system (20).
Preventive medicine
Preventive medicine developed as a branch of medicine distinct
from public health. By definition, preventive medicine i: applied to
"healthy" people, customarily by actions affectinc large numbers or
populations. Its primary objective is preventior of disease and
promotion of health.
The early triumphs of preventive medicine were in the field o
bacterial vaccines and antisera at the turn of the century whicl led
to the conquest of a wide spectrum of specific diseases Declines
took place in the morbidity and mortality fron diphtheria, tetanus,
typhoid fever and others. Later, the introduction of tissue culture of
viruses led to the development o anti-viral vaccines, e.g., polio
vaccines (1955, 1960). The eradication of smallpox (the last case
of smallpox occurred ir Somalia in 1977) is one of the greatest
triumphs of preventive medicine in recent times. The search for
better and newei vaccines (e.g., against malaria, leprosy, syphilis
and othei parasitic diseases and even cancer) continues.
Preventive medicine did not confine itself to vaccination anc
quarantine. Discoveries in the field of nutrition have added i new
dimension to preventive medicine. New strategies have been
developed for combating specific deficiencies' as foi example,
nutritional blindness and iodine deficiency disorders The
recognition of the role of vitamins, minerals, proteins anc other
nutrients, and more recently dietary fibre emphasize the nutrition
component of preventive medicine.
Another glorious chapter in the history of preventive medicine
is the discovery of synthetic insecticides such as DDT HCH,
malathion and others. They have brought abou fundamental
changes in the strategy in the control of vector borne diseases (e.g.,
malaria, leishmaniasis, plague, rickettsia diseases) which have been
among the most important world wide health problems for many
years. Despite insecticide resistance and environmental pollution
mishaps (e.g., Bhopa tragedy in India in 1984), some of the
chemical insecticides sucr as DDT still remain unchallenged in the
control of disease.
The discovery of sulpha drugs, anti-malarials, antibiotics antitubercular and anti-leprosy drugs have all enrichec preventive
medicine. Chemoprophylaxis and mass druc treatment have
become important tools of preventive medicine The pattern of
disease in the community began to change with improved control
of infectious diseases through both preventior and treatment, and
people are now living for longer years especially those in
developing countries.
A new concept - concept of disease eradication - began tc take
shape. This concept found ready application in the eradication of
smallpox. Eradication of certain other disease: (e.g., measles,
tetanus, guinea worm and endemic goitre) are or the anvil.
Another notable development in the 20th century is the
development of "screening" for the diagnosis of disease in it;
presymptomatic stage (21). In the 1930s, the two mos commonly
used tests were the serologic blood test for syphilis and the chest
X-ray for tuberculosis. As the number of screening tests increased,
the concept of screening for individual disease: entered the
multiphasic epoch in early 1950s. In spite of the fac that the utility
of screening has been increasingly debated ir recent years,
screening for disease among apparently healths
____________________________________MODERN MEDI
people has remained an important part of preventive medicine. An
offshoot of the screening is screening for "risk factors" of disease
and identification of "high risk groups". Since we do not have
specific weapons against chronic diseases, screening and regular
health-checkups have acquired an important place in the early
detection of cancer, diabetes, rheumatism and cardiovascular
disease, the so-called "diseases of civilization".
Preventive medicine is currently faced with the problem of
"population explosion" in developing countries where population
over-growth is causing social, economic, political and
environmental problems. This is another kind of prevention prevention of a problem that demands a mass attack, if its benefits
are to accrue in the present and succeeding generations.
Consequently, research in human fertility and contraceptive
technology has gained momentum. Genetic counselling is another
aspect of the population problem that is receiving attention.
Preventive medicine has become a growing point in medicine
(21). Advances in the field of treatment in no way has diminished
the need for preventive care nor its usefulness. Preventive measures
are already being applied not only to the chronic, degenerative and
hereditary diseases but also to the special problems of old age. In
fact, as medical science advances, it will become more and more
preventive medical practice in nature. The emergence of preventive
paediatrics, geriatrics and preventive cardiology reflect newer
trends in the scope of preventive medicine.
Scientific advances, improved living standards and fuller
education of the public have opened up a number of new avenues
to prevention. Three levels of prevention are now recognized:
primary, intended to prevent disease among healthy people;
secondary, directed towards those in whom the disease has already
developed; and tertiary, to reduce the prevalence of chronic
disability consequent to disease. Preventive medicine ranges far
beyond the medical field in the narrow sense of the word. Besides
communicable diseases, it is concerned with the environmental,
social, economic and more general aspects of prevention. Modern
preventive medicine has been defined as "the art and science of
health promotion, disease prevention, disability limitation and
rehabilitation". It implies a more personal encounter between the
individual and health professional than public health. In sum,
preventive medicine is a kind of anticipatory medicine (22).
Social medicine
Social medicine has been primarily a European speciality. The
seeds that medicine is a social science were sown late in the 19th
century by pioneers such as Neumann (1847) and Virchow (1848).
But their ideas were far too ahead of their time. The germ theory of
disease and discoveries in microbiology checked the development
of these ideas.
In 1911, the concept of social medicine was revived by Alfred
Grotjahn (1869-1931) of Berlin who stressed the importance of
social factors in the aetiology of disease, which he called "social
pathology". Others called it geographical pathology and population
pathology. In 1912 Rene Sand had founded the Belgian Social
Medicine Association. Developments in the field of social sciences
(e.g., sociology, psychology, anthropology) rediscovered that man
is not only a biological animal, but also a social being, and disease
has social causes, social consequences and social therapy. The
ideas of social medicine spread to other countries. John Ryle and
his group in England were influenced by these ideas and visualized
social medicine as an evolution of medicine. They promoted the
concept of social medicine in England. A Chair of social medicine
was set up at Oxford in 1942 followed by similar others in other
Universities in England.
Social medicine has varying meanings attached to its label. By
was stirred leading to a new awakening that the health gap between
rich and poor within countries and between countries should be
narrowed and ultimately eliminated. It is conceded that the
neglected 80 per cent of the world's population too have an equal
claim to health care, to protection from the killer diseases of
childhood, to primary health care for mothers and children, to
treatment for those ills that mankind has long ago learnt to control,
if not to cure (31). Against this background, in 1981, the members
of the WHO pledged themselves to an ambitious target to provide
Health for All by the year 2000, that is attainment of a level of
health that will permit all peoples "to lead a socially and
economically productive life" (32). Currently public health, along
with other medical sciences and other health-related sectors is
engaged in this broad field of effort. This theme is amplified in the
following pages.
IV. MEDICAL REVOLUTION
State of the art
Medicine has moved from the organism to organ, and from the
organ to the cell, and from the cell to molecular properties. The
discovery of the biological role of nucleic acids, the uncovering of
the genetic code and its role in regulating life processes are
marvellous discoveries in recent years. Medicine has acquired a
vast body of knowledge and has become highly technical. It has
acquired new capabilities to modify and perhaps control the
capacities and activities of men by direct intervention into and
manipulation of their bodies and minds, viz. genetic counselling,
genetic engineering, prenatal diagnosis of sex, prenatal diagnosis
of genetic diseases, in vitro fertilization, the prospect of cloning
(the asexual reproduction of unlimited number of genetically
identical individuals from a single parent), organ transplantation,
the use of artificial kidney machine, the development of an
artificial heart, the practice of psychosurgery, etc. The data
presented show that modern medicine has entered a new
evolutionary stage with the promise of continued improvements in
medical capabilities to preserve life, if not merely to solve
problems of sickness.
Failure of medicine
Despite spectacular biomedical advances and massive
expenditures, death rates in the developed countries have remained
unchanged; and also life expectancy. Today, a great scepticism
surrounds medical care (33). Like so many other institutions in
contemporary society medicine has come under heavy fire.
Medicine, as practised today, has begun to be questioned and
criticised. Some critics have even described modern medicine as a
threat to health. Their argu/nents have been based on certain facts
such as: (a) with increased medical costs has not come increased
benefits in terms of health (b) despite spectacular advances in
medicine, the threat posed by certain major diseases such as
malaria, schistosomiasis, leprosy, filaria, trypanosomiasis and
leishmaniasis either has not lessened or has actually increased (c)
the expectation of life has remained low and infant and child
mortality rates high in many developing countries, despite
advances in medicine (d) historical epidemiological studies
showed that significant improvements in longevity had been
achieved through improved food supplies and sanitation long
before the advent of modern drugs and high technology, (34). (e)
there is no equity in the distribution of health services, resulting in
limited access to health care for large segments of the world's
population, and (f) modern medicine is also attacked for its elitist
orientation even in health systems adapted to overcome social
disparities (35).
High-technology medicine seems to be getting out of hand and
leading health systems in the wrong direction i.e., away from the
health promotion for the many and towards expensive treatment
for the few. For example, in the developing countries, the tendency
has been to follow the Western models of medical
London.
2.Dubos, R.J. (1969). Man, Medicine and Environment. New American Library,
New York.
3.Jaggi, O.P. (1973). Indian System of Medicine, Atma Ram and Sons,
4.Gokhale, B.V. (1960). Swasth Hind, 4, 165.
5.Banerjee, J.N. (1966). Ind. J. Med. Edu., 5,79
6.Bhatia, S.L. (1957). Ind. J. Hist. Med., 2,70
7.Parke-Davis (1961). Great Moments in Medicine. A History of Medicine in
pictures, Parke-Davis & Co.
8.Kutumbiah, R (1956). Ind.J.Hist.Med., 2,6
9.Kishore, Jugal (1974). Swasth Hind, 18,36
10.WHO (1984). World Health, July 1984
11.Smith, A.J. (1974). Brit.Med.J., 2, 367
12.Diamond, E.G. (1971). JAMA 218, 1558
13.WHO (1970). World Health, May 1970.
14.Anderson, C.L. etal (1978). Community Health, C.V. Mosby.
15.Kark, S.L. (1974). Epidemiology and Community Medicine, Appleton Century
Crofts.
16.Reiser, S.L. (1980). World Health Forum, 1, 103.
17.Guthrie Douglas (1947). A History of Medicine, Thomas Nelson & Sons,
London
18.Hobson, W. (1965). World Health and History, Oxford University Press,
London.
19.Brockington, C.F. (1967). World Health, Churchill, London.
20.Noble, John (1976). Primary Care and the Practice of Medicine, Boston, Little,
Brown & Co.
21.Norton Alan (1969). The New Dimensions of Medicine, 20th Century Studies,
London, Hodder & Stoughton.
1.Clark
2.Crew. F.A.E. (1960). Med. Edu. Bull, No.2, WHO, SEARO, New Delhi.
3.Stieglitz, Edward J. (1949). In: Social Medicine, Its Derivatives and Objectives,
26.WHO (2003), The World Health Report 2003, Shaping the future.
27.UNDP, Human Development Report 2003, Millennium Developmen Goals : A
compact among nations to end human poverty, Oxfon University Press.
Concept of
Health
and Disease
"Health is NOT mainly an issue of doctors, social services and hospitals. It is an issue of social justice."
CONCEPT
OF HEALTH
1. Biomedical concept
Traditionally, health has been viewed as an "absence of
disease; and if one was free from disease; then the person was
considered heaithy. This concept, known as the "biomedical
concept has the basis in the "germ theory of disease" which
dominated medical thought at the turn of the 20th century. The
medical profession viewed the human body as a machine,
disease as a consequence of the breakdown of the machine
and one of the doctor's task as repair of the machine (4). Thus
health, in this narrow view, became the ultimate goal of
medicine.
The criticism that is levelled against the biomedical concept
,s that it has minimized the role of the environmental, social,
psychological and cultural determinants of health. The
biomedical model, for all its spectacular success in treating
disease, was found inadequate to solve some of the major
health problems of mankind (e.g., malnutrition, chronic
diseases, accidents, drug abuse, mental illness, environmental
pollution, population explosion) by elaborating the medical
technologies. Developments in medical and social sciences led
to the
conclusion that the biomedical concept of health was
inadequate,
_ _ . . .
'
^
"
Deficiencies in the biomedical concept gave rise to other
concepts. The ecologists put forward an attractive hypothesis
which viewed health as a dynamic equilibrium between man
and his environment, and disease a maladjustment of the
human organism to environment. Dubos (5) defined health
saying : "Health implies the relative absence of pain and
discomfort and a continuous adaptation and adjustment to the
environment to ensure optimal function". Human ecological
and
cultural adaptations do determine not only the occurrence
of disease b
also the availability of food and the population
explosion. The ecological concept raises two issues, viz.
imperfect man and imperfect environment. History argues
strongly that improvement in human adaptation to natural
environments can lead to longer life expectancies and a better
quality of life - even in the absence of modern health delivery
services (6).
CHANCING CONCEPTS
An understanding of health is the basis of all health care.
Health is not perceived the same way by all members of a
_______________________________DEFINITIONS OF HE
3. Psychosocial concepts
Contemporary developments in social sciences revealed that
health is not only a biomedical phenomenon, but one which is
influenced by social, psychological, cultural, economic and
political factors of the people concerned (6). These factors must be
taken into consideration in defining and measuring health. Thus
health is both a biological and social phenomenon.
4. Holistic concept
The holistic model is a synthesis of all the above concepts. It
recognizes the strength of social, economic, political and
environmental influences on health. It has been variously described
as a unified or multidimensional process involving the well-being
of the whole person in the context of his environment. This view
corresponds to the view held by the ancients that health implies a
sound mind, in a sound body, in a sound family, in sound
environment. The holistic approach implies that all sectors of
society have an effect on health, in particular, agriculture, animal
husbandry, food, industry, education, housing, public works,
communications and other sectors (7). The emphasis is on the
promotion and protection of health.
DEFINITIONS OF HEALTH
"Health" is one of those terms which most people find it
difficult to define although they are confident of its meaning.
Therefore, many definitions of health have been offered from time
to time, including the following :
a. "the condition of being sound in body, mind or spirit,
especially freedom from physical disease or pain"
(Webster);
b. "soundness of body or mind; that condition in which its
functions are duly and efficiently discharged" (Oxford
English Dictionary);
c. "a condition or quality of the human organism
expressing the adequate functioning of the organism in
given conditions, genetic and environmental" (8);
d. "a modus vivendi enabling imperfect men to achieve a
rewarding and not too painful existence while they cope
with an imperfect world" (9);
e. "a state of relative equilibrium of body form and
function which results from its successful dynamic
adjustment to forces tending to disturb it. It is not passive
interplay between body substance and forces impinging
upon it but an active response of body forces working
toward readjustment" (Perkins).
WHO definition
The widely accepted definition of health is that given by the
World Health Organization (1948) in the preamble to its
constitution, which is as follows :
"Health is a state of complete physical, mental and social
wellbeing and not merely an absence of disease or
infirmity"
In recent years, this statement has been amplified to include the
ability to lead a "socially and economically productive life" (7).
The WHO definition of health has been criticised as being too
broad. Some argue that health cannot be defined as a "state" at all,
but must be seen as a process of continuous adjustment to the
changing demands of living and of the changing meanings we give
to life. It is a dynamic concept. It helps people live well, work well
and enjoy themselves. The WHO definition of health is therefore
considered by many as an idealistic goal than a realistic
proposition. It refers to a
^_____________________________CONCEPT OF WELLBEING 15
6. Vocational dimension
The vocational aspect of life is a new dimension. It is part of
human existence. When work is fully adapted to human goals,
capacities and limitations, work often plays a role in promoting
both physical and mental health. Physical work is usually
associated with an improvement in physical capacity, while goal
achievement and self-realization in work are a source of
satisfaction and enhanced self-esteem (18).
The importance of this dimension is exposed when individuals
suddenly lose their jobs or faced with mandatory retirement. For
many individuals, the vocational dimension may be merely a
source of income. To others, this dimension represents the
culmination of the efforts of other dimensions as they function
together to produce what the individual considers life "success"
(11).
7. Others
A few other dimensions have also been suggested such as (19):
-philosophical dimension
-cultural dimension
-socio-economic dimension
-environmental dimension
-educational dimension
-nutritional dimension
-curative dimension
-preventive dimension
A glance at the above dimensions shows that there are many
"non-medical" dimensions of health, e.g., social, cultural,
educational, etc. These symbolize a huge range of factors to which
other sectors besides health must contribute if all people are indeed
to attain a level of health that will permit them to lead a socially
and economically productive life.
POSITIVE HEALTH
Health in the broad sense of the world does not merely mean
the absence of disease or provision of diagnostic, curative and
preventive services. It also includes as embodied in the WHO
definition, a state of physical, mental and social well-being. The
harmonious balance of this state of the human individual integrated
into his environment, constitutes health, as defined by WHO.
The state of positive health implies the notion of "perfect
functioning" of the body and mind. It conceptualizes health
biologically, as a state in which every cell and every organ is
functioning at optimum capacity and in perfect harmony with the
rest of the body; psychologically, as a state in which the individual
feels a sense of perfect well-being and of mastery over his
environment, and socially, as a state in which the individual's
capacities for participation in the social system are optimal (20).
These ideas were widely ventilated some years ago but now appear
slightly ridiculous (21).
Dubos (5) said, "The concept of perfect positive health cannot
become a reality because man will never be so perfectly adapted to
his environment that his life will not involve struggles, failures and
sufferings". Positive health will, therefore, always remain a mirage,
because everything in our life is subject to change (22). Health in
this context has been described as a potentiality - the ability of an
individual or a social group to modify himself or itself continually,
in the face of changing conditions of life. In working for positive
health the doctor and the community health expert are in the same
position as the gardener or farmer faced with insects, moulds and
weeds. Their work is never done (22).
3. Quality of life
Much has been said and written on the quality of life in recent
years. It is the "subjective" component of wellbeing. "Quality of
life" was defined by WHO (27) as: "the condition of life resulting
from the combination of the effects of the complete range of
factors such as those determining health, happiness (including
comfort in the physical environment and a satisfying occupation),
education, social and intellectual attainments, freedom of action,
justice and freedom of expression".
A recent definition of quality of life is as follows (24): "a
composite measure of physical, mental and social wellbeing as
perceived by each individual or by group of individuals - that is to
say, happiness, satisfaction and gratification as it is experienced in
such life concerns as health, marriage, family work, financial
situation, educational opportunities, self-esteem, creativity,
belongingness, and trust in others".
Thus, a distinction is drawn between the concept of "level of
living" consisting of objective criteria and of "quality of life"
comprising the individual's own subjective evaluation of these. The
quality of life can be evaluated by assessing a person's subjective
feelings of happiness or unhappiness about the various life
concerns.
People are now demanding a better quality of life. Therefore,
governments all over the world are increasingly concerned about
improving the quality of life of their people by reducing morbidity
and mortality, providing primary health care and enhancing
physical, mental and social well-being. It is conceded that a rise in
the standard of living of the people is not enough to achieve
satisfaction or happiness. Improvement of quality of life must also
be added, and this means increased emphasis on social policy and
on reformulation of societal goals to make life more livable for all
those who survive.
Physical quality of life index
As things stand at present, this important concept of quality of
life is difficult to define and even more difficult to measure (28).
Various attempts have been made to reach one composite index
from a number of health indicators. The "Physical quality of life
index" is one such indexjTlt consolidates thre^l indicators, viz.
infant mortality, life expectancy at age one, and^ literacy. These
three components measure the results ratheVj" than inputs. As
suclvthey lend themselves to international anch national
comparison) ^--0 ^jS^l " ^ /f5)
For each component, (the performance of individual countries
is placed on a scare of 0 to 100, where 0 represents an absolutely
defined "worst" performance, and 100 represents an absolutely
defined "best" performance) The composite index is calculated by
averaging the three indicators, giving equal weight to each of them.
The resulting PQLI thus also is scaled 0 to 100.
It may be mentioned that PQLI has not taken per capita GNP
into consideration, showing thereby that "money is not everything".
For example, the oil-rich countries of Middle East xwith high per
capita incomes have in fact not very high PQLIs. At the other
extreme, Sri Lanka and Kerala state in India have low per capita
incomes with high PQLIs. In short,(PQLI does not measure
economic growth; it measures the results of social, economic and
political policies. It is intended to complement, not replace^GNP
(29). The ultimate objective is to attain a PQLI of lOO)
Human Development Index
Human development index (HDI) is defined as "a composite
index combining indicators representing three dimensions longevity (life expectancy at birth); knowledge (adult literacy rate
and mean years of schooling); and income
55
-inn = 0.55
_______________________________DETERMINANTS OF HEALTH
DETERMINANTS OF HEALTH
Health is multifactorial. The factors which influence heal lie
both within the individual and externally in the society which he
or she lives. It is a truism to say that what man is ar to what
diseases he may fall victim depends on a combinatic of two sets
of factors - his genetic factors and tl environmental factors to
which he is exposed. These facto interact and these interactions
may be health-promoting < deleterious. Thus, conceptually, the
health of individuals an whole communities may be considered to
be the result of mar interactions. Only a brief indication of the
more importai determinants or variables are shown in Fig. 3.
1. Biological determinants
The physical and mental traits of every human being are to
some extent determined by the nature of his genes at the moment
of conception. The genetic make-up is unique in that it cannot be
altered after conception. A number of diseases are now known to
be of genetic origin, e.g., chromosomal anomalies, errors of
metabolism, mental retardation, some types of diabetes, etc. The
state of health, therefore depends partly on the genetic constitution
of man. Nowadays, medical genetics offers hope for prevention
and treatment of a wide spectrum of diseases, thus the prospect of
better medicine and longer, healthier life. A vast field of
knowledge has yet to be exploited. It plays a particularly important
role in genetic screening and gene therapy.
Thus, from the genetic stand-point, health may be defined as
that "state of the individual which is based upon the absence from
the genetic constitution of such genes as correspond to characters
that take the form of serious defect and derangement and to the
absence of any aberration in respect of the total amount of
chromosome material in the karyotype or stated in positive terms,
from the presence in the genetic constitution of the genes that
correspond to the normal characterization and to the presence of a
normal karyotype" (12).
The "positive health" advocated by WHO implies that a person
should be able to express as completely as possible the
potentialities of his genetic heritage. This is possible only when the
person is allowed to live in healthy relationship with his
environment - an environment that transforms genetic potentialities
into phenotypic realities (22).
2. Behavioural and socio-cultural conditions
The term "lifestyle" is rather a diffuse concept often used to
denote "the way people live", reflecting a whole range of social
values, attitudes and activities (32). It is composed of cultural and
behavioural patterns and lifelong personal habits (e.g., smoking,
alcoholism) that have developed through processes of socialization.
Lifestyles are learnt through social interaction with parents, peer
groups, friends and siblings and through school and mass media.
Health requires the promotion of healthy lifestyle. In the last 20
years, a considerable body of evidence has accumulated which
indicates that there is an association between health and lifestyle of
individuals (33). Many current-day health problems especially in
the developed countries (e.g., coronary heart disease, obesity, lung
cancer, drug addiction) are associated with lifestyle changes. In
developing countries such as India where traditional lifestyles still
persist, risks of illness and death are connected with lack of
sanitation, poor nutrition, personal hygiene, elementary human
habits, customs and cultural patterns.
It may be noted that not all lifestyle factors are harmful. There
are many that can actually promote health. Examples include
adequate nutrition, enough sleep, sufficient physical activity, etc.
In short, the achievement of optimum health demands adoption of
healthy lifestyles. Health is both a consequence of an individual's
lifestyle and a factor in determining it (32).
3. Environment
It was Hippocrates who first related disease to environment,
e.g., climate, water, air, etc. Centuries later, Pettenkofer in
Germany revived the concept of disease-environment association.
Environment is classified as "internal" and "external". The
_________________________________ECOLOGY OF HEAL
usually show a higher incidence of illhealth and death. For many,
loss of work may mean loss of income and status. It can cause
psychological and social damage.
(iv) Political system : Health is also related to the country's
political system. Often the main obstacles to the implementation of
health technologies are not technical, but rather political. Decisions
concerning resource allocation, manpower policy, choice of
technology and the degree to which health services are made
available and accessible to different segments of the society are
examples of the manner in which the political system can shape
community health services (36). The percentage of GNP spent on
health is a quantitative indicator of political commitment.
Available information shows that India spends about 3 per cent of
its GNP on health and family welfare (37). To achieve the goal of
health for all, WHO has set the target of at least 5 per cent
expenditure of each country's GNP on health care. What is needed
is political commitment and leadership which is oriented towards
social development, and not merely economic development. If
poor health patterns are to be changed, then changes must be made
in the entire sociopolitical system in any given community. Social,
economic and political actions are required to eliminate health
hazards in people's working and living environments.
5. Health services
The term health and family welfare services cover a wide
spectrum of personal and community services for treatment of
disease, prevention of illness and promotion of health. The purpose
of health services is to improve the health status of population. For
example, immunization of children can influence the
incidence/prevalence of particular diseases. Provision of safe water
can prevent mortality and morbidity from water-borne diseases.
The care of pregnant women and children would contribute to the
reduction of maternal and child morbidity and mortality. To be
effective, the health services must reach the social periphery,
equitably distributed, accessible at a cost the country and
community can afford and socially acceptable (7). All these are
ingredients of what is now termed "primary health care", which is
seen as the way to better health.
Health services can also be seen as essential for social and
economic development. It is well to remind ourselves that "health
care does not produce good health" (38). Whereas, there is a strong
correlation between GNP and expectation of life at birth, there is
no significant correlation between medical density and expectation
of life at birth (39). The most we can expect from an effective
health service is good care (38). The epidemiological perspective
emphasizes that health services, no matter how technically elegant
or cost-effective, are ultimately pertinent only if they improve
health (40).
6. Aging of the Population
By the year 2020, the world will have more than one billion
people aged 60 and over and more than two - thirds of them living
in developing countries. Although the elderly in many countries
enjoy better health than hitherto, a major concern of rapid
population aging is the increased prevalence of chronic diseases
and disabilities both being conditions that tend to accompany the
aging process and deserve special attention.
7. Gender
The 1990s have witnessed an increased concentration on
women's issues. In 1993, the Global Commission on Women's
Health was established. The commission drew up an agenda for
action on women's health covering nutrition, reproductive health,
the health consequences of violence, aging, lifestyle
(0 |,,)
TABLE 1
Comparison of Kerala and all-India Health Statistics
Kerala
Death rate/1000 (2002)
Rural birth rate (2002)
Infant mortality rate (2002)
Annual growth rate, per cent (2001)
Life expectancy at birth
2001-06 (Projection)
Male
Female
Literacy rate, per cent (2001)
Female literacy rate (2001)
Mean age at marriage females (1999)
Per capita income (2000-01)
Doctor-population ratio (1991)
All-India
6.4
8.1
16.8
10
0.9
66.5
25.0
64
1.93
61.5
71.7
75
90.92
87.86
22.1
Rs. 21046
1:7213
64.1
65.4
65.38
54.16
19.5
Rs. 16707
1:2148
_______________________________INDICATORS OF HEALTH 23
4.Nutritional status indicators
5.Health care delivery indicators
6.Utilization rates
7.Indicators of social and mental health
8.Environmental indicators
9.Socio-economic indicators
10.Health policy indicators
11.Indicators of quality of life
12.Other indicators
y <r\. j_
as 250 times higher. This indicates the magnitude of the gaj and
the room for improvement.
Qe) Under-5 proportionate mortality rate] : It is thi proportion
of total deaths occurring in the under-5 age group Thisjrate can be
used tcfreflect both infant and child mortalit ratesjn communities
with poor hygiene, the proportion ma e'xceed 60 per cent. In some
European countries, th proportion is less than 2 per cent. High rate
reflects high birt rates, high child mortality rates and shorter life
expectanc (60).
(a)Maternal (puerperal) mortality rate : Matern< (puerperal)
mortality accounts for the greatest proportion c deaths among
women of reproductive age in most of th developing world,
although its importance is not alwav evident from official
statistics (61). There are enormot variations in maternal
mortality rate according to country: level of socioeconomic
status.
(b)Disease-specific mortality : Mortality rates can b computed
for specific diseases. As countries begin to extricai themselves
from the burden of communicable diseases, number of other
indicators such as deaths from cance cardiovascular diseases,
accidents, diabetes, etc have emerge as measures of specific
disease problems.
(h) Proportional mortality rate : The simplest measures <
estimating the burden of a disease in the community proportional
mortality rate, i.e., the proportion of all deatl currently attributed
to it. For example, coronary heart diseai is the cause of 25 to 30
per cent of all deaths in most westei countries. The proportional
mortality rate from communicab diseases has been suggested as a
useful health status indicate it indicates the magnitude of
preventable mortality.
Mortality indicators represent the traditional measures health
status. Even today they are probably the most oftt used indirect
indicators of health. As infectious diseases ha\ been brought under
control, mortality rates have declined very low levels in many
countries. Consequently mortali indicators are losing their
sensitivity as health indicators developed countries. However,
mortality indicators continue be used as the starting point in
health status evaluation.
1. Mortality indicators
\Lr^\>?
[(a) Crude death ratenJhis is consideredja fair indicator of
the comparative heajtfijof the people.CJt is defined as the
5
number of deaths per 1000 population per year in a given,
f| communitO. It indicates the rate at which people are dying.
Strictly speaking, health should not be measured by the
number of deaths that occur in a community. But in many
countries, the crude death rate is the only available indicator of
health {Whe n used for international comparison, the usefulness
, of the crude death rate is restricted because it is influenced by
-^ the age-sex composition of the population) Although not a
/ perfect measure of health status, a decrease in death rate
provides a good tool for assessing the overall health
improvement in a population. Reducing the number of deaths
in the population is an obvious goal of medicine and health
care, and success or failure to do so is a measure of a nation's
commitment to better health.
(b) Expectation of life : Life expectancy at birth is "the
average number of years that will be lived by those born alive
into a population if the current age-specific mortality rates
persist". Life expectancy at birth is highly influenced by the
infant mortality rate where that is high. Life expectancy at the
age of 1 excludes the influence of infant mortality, and life
expectancy at the age of 5 excludes the influence of child
mortality. Life expectancy at birth is used most frequently (60).
It is estimated for both sexes separately. An increase in the
expectation of life is regarded, inferentially, as an improvement
in health status.
. LLife expectancy is a good indicator of socioeconomic development 2. Morbidity indicators
in general. As an indicator of long-term survival,
To describe health in terms of mortality rates only
\ it can be considered as a positive health indicator. It has been
misleading. This is because, mortality indicators do not reve the
adopted as a global health indicator"]
burden of illhealth in a community, as for example menl illness
[c) Infant mortality rate^ Infant mortality rate is the ratio of
and rheumatoid arthritis. Therefore morbidity indicate are used
deaths under 1 year of age in a given year to the total number
to supplement mortality data to describe the heal status of a
of live births in the same year; usually expressed as a rate per
population. Morbidity statistics have also their ov drawback;
1000 live births (59)lh. is one of the most universally accepted
they tend to overlook a large number of conditio which are
indicators of health status not only of infants, but also of whole
subclinical or inapparent, that is, the hidden part the iceberg of
T| population and of the socioeconomic conditions under which >.
disease.
they live. In addition, the infant mortality rate is a sensitive I indicator
The following morbidity rates are used for assessing illheal in
of the availability, utilization and effectiveness of health care,
the
community (62).
particularly perinatal carej
a. incidence and prevalence
f(d) Child mortality rate : Another indicator related to the
overall health status is the early childhood (1-4 years)
b. notification rates
-^x mortality ratej It is defined as the number of deaths at ages 1 -4
c. attendance rates at out-patient departments,
, Vears in a given year, per 1000 children in that age group at the
health centres, etc.
mid-point of the year concerned. It thus excludes infant
d. admission, readmission and discharge rates
mortality.
e. duration of stay in hospital and
Apart from its correlation with inadequate MCH services, it is
f. spells of sickness or absence from work or school.
also related to insufficient nutrition, low coverage by immunization
and adverse environmental exposure and other exogenous agents. 3. Disability rates
Whereas the IMR may be more than 10 times higher in the least
Since death rates have not changed markedly in rece years,
developed countries than in the developed countries, the child
despite massive health expenditures, disability rat related to
mortality rate may be as much
illness and injury have come into use to suppleme
-----------;------ vY^
----------mortality and morbidity indicators. The disability rates are based
on the premise or notion that health implies a full range of daily
activities. The commonly used disability rates fall into two groups:
(a) Event-type indicators and (b) person-type indicators (15,63).
(a) Event-type indicators :
i) Number of days of restricted activity
ii) Bed disability days
iii) Work-loss days (or school loss days) within a specified
period
_________________________________INDICATORS OF HEALTH 25
people live. They include indicators relating to pollution of air and water,
radiation, solid wastes, noise, exposure to toxic substances in food or
drink. Among these, the most useful indicators are those measuring the
proportion of population having access to safe water and sanitation
facilities, as for example, percentage of households with safe water in the
home or within 15 minutes' walking distance from a water standpoint or
protected well; adequate sanitary facilities in the home or immediate
vicinity (60).
9. Socio-economic indicators
These indicators do not directly measure health. Nevertheless, they are
of great importance in the interpretation of the indicators of health care.
These include :
a. rate of population increase
b. per capita GNP
c. level of unemployment
d. dependency ratio
e. literacy rates, especially female literacy rates
f. family size
g. housing: the number of persons per room
h. per capita "calorie" availability
(c)Health for All indicators : For monitoring progress towards the goal
of Health for All by 2000 AD, the WHO has listed the following four
categories of indicators (Table 2).
TABLE 2
Indicators selected for monitoring progress towards Health for All
(1) Health policy indicators:
-political commitment to Health for All
-resource allocation
-the degree of equity of distribution of health services
-community involvement
-organizational framework and managerial process
(2) Social and economic indicators related to health:
-rate of population increase
-GNP or GDP
-income distribution
-work conditions
-adult literacy rate
-housing
-food availability
(3) Indicators for the provision of health care:
-availability
-accessibility
-utilization
-quality of care
(4) Health status indicators:
-low birth weight (percentage)
-nutritional status and psychosocial development of children
-infant mortality rate
-child mortality rate (1-4 years)
-life expectancy at birth
-maternal mortality rate
-disease specific mortality
-morbidity - incidence and prevalence
-disability prevalence
Source (60)
(d) Millennium Development Goal Indicators
The
Millennium Development Goal adopted by the United Nations n the year
2000 provides an opportunity for concerted action :o improve global
health. The health related goals and their ndicators of progress are listed
in Table 3.
Table 3
Health-related Millennium Development Goals, and indicators
Goal: 1. Eradicate extreme poverty and hunger
Indicator: 4. Prevalence of underweight children under five years of
age 5. Proportion of population below minimum level of dietary
energy consumption Goal: 4. Reduce child mortality
Indicator: 13. Under-five mortality rate
1.Infant mortality rate
2.Proportion of 1-year-old children immunized against
measles
Goal: 5. Improve maternal health
Indicator: 16. Maternal mortality ratio
17. Proportion of births attended by skilled health personnel
Goal: 6. Combat HIV/AIDS, malaria and other diseases
Indicator: 18. HIV prevalence among young people aged 15 to 24
years
1.Condom use rate of the contraceptive prevalence rate
2.Number of children orphaned by HIV/AIDS Indicator:
21. Prevalence and death rates associated with malaria
1.Proportion of population in malaria-risk areas using
effective malaria prevention and treatment measures
2.Prevalence and death rates associated with tuberculosis
3.Proportion of tuberculosis cases detected and cured
under Directly Observed Treatment, Short-course
(DOTS)
Goal: 7. Ensure environmental sustainability
Indicator: 29. Proportion of population using solid fuel
Indicator: 30. Proportion of population with sustainable access to an
improved water source, urban and rural Indicator: 31. Proportion of
urban population with access to improved sanitation Goal: 8.
Develop a global partnership for development
Indicator: 46. Proportion of population with access to affordable
________________essential drugs on a sustainable basis______________
Source : (60 a)
growth rates less than 0.5 per cent, and some have already
achieved zero population growth rate (e.g., Austria, Belgium,
Federal Republic of Germany and the UK). The rest of the world
continues to reproduce at a prodigious rate. Rates over 2.4 per cent
have occurred in some African (e.g., Nigeria, Zambia, Congo) and
Middle East (e.g., UAE, Libya, Saudi Arabia, Iraq) countries. In
India, the current growth rate is about 1.85 per cent. These
countries are now facing the population problem.
The population in developing countries is a "young"
population; the proportion of persons under 15 years of age is
about 32.6 per cent, compared to about 20.2 per cent in developed
countries. The proportion of people over 65 years in developing
countries is about 5.1 per cent, compared to 13.2 per cent in the
developed countries. The social and economic backlashes of this
age distribution are being felt in both the developing and
developed countries - the former having to bear the heavy burden
of providing for a population which is mainly young; and the latter
having to deal with the problems of aging.
3. Contrasts in health (Health gap)
While accurate statistical data are difficult to obtain, even
perfunctory glance at available data (Table 4 and Fig. 4) are
sufficient to illustrate the wide health gap between population in
the developed and developing countries.
Table 4 shows that the present gap in life expectancy at birth
between developed and developing countries is 15-20 years.
Developed countries are characterised by longer life expectancy
and lower infant and child mortality rates, and the opposite is true
of developing countries.
TABLE 4
Selected health and socio -economic indicators
Least
developed
countries
Other
Developed
developing countries
countries
49
62
78
99
62
158
90
890
440
13
1.4
8.4
25.2
2.2
9.6
74.2
277
1154
28214
14
53.3
2099
62
74.5
2663
78
97
3371
100
44
52
100
CONCEPT OF CAUSATION 29
Each country will have to develop a health policy of its own
aimed at defined goals, for improving the people's health, in the
light of its own problems, particular circumstances, social and
economic structures, and political and administrative mechanisms.
Among the crucial factors affecting realization of these goals are: a
political commitment; financial implications; administrative
reforms; community participation and basic legislation (76).
A landmark in the development of health policy was the worldwide adoption of the goal of HFA by 2000 AD. A further landmark
was the Alma-Ata Declaration (1978) calling on all governments
to develop and implement primary health care strategies to attain
the target of HFA by 2000 AD and more recently, Millennium
Development Goals.
Health services research
Health research has several ramifications. It may include (a)
Biomedical research, to elucidate outstanding health problems
and develop new or better ways of dealing with them; (b)
Intersectoral research, for which relationships would have to be
established with the institutions concerned with the other sectors,
and (c) Health services research or health practice research (now
called "health systems research").
The concept of health services research (HSR) was developed
during 1981-1982. It has been defined as "the systematic study of
the means by which biomedical and other relevant knowledge is
brought to bear on the health of individuals and communities under
a given set of conditions" (77). HSR is wide in scope. It deals with
all aspects of management of health services, viz. prioritization of
health problems, planning, management, logistics and delivery of
health care services. It deals with such topics as manpower,
organization, the utilization of facilities, the quality of health care,
cost-benefit and cost-effectiveness (78).
Thousands of people suffer morbidity, mortality and disability
not because of deficiencies in biomedical knowledge but as a
result of the failure to apply this knowledge effectively. Health
services research aims to correct this failure (79).
The concept of HSR is holistic and multidisciplinary. The
prime purpose of HSR is to improve the health of the people
through improvement not only of conventional health services but
also of other services that have a bearing on health. HSR is
essential for the continuous evolution and refinement of health
services (77).
CONCEPT OF DISEASE
There have been many attempts to define disease. Webster
defines disease as "a condition in which body health is impaired, a
departure from a state of health, an alteration of the human body
interrupting the performance of vital functions". The Oxford
English Dictionary defines disease as "a condition of the body or
some part or organ of the body in which its functions are disrupted
or deranged". From an ecological point of view, disease is defined
as "a maladjustment of the human organism to the environment"
(80). From a sociological point of view, disease is considered a
social phenomenon, occurring in all societies (81) and defined and
fought in terms of the particular cultural forces prevalent in the
society. The simplest definition is, of course, that disease is just the
opposite of health - i.e., any deviation from normal functioning or
state of complete physical or mental well-being - since health and
disease are mutually exclusive. These definitions are considered
inadequate because they do not give a criterion by which to decide
when a disease state begins, nor do they lend themselves to
measurement of disease.
The WHO has defined health but not disease. This is because
disease has many shades ("spectrum of disease") ranging from
inapparent (subclinical) cases to severe manifest illness. Some
diseases commence acutely (e.g., food poisoning), and some
insidiously (e.g., mental illness, rheumatoid arthritis). In some
diseases, a "carrier" state occurs in which the individual remains
outwardly healthy, and is able to infect others (e.g., typhoid fever).
In some instances, the same organism may cause more than one
clinical manifestation (e.g., streptococcus). In some cases, the same
disease may be caused by more than one organism (e.g.,
diarrhoea). Some diseases have a short course, and some a
prolonged course. It is easy to determine illness when the signs and
symptoms are manifest, but in many diseases the border-line
between normal and abnormal is indistinct as in the case of
diabetes, hypertension and mental illness. The end-point or final
outcome of disease is variable - recovery, disability or death of the
host.
Distinction is also made between the words disease, illness and
sickness which are not wholly synonymous. The term "disease"
literally means "without ease" (uneasiness) -disease, the opposite
of ease - when something is wrong with bodily function. "Illness"
refers not only to the presence of a specific disease, but also to the
individual's perceptions and behaviour in response to the disease,
as well as the impact of that disease on the psychosocial
environment (82). "Sickness" refers to a state of social dysfunction.
Susser (83) has suggested the following usage:
Disease is a physiological/psychological dysfunction;
Illness is a subjective state of the person who feels aware of
not being well;
Sickness is a state of social dysfunction, i.e., a role that the
individual assumes when ill ("sickness role").
The clinician sees people who are ill rather than the diseases
which he must diagnose and treat (84). However, it is possible to
be victim of disease without feeling ill, and to be ill without signs
of physical impairment. In short, an adequate definition of disease
is yet to be found - a definition that is satisfactory or acceptable to
the epidemiologist, clinician, sociologist and the statistician.
CONCEPT OF CAUSATION
Up to the time of Louis Pasteur (1922-1895), various concepts
of disease causation were in vogue, e.g., the supernatural theory of
disease, the theory of humors, the concept of contagion, miasmatic
theory of disease, the theory of spontaneous generation, etc.
Discoveries in microbiology marked a turning point in our
aetiological concepts .
Germ theory of disease
Mention has already been made about the germ theory of
disease in chapter 1. This concept gained momentum during the
19th and the early part of 20th century. The emphasis had shifted
from empirical causes (e.g., bad air) to microbes as the sole cause
of disease. The concept of cause embodied in the germ theory of
disease is generally referred to as a one-to-one relationship
between causal agent and disease. The disease model accordingly
is :
Disease agent > Man > Disease
The germ theory of disease, though it was a revolutionary
concept, led many epidemiologists to take one-sided view of
disease causation. That is, they could not think beyond the germ
theory of disease. It is now recognized that a disease is rarely
caused by a single agent alone, but rather depends upon a number
of factors which contribute to its occurrence. Therefore modern
medicine has moved away from the strict adherence to the germ
theory of disease.
Epidemiological triad
The germ theory of disease has many limitations. For example,
it is well-known, that not everyone exposed to tuberculosis
develops tuberculosis. The same exposure, however, in an
undernourished or otherwise susceptible person may result in
clinical disease. Similarly, not everyone exposed to betahaemolytic streptococci develops acute rheumatic fever. There are
other factors relating to the host and environment which are
equally important to determine whether or not disease will occur in
the exposed host. This demanded a broader concept of disease
causation that synthesized the basic factors of agent, host and
environment (Fig. 5).
Environment
Agent
Host
FIG. 5
Epidemiological triad
The above m^del - agent, host and environment - has been in
use for many years. It helped epidemiologists to focus on different
elates of factors, especially with regard to infectious diseases (H5).
Multifactorial causation
The concept that disease is due to multiple factors is not a new
one. Pettenkofer of Munich (1819-1901) was an early proponent of
this concept. But the "germ theory of disease" or "single cause
idea" in the late 19th century overshadowed the multiple cause
theory.
As a result of advances in public health, chemotherapy,
antibiotics and vector control communicable diseases began to
decline - only to be replaced by new types of diseases, the so-called
"modern" diseases of civilization, e.g., lung cancer, coronary heart
disease, chronic bronchitis, mental illness, etc. These diseases
could not be explained on the basis of the germ theory of disease
nor could they be prevented by the traditional methods of isolation,
immunization or improvements in sanitation. The realization began
to dawn that the "single cause idea" was an oversimplification and
that there are other factors in the aetiology of diseases - social,
economic, cultural, genetic and psychological which are equally
important. As already mentioned, tuberculosis is not merely due to
tubercle bacilli; factors such as poverty, overcrowding and
malnutrition contribute to its occurrence. The doctrine of one-toone relationship between cause and disease has been shown to be
untenable, even for microbial diseases, e.g., tuberculosis, leprosy.
It is now known that diseases such as coronary heart disease
and cancer are due to multiple factors. For example, excess of fat
intake, smoking, lack of physical exercise and obesity are all
involved in the pathogenesis of coronary heart disease. Most of
these factors are linked to lifestyle and human behaviour.
Epidemiology has contributed significantly to our present day
understanding of multifactorial causation of disease. Medical men
are looking "beyond the "germ theory" of disease into the total life
situation of the patient and the community in search of multiple (or
risk) factors of disease.
Therefore new models of disease causation have been
developed (e.g., multifactorial causation, web of causation)
-------------------------- f
PERIOD OF PRE- PATHOGENESIS
-------- f
PERIOD OF PATHOGENESIS
DISEASE PROCESS
Host
And
Environmental Factors
(known and unknown)
Bring agent and
host together or
produce a disease
provoking stimulus
Chronic state
Defect
Dli lability
Illnes
Clinical horizon
1
. hum
hos
LEVELS OF
PREVENTION
MODES OF
INTERVENTION
In th
PRIMARY PREVENTION
HEALTH '
SPECIFIC
PROMOTION PROTECTION
RECOVERY
_____________
t
PRETENTION
TERTIARY PREVENTION
ARIIITATION
RFH
REHABILITATION
FIG. 7
Natural history of disease (From Preventive Medicine for the Doctor in His
Community, by Leavell & Clark with permission of McGraw-Hill Book Co.)
4. Chemical agents:
(i) Endogenous: Some of the chemicals may be produced in the
body as a result of derangement of function, e.g., urea (ureamia),
serum bilirubin (jaundice), ketones (ketosis), uric acid (gout),
calcium carbonate (kidney stones), etc: (ii) Exogenous: Agents
arising outside of human host, e.g., allergens, metals, fumes, dust,
gases, insecticides, etc. These may be acquired by inhalation,
ingestion or inoculation.
5. Mechanical agents:
Exposure to chronic friction and other mechanical forces may
result in crushing, tearing, sprains, dislocations and even death.
6. Absence or insufficiency or excess of a factor necessary to
health:
These may be (i) Chemical factors: e.g., hormones (insulin,
oestrogens, enzymes (ii) Nutrient factors: given under (2) above
(iii) Lack of structure: e.g., thymus (iv) Lack of part of structure,
e.g., cardiac defects (v) Chromosomal factors, e.g., mongolism,
turner's syndrome, and (vi) Immunological factors, e.g.,
agammaglobulinaemia.
7. Social agents:
It is also necessary to consider social agents of disease.
4. Chemical agents:
(i) Endogenous: Some of the chemicals may be produced in the
body as a result of derangement of function, e.g., urea (ureamia),
serum bilirubin (jaundice), ketones (ketosis), uric acid (gout),
calcium carbonate (kidney stones), etc: (ii) Exogenous: Agents
arising outside of human host, e.g., allergens, metals, fumes, dust,
gases, insecticides, etc. These may be acquired by inhalation,
ingestion or inoculation.
5. Mechanical agents:
Exposure to chronic friction and other mechanical forces may
result in crushing, tearing, sprains, dislocations and even death.
6. Absence or insufficiency or excess of a factor necessary to
health:
These may be (i) Chemical factors: e.g., hormones (insulin,
oestrogens, enzymes (ii) Nutrient factors: given under (2) above
(iii) Lack of structure: e.g., thymus (iv) Lack of part of structure,
e.g., cardiac defects (v) Chromosomal factors, e.g., mongolism,
turner's syndrome, and (vi) Immunological factors, e.g.,
agammaglobulinaemia.
7. Social agents:
It is also necessary to consider social agents of disease.
_____________________________ENVIRONMENTAL FACTORS
:
b. Biological environment:
The biological environment is the universe of living thin
which surrounds man, including man himself. The living thin are
the viruses and other microbial agents, insects, rodem animals
and plants. These are constantly working for the-survival, and in
this process, some of them act as diseasi producing agents,
reservoirs of infection, intermediate ho; and vectors of disease.
Between the members of the ecologic system (which includes
man) there is constant adjustment at readjustment. For the most
part, the parties manage to effect harmonious inter-relationship,
to achieve a state of peace! co-existence, even though this may
not be always endurin When for any reason, this harmonious
relationship disturbed, ill health results. In the area of biologic
environment also, preventive medicine has been high successful
in protecting the health of the individual and of tl community.
c. Psychosocial environment:
It is difficult to define "psychosocial environment" agair the
background of the highly varied social, economic ai cultural
contexts of different countries and their soc standards and value
systems. It includes a complex psychosocial factors which are
defined as "those facte affecting personal health, health care and
community we being that stem from the psychosocial make-up
of individui and the structure and functions of social groups"
(62). Th include cultural values, customs, habits, beliefs, attitudf
morals, religion, education, lifestyles, community life, heal
services, social and political organization.
In addition to this broad aspect of psychosoc environment,
man is in constant interaction with that part the social
environment known as "people". He is a member a social group,
the member of a family, of a caste, of community and of a
nation. Between the individual and otr members of the group,
there can be harmony or disharmor interests and points of view
that are shared or that are conflict. The behaviour of one
individual can affect oth< more or less directly; conflict and
tension between t individual and the group as a whole or
between the individi and other members of the group can yield
great distress. T law of the land, customs, attitudes, beliefs,
traditions, regulate the interactions among groups of individuals
a families.
The impact of social environment has both positive a
negative aspects on the health of individuals and communitii A
favourable social environment can improve health, provi
opportunities for man to achieve a sense of fulfilment, and a to
the quality of life. Therefore, customs and traditic favouring
health must be preserved. Beneficial soc behaviour (e.g.,
community participation) should be restor where it has
disappeared due to social changes.
Psychosocial factors can also affect negatively man's hea and
well-being. For example, poverty, urbanization, migrati and
exposure to stressful situations such as bereaveme desertion,
loss of employment, birth of a handicapped ch may produce
feelings of anxiety, depression, anger, frustratic and so forth;
and these feelings may be accompanied physical symptoms such
as headache, palpitations a sweating. But these emotional states
also produce changes the endocrine, autonomic and motor
systems, which, prolonged and in interaction with genetic and
personal factors, may lead to structural changes in various bod
organs. The ' resulting psychosomatic disorders inclu conditions
such as duodenal ulcer, bronchial asthn hypertension, coronary
heart disease, mental disorders a socially deviant behaviour
(e.g., suicide, crime, violence, dr
risk factors such as age, sex, race, family history and genetic
factors are not subject to change. They act more as signals in
alerting health professionals and other personnel to the possible
outcome (91).
Risk factors may characterise the individual, the family, the
group, the community or the environment. For example, some of
the individual risk factors include age, sex, smoking, hypertension,
etc. But there are also collective community risks - for example,
from the presence of malaria, from air pollution, from substandard
housing, or a poor water supply or poor health care services. The
degree of risk in these cases is indirectly an expression of need.
Therefore it is stated that a risk factor is a proxy for need indicating the need for promotive and preventive health services.
Epidemiological methods (e.g., case control and cohort studies)
are needed to identify risk factors and estimate the degree of risk.
These studies are carried out in population groups among whom
certain diseases occur much more frequently than other groups. By
such comparative studies, epidemiologists have been able to
identify smoking as a risk for lung cancer; high serum cholesterol
and high blood pressure as risk factors for coronary heart disease.
The contribution of epidemiology in the identification of risk
factors has been highly significant. Risk factors associated with
some major disease groups are as shown in Table 5.
TABLE 5
Prominent Risk Factors
Disease
Risk factors
Heart disease
TABLE 6
Guidelines for defining "at-risk" groups
a. Biological situation:
-age group, e.g., infants (low birth weight), toddlers, elderly
-sex, e.g., females in the reproductive age period
-physiological state, e.g., pregnancy, cholesterol level, high
blood pressure
-genetic factors, e.g. family history of genetic disorders
-other health conditions (disease, physical functioning,
unhealthy behaviour)
b. Physical situation:
-rural, urban slums
-living conditions, overcrowding
-environment: water supply, proximity to industries
c. Sociocultural and cultural situation:
-social class
-ethnic and cultural group
-family disruption, education, housing
-customs, habits and behaviour (e.g., smoking, lack of
exercise, over-eating, drug addicts)
-access to health services
-lifestyles and attitudes
_______________________________CONCEPTS OF CONTROL
35
malnutrition, mental illness) the unknown morbidity (i.e., the
submerged portion of the iceberg) far exceeds the known
morbidity. The hidden part of the iceberg thus constitutes an
important, undiagnosed reservoir of infection or disease in the
community, and its detection and control is a challenge to modern
techniques in preventive medicine. One of the major deterrents in
the study of chronic diseases of unknown aetiology is the absence
of methods to detect the subclinical state - the bottom of the
iceberg (95).
Source (94)
Modern epidemiology is concerned with the identification
of risk factors and high-risk groups in the population. Since
resources are scarce, identification of those at risk is
imperative. It helps to define priorities and points to those most
in need of attention. The knowledge of risk factors and risk
groups can be used to prevent disease in so far as we are able
to
remove
or
minimise
the
risk.
M
Spectrum of disease
V_^
The term "spectrum of disease" is a graphic representation of
variations in the manifestations of disease. It is akin to the
spectrum of light where the colours vary from one end to the other
but difficult to determine where one colour ends and the other
begins. At one end of the disease spectrum are subclinical
infections which are not ordinarily identified and at the other end
are fatal illnesses. In the middle of the spectrum lie illnesses
ranging in severity from mild to severe. These different
manifestations are simply reflections of individuals' different
states of immunity and receptivity. Leprosy is an excellent
example of the spectral concept of disease. For almost every
disease there exists a spectrum of severity, with few exceptions
such as rabies. In infectious diseases, the spectrum of disease is
also referred to as the "gradient of infection".
The sequence of events in the spectrum of disease can be
interrupted by early diagnosis and treatment or by preventive
measures which if introduced at a particular point will prevent or
retard the further development of the disease. The concept of
spectrum of disease provides for inclusion of all cases, both
subclinical and clinical, in the study of disease.
Iceberg of disease
/^A /
A concept closely related to the spectrum of disease is the
concept of the iceberg phenomenon of disease .[According to this
concept, disease in a community may be compared with an iceberg
(Fig. 9). The floating tip of the iceberg represents what the
physician sees in the community, i.e., clinical cases. The vast
submerged portion of the iceberg represents the hidden mass of
disease, i.e., latent, inapparent, presymptomatic and undiagnosed
cases and carriers in the community. The "waterline" represents
the demarcation between apparent and inapparent disease^
In Qnm> Hkoacoc to n
hunortoncinn
Hiaho+oc
anaomia
CONCEPTS OF CONTROL
'Disease control
v
The term "disease control" describes (ongoing) operations
aimed at reducing:
i. the incidence of disease
ii. the duration of disease, and consequently the risk of
transmission
iii. the effects of infection, including both the physical and
psychosocial complications; and
.
iv. the financial burden to the community. /
y
Control activities may focus on primary prevention or
secondary prevention, most control programmes combine the two.
The concept of tertiary prevention is comparatively less relevant to
control efforts.
In disease control, the disease "agent" is permitted to persist
in the community at a level where it ceases to be a public
health-^prablem according to the tolerance of the local
populatioty/(A state of equilibrium becomes established
between the^ disease agent, host and environment components
of the disease process. An excellent embodiment of this
concept is malaria control, which is distinct from malaria
eradication)
^ *Disease elimination f<-l I *,'
//Between control and eradication, an intermediate goal has biien
described, called "regional elimination" (92). The term
"elimination" is used to describe interruption of transmission of
disease, as for example, elimination of measles, polio and
diphtheria from large geographic regions or areas (31). Regional
elimination is now seen as an important precursor of eradication
(96).
Disease eradication
Eradication literally means to "tear out by roots". Eradication of
disease implies termination of all transmission of infection by
extermination of the infectious agent (31). As the name implies,
eradication is an absolute process, and not a relative goal. It is
"all or none phenomenon". The word
*
Sentinel surveillance agencies could be interested and
competent physicians (or institutions) in selected areas to report
the cases of disease in their areas. This system would provide more
valuable and detailed information than could be obtained from the
traditional notification system (104). Finally, these sentinel sites
could be developed into a notification system for providing more
detailed information, which, in some settings, may be less costly
than developing and maintaining an ongoing notification system.
Evaluation of control
Evaluation is the process by which results are compared with
the intended objectives, or more simply the assessment of how
well a programme is performing. Evaluation should always be
considered during the planning and implementation stages of a
programme or activity. Evaluation may be crucial in identifying
the health benefits derived (impact on morbidity, mortality,
sequelae, patient satisfaction). Evaluation can be useful in
identifying performance difficulties. Evaluation studies may also
be carried out to generate information for other purposes, e.g., to
attract attention to a problem, extension of control activities,
training and patient management, etc. The principles of evaluation
are discussed in chapter 20.
CONCEPTS OF PREVENTION
The goals of medicine are to promote health, to preserve health,
to restore health when it is impaired, and to minimize suffering and
distress. These goals are embodied in the word "prevention" (31).
Successful prevention depends upon a knowledge of causation,
dynamics of transmission, identification of risk factors and risk
groups, availability of prophylactic or early detection and treatment
measures, an organization for applying these measures to
appropriate persons or groups, and continuous evaluation of and
development of procedures applied (105).
It is not necessary (although desirable) to know everything
about the natural history of a disease to initiate preventive
measures. Often times, removal or elimination of a single known
essential cause may be sufficient to prevent a disease. The
objective of preventive medicine is to intercept or oppose the
"cause" and thereby the disease process. This epidemiological
concept permits the inclusion of treatment as one of the modes of
intervention (42).
Levels of prevention
In modern day, the concept of prevention has become broadbasedf It has become customary to define prevention in
_____________________________CONCEPTS OF PREVENTION 37
terms of four level:
S /N
1.primordial prevention i <*>
2.primary prevention
*
3.secondary prevention
4.tertiary prevention
' wgj "
Va ^ 'Mft**"
These levels of prevention are siK)\^^n^ig#-4i-fel^:iQjJ*D
the natural history of disease^ Authorities on preventive medicine
do not agree on the precise boundaries between these levels, but
that does not minimise their importance. For example, the supply
of food supplements to a family could be primary prevention for
some members, and secondary prevention (curative) for others
(10). These differences of opinion are more semantic than
substantive (31). A general discussion of these concepts is given
below:
1. Primordial prevention
Primordial prevention, a new concept, is receiving special
attention in the prevention of chronic diseases. This is primary
prevention in its purest sense (107), that is, prevention of the
emergence or development of risk factors in countries or
population groups in which they have not yet appeared (106). For
example, many adult health problems (e.g., obesity, hypertension)
have their early origins in childhood, because this is the time when
lifestyles are formed (for example, smoking, eating patterns,
physical exercise). In primordial prevention, efforts are directed
towards discouraging children from adopting harmful lifestyles
(108). The main intervention in primordial prevention is through
individual and mass education (106).
2. Primary prevention
w^^u
Primary prevention can be defined as "action taken prior to the
onset of disease, which removes the possibility that a disease will
ever occur". It signifies intervention in the prepathogenesis phase
of a disease or health problem (e.g., low birth weight) or other
departure from health. Primary prevention may be accomplished
by measures designed to promote general health and well-being,
and quality of life of people or by specific protective measures.
These are discussed in detail elsewhere under "Mode of
Intervention".
Primary prevention is far more than averting the occurrence of
a disease and prolonging life. It includes the concept of "positive
health", a concept that encourages achievement and maintenance
of "an acceptable level of health that will enable every individual
to lead a socially and economically productive life". It concerns an
individual's attitude towards life and health and the initiative he
takes about positive and responsible measures for himself, his
family and his community.
The concept of primary prevention is now being applied to the
prevention of chronic diseases such as coronary heart disease,
hypertension and cancer based on elimination or modification of
"risk factors" of disease. The WHO has recommended the
following approaches for the primary prevention of chronic
diseases where the risk factors are established (106) :
a. population (mass) strategy
b. high-risk strategy
a. Population (mass) strategy:
Another preventive approach is "population strategy" which is
directed at the whole population irrespective of individual risk
levels. For example, studies have shown that even a small
reduction in the average blood pressure or serum cholesterol of a
population would produce a large reduction in the incidence of
cardiovascular disease (108). The population approach is directed
towards socio-economic, behavioural and lifestyle changes (108).
____________________________CONCEPTS OF PREVENTION 37
terms of four level:
>V j~\
1.primordial prevention
>^
2.primary prevention
^~
3.secondary prevention
4. tertiary prevention
' \p\^Si^i--f- V lf^<t*Vft^
These levels of prevention are slvjwfriftj^A'MtfiwlsSJiSitfio
the natural history of disease^ Authorities on preventive medicine
do not agree on the precise boundaries between these levels, but
that does not minimise their importance. For example, the supply
of food supplements to a family could be primary prevention for
some members, and secondary prevention (curative) for others
(10). These differences of opinion are more semantic than
substantive (31). A general discussion of these concepts is given
below:
1. Primordial prevention
Primordial prevention, a new concept, is receiving special
attention in the prevention of chronic diseases. This is primary
prevention in its purest sense (107), that is, prevention of the
emergence or development of risk factors in countries or
population groups in which they have not yet appeared (106). For
example, many adult health problems (e.g., obesity, hypertension)
have thejr early origins in childhood, because this is the time when
lifestyles are formed (for example, smoking, eating patterns,
physical exercise). In primordial prevention, efforts are directed
towards discouraging children from adopting harmful lifestyles
(108). The main intervention in primordial prevention is through
individual and mass education (106).
2. Primary prevention
Primary prevention can be defined as "action taken prior to the
onset of disease, which removes the possibility that a disease will
ever occur". It signifies intervention in the prepathogenesis phase
of a disease or health problem (e.g., low birth weight) or other
departure from health. Primary prevention may be accomplished
by measures designed to promote general health and well-being,
and quality of life of people or by specific protective measures.
These are discussed in detail elsewhere under "Mode of
Intervention".
Primary prevention is far more than averting the occurrence of
a disease and prolonging life. It includes the concept of "positive
health", a concept that encourages achievement and maintenance
of "an acceptable level of health that will enable every individual
to lead a socially and economically productive life". It concerns an
individual's attitude towards life and health and the initiative he
takes about positive and responsible measures for himself, his
family and his community.
The concept of primary prevention is now being applied to the
prevention of chronic diseases such as coronary heart disease,
hypertension and cancer based on elimination or modification of
"risk factors" of disease. The WHO has recommended the
following approaches for the primary prevention of chronic
diseases where the risk factors are established (106) :
a. population (mass) strategy
b. high-risk strategy
a. Population (mass) strategy:
Another preventive approach is "population strategy" which is
directed at the whole population irrespective of individual risk
levels. For example, studies have shown that even a small
reduction in the average blood pressure or serum cholesterol of a
population would produce a large reduction in the incidence of
cardiovascular disease (108). The population approach is directed
towards socio-economic, behavioural and lifestyle changes (108).
4. Disability limitation
* When a patient reports late in the pathogenesis phase, the mode of
intervention is disability limitation. The objective of this
intervention is to prevent or halt the transition of the disease
process from impairment to handicap^)
Disability prevention:
Another concept is ("disability prevention". It relates to all , the
levels of prevention: (a) reducing the occurrence of
40 CONCEPT OF HEALTH AND DISEASE_____________________produces its own pattern of disease. The truth of this will be
obvious when one compares the leading causes of death in the
developed countries at the beginning of this century and now
(Table 7).
TABLE 7
Leading Causes of Death in the United States
1900 and 1994
Per cent of deaths
from all causes
Cause of death
1900
Pneumonia and influenza
Tuberculosis
Diarrhoea and enteritis
Heart disease
Cerebrovascular disease
Chronic nephritis
Accidents
Cancer
Certain diseases of infancy
Diphtheria
11.8
11.3
8.3
8.0
6.2
4.7
4.2
3.7
3.6
2.3
1994
Heart disease
Cancer
Cerebrovascular disease
Accidents
Chronic obstructive pulmonary disease
Pneumonia and influenza
Diabetes
Suicide
Chronic liver diseases and cirrhosis
HIV infection
All other causes
32.1
23.5
6.8
3.9
4.5
3.6
2.4
1.4
1.1
1.8
18.9
___________________________________POPULATION MEDICINE 41
fublic health
tjjf fThe term "public health" came into general use around ri|Al8W7"It
arose from the need to protect "the public" from the Spread of
communicable diseases. Later, it appeared in 1848 in the name of a
law, the Public Health Act in England to crystallise the efforts
organized by society to protect, promote, and restore the people's
health. J
In 1920, C.E.A. Winslow, a former professor of public health at
Yale University, gave the oft-quoted definition of public health.
(The WHO Expert Committee on Public Health Administration,
adapting Winslow's earlier definition, has defined it as (124):
"the science and art of preventing disease, prolonging life,
and promoting health and efficiency through organized
/& community effort&for the sanitation of the environment,
\J ^ JS-H, the control of communicable infections, the education of
(Ik) the individual in personal hygiene, the organization of
^>f medical and nursing services for early diagnosis and
preventive treatment of disease, and the development of
social machinery to ensure for every individual a standard
of living adequate for the maintenance of health, so
organizing these benefits as to enable every citizen to
realize his birthright of health and longevity".
Whereas in developing countries such as India, public health
has not made much headway in terms of sanitary reforms and
control of communicable diseases, it has made tremendous strides
in the industrialized western countries resulting in longer
expectation of life and significant decline in death rates. As a result
of improvements in public health during the past 50 or 60 years,
public health in the developed countries has moved from sanitation
and control of communicable diseases (which have been largely
controlled) to preventive, therapeutic and rehabilitative aspects of
chronic diseases and behavioural disorders.
A EURO symposium in 1966 (59) suggested that the definition
of public health should be expanded to include the organization of
medical care services. This was endorsed by another Expert
Committee of WHO in 1973 (125). Thus modern public health also
includes organization of medical care, as a means of protecting and
improving the health of people (126). Since the organization of
public health tends to be determined by cultural, political and
administrative patterns of the countries, there is a wide mosaic of
organizational arrangements.
Public health, in its present form, is a combination of scientific
disciplines (e.g., epidemiology, biostatistics, laboratory sciences,
social sciences, demography) and skills and strategies (e.g.,
epidemiological investigations, planning and management,
interventions, surveillance, evaluation) that are directed to the
maintenance and improvement of the health of the people (126).
With the adoption of the goal of "Health for All", a new public
health is now evident world-wide, which may be defined as:
"the organized application of local, state, national and
international resources to achieve "Health for All", i.e.,
attainment by all people of the world by the year 2000 of a
level of health that will permit them to lead a socially and
economically productive life".
Although the term "public health" has lost its original meaning,
the term is still widely used. Terms like preventive medicine, social
medicine and community medicine are used as synonyms for
public health. Public health is not only a discipline but has become
a "social institution" (31) created and maintained by society to do
something about the death rate and sanitary conditions and many
other matters relating to life and death (127). In this sense public
health is both a body of knowledge and also a means to apply that
knowledge.
Preventive medicine
Preventive medicine developed as a branch of medicine distinct
from public health, based on aetiology. It is, by definition, applied
to "healthy" people. It scored several successes in the prevention of
communicable diseases based on immunization, so much so, in its
early years, preventive medicine was equated with the control of
infectious diseases. A brief account of the advances made in
preventive medicine is given in chapter 1.
As concepts of the aetiology of disease changed through time,
so too have the techniques and activities of preventive medicine.
Preventive medicine is no longer concerned, as it used to be, with
immunization, important though it may be. The concept of
preventive medicine has broadened to include health promotion,
treatment, and prevention of disability as well as specific
protection (42). Preventive medicine has thus come to include both
specific medical measures (e.g., immunization), as well as general
health promotional measures (e.g., health education). Within this
change in the definition and scope of preventive medicine, it has
become clear that promoting health and preventing illness involve
responsibilities and decisions at many levels - individual, public
and private; and that these efforts are applied to whole population
or to segments. In this, preventive medicine has become akin to
public health.
Preventive medicine has become a growing point in medicine
(128). It has branched into newer areas such as screening for
disease, population control, environmental control, genetic
counselling and prevention of chronic diseases. Community
prevention and primordial prevention (see page 37) are relatively
new concepts which are being applied in the community control of
coronary heart disease, hypertension and cancer with palpable
success (106). The emergence of preventive paediatrics, preventive
geriatrics and preventive cardiology are relatively new dimensions
of prevention.
Since preventive medicine has increasingly tended to be applied
to the organized health activities of the community (59), the term
"preventive medicine" is regarded as synonymous with public
health. Both terms often appear in combination (e.g., MaxcyRosenau Textbook of "Public Health and Preventive Medicine").
Associated with the concept of public health, preventive
medicine has been defined as meaning "not only the organized
activities of the community to prevent occurrence as well as
progression of disease and disability, mental and physical, but also
the timely application of all means to promote the health of
individuals, and of the community as a whole, including
prophylaxis, health education and similar work done by a good
doctor in looking after individuals and families" (59). In this the
goals of preventive medicine and public health have become
identical, i.e., Health for All. In line with this extension of the
scope of preventive medicine, it is now customary to speak of
primary, secondary and tertiary levels of prevention (59). The
cornerstone of preventive medicine is, however, "primary
prevention".
Community health
The term "community health" has replaced in some countries,
the terms public health, preventive medicine and social medicine.
A EURO symposium in 1966 (59) defined community health as
including "all the personal health and environmental services in
any human community, irrespective of whether such services were
public or private ones". In some instances, community health is
used as a synonym for "environmental health". It is also used to
refer to "community health care". Therefore, a WHO Expert
Committee in 1973 (125) observed that without further
qualification, the term
I.Congenital
References
1.Evang, K. (1967) In: Health of Mankind, Ciba Foundation, 100th
symposium, Churchill, London.
2.WHO (1979). Health for All, Sr.No.2
3.WHO (1980). WHO Chr., 34 (2) 80
4.Ahmed, and Coelho, (1979). Toward a New Definition of Health,
Pleum, N. Y.
5.Dubos, R. (1965). Man Adapting, New Haven, Yale Uni.Press
DISEASE CLASSIFICATION 45
D.
2.WHO (1984). Health for All, Ser.No.9
3.WHO (1984). Health Planning and Management Glossary. Reg.Health
Paper 2, SEARO, New Delhi.
4.WHO (1981). Health for All, Sr.No.6
5.Hogarth, J. (1978). Glossary for Health Care Terminology, Public
Health in Europe-4
6.WHO (1981). Health for All, Sr.No.4
60 a.WHO (2003), World Health Report 2003, Shaping the future.
1.WHO (1987). Evaluation of the Strategy for HFA by the year 2000;
Seventh Report on the World Health Situation, Vol.1.
2.WHO (1976). Techn. Rep.Ser., No.587
3.Wilson, R.W. and T.F. Drury (1984). Ann Rev. Pub.Health. 5:83-106
4.Last, John M., A Dictionary of Epidemiology, Third Ed. (1995), Ox.U.P.
5.UN Dept. of Economic and Social Affairs (1978). Social Indicators,
Statistical Paper Series M.No.63
6.Sheehan, and Hopkins, (1979). Basic needs performance, ILO,
Geneva
7.WHO (1971). Techn.Rep. Ser., No.472
68. WHO, World Health Report 1998, Report of Director-General WHO
68a. UNDP (2002), Human Development Report 2002, Deepening
Democracy in a fragmented world. 68b. UNICEF (2001), State of
World's Children 2001 68 c.WHO (2002), World Health Report 2002,
Reducing Risks, Promoting
Healthy Life.
1.WHO (1997), World Health Report 1997, Conquering suffering,
Enriching humanity Report of the Director-General WHO.
2.Lee PR. and RE. Franks (1977). Preventive Medicine, 6, 209: 226
3.WHO (1972). Techn.Rep.Ser.No.499
4.WHO (1980). Information systems for health services, Public Health in
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5.WHO (1987). Techn.Rep.Ser,No.746
6.Kohn,R. (1983). The health centre concept in primary health care,
Public health in Europe-22, Regional Office for Europe
7.WHO (1981). Health for All, Sr.No.5
8.WHO (1980). Sixth Report, World Health Situation
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Techn.Publ.l, New Delhi
10.Grundy, F.and W.A. Reinke (1973). Health Practice Research and
Formalized Management Methods, WHO, Geneva
11.WHO (1979). WHO Chr, 33(2)49
12.Gregg Alan (1956). Amer. J. Public Health, 46: 1384
13.Suchman, E.A. (1963). Sociology and the field of Public Health, Russel
Sage Foundation, New York
14.Ouslander, J.G. and J.C. Beck (1982). Ann.Reu.Pub/ic Health, 3:58
15.Susser, M.W. and Waston, W. (1971). Sociology in Medicine, 2nd ed.
London, Oxford University Press
16.Le Riche, W.H. and Jean Milner (1971). Epidemiology as Medical
Ecology, Churchill Livingstone, Edinburgh
17.Mausner, J.S. and Kramer, S. (1985). Mausner and Bahn:
Epidemiology-An Introductory Text, Saunders
18.MacMahon, B.and Pugh, T.F. (1970). Epidemiology: Principles and
Methods, Boston: Little, Brown
19.Stallones, R.A. (1971). Environmental Ecology and Epidemiology,
PAHO Scientific Publ.No.231
20.Suchman, E.A. (1970). Arch.Enu. Health, 20:105
21.WHO (1980). WHO Chr., 34(5)189
22.WHO (1979). Techn.Rep.Ser.,No.636
23.Backett, E.M. et al (1984). The risk approach to health care, Public
health papers No. 76
24.Fielding, J.E. (1984). Ann.Reu.Pub/ic Health, 5:239
25.WHO (1977). WHO Chr., 31:150
26.WHO (1976). Tech.Rep.Ser.No.593
27.Lilienfeld, A.M. and Lilienfeld, D. (1979). Foundations of
Epidemiology, New York, Oxford University Press
28.Stuart-Harris, Charles (1981). World Health Forum, 2 (2) 305
29.Henderson, D.A. (1987). World Health Forum, 8 (3) 283
30.Soper, F.L. (1962). Am.J.Public Health, 52:724-745
31.WHO (1972). Heafth Hazards of the Human Environment, WHO
Geneva
32.WHO (1981). Tech.Rep.Ser.,No.666
33.Raska, K. (1966). WHO Chr, 20, 315
Principles of Epidemiology
and Epidemiologic Methods
"I keep six honest serving men; they taught me all I know.
Their names are what, why, when, how, where and who."
Aims of epidemiology
According to the International Epidemiological Association
(IEAfTepidemiology has three main aims (5):
*. toUescribe the distribution and magnitude of health and pjl
disease problems in human populations
Epidemiological Approach
b\ to identify aetiological factors (risk factors) in the
The epidemiological approach to problems of health and
pathogenesis of disease; and
disease is based on two major foundations:
c. to provide the data essential to the planning, implementation
a. Asking questions
and evaluation of services for the prevention, control and
b. Making comparison
treatment of disease and to the setting up of priorities among
those services^ v. <*\ >( *3
In order to fulfil these aims, three rather different classes of '\ a. Asking questions :
epidemiological studies may be mentioned: descriptive studies, '/ Epidemiology has been defined as "a means of learning or asking
questions....and getting answers that lead to further questions"
analytical studies, and experimental or intervention studies (6).
(10). For example, the following questions could be asked (11) :
These studies are described in the following pages.
The ultimate aim of epidemiology is to lead to effective action :
RELATED TO HEALTH EVENTS
a. to eliminate or reduce the health problem or its
a. What is the event ? (the problem)
consequences; and
b. What is its magnitude?
b. to promote the health and well-being of society as a
c. Where did it happen?
whole.
d. When did it happen?
Epidemiology and clinical medicine
e. Who are affected?
The basic difference between epidemiology and clinical
f. Why did it happen?
medicine is that in epidemiology, the unit of study is a "defined
population" or "population at risk"; in clinical medicine, the unit of
RELATED TO HEALTH ACTION
study is a "case" or "cases". In clinical medicine, the
a. What can be done to reduce this problem and its
consequences ?
a. Measurement of mortality
Measurement of morbidity
Measurement of disability
Measurement of natality
Measurement of the presence, absence or distribution
of the characteristic or attributes of the disease
f. Measurement of medical needs, health care facilities,
utilization of health services and other health-related
events
g. Measurement of the presence, absence or distribution
of the environmental and other factors suspected of
causing the disease.
h. Measurement of demographic variables
Inspite of a wide range of presently available measurements,
there are many areas which are not fully covered. As for example,
measurement of the Psycho-social aspects of health and disease.
The components of well-being need to be better identified.
The basic requirements of measurements are validity,
reliability, accuracy, sensitivity and specificity. These are
discussed in the next chapter. Finally, measurement errors are
unavoidable, no matter where and by whom measurements are
taken. The purpose of quality control in measurement is, therefore,
not to eliminate errors, but to reduce them as much as possible or
at least to an acceptable level.
In the above connection, the following terminology needs
explanation: (a) Variate: Any piece of information referring to the
patient or his disease is called a variate. A variate can be discrete,
that is it can be present or absent, e.g., cancer lung, broken leg, or
rash in measles or it can be continuously distributed, e.g., blood
pressure, serum cholesterol, height, etc. (b) Circumstance: Any
factor in the environment that might be suspected of causing a
disease, e.g., air pollution, polluted water, etc (9).
The frequency of a discrete variable or circumstance can be
expressed as a rate in relation to population. The frequency oi
continuously distributed variables or circumstances is expressed in
the form of a frequency distribution using the summarising indices
of mean, centiles, standard deviations, etc.
Tools of measurement
The epidemiologist usually expresses disease magnitude as a
rate, ratio or proportion. A clear understanding of the term is
required for proper interpretation of epidemiological data. The
basic tools of measurement in epidemiology are :
1.Rates
2.Ratios, and
3.Proportions
1. RATE:
When we say there were 500 deaths from motor vehicle
accidents in City A during 1985, it is just nothing more thar
counting deaths in that city during that particular year. Such E
statement might be sufficient for the municipal administrator tc
provide necessary health services. But it conveys no meaninc to an
epidemiologist who is interested in comparing the frequency of
accidents in City A with that in City B. To allow such
comparisons, the frequency must be expressed as a rate.
A rate measures the occurrence of some particular even
(development of disease or the occurrence of death) in c
population during a given time period. It is a statement of tht risk
of developing a condition. It indicates the change in somt event
that takes place in a population over a period of time. Ar
2. RATIO:
yfl^^M/>TJl
x\
x : y or )
y J
EM
xj
Example 1:
The ratio of white blood cells relative to red cells is 1:600 or
1/600, meaning that for each white cell, there are 600 red
cells.
Example 2:
The number of children with scabies at a certain time
The number of children with malnutrition at a certain time
Approximate interval
between onset and
death
DEATH
'
*2V<aJLt^-*
Diseases with
Crude
death
rate
0-1
1-4
5-7
8-44
45-64
15.2
13.5
0.6
0.4
1.5
10.7
Age -specific
9.9
22.6
1.0
0.5
1A '
-----
TABLE 1
Crude and Age-specific Death Rates
Popula
-tion
?---- '^
3.6
18.8
61.1
J
4i Proportional mortality rate (Ratio)
Mt is sometimes useful to know what proportion of tot* deaths
are due to a particular cause (e.g., cancer) or whe proportion of
deaths are occurring in a particular age grouj (e.g., above the age
of 50 years)|fProportional mortality rati expresses the "number of
deaths due to a particular cause (o in a specific age group) per 100
(or 1000) total deaths\ Thu: we have:
(a) Proportional mortality from a specific disease
i ^?Number of deaths from the specific disease
in a year
= ------------------------------------------------ X100
Total deaths from all causes in that year
variables such as income, religion, race, housing, etc. Specific death . x>t?
= ------------------------------------------------------ xl00]
rates can help us to identify particular groups or groups "at risk", for
Total number of deaths during the same period
preventive i action. They permit comparisons between different
causes within the same population. Specific death rates are obtained
(c) Proportional mortality rate for aged 50 years and above
mainly in countries in which a satisfactory civil registration system
Number of deaths of persons aged 50
operates and in which a high proportion of deaths is certified
years and above
medically.
= ------------------------------------------------ X 100
Table 2 illustrates how some specific death rates in common
Total deaths of all age groups in that year
use are computed :
__
TABLE 2
Specific Death Rates
=
.
Number of deaths from tuberculosis during a calendar year
= ----------------------------------------------------------------- X 1,000
Mid-year population
1.
2.
3.
4.
5.
Deaths in January X 12
---------------------------- X 1,000
Mid-year population
------------------------------- X 1,000
Mid-year population
X 1,000
_____________________________DIRECT STANDARDIZATION 53
Proportional mortality rate is computed usually for a broad
disease group (such as communicable diseases as a whole) and for
a specific disease of major public health importance, such as
cancer or coronary heart disease in industrialized countries (14).
Proportional rates are used when population data are not
available. Since proportional mortality rate depends upon two
variables, both of which may differ, it is of limited value in
making comparison between population groups or different time
periods. However, proportional rates are useful indicators within
any population group of the relative importance of the specific
disease or disease group, as a cause of death. Mortality from
communicable diseases is especially important as it relates mostly
to preventable conditions. Since the prevailing causes of death
vary according to age and sex, it is desirable to compute
proportionate mortality separately for each age and sex group in
order to determine measures directed to particular age-sex groups
for the reduction of preventable mortality (14). Proportional
mortality rate does not indicate the risk of members of the
population contracting or dying from the disease.
Survival rate
Q^ \ J%V*$
population is obtained; these are added together for all the age
groups, to give the total expected deaths. The final operation is
to divide the "expected" total number of deaths by the total of
the standard population, which yields the standardized or ageadjusted rate.
*
Example 1
Example 1 shows: (a) the computation of age-specific death
rates per 1000 population for city X (Table 3); and (b) application
of these rates to a standard population to obtain the "expected
deaths" and the standardized or age-adjusted death rate (Table 4).
TABLE 3
Calculation of Age-specific death rates for City X
DIRECT STANDARDIZATION
Deaths in
the year
Age -specific
death rates
60
15.0
4,000
1-4
5-14
15-19
20-24
25-34
35-44
45-54
55-64
4,500
4,000
5,000
4,000
8,000
9,000
8,000
7,000
20
12
15
16
25
48
100
150
53,500
446
4.4
3.0
3.0
4.0
3.1
5.3
12.5
21.4
TABLE 4
Calculation of the Standardized death rate for City X
Mid-year
population
per 1000
Age
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Age
-----''----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Standard
population
---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Age-specific
death rates
per 1000
Expected
deaths
2,400
15.0
1-4
9,600
4.4
42.24
5-14
19,000
3.0
57
9,000
3.0
27
20-24
8,000
4.0
32
25-34
14,000
3.1
43.4
35-44
12,000
5.3
63.6
45-54
11,000
12.5
137.5
55-64
8,000
21.4
171.2
15-19
93,000
609.94
609.94
Standardized
36
93,000
*
X IUUU o.oo
CONTROLS
40-49
400
50-59
500
100
10
10
400
40
10
Total
1,000
500
210
42
500
90
18 i
No.
Heavy
smoker
s200
*c-*r>
Observed deaths
_
*SMR = -------- ;-^ X nn
100
Expected deaths
Total
subjects
500
Age
%
No. Heavy
smokers
50
100
50
%
50
Source (5)
Age adjustments were carried out (a) first, by combining the
number of subjects in both the age groups (500+500=1,000) to
create a standard population, and (b) applying the observed agespecific proportions of heavy smokers (i.e., 50% and 10% in both
cases and controls) to the same standard population. The results (or
"expected" values) are shown in Table 6, which shows that the age
adjusted proportions of heavy smokers are identical (30%) for
cases and controls. The previously observed difference is explained
entirely by the difference in age composition.
Subjects
40-49
500
50-59
500
Total
1000
Standardized rates
Expected
CASES
500 X 50
100 500
X 10
100
300
500 X 50
100 500
X 10
- ^f)
= 250 =
50
v Iflfl
100
300
y mn
1000
If the ratio had value greater than 100, then the occupation
would appear to carry a greater mortality risk than that of the
whole population. If the ratio had value less than 100, then the
occupation risks of mortality would seem to be proportionately less
than that for the whole population.
Table 7 shows that the mortality experience of coal workers
was 129 per cent, which meant that their mortality was 29 per cent
more than that experienced by the national population. Values over
100 per cent represent an unfavourable mortality experience and
those below 100 per cent relatively favourable mortality
experience. Table 7 displays the calculations
TABLE 7
Calculation of the SMR for Coal workers
Age
25-34
35-44
45-54
55-64
TABLE 6
Age-adjusted proportions
Age
300
3D
1000
National
population
death rates
per 1000
Coal
worker
population
Observed
deaths
Expec
deatr
3.0
5.0
8.0
25.0
300
*
0.9
400
*
2.0
200
*
1.6
100
*
2.5
1,000
9
7.0
SMR = 9/7x100=129 * It is not
only the total for the
necessary to know these values; whole agerange is required
The SMR has the advantage over the direct method of age
adjustment in that it permits adjustment for age and other factors
where age specific rates are not available or are unstable because
of small numbers. One needs to know only the number of persons
in each age group in the study population and the age specific rates
of the national population (or other reference population). It is
possible to use SMR if the event of interest is occurrence of
disease rather than death.
2. Other standardization techniques
(a) A more complicated method of indirect adjustment which
yields absolute age adjusted rate, involves the calculation of an
index death rate and a standardizing factor for each population of
interest. The reader is referred to A.B. Hill's "Principles of Medical
Statistics", (b) Life table is an age-adjusted summary of current allcauses mortality, (c) Regression techniques: These are an efficient
means of standardization (d) Multivariate analysis: A computer,
using regression or similar methods, can standardize for many
variables simultaneously (16).
MEASUREMENT OF MORBIDITY
Morbidity has been defined as "any departure, subjective or
(T7\
INCIDENCE
)g>-or-&aag______________________PREVALENCE 55
O-----------------------------------case 3
O--------------
case 4
O--------------------------------------- case 5
O------O---------- case 7
case 6
O-----------------case 8
Jan 1
Dec 31
O Start of illness
---- Duration of illness
_____________________________EPIDEMIOLOGIC METHODS
element of duration reflects the prognostic factors, and incidence
reflects the causal factors. Therefore incidence rates should be
optimally used in the formulation and testing of aetiological
hypotheses. When incidence rates are not available, prevalence
rates (which are readily obtainable) may have to be used, but the
contribution of duration element always has to be assessed.
Uses of prevalence
(a) Prevalence helps to estimate the magnitude of health/
disease problems in the community, and identify potential highrisk populations (b) Prevalence rates are especially useful for
administrative and planning purposes, e.g., hospital beds,
manpower needs, rehabilitation facilities, etc.
EPIDEMIOLOGIC METHODS
The primary concern of the epidemiologist is to study.,, disease
occurrence in people, who during the course of their V lives are
exposed to numerous factors and circumstances, some of which may
have a role in disease aetiology. Unlike the clinician or the laboratory
investigator who is able to study disease conditions more precisely,
the epidemiologist employs carefully designed research strategies to
explore disease aetiolow^T^ \fc>*^M
^Epidemiological studies can-Jbe classified as observational
studTes and experimental studies with further subdivisions :
[j.. Observational studies^
fa
A>
Populations as
unit of study
(ii) Cross-sectional or Prevalence, with
Individuals as
unit of study
(iii)Case-control
or Case-reference, with Individuals as
unit of study
/' or Follow-up,
with Individuals
as unit of study
2. Experimental studies Intervention studies
a. Randomized
/^or Clinical
with Patients as
controlled trials (
trials
unit of study
b. Field trials or
Community
with Healthy
intervention
people as
studies
unit of study
c. Community trials,\
with
* \) s^O^f^&S
Communities
\as unit of study
TABLE 9
Characteristics frequently examined in
descriptive studies
Time
Place
Perso r
Year, season
Climatic zones
Age
Birth order
Month, week
Country, region
Sex
Family size
Day, hour of
onset,
Urban/rural Local
community
Marital
state
Height
Weight
Duration
Towns
Cities
Institutions
Occupation
Social status
Education
Blood pressure
Blood cholesterol
Personal habits
TIME DISTRIBUTION
The pattern of disease may be described by the time of its
occurrence, i.e., by week, month, year, the day of the week, hour
of onset, etc. It raises questions whether the disease is seasonal in
occurrence; whether it shows periodic increase or decrease; or
whether it follows a consistent time trend. Such studies may yield
important clues about the source or aetiology of the disease,
thereby suggesting potential preventive measures. Epidemiologists
have identified three kinds of time trends or fluctuations in disease
occurrence.
I.Short-term fluctuations
II.Periodic fluctuations, and
III.Long-term or secular trends
I. Short-term fluctuations
The best known short-term fluctuation in the occurrence of a
disease is an epidemic. According to modern concepts an epidemic
is defined as "the occurrence in a community or region of cases of
an illness or other health-related events clearly in excess of normal
expectancy". The community or region, and the time period in
which the cases occur, are specified precisely. Epidemicity is thus
relative to usual frequency of the disease in the same area, among
the specified population, at the same season of the year (2). The
data in Table 10 illustrate this point.
Types of epidemics
Three major types of epidemics may be distinguished.
A. Common - source epidemics
(a)Single exposure or "point source" epidemics.
(b)Continuous or multiple exposure epidemics
B. Propagated epidemics
Person-to-person
Arthropod vector
Animal reservoir
C. Slow (modern) epidemics
A graph of the time distribution of epidemic cases is called the
"epidemic curve" (fig 4). The epidemic curve may suggest: (1) a
time relationship with exposure to a suspected source, (2) a
cyclical or seasonal pattern suggestive of a particular infection, and
common source or propagated spread of the disease.
A. Common -source epidemics
(af Common -source, single exposure epidemics
rThese are also known as "point-source" epidemics. The
exposure to the disease agent is brief and essentially simultaneous,
the resultant cases all develop within one incubation period of the
disease^(e.g., an epidemic of food
DESCRIPTIVE EPIDEMIOGY
poisoning). Fig 4 illustrates a common-source, single exposure
epidemic. The curve has usually one peak. One point of interest is
the "median incubation period", it is the time required for 50 per
cent of the cases to occur following exposure.
May
June
July
August
September
October
November
December
Total
1988
3617
3994
5891
7015
8912
11324
17616
16499
4075
2108
2129
2112
84792
1990
892
824
1890
5053
7484
6641
5867
4323
2383
1715
2261
1318
40601
1992
765
749
1595
4458
7602
6633
6107
6263
2820
2189
2335
1656
43172
1994
1155
1283
2312
4020
6813
7011
10377
10430
4522
2400
1823
1288
53434
Source (25)
(ii) Cyclic trend : Some diseases occur in cycles spread over
short periods of time which may be days, weeks, months or
years. For example, measles in the pre-vaccination era appeared
in cycles with major peaks every 2-3 years and rubella every 6-9
years. This was due to naturally occurring variations in herd
immunity. A build-up of susceptibles is again required in the
"herd" before there can be another attack. Influenza pandemics
are known to occur at intervals of 7-10 years, due to antigenic
variations. Non-infectious conditions may also show periodic
fluctuations, e.g., automobile accidents in US are more frequent
on week-ends, especially Saturdays. A knowledge of cyclicity of
disease is useful in that it may enable 1 communities to defend
themselves.
. Long-term or secular trends
v [The term "secular trend" implies changes in the occurrence ,
pfdisease (i.e., a progressive increase or decrease) over a long
'period of time, generally several years or decades.. Although it
may have short-term fluctuations imposed on it, a secular trend
implies a consistent tendency to change in a particular direction
or a definite movement in one direction. Examples include
cqronary heart disease, lung cancer and diabetes which have
shown a consistent upward trend in the developed countries
during the past 50 years or so, followed by a decline of such
diseases as tuberculosis, typhoid fever, diphtheria and
Interpretation 6#Time-trends :
By surveillance or monitoring of time trends, the
epidemiologist seeks which diseases are increasing, which
PLACE DISTRIBUTION 61
National variations
It is obvious that variations in disease occurrence must also exist
within countries or national boundaries. For example the distribution
of endemic goitre, lathyrism, fluorosis, guinea-worm disease,
leprosy, malaria, nutritional deficiency diseases have all shown
variations in their distribution in India, with some parts of the
country more affected and others less affected or not affected at all.
Such situations exist in every country. One of the functions of
descriptive epidemiology is to provide data regarding the type of
disease problems and their5-magnitude in terms of incidence,
prevalence and mortality rates. Such information is needed to
demarcate the affected , areas and for providing appropriate health
care services.
WW
Rural-urban variations
Rural/urban variations in disease distribution are well known.
Chronic bronchitis, accidents, lung cancer, cardiovascular diseases,
mental illness and drug dependence are usually more frequent in
urban than in rural areas. On the other hand, skin and zoonotic
diseases and soil-transmitted helminths may be more frequent in
rural areas than in urban areas. Death rates, especially infant and
maternal mortality rates, are higher for rural than urban areas.
These variations may be due to differences in population density,
social class, deficiencies in medical care, levels of sanitation,
education and environmental factors. The epidemiologist seeks to
define groups which are at higher risk for particular diseases, and
provides guidelines to the health administrator for their prevention
and control.
Local distributions
Inner and outer city variations in disease frequency are well
known. These variations are best studied with the aid of 'spot maps'
or 'shaded maps'. These maps show at a glance areas of high or low
frequency, the ^boundaries and patterns of disease distribution. For
examplef if the map shows "clustering" of cases, it may suggest a
common source of infection or a ftcommon risk factor shared by all
the cases. It was by such a tudy (spot map of fatal cases)/John
Snow of England in his classic investigation of cholera epidemic in
1854 in the Golden ) Square district of London^'Vas able to focus
attention on the common water pump in Broad street as the source
of infection (Fig. 6). Based on his descriptive findings, Snow was
able to hypothesize that cholera was a water-borne disease, long
before the birth of bacteriology^ It was by a spot map by "place of
employment" Maxcy hypothesized a rodent reservoir for typhus
fever in 1920s which led to the discovery that typhus fever was not
a single disease entity, as it was earlier thought. More recently, the
evidence of case clustering based on sexual contact or blood
product use provided the clue that AIDS (Acquired Immune
Deficiency Syndrome) was an infectious disease.
In short the geographic differences in disease occurrence is an
important dimension of a descriptive study. These differences are
determined by the agent, host and environmental factors. The
classic example of place-related diseases include yellow fever,
schistosomiasis, sleeping sickness and endemic goitre. There have
also been studies on asthma, cancer, cardiovascular diseases, blood
groups and abnormal
PERSON DISTRIBUTION 63
make their interpretation difficult : (a) small numbers of
observations are a frequent source of bimodality; (b) the absence of
bimodality does not signify that data have come from a
homogeneous source.
(b) Sex : Sex is another host characteristic which is often
studied in relation to disease, using such indices as sex-ratio,
sex-specific morbidity and mortality rates. It has been found
that certain chronic diseases such as diabetes, hyperthyroidism
and obesity are strikingly more common in women than in
men, and diseases such as lung cancer and coronary heart
disease are less frequent in women.
Variations in disease frequency between sexes have been
ascribed to (a) basic biological differences between the sexes,
including sex-linked genetic inheritance, and (b) cultural and
behavioural differences between the sexes (e.g., smoking,
automobile use, alcoholism) due to different roles in social setting.
In fact, it is the 4:1 male to female ratio in lung cancer that has
helped to identify cigarette smoking as a causal factor. Even larger
differences exist in, for example, duodenal ulcer and coronary
heart disease, that are as yet unexplained (30).
(a)Ethnicity : Differences in disease occurrence have been
noted between population subgroups of different racial and
ethnic origin. These include tuberculosis, essential
hypertension, coronary heart disease, cancer, and sickle cell
anaemia. These differences, whether they are related to genetic
or environmental factors, have been a stimulus to further
studies.
(b)Marital status : In countries where studies on mortality in
relation to martial status have been conducted, it was found that
mortality rates were always lower for married males and
females than "for the unmarried, of the same age and sex.
According to demographers and sociologists, the reason for this
phenomenon may be found in the fact that marriages are
selective with respect to the health status of persons, for those
who are healthy are more likely to get married with the result
that the risk of dying is also less. Besides, married persons are
generally more secure and protected and they usually lead a
more sober life than those who are unmarried. All these factors
are thought to contribute to lower mortality rates among
married persons.
Martial status can be a risk factor for some diseases and
conditions. The observation that cancer cervix is rare in nuns led to
the hypothesis regarding marital status and cancer cervix. Further
studies led to the suggestion that cancer cervix may be associated
with multiple sexual contacts and promiscuity. This in turn raised
the possibility of a possible infectious agent transmitted venereally.
Although the viral aetiology of cancer cervix is not yet proved, this
chain of thinking serves to illustrate how an observation can be a
starting point of an epidemiological enquiry.
(e) Occupation ; It is now well recognized that man's
occupation from which he earns his livelihood has an
important bearing on his health status. Occupation may alter
the habit pattern of employees e.g., sleep, alcohol, smoking,
drug addiction, night shifts etc. It is obvious that persons
working in particular occupations are exposed to particular
types of risks. For instance, while workers in coal mines are
more likely to suffer from silicosis, those in sedentary
occupations face the risk of heart disease.
(f) Social class : Epidemiological studies have shown that
health and diseases are not equally distributed in social classes.
Individuals in the upper social classes have a longer life
expectancy and better health and nutritional status than those
in the lower social classes. Certain diseases (e.g., coronary
heart disease, hypertension, diabetes) have shown a higher
prevalence in upper classes than in the lower classes. Social
class differences have also been observed in mental illness and
- is an
An improved formulation :
"The smoking of 30-40 cigarettes per day causes lung
cancer in 10 per cent of smokers after 20 years of exposure"
The improved formulation suggests data needed to test the
hypothesis, i.e., the number of cigarettes smoking per day, years of
exposure, and so on. The success or failure of a research project
frequently depends upon the soundness of the hypothesis (12).
Uses of descriptive epidemiology
' ^Descriptive studies : (a) provide data regarding the magnitude of
the disease load and types of disease problems in the community in
terms of morbidity and mortality rates and ratios (b) provide clues
to disease aetiology, and help in the formulation of an aetiological
hypothesis. That is, the existence of a possible causal association
between a factor and a disease is usually recognized in descriptive
studies. Thus, if the disease is observed to be more frequent in a
particular group than in others, hypotheses are formulated to
explain the increased frequency (c) provide background data for
planning, organizing and evaluating preventive and curative
services, and (d) they contribute to research by describing
variations in disease occurrence by time, place and person^
^*V_
ANALYTICAL EPIDEMIOLOGY
jAnalytical studies are the second major type of epidemiological
studies. In contrast to descriptive studies that look at entire
populations, in analytical studies, the subject of interest is the
individual within the population. The object is not to formulate, but
to test hypotheses. ^Nevertheless,^ although individuals are
evaluated in analytical studies, the inference is not to individuals,
but to the population from which they are selected.
Analytical studies comprise two distinct types of observational
studies :
a. case control study
b. cohort study
From each of these study designs, one can determine :
a. whether or not a statistical association exists between
a disease and a suspected factor; and
b. if one exists, the strength of the Association
A schematic design of case control and cohort studies is shown
in Fig.8.
ANALYTICAL EPIDEMIOLOGY
CASE-CONTROL STUDY
Present
Absent
Individual Exposed to
Particular Factor(s)
Individual Unexposed to
Particular Factor(s)
individuals wnn
Particular Disease
Particular Disease
i
J
) Controls
PROSPECTIVE (Cohort)
STUDY
absence
of
particular
TIME
FIG.8
Schematic diagram of the design of case control and cohort studies
yj \ IS
CASE CONTROL STUDY
<* ^-^
\ Case control studies, often called "retrospective studies" are a
common first approach to test causal hypothesis. In recent years, the
case control approach has emerged as a permanent method of
epidemiological investigation}. The case control method has three
distinct features :
a. both exposure and outcome (disease) have occurred
before the start of the study
b. the study proceeds backwards from effect to cause; and
c. it uses a control or comparison group to support or
refute an inference
/"-*4/\
By definition/ a case control study irivolves two populations cases and controls. In case control studies, the unit is the individual
rather than the group. The focus is on a disease or some other health
problem that has already developed Wy\
Case control studies are basically comparison studies. Cases
and controls must be comparable with respect to known
"confounding factors" such as age, sex, occupation, social status,
etc. The questions asked relate to personal characteristics and
antecedent exposures which may be responsible for the condition
studied. For example, one can use as "cases" the immunized
children and use as "controls" un-immunized children and look for
factors of interest in their past histories. Case control studies have
been used effectively for studies of many cancers, and other
serious conditions such as cirrhosis of the liver, lupus
erythematosis, and congestive heart failure.
The basic design of a case control study is shown in Table 11.
It is a 2 x 2 table which provides a very useful framework to
discuss the various elements which make up a case control study.
To illustrate, if it is our intention to test the hypothesis that
"cigarette smoking causes lung cancer", using the case control
method, the investigation begins by assembling a group of lung
cancer cases (a+c), and a group of suitably matched controls
(b+d). One then explores the past history of these two groups for
the presence or absence of smoking, which is suspected to be
related to the occurrence of cancer lung. If the frequency of
smoking, a/(a+c) is higher in cases than in controls b/(b + d), an
association is said to exist between smoking and lung cancer. Case
control studies have their major use in the chronic disease problem
when the causal pathway may span many decades.
-"v
K J
IftDLE 1 J.
study
Cases
(Disease present)
Control (Disease
absent)
ac
a+c
b
d
b+d
Basic steps
There are four basic steps in conducting a case control
study :
1.Selection of cases and controls
2.Matching
3.Measurement of exposure, and
4.Analysis and interpretation
TABLE 12
A case control study of smoking and lung cancer
Cases (with
lung cancer)
33
(a)
55
(b)
Non-smokers
2
(c)
27
(d)
35
(a+c)
82
(b+d)
Total
u---------------------------
Source (34).
Exposure rates:
a. Cases = a/(a+c) = 33/35 = 94.2 per cent
b. Controls = b/(b+d) = 55/82 = 67.0 per cent
P < 0.001
Table 12 shows that the frequency rate of lung cancer was
definitely higher among smokers than among non-smokers. The
next step will be to ascertain whether there is a statistical
association between exposure status and occurrence of lung
cancer. This question can be resolved by calculating the P value,
which in this case is less than 0.001.
The particular test of significance will depend upon the
variables under investigation. If we are dealing with discrete
variables, as in the present case (smoking and lung cancer;
exposure and disease) the results are usually presented as rates or
proportions of those present or absent in the study and in the
control group. The test of significance usually adopted is the
standard error of difference between two proportions or the Chisquare test. On the other hand, if we are dealing with continuous
variables (e.g., age, blood pressure), the data will have to be
grouped and the test of significance used is likely to be the
standard error of difference between two means, or the test.
According to convention, if P is less than or equal to 0.05, it is
regarded as "statistically significant". The smaller the P value, the
greater the statistical significance or probability that the
association is not due to chance alone. However, statistical
association (P value) does not imply causation. Statement of P
value is thus an inadequate, although common end-point of case
control studies.
(b) ESTIMATION OF RISK
The second analytical step is estimation of disease risk
associated with exposure. It should be noted (Table 12) that if
the exposure rate was 94.2 per cent in the study group, it does
not mean that 94.2 per cent of those smoked would develop
lung cancer. The estimation of disease risk associated with
exposure is obtained by an index known as "Relative Risk"
(RR) or "risk ratio", which is defined as the ratio between the
incidence of disease among exposed persons and incidence
among non-exposed. It is given by the formula:
_.
I Relative risk =
***-1
0
'W^
/TN
<?
ADVANTAGES
1.Relatively easy to carry out
2.Rapid and inexpensive (compared with cohort studies)
3.Require comparatively few subjects
.4. Particularly suitable to investigate rare diseases or diseases about
which little is known. But a disease which is rare in the general
population (e.g., leukaemia in adolescents) may not ) - be rare in
special exposure group (e.g. prenatal X-rays).
J 5. No risk to subjects
S. Allows the study of several different aetiological factors (e.g.,
smoking, physical activity and personality characteristics in L Q
myocardial infarction)
I 7. Risk factors can be identified. Rational prevention and control
programmes can be established
1.No attrition problems, because case control studies do not require
follow-up of individuals into the future
2.Ethical problems minimal
DISADVANTAGES
1.Problems of bias relies on memory or past records, the accuracy
of which may be uncertain; validation of information obtained is
difficult or sometimes impossible
2.Selection of an appropriate control group may be difficult
3.We cannot measure incidence, and can only estimate the
relative risk
4.Do not distinguish between causes and associated factors
5.Not suited to the evaluation of therapy or prophylaxis of
disease
6.Another major concern is the representativeness of cases ana\
controls
Source (35,36)
I
Examples of case control studies
Case control studies have provided much of the current base of
knowledge in epidemiology. Some of the early case control studies
centred round cigarette smoking and lung cancer (34,37,38).
Recent studies include: maternal smoking and congenital
malformations (39), radiation and leukaemia (40), oral
contraceptive use and hepatocellular adenoma (41), herpes simplex
and Bell palsy (42), induced abortion and spontaneous abortion
(43), physical activity and coronary death (44), artificial
sweeteners and bladder cancer (45), etc.
A few studies are cited in detail:
Example 1: Adenocarcinoma of the vagina (26)
An excellent example of a case control study is
adenocarcinoma of the vagina in young women. It is not only a
rare disease, but also the usual victim is over 50 years of age.
There was an unusual occurrence of this tumor in 7 young women
(15 to 22 years) born in one Boston hospital between 1966 and
1969. The apparent "time clustering" of cases - 7 occurring within
4 years at a single hospital - led to this enquiry. An eighth case
occurred in 1969 in a 20 year old patient who was treated at
another Boston hospital in USA.
The cause of this tumor was investigated by a case control
study in 1971 to find out the factors that might be associated with
this tumor. As this was a rare disease, for each case, four matched
controls were put up. The controls were identified
from the birth records of the hospital in which each case was born.
Female births occurring closest in time to each patient were
selected as controls. Information was collected by personal
interviews regarding (a) maternal age (b) maternal smoking (c)
antenatal radiology, and (d) diethyl-stilboestrol (DES) exposure in
foetal life. The results of the study are shown in Table 14 which
shows that cases differed significantly from the controls in their
past history. Seven of the eight cases had been exposed to DES in
foetal life. This drug had been given to their mothers during the
first trimester of pregnancy to prevent possible miscarriage. But
none of the mothers in the control group had received DES. Since
this study, more cases have been reported and the association with
DES has been confirmed. The case control method played a critical
role in revealing exposure to DES in utero as the cause of vaginal
adenocarcinoma in the exposed child 10-20 years later.
TABLE 14
Association between maternal DES therapy and
adenocarcinoma of vagina amongst female offspring
Information
acquired
retrospectively
Maternal age
Maternal smoking
Antenatal radiology
Oestrogen exposure
Cases
Controls
Significance
(8)
(32)
level
26.1
29.3
n.s.
7
1
7
21
4
-
n.s.
n.s.
P< 0.00001
Source (26).
Example 2: Oral contraceptives and thromboembolic disease
(46,47)
By August 1965, the British Committee on Safety of Drugs had
received 249 reports of adverse reactions and 16 reports of death
in women taking oral contraceptives. It became apparent that
epidemiological studies were needed to determine whether women
who took oral contraceptives were at greater risk of developing
thromboembolic disease.
In 1968 and 1969, Vassey and Doll reported the findings of
their case control studies in which they interviewed women who
had been admitted to hospitals with venous thrombosis or
pulmonary embolism without medical cause and compared the
history with that obtained from other women who had been
admitted to the same hospital with other diseases and who were
matched for age, marital status and parity.
It was found that out of 84, 42 (50%) of those with venous
thrombosis and pulmonary embolism had been using oral
contraceptives, compared with 14% of controls (Table 15). The
studies confirmed that taking the pill and having pulmonary
embolism co-existed more frequently than would be expected by
chance. The relative risk of users to non-users was 6.3:1. That is,
the investigators found that users of oral contraceptives were about
6 times as likely as non-users to develop thromboembolic disease.
TABLE 15
Case control studies on the safety of oral contraceptives
Per cent who
No.________________________________used oral
______________________________________contraceptives
Cases (venous
thrombosis and
pulmonary embolism)
84
50
Controls
168
14
Source (46,47).
_______________________________________COHORT STUDY 69
Example 3 : Thalidomide tragedy (48)
Thalidomide was first marketed as a safe, non-barbiturate
hypnotic in Britain in 1958. In 1961, at a congress of
Gynaecologists, attention was drawn to the birth of a large number
of babies with congenital abnormalities, which was previously
rare. In the same year, if was suggested that thalidomide might be
responsible for it.
A retrospective study of 46 mothers delivered of deformed
babies showed that 41 were found to have thalidomide during their
early pregnancy. This was compared with a control of 300 mothers
who had delivered normal babies; none of these had taken
thalidomide. Laboratory experiments confirmed that thalidomide
was teratogenic in experimental studies (48).
IP)
COHORT STUDY
i Cohort study is another type of analytical (observational) sftfdy
which is usually undertaken to obtain additional evidence to refute or
support the existence of an association between suspected cause and
disease. Cohort study is known by a variety of names : prospective
study.Jongitudinal study, incidence study, and forward-looking study.
The most widely used term, however, is "cohort study" (4).
ffhe distinguishing features of cohort studies are :
a. the cohorts are identified prior to the appearance of
the disease under investigation
b. the study groups, so defined, are observed over a
period of time to determine the frequency of disease
X'V J
among them
c. the study proceeds forward from cause to effect. I
Concept of cohort
yes
no
Total
a+b
c+d
______________________________________COHORT STUDY 71
information (e.g., dose of radiation, kinds of surgery, or details of
medical treatment) can be obtained only from medical records (c)
Medical examination or special tests : Some types of information
can be obtained only by medical examination or special tests, e.g.,
blood pressure, serum cholesterol, ECG. (d) Environmental
surveys : This is the best source for obtaining information on
exposure levels of the suspected factor in the environment where
the cohort lived or worked. In fact, information may be needed
from more than one or all of the above sources.
Information about exposure (or any other factor related to the
development of the disease being investigated) should be collected
in a manner that will allow classification of cohort members :
(a)according to whether or not they have been exposed to the
suspected factor, and
(b)according to the level or degree of exposure, at least in broad
classes, in the case of special exposure groups (Table 17).
In addition to the above, basic information about demographic
variables which might affect the frequency of disease under
investigation, should also be collected. Such information will be
required for subsequent analysis.
3. Selection of comparison groups
There are many ways of assembling comparison groups :
(a) Internal comparisons:
In some cohort studies, no outside comparison group is
required. The comparison groups are in-built. That is, single cohort
enters the study, and its members may, on the basis of information
obtained, be classified into several comparison groups according to
the degrees or levels of exposure to risk (e.g., smoking, blood
pressure, serum cholesterol) before the development of the disease
in question. The groups, so defined, are compared in terms of their
subsequent morbidity and mortality rates. Table 17 illustrates this
point. It shows that mortality from lung cancer increases with
increasing number of cigarettes smoked reinforcing the conclusion
that there is valid association between smoking and lung cancer.
TABLE 17
Age standardized death rates per 100,000 men per year by
amount of current smoking
:^^\m: -: ::rM:f:;^;-:;;; ::^:~r^7r<
Classification of
exposure (cigarettes)
1/2 pack
1/2-1 pack
1-2 packs
2 packs +
No. of deaths
Death rate
24
84
90
97
95.2
107.8
229.2
264.2
Source (5).
(b) External comparisons:
When information on degree of exposure is not available, it is
necessary to put up an external control, to evaluate the experience
of the exposed group, e.g., smokers and non-smokers, a cohort of
radiologists compared with a cohort of ophthalmologists, etc. The
study and control cohorts should be similar in demographic and
possibly important variables other than those under study.
(c) Comparison with general population rates :
If none is available, the mortality experience of the exposed
group is compared with the mortality experience of the general
population in the same geographic area as the exposed people, e.g.,
comparison of frequency of lung cancer among uranium
Developed
Smoking
lung cancer
lung cancer
70
(a)
3
(c)
6930
(b)
2997
(d)
Yes
No
Total
7000
(a + b)
3000
(c + d)
cidence rates :
(a)among smokers
= 70/7000 = 10 per 1000
(b)among non-smokers
= 3/3000 = 1 per 1000
Statistical significance : P < 0.001
1
i) Estimation ofj risk :
Having calculated the incidence rates, the next step is to
>timate the risk of outcome (e.g., disease or death) in the
<posed and non-exposed cohorts. This is done in terms of
vo well-known indices: (a) relative risk, (b) attributable risk.
Q V,%*\^RELATIVE RISK
Relative risk (RR) is the ratio of the incidence of the disease Dr
death) among exposed and the incidence among non-xposed.
Some authors use the term "risk ratio" to refer to slative risk.
Incidence of disease (or death) among exposed
\
RR= ---------------------------------------------------------------- \
Incidence of disease (or death) among non-exposed J
In our hypothetical example (Table 18)
. , ./jAftf
RR of lung cancer = 4p = 10
V Estimation of relative risk (RR) is important in aetiological
inquiries. It is a direct measure (or index) of the "strength" of ;he
association between suspected cause and effect/A relative i^k of
one indicates no association; relative risk greater than :>ne
suggests "positive" association between exposure and the disease
under study. A relative risk of 2 indicates that the incidence rate of
disease is 2 times higher in the exposed group as compared with
the unexposed. Equivalently, this represents a 100 per cent
increase in risk. A relative risk of 0.25 indicates a 75% reduction
in the incidence rate in exposed individuals as compared with the
unexposed (35). It is often useful to consider the 95 per cent
confidence interval of a relative risk since it provides an indication
of the likely and maximum levels of risk.
In our hypothetical example (Table 18), the relative risk is 10. It
implies that smokers are 10 times^at greater risk of developing lung
cancer than non-smokers.{The larger the RR, the greater the
"strength" of the association between the Suspected factor and
disease. It may be noted that risk does not necessarily imply causal
association's \
ATTRIBUTABIE RISK
Non-smokers
10
Non-exposed to suspected
causal factor (b)
74(c)
224
Total population
Individual RR
Population AR
-if)
^i.'MJ
Source (58).
30-39
Ages
40-44
Relative risk
2.8
2.8
Attributable risk
3.5
20.0
Source (62).
Death rate/1000
Smokers Non-smokers
RR
^ABLE !22
C/Main differences between case control and cohort studies
AR(%)
Lung cancer
0.90
0.07
12.86
92.2
CHD
4.87
4.22
1.15
13.3
Cohort study
greatest confidence that the groups are comparable so that like can
be compared with like. It ensures that the investigator has no
control over allocation of participants to either study or control
group, thus eliminating what is known as "selection bias". In other
words, by random allocation, every individual gets an equal
chance of being allocated into either group or any of the trial
groups.
It is crucial that both the groups should be alike with regard to certain
variables or characteristics that might affect the outcome of the
experiment (e.g., age, sex), the entire study population can be stratified
into subgroups according to the variable, and individuals within each
subgroup can then be randomly allocated into study and control groups. It
is always desirable to check that the groups formed initially are basically
similar in composition/Randomization is done only after the | participant
has enterechthe study, that is after having been *l pafo qualified for the
trial and has given his informed consent to 4/ participate in the
studyARandomization is best done by using a table of random numbers
(see chapter 16).
The essential difference between a randomized controlled trial
and an analytical study is that in the latter, there is no
randomization because a differentiation into diseased and nondiseased (exposed or non-exposed) groups has already taken place.
The only option left to ensure comparability in analytical studies is
by matching.
4. Manipulation :
Having formed the study and control groups, the next step is to
intervene or manipulate the study (experimental) group by the
deliberate application or withdrawal or reduction of the suspected
causal factor (e.g., this may be a drug, vaccine, dietary component,
a habit, etc) as laid down in the protocol.
This manipulation creates an independent variable (e.g., drug,
vaccine, a new procedure) whose effect is then determined by
measurement of the final outcome, which constitutes the
dependent variable (e.g., incidence of disease, survival time,
recovery period).
5. Follow -up:
This implies examination of the experimental and control group
subjects at defined intervals of time, in a standard manner, with
equal intensity, under the same given circumstances, in the same
time frame till final assessment of outcome. The duration of the
trial is usually based on the expectation that a significant
difference (e.g., mortality) will be demonstrable at a given point in
time after the start of the trial. Thus the follow-up may be short or
may require many years depending upon the study undertaken.
')[ It may be mentioned that some losses to follow-up are inevitable
due to factors, such as death, migration and loss of interest. This is
known as attrition. If the attrition is substantial, it may be difficult
to generalise the results of the study to the reference population.
Every effort, therefore, should be made to minimise the losses to
follow-up. \
6. Assessment:
The final step is assessment of the outcome of the trial in terms
of (a) positive results : that is, benefits of the experimental measure
such as reduced incidence or severity of the disease, cost to the
health service or other appropriate outcome in the study and
control groups, (b) negative results : that is, severity and frequency
of side-effects and complications, if any, including death. Adverse
effects may be missed if they are not sought.
The incidence of positive/negative results is rigorously
compared in both the groups, and the differences, if any, are tested
for statistical significance. Techniques are available for
' the analysis of data as they are collected (sequential analysis), but it
is more useful to analyse the results at the end of the trial.
Bias may arise from errors of assessment of the outcome due to
human, element. These may be from three sources : First, there
may be bias on the part of the participants, who may subjectively
feel better or report improvement if they knew they were receiving
a new form of treatment. This is known as "subject variation".
Secondly there may be observer bias, that is the investigator
measuring the outcome of a therapeutic trial may be influenced if
he knows beforehand the particular procedure or therapy to which
the patient has been subjected. This is known as "observer bias."
Thirdly, there may be bias in evaluation - that is, the investigator
may subconsciously give a favourable report of the outcome of the
trial. Randomization cannot guard against these sorts of bias, nor
the size of the sample. In order to reduce these problems, a
technique known as "blinding" is adopted, which will ensure that
the outcome is assessed objectively.
k_>5>.Blinding : Blinding can be done in three ways -(a) SINGLE
BLIND TRIAL : The trial is so planned that the participant is not
awaje whethekhe belongs to the study group or control group (B)
pOUBLE'BLIND TRIAL : The trial is so planned that neither the
doctor nor the participant is aware of the group allocation and the
treatment received HC) TRIPLE BLIND TRIAL : This goes one
step further. The participant, the investigator and the person
analysing the data are all "blind". Ideally, of course, triple blinding
should be used; but the double blinding is the most frequently used
method when a blind trial is conducted (4). When an outcome such
as death is being measured, blinding is not so essential.
SOME STUDY DESIGNS
It is useful to consider here some of the study designs of
controlled trials :
1. Concurrent parallel study design
In this situation (Fig 10-a), comparisons are made between two
randomly assigned groups, one group exposed to specific
treatment, and the other group not exposed. Patients remain in the
study group or the control group for the duration of the
investigation.
a
Random
Assignment
Patients
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________________________________NON-RANDOMIZED TRIALS 79
2. Natural experiments
Where experimental studies are not possible in human
populations, the epidemiologist seeks to identify "natural
circumstances" that mimic an experiment. For example, in respect
of cigarette smoking, people have separated themselves "naturally"
into two groups, smokers and non-smokers. Epidemiologists have
taken advantage of this separation and tested hypothesis regarding
lung cancer and cigarette smoking. Other populations involved in
natural experiments comprise the following groups : (a) migrants
(b) religious or social groups (c) atomic bombing of Japan (d)
famines (e) earthquakes, etc. A major earthquake in Athens in 1981
provided a "natural experiment" to epidemiologists who studied the
effects of acute stress on cardiovascular mortality. They showed an
excess of deaths from cardiac and external causes on the days after
the major earthquake, but no excess deaths from other causes (84).
Q1 f John Snow's discovery that cholera is a water-borne disease
NON-RANDOMIZED TRIALS
was the outcome of a natural experiment. Snow in his "grand
Although the experimental method is almost always to beV experiment" identified two randomly mixed populations, alike in
preferred, it is not always possible for ethical, administrative and other important respects, except the source of water supply in their
other reasons to resort to a randomized controlled trial in human households. The results of the experiment are given in Table 23.
beings. For example, smoking and lung cancer and induction of
cancer by viruses have not lent themselves to direct experimentation
TABLE 23
in human beings. Secondly, some preventive measures can be
Deaths from cholera per 10,000 houses and sources of water
applied only to groups or on a community-wide basis (e.g.,
supply of these houses, London 1853
community trials of water fluoridation). Thirdly, when disease
frequency is low and the natural history long (e.g., cancer cervix) Sources of
Deaths from
Deaths in
Number of
cholera
each 10,000
randomized controlled trials require follow-up of thousands of water supply
houses
houses
people for a decade or more. The cost and logistics are often
prohibitive. These trials are rare. In such situations, we must depend Southwark &
upon other study designs - these are referred to as non-randomized Vauxhall Co.
40,046
315
1263
Lambeth Co.
(or non-experimental) trials.
Where the approach is sophisticated in randomized controlled
trials, it is rather crude in non-randomized trials. As there is no
randomization in non-experimental trials, the degree of
comparability will be low and the chances of a spurious result
higher than where randomization had taken place. In other words,
the validity of causal inference remains largely a matter of extrastatistical judgement. Nevertheless, vital decisions affecting public
health and preventive medicine
26,107
98
37
1970
1971
564
14620
464
12454
....................
|
-17.7
-14.8
1970
1971
% change
564
1426
464
1429
-17.7
0.2
14620
39980
12454
40396
-14.8
1.0
Model in which one factor is shown to lead to more than one disease
(ii) Multifactorial causation :
The causal thinking is different when we consider a noncommunicable disease or condition (e.g., CHD) where the
aetiology is multifactoriaH)Two models are presented in Figures
14 and 15 to explain the* complex situation. In one model (Fig
14), there are alternative causal factors (Factors 1,2 and 3) each
acting independently. This situation is exemplified in lung cancer
where more than one aetiological factor (e.g., smoking, air
pollution, exposure to asbestos) can produce the disease
independently. It is possible as our knowledge of cancer increases,
we may discover a common biochemical event at the cellular level
that can be produced by each of the factors. The cellular or
molecular factor will then be considered necessary as a causal
factor (4).
In the second model (Fig 15) the causal factors act cumulatively
to produce disease. This is probably the correct model for many
diseases. It is possible that each of the several factors act
independently, but when an individual is exposed to 2 or more
factors, there may be a synergistic effect.
criteria.
1.Temporal association
2.Strength of association
3.Specificity of the association
4.Consistency of the association
5.Biological plausibility
6.Coherence of the association
The Surgeon-General's Report (1964) states that the causal
significance of an association is a matter of judgement which goes
beyond any statement of statistical probability. To judge or
evaluate the causal significance of an association, all the above
criteria must be utilized, no one of which by itself is self-sufficient
or a sine qua- non for drawing causal inferences from statistical
associations, but each adds to the quantum of evidence, and all put
together contribute to a probability of the association being causal.
ASSOCIATION BETWEEN CIGARETTE SMOKING
AND LUNG CANCER
Cigarette smoking and lung cancer hypothesis provides an
excellent example to illustrate the epidemiological criteria for
establishing whether or not an observed association plays a causal
role in the aetiology of a disease. The data fulfilling the criteria
were covered adequately in Smoking and Health, the initial report
of the Advisory Committee to the Surgeon General of the Public
Health Service in 1964 (88). The later reports of US Public Health
Service from 1964-1973, and similar other reports (e.g., Report of
the Royal College of Physicians, London : Smoking or Health,
1977) summarised newer data supporting the validity of the
hypothesis. Let us examine the cigarette smoking and lung cancer
hypothesis in the light of the above criteria.
1. Temporal association
This criterion centres round the question: Does the suspected
cause precede the observed effect ? A causal association requires
that exposure to a putative cause must precede temporarily the
onset of a disease which it is purported to produce to allow for any
necessary period of induction and latency. This requirement is
basic to the causal concept.
In certain acute diseases such as water and food-borne
outbreaks, discovery of temporal sequence of two variables (e.g.,
drinking contaminated water and diarrhoea) is not often a serious
problem. However, in many chronic diseases, because of insidious
onset and ignorance of precise induction periods, it becomes hard
to establish a temporal sequence as to which came first - the
suspected agent or the disease, because one is dealing with a
continuous evolving process.
Lung cancer occurs in smokers of long-standing; this satisfies
the temporal requirement. Further, the increase in consumption of
cigarettes preceded by about 30 years the increase in death rates
from lung cancer. These observations are compatible with the long
latent period characteristic of carcinogenesis.
2. Strength of association
The strength of association is based on answers to two
questions:
a. Relative risk - is it large ?
b. Is there a dose -response, duration -response relationship ?
In general, the larger the relative risk, the greater the likelihood
of a causal association. Furthermore, the likelihood of a causal
relationship is strengthened if there is a biological gradient or
dose-response relationship - i.e., with increasing levels of exposure
to the risk factor, an increasing rise in
Source (60)
Non-smokers
Relative risk j
0.07
0.07
0.07
6.7
12.3
23.7
Cessation experiment:
Another piece of evidence is provided by the cessation
experiment. Table 27 shows the Mortality ratios in ex-cigarette
smokers by number of years stopped smoking among British
doctors. The results confirmed that the mortality ratios were
reduced in a way that would be expected if smoking were the
cause of the disease. This is a strong point in the evidence
favouring the hypothesis.
TABLE 27
Lung cancer mortality ratios in ex-cigarette - smokers, by
number of years stopped smoking, British physicians
Years stopped smoking
Still smoking
1-4
5-9
10-14
15 +
Non-smokers
Mortality ratio
15.8
16.0
5.9
5.3
2.0
1.0
Source (58)
3. Specificity of the association
The concept of specificity implies a "one-to-one" relationship
between the cause and effect. In the recent past, much of the
controversy over cigarette smoking and lung cancer centred round
lack of specificity of the association. That is, cigarette smoking is
linked with not only lung cancer but several others such as
coronary heart disease, bronchitis, emphysema, cancer cervix, etc.
This was used, for several years, as an argument against the
acceptance of the association as causal. It is true that cigarette
smoking is associated with so many diseases reflecting an apparent
lack of specificity, but that cannot be a strong argument, so as to
dismiss the causal
. :
Expected
deaths
(E)
170.3
89.5
14.0
37.0
105.1
111.6
6,430.7
207.8
15,653.9
Observed
Mortality
deaths (O)
ratio (O/E
1,833
546
75
152
294
216
11,177
213
23,223
10.8
6.1
5.4
4.1
2.8
1.9
1.7
1.0
17
Source (36)
The concept of specificity cannot be entirely dissociate from
the concept of association. It has been estimated the about 80-90
per cent of lung cancer can be attributed t cigarette smoking. To
say this, it is assumed that the associatio between smoking and
lung cancer is causal. Under the headin of specificity, two more
observations require comment: (a) nc everyone who smokes
develops cancer, and (b) not everyon who develops lung cancer
has smoked. The first apparer paradox is related to the
multifactorial nature of lung cancer, may well be that there are
other factors as yet unidentifie which must be present in
conjunction with smoking for lun cancer to develop. As for lung
cancer in non-smokers, it i known that there are factors other than
smoking which increas the risk of lung cancer such as
occupational exposure t chromates, asbestos, nickel, uranium and
exposure to ai pollution. Deviations from one-to-one relationship
betwee cigarette smoking and lung cancer therefore cannot be
said t rule out a causal relationship.
4. Consistency of the association
The association is consistent if the results are replicatei when
studied in different settings and by different methods That is,
evidence from a single study is seldom sufficient t< establish
"causal" association. If there is no consistency, it wi weaken a
causal interpretation.
A consistent association has been found between cigarett
smoking and lung cancer. More than 50 retrospective studie and
at least nine prospective studies in different countries hav shown a
consistent association between cigarette smoking am subsequent
development of lung cancer, lending support to ; causal
association.
Biological plausibility
Causal association is supported if there is biological
jdibility to the association, that is, the association agrees with
rrent understanding of the response of cells, tissues, organs,
id systems to stimuli. For example, the notion that food
take and cancer are interrelated is an old one. The positive
isociation of intestine, rectum and breast cancers is
ologically logical, whereas the positive association of food
id skin cancer makes no biological sense suggesting that
rength of association by itself does not imply causality. This is
tie of the pitfalls of correlation studies. Further, the criterion of
iological plausibility should not be applied rigidly. That is,
fen if a biological mechanism cannot be postulated, it does
ot rule out the possibility of a cause and effect relationship,
>r it may be merely due to the limits of current knowledge.
The cigarette smoking and lung cancer hypothesis is
iologically plausible. It is not hard to visualize the inhalation
if hot smoke into the lungs and deposition of a chemical
arcinogen over a period of time probably building itself up to
i threshold level and initiating neoplastic changes in the lungs.
Experimental studies in animals have strengthened the
ividence for the aetiological role of cigarette smoking,
ilthough one cannot directly translate the results of such
;tudies in humans. Many such studies have shown that lung
:ancer can be produced by tracheo-bronchial implantation of
:obacco extracts or by inhalation of cigarette smoke or of
aerosols of its constituents. Carcinogenic substances have been
isolated from cigarette smoke, although the precise carcinogens
responsible for lung cancer in man are unknown. The
biological credibility, in fact, provides a convincing evidence in
favour of a causal association.
6. Coherence of the association
A final criterion for the appraisal of causal significance of an
association is its coherence with known facts that are thought to be
relevant. For example, the historical evidence of the rising
consumption of tobacco in the form of cigarettes and the rising
incidence of lung cancer are coherent. Male and female
differences in trends of lung cancer death rates are also coherent
with the more recent adoption of cigarette smoking by women.
Death rates rose first in males and are now increasing relatively
more rapidly in females. The fall in the relative risk of lung cancer
when cigarette smoking is stopped, and the occurrence of lung
cancer from occupational exposure to other carcinogens such as
asbestos and uranium and the demonstrated increase in lung
cancer risk when workers exposed to these substances also
smoked, enhance the significance of a causal association.
In conclusion, it may be stated that the association between
cigarette smoking and lung cancer can never be proved by a direct
experiment on humans. It is an illusory and virtually unattainable
goal. It is well known that epidemiology depends heavily on
inferences drawn from observations rather than on the ultimate
experiment. The nearest approach to "scientific proof", therefore is
the vast body of convincing evidence we have accumulated during
the past few years meeting all the criteria proposed for judging the
causality of such associations.
USES OF EPIDEMIOLOGY
While the study of disease distribution and causation remains
central to epidemiology; the techniques of epidemiology have a
wider application covering many more important areas relating not
only to disease but also health and health services. In more
utilitarian terms, epidemiology has been
defined
as
"a
means of learning, or asking
ENDEMIC (/Q((5S\
f OPPORTUNISTIC INFECTION:
This is infection by an organism"(s) that takes the opportunity
provided by a defect in host defence to infect the host and hence
cause disease. The organisms include Herpes simplex,
Cytomegalovirus, Toxoplasma, M. tuberculosis, M. avium
intracellular, Pneumocystis, etc. (For example, opportunistic
infections are very common in AIDS). Infection by an organism
that is not normally pathogenic, but can cause disease if resistance
is lowered. ]
MODES OF TRANSMISSION 89
a carrier. For example, in polio the infection may remain
subclinical and the person may act as a temporary carrier by
virtue of shedding the organism. On the other hand, in
tuberculosis, most persons with positive tuberculin test do not
actively disseminate tubercle bacilli and therefore are not labelled
as carrier (36).
B. By Duration : (a) TEMPORARY CARRIERS :
Temporary carriers are those who shed the infectious agent for
short periods of time. In this category may be included the
incubatory, convalescent and healthy carriers, (b) CHRONIC
CARRIERS : A chronic carrier is one who excretes the
infectious agent for indefinite periods. Chronic carrier state
occurs in a number of diseases, e.g., typhoid fever, hepatitis B,
dysentery, cerebro-spinal meningitis, malaria, gonorrhoea, etc.
Chronic carriers are far more important sources of infection
than cases. The longer the carrier state, the greater the risk to
the community. Some carriers excrete the infectious agent only
intermittently and some continuously. The duration of the
carrier state varies with the disease. In typhoid fever and
hepatitis B, the chronic carrier state may last for several years;
in chronic dysentery, it may last for a year or longer. In
diphtheria, the carrier state is associated with infected tonsils;
in typhoid fever with gall bladder disease. Chronic carriers are
known to reintroduce disease into areas which are otherwise
free of infection (e.g., malaria). Therefore their early detection
and treatment are essential to limit the spread of infection.
Carriers of avirulent organisms are called pseudo-carriers.
Pseudo-carriers are not important epidemiologically.
C. By Portal of Exit : Carriers may also be classified
according to the portal of exit of the infectious agent. Thus we
have urinary carriers, intestinal carriers, respiratory carriers,
nasal carriers, etc. Skin eruptions, open wounds and blood are
also portals of exit. In typhoid fever, the urinary carrier is more
dangerous than an intestinal carrier. A typhoid carrier working
in a food establishment or water works is more dangerous than
a typhoid carrier working in an office establishment. Thus the
portal of exit and the occupational status of the carrier are
important epidemiological considerations.
2. Animal reservoir
The source of infection may sometimes be animals and birds.
These, like the human sources of infection, may be cases or carriers.
The diseases and infections which are transmissible to man from
vertebrates are called zoonoses. There are over 100 zoonotic
diseases which may be conveyed to man from animals and birds.
The best known examples are rabies, yellow fever and influenza.
The role of pigs and ducks in the spread of epidemic and pandemic
influenza both as reservoirs, carriers and "amplifying hosts" is now
well established. Pigeons in cities can lead to infection with
chlamydia; dust mites fromy them can cause allergy in man.
Ornithosis and arboviruses can ' be transmitted to man from various
birds. Wild birds, in particular, are important hosts in the
transmission cycles of most of the mosquito-borne encephalitis and
several mosquito-borne undifferentiated febrile diseases (102).
Histoplasmosis is carried all over the world by birds (110). As birds
migrate from one locality to another they may carry ticks infected
with viruses and rickettsiae that may cause disease in humans. In
short, the migrations and movements of animals and birds may
carry serious epizootiological and epidemiological risks. There is
evidence that genetic recombination between animal and human
viruses might produce "new" strains of viruses (e.g., influenza
viruses).
3. Reservoir in non-living things
Soil and inanimate matter can also act as reservoirs of
infection. For example, soil may harbour agents that cause
tetanus, anthrax, coccidioidomycosis and mycetoma.
MODES OF TRANSMISSION
Communicable diseases may be transmitted from the reservoir
or source of infection to a susceptible individual in many different
ways, depending upon the infectious agent, portal of entry and the
local ecological conditions. As a rule, an infectious disease is
transmitted by only one route, e.g., typhoid fever by vehicle
transmission and common cold by direct contact. But there are
others which may be transmitted by several routes e.g., AIDS,
salmonellosis, hepatitis B, brucellosis, Q fever, tularemia etc. The
multiple transmission routes enhance the survival of the infectious
agent. The mode of transmission of infectious diseases may be
classified as below (2,100).
A
DIRECT TRANSMISSION
1.Direct contact
2.Droplet infection
3.Contact with soil
4.Inoculation into skin or mucosa
5.Transplacental (vertical)
INDIRECT TRANSMISSION
1.Vehicle-borne
2.Vector-borne
a. Mechanical
b. Biological
3. Air-borne
a. Droplet nuclei
b. Dust
1.Fomite -borne
2.Unclean hands and fingers
iespiicuory mucosa ui
B. Indirect transmission
This embraces a variety of mechanisms including the traditional
5 F's - "flies, fingers, fomites, food and fluid". An essential
requirement for indirect transmission is that the infectious agent
must be capable of surviving outside the human host in the
external environment and retain its basic properties of
pathogenesis and virulence till it finds a new host. This depends
upon the characteristics of the agent, the inanimate object and the
influence of environmental factors such as temperature and
humidity. If the disease agent acquires drug resistance, it will
further facilitate its spread. Indirect transmission can occur in a
variety of settings :
1. Vehicle-borne
Vehicle-borne transmission implies transmission of the
infectious agent through the agency of water, food (including
raw vegetables, fruits, milk and milk products), ice, blood,
serum, plasma or other biological products such as tissues and
organs. Of these water and food are the most frequent vehicles
of transmission, because they are used by everyone. The
infectious agent may have multiplied or developed in the
vehicle (e.g., S. aureus in food) before being transmitted; or
only passively transmitted in the vehicle (e.g., hepatitis A virus
in water). Diseases transmitted by water and food include
chiefly infections of the alimentary tract, e.g., acute diarrhoeas,
typhoid fever, cholera, polio, hepatitis A, food poisoning and
intestinal parasites. Those transmitted by blood include
hepatitis B, malaria, syphilis, brucellosis, trypanasomes
(Chaga's
disease),
infectious
mononucleosis
and
cytomegalovirus infection (114). Organ transplantation may
result in the introduction of the disease agent such as
cytomegalovirus in association with kidney transplants.
,
The epidemiological features of vehicle transmission are!y (a)
if the dose of contamination is heavy, the outbreak may be"
explosive as in the case of cholera and hepatitis A epidemics
(b) cases are initially confined to those who are exposed to the
contaminated vehicle, in some infections (c) when secondary cases
occur, the primary case may be obscured (d) the distafice travelled
by the infectious agent may be great, e.g., outbreaks of food
poisoning (e) it is not always possible to isolate the infectious
agent in the incriminated vehicle, e.g., typhoid bacilli in
contaminated water (f) when the vehicle is controlled or
withdrawn, the epidemic subsides, e.g., epidemics of cholera, and
(g) the common source of infection is often traceable.
2. Vector-borne
In infectious disease epidemiology, vector is defined as an
arthropod or any living carrier (e.g., snail) that transports an
infectious agent to a susceptible individual. Transmission by a
vector may be mechanical or biological. In the latter case, the
disease agent passes through a developmental cycle or
multiplication in the vector.
Epidemiological classification of vector-borne diseases :
I. By vector :
a) Invertebrate type : Arthropod vectors fall into seven
orders largely
(1) Diptera - flies and mosquitoes ~
(2) Siphonaptera - fleas w
(3) Orthoptera
- cockroaches * j
(4) Anoplura - sucking
lice
(1)Hemiptera - Bugs, including kissing bugs
(2)Acarina - ticks and mites
(3)Copepoda - cyclops
b) Vertebrate type - Mice, rodents, bats
II. By transmission chain :
Vector-borne diseases are classified under heterogeneous
infection chain and involve three principal patterns :
a) Man and a non-vertebrate host
1)Man-arthropod-man (malaria)
2)Man-snail-man (schistosomiasis)
b) Man, another vertebrate host, and a non-vertebrate host
1)Mammal-arthropod-man (plague)
2)Bird-arthropod-man (encephalitis)
c) Man and 2 intermediate hosts
1)Man-cyclops-fish-man (fish tape worm)
2)Man-snail-fish-man (Clonorchis sinensis)
3)Man-snail-crab-man (Paragonimiasis)
III. By methods in which vectors transmit agent:
a)Biting
b)Regurgitation
c)Scratching-in of infective faeces
d)Contamination of host with body fluids of vectors
IV By methods in which vectors are involved in the
transmission and propagation of parasites :
(a) Mechanical transmission : The infectious agent is
mechanically transported by a crawling or flying arthropod through
soiling of its feet or proboscis; or by passage of organisms through
its gastro-intestinal tract and passively excreted. There is no
development or multiplication of {he infectious agent on or within
the vector ^()V, ^ . \< Qj (K
Y"^$) ^Biological transmission : (The infectious agent undergoing
replication or development or both in vector and requires an
incubation period before vector can transmit. Biological
transmission is of three types : (i) Propagative : The ^Sgent merely
multiplies in vector, but no change in form, e.g., plague bacilli in
rat fleas (ii) Cydo -propagative : The agent
SUSCEPTIBLE HOST 9
changes in form and number, e.g., malaria parasites in mosquito
(iii) Cyclo-developmental : The disease agent undergoes only
development /but no multiplication, e.g., microfilaria in
mosquito}) \j"^Wk Mr- ^^nO
When the infectiousagent is transmitted vertically from the
infected female to her progeny in the vector, it is known as
transovarial transmission. Transmission of the disease agent from
one stage of the life cycle to another as for example nymph to adult
is known as trans -stadial transmission ^J^t Op
The factors which influence the ability of vectors to transmit
disease are : (a) host feeding preferences (b) infectivity, that is
ability to transmit the disease agent (c) susceptibility, that is ability
to become infected (d) survival rate of vectors in the environment
(e) domesticity, that is degree of association with man, and (f)
suitable environmental factors. Seasonal occurrence of some
diseases (e.g., malaria) may be related to intense breeding and
thereby greater density of the insect vector during certain periods
of the year.
3. Airborne
Successful parasitism
(1)Droplet nuclei : "Droplet nuclei" are a type of particles
Four stages have been described in successful parasitism : (a)
implicated in the spread of airborne infection. They are tiny
First, the infectious agent must find a PORTAL OF ENTRY by
particles (1-10 microns range) that represent the dried residue
which it may enter the host. There are many portals of entry, e.g.,
of droplets (2). They may be formed by (a) evaporation of
respiratory tract, alimentary tract, genitourinary tract, skin, etc.
droplets coughed or sneezed into the air or (b) generated
Some organisms may have more than one portal of entry, e.g.,
purposefully by a variety of atomising devices (aerosols). They
hepatitis B, Q fever, brucellosis, (b) On gaining entry into the host,
may also be formed accidentally in microbiological
the organisms must reach the appropriate tissue or "site of election"
laboratories, in abattoirs, rendering plants or autopsy rooms
in the body of the host where it may find optimum conditions for
(100). The droplet nuclei may remain airborne for long periods
its multiplication and survival, (c) Thirdly, the disease agent must
of time, some retaining and others losing infectivity or
find a way out of the body (portal of exit) in order that it may reach
virulence. They not only keep floating in the air but may be
a new host and propagate its species. If there is no portal of exit,
disseminated by air currents from the point of their origin.
the infection becomes a dead-end infection as in rabies, bubonic
Particles in the 1 -5 micron range are liable to be easily drawn
plague, tetanus and trichinosis, (d) After leaving the human body,
into the alveoli of the lungs and may be retained there. Diseases
the organism must survive in the external environment for
spread by droplet nuclei include tuberculosis, influenza,
sufficient period till a new host is found. In addition, a successful
chickenpox, measles, Q fever and many respiratory infections.
disease agent should not cause the death of the host but produce
(Not considered airborne are droplets and other large particles
only a low-grade immunity so that the host is vulnerable again and
which promptly settle out). Mention must also be made of the
again to the same infection. The best example is common cold
role of airborne spread of toxic air pollutants including "smog"
virus.
resulting in air pollution epidemics.
/V*7\
(2)Dusr : Some of the larger droplets which are expelled during i Incubation period
,V An infection becomes apparent only after a certain
talking, coughing or sneezing, settle down by their sheer weight
.N incubation period, which is defined as "the time interval
on the floor, carpets, furniture, clothes, bedding, linen and other
objects in the immediate environment and become part of the
iJ between invasion by an infectious agent and appearance of the
dust. A variety of infectious agents (e.g.,^ streptococci, other
rj^irst sign or symptom of the disease in questionTfi?,). During the
pathogenic bacteria, viruses and fungal spores) and skin
^ijicubation period, the infectious agent undergoes
squamae have been found in the dust of hospital wards and
i* multiplication in the host. When a sufficient density of the
living rooms. Some of them (e.g., tubercle, bacilli) may survive
disease agent is built up in the host, the health equilibrium is
in the dust for considerable periods underi optimum conditions
disturbed and the disease becomes overt. Also of interest to the
of temperature and moisture. During the act of sweeping,
epidemiologist is the median incubation period, defined as
dusting and bed-making, the dust is released into the air and
the time required for 50 per cent of the cases to occur following
becomes once again airborne. Dust particles may also be blown
exposure. These concepts are explained in Fig. 18. The factors
from the soil by wind; this may include fungal spores.
which determine the incubation period include the generation
Coccidioidomycosis is an example of a disease spread through
time of the particular pathogen, infective dose, portal of entry
airborne transmission of fungal spores (36). Other diseases
and individual susceptibility. As a rule, infectious diseases are
carried by infected dust include streptococcal and
not communicable during the incubation period, but there are
staphylococcal infection, pneumonia, tuberculosis, Q-fever and
exceptions, as for example, measles, chickenpox, whooping
psittacosis. Airborne dust is primarily inhaled, but may settle on
cough and hepatitis A are communicable during the later part
uncovered food and milk. This type of transmission is most
of the incubation period.
common in hospital-acquired (nosocomial) infection.
The length of the incubation period is characteristic of each
disease. There is a minimum incubation period for every disease
4. Fomite-borne
before which no illness can occur. That is, incubation period varies
Fomites (singular; fomes) are inanimate articles or substances
for different infectious diseases, and also from one person to
other than water or food contaminated by the infectious discharges
another with the same disease. In some, the incubation period is
from a patient and capable of harbouring and transferring the
very short ranging from a few hours to 2-3
infectious agent to a healthy person. Fomites include soiled
clothes, towels, linen, handkerchiefs,
closed group, there is an initial primary case. The primary case V/*
is followed by 2 or 3 secondary cases within a short time /The
gap in time between the onset of the primary case ana the Vsecondary case is called the "serial interval'l By collecting
information about a whole series of such onsets, we get a
distribution of secondary cases from which we can guess the j
incubation period of disease.
-.
Generationtime')
Another concept in infectious- disease epidemiology' is "generation time". It is defined asf'the interval of time between / -receipt of infection by
a host ana""fnaximal infectivity of thatx,, host" (2). In general, generation time is roughly equal to the hg incubation period. However, these two
terms are not the same. The time of maximum communicability may precede or follow the incubation period7_jFor example, in mumps,
communicability appears to reach its height about 48 hours before the onset of swelling of the salivary glands (36). With person-to-person
transmission of infection, the interval between cases is determined by the generation time (2). A further difference is that the term "incubation
period" can only be applied to infections that result in manifest disease, whereas "generation time" refers to transmissions of infection, whether
clinical or subclinical (36).
/
Communicable period
DVVM
vjjOTie
communicable
period
is
tlefined
as
"the
time
during
wMch
an
infectious
agent
may
be
transferred
directly
or
indirectly
from
an
infected
person
to
another
person,
from
an
dnfected
animal
to
man,
or
from^n
infected
person
to
an
animal,
including
arthropods"jfJ^l^ommunicability
varies
in
different
diseases.
Some
diseases-are
more
communicable
during
the
incubation
period
than
during
actual
illness.
Communicability
of
some
diseases
can
be
reduced
by
early
i,
diagnosis
and
treatment.
[An
imp^ojtant
measure
of
ry
communicability is Secondary Attack Rate?!
\-J \
Secondary attack rate
K
v*J)
Secondary
attack
rate
(SAR)
is
exposed
persons
developing
the
disease
incubation
period,
following
exposure
It is given by the formula :
y^
Number of exposed persons developing
S
the disease within the range of the
(
incubation period
C U-'
> SAR= ---------------------------------------------- X100
?'
\
Total number of exposed/"susceptible" .
/"-v-i
/
contacts
Jm*\
{&!t
defined
within
to
as
the
the
"the
number
range
of
primary
of
the
case\(4).
The denominator consists of all persons who are exposed to the case. More specifically, the denominator may be restricted only to
"susceptible" contacts, if means are available to
HOST DEFENCES 93
distinguish the susceptible persons from the immune (4). The
primary case is excluded from both the numerator and
denominator.
Supposing there is a family of 6 consisting of 2 parents (already
immune) and 4 children who are susceptible to a specific disease,
say measles. There occurs a primary case and within a short time 2
secondary cases among the remaining children. The secondary
attack rate is 2/3 or 66.6 per cent. The primary case is excluded
from both numerator and denominator.
Secondary attack rate is limited in its application to infectious
diseases in which the primary case is infective for only a short
period of time measured in days (e.g., measles and chickenpox).
When the primary case is infective over a long period of time (e.g.,
tuberculosis), duration of exposure is an important factor in
determining the extent of spread (13). It is indicated by the
formula :
Number of contacts developing
rj \C^
tuberculosis
\ ^
SAR = ---------------------------------
x ioo|
.y tn
\t"T
SPECIFIC DEFENCES
Specific defences come into play, once microorganisms have
breached local defence mechanisms. By virtue of these defences,
the host is able to recognize, destroy and eliminate antigenic
material (e.g., bacteria, viruses, proteins, etc.) foreign to his own.
A person is said to be immune when he possesses "specific
protective antibodies or cellular immunity as a result of previous
infection or immunization, or is so conditioned by such previous
experience as to respond adequately to prevent infection and/or
clinical illness following exposure to a specific infectious agent"
(100).
The specific defences may be discussed for convenience under
the following heads :
1. Active immunity
(1)Humoral immunity
(2)Cellular immunity
(3)Combination of the above
2. Passive immunity
(1)Normal human Ig
(2)Specific human Ig
(3)Animal antitoxins or antisera
1. Active Immunity
It is the immunity which an individual develops as a result of
infection or by specific immunization and is usually associated
with presence of antibodies or cells having a specific action on the
microorganism concerned with a particular infectious disease or on
its toxin (100). In other words, active immunity depends upon the
humoral and cellular responses of the host. The immunity
produced is specific for a particular disease, i.e., the individual in
most cases is immune to further infection with the same organism
or antigenically related organism for varying periods depending
upon the particular disease.
.
f Active immunity may be acquired in 3 ways :
(a)following clinical infection, e.g., chickenpox, rubella and
measles.
(b)following subclinical or inapparent infection, e.g., polio and
diphtheria.
(c)following immunization with an antigen which may be a
killed vaccine, a live attenuated vaccine or toxoid. ")
The Immune Response
(a) PRIMARY RESPONSE : When an antigen is administered
for the first time to an animal or human who has never been
exposed to it, there is a latent period of induction of 3 to 10 days
before antibodies appear in the blood (Fig. 19). The antibody that
is elicited first is entirely of the IgM type. The IgM antibody titre
rises steadily during the next 2-3 days or more, reaches a peak
level and then declines almost as fast as it developed. Meanwhile,
if the antigenic stimulus was sufficient, IgG antibody appears in a
few days. IgG reaches a peak in 7-10 days and then gradually falls
over a period of weeks or months (Fig.19).
The nature and extent of primary response to an antigen is
determined by a number of factors, e.g., dose of antigen, nature of
antigen, route of administration, adjuvants, nutritional status of the
host, etc (116). For example, with small doses of antigen, only
IgM type of response may be induced, and successive small doses
of antigen at suitable intervals may also induce IgM antibody. The
antigenic dose required for the induction of IgG is about 50 times
that which is required to induce IgM antibody.
IMMUNIZING AGENTS
2. Passive immunity
When antibodies produced in one body (human or animal) are
transferred to another to induce protection against disease, it is
known as passive immunity. In other words, the body does not
produce its own antibodies but depends upon ready-made
antibodies. Passive immunity may be induced :
(a)by administration of an antibody-containing preparation
(immune globulin or antiserum)
(b)by transfer of maternal antibodies across the placenta. Human
milk also contains protective antibodies, (IgA).
(c)by transfer of lymphocytes, to induce passive cellular
immunity - this procedure is still experimental.
Passive immunity differs from active immunity in the following
respects : (a) immunity is rapidly established (b) immunity
produced is only temporary (days to months) till the antibody is
eliminated from the body, and (c) there is no education of the
reticulo-endothelial system.
Passive immunization is useful for individual who cannot form
antibodies, or for the normal host who takes time to develop
antibodies following active immunization.
[Herd Immunity
\/-A^/f%)
It is the level of resistance dfa community or group of people to
a particular diseasjpf 122). According to another source (123) herd
immunity implies group protection beyond that afforded by the
protection of immunized individuals. That is, it concerns the
freedom from infection of individuals within a herd by sole virtue
of the influence of the herd structure on the transmission among
individuals. Thus there is an unfortunate confusion over the
definition of herd immunity
fflferd immunity provides an immunological barrier to the
spread of disease in the human herd. For example, when an
infectious disease is introduced into a "virgin" population, that is,
population with a very low or no immunity, the attack and case
fatality rates tend to be very high involving practically all
susceptibles as it had happened in the very severe measles
epidemic in the Faroe islands, in 1854, where the population had
no previous experience of measles. The epidemic wave declined
with a|uuld-up of herd immunity following natural
[ Elements wfrfeh contribute to herd immunity are (a) occurrence
of clinical and subclinical infection in the herd, (b) immunization
of the herd and (c) herd structure. Herd structure is never constant.
It is subject to constant variation because of new births, deaths and
population mobility. An on-going immunizationjjrogramme will
keep up the herd immunity at a very high levelj j^-^S f\
The herd structure includes-rfot only the hosts (population)
belonging to the herd species but also the presence and distribution
of alternative animal hosts and possible insect vectors as well as
those environmental and social factors that favour or inhibit the
spread of infection from host to host. The herd structure thus plays
a decisive role in the immunity status of the herd.
If the herd immunity is sufficiently high, the occurrence of an
epidemic is regarded as highly unlikely. If that high level of
immunity is maintained and stepped up, by an on-going
immunization programme, to the point where the susceptible
persons are reduced to a small proportion of the population, it may
lead (but not necessarily) to elimination of the disease in due
course. This has been achieved in such diseases as diphtheria and
poliomyelitis. In the case of smallpox, however,
TABLE 29
Immunizing Agents
VACCINES
J<
Live
attenuated
vaccines
Inactivated
or killed
vaccines
,_
BCG
Typhoid oral
Plague
Oral polio
Yellow fever
Measles
Rubella
Mumps
Influenza
Epi. typhus
Typhoid
Cholera
Pertussis
C.S. meningitis
Plague
Rabies
Salk (polio)
Influenza
Hepatitis B
Japanese
encephalitis _
KFD
Diphtheria
Toxoids
1_ Tetanus
IMMUNO-
GLOBULINS
Human
Immunoglobulins
P Hepatitis A
TABLE 30
Vaccine dose
Bacterial
Antibody
persistence (immunity)
Booster needed
Revaccination
Latency
Oncogenicity
Viral
Attenuated
Vaccines
Low
(replicates)
Killed
Vaccines
High
Long
Infrequently
Possible
Possible
?
Short
Frequently
None
None
None
Rickettsial
TABLE 31
Milestones in vaccination
Bacterial
1798
1885
- 1892
1913
Viral
ju m >
Bacterial
OBWJ
Measles
Rabies
Tetanus
Mumps
Human normal Ig
Hepatitis B
Varicella
Diphtheria
Human specific Ig
Diphtheria
Non -human
Tetanus
(Antisera)
Gas gangrene
Bacterial
Botulism
__ Rabies
Viral
r
~ b.
Inactivated or killed vaccines :
Organisms killed by heat or chemicals, when infected into the
body stimulate active immunity. They are usually safe but
generally, less efficacious than live vaccines. For example, cholera
vaccine offers only 50 per cent protection. The efficacy of 3 doses
of pertussis vaccine is about 80 per cent in the first three years, and
almost nil 12 years after immunization. Killed vaccines usually
require a primary series of 2 or 3 doses of vaccine to produce an
adequate antibody response, and in most cases "booster" injections
are required. The duration of immunity following the use of
inactivated vaccines varies from months to many years. Inactivated
polio vaccine has been quite an effective vaccine, the widespread
use of which in certain countries has led to the elimination of the
disease. Killed vaccines are usually administered by subcutaneous
or intramuscular route. The only absolute contraindication to their
administration is a severe local or general reaction to a previous
dose.
Some features of attenuated versus inactivated (killed) vaccines
are listed in table 30 and some of the very important developments
in the field of vaccines are listed in table 31.
Smallpox vaccine
Rabies vaccine
Cholera vaccine
Toxin/antitoxin immunization against
diphtheria
*1921 - BCG
*1923 - Diphtheria Toxoid
*1923 - Pertussis vaccine
*1927 - Tetanus toxoid
-1937
- Influenza vaccine
-1937
- Yellow fever vaccine (17 D)
1949
- Mumps vaccine
v
1954 - Salk's Polio vaccine
* 1957 - Sabin live oral Polio vaccine
**J
* 1960 - Measles vaccine
*
1962 - Rubella vaccine
^0
1968 - Type C meningococcus vaccine
f...
1971 - Type A meningococcus vaccine
-jA
1976 - Hepatitis B vaccine
-._/- Diseases subject to the I.H.R. for which vaccination may be
required.
* The six vaccines recommended in childhood by WHO for
inclusion in the EPI.
Source WHJFeb - March 1977.
c. Toxoids:
Certain organisms produce exotoxins, e.g., diphtheria and
tetanus bacilli. The toxins produced by these organisms are
detoxicated and used in the preparation of , vaccines. The
antibodies produced neutralise the toxic moiety produced during
infection, rather than act upon the organisms. In general, toxoid
preparations are highly efficacious and safe immunizing agents.
d. Cellular fractions:
Vaccines, in certain instances, are prepared from extracted
cellular fractions, e.g., meningococcal vaccine from the
polysaccharide antigen of the cell wall, the pneumococcal vaccine
from the polysaccharide contained in the capsule of the organism
and hepatitis B polypeptide vaccines. Although the duration of
experience with these vaccines is limited, their efficacy and safety
appear to be high.
e. Combinations:
If more than one kind of immunizing agent is included in the
vaccine, it is called a mixed or combined vaccine. The aim of
combined vaccines is to simplify administration, reduce costs and
minimise the number of contacts of the patient with the health
system. The following are some of the well-known combinations :
DPT (Diphtheria-pertussis-tetanus) DT
(Diphtheria-tetanus) DP
(Diphtheriapertussis)
IMMUNOGLOBULINS
DPT and typhoid vaccine
MMR (Measles, mumps and rubella)
DPTP (DPT plus inactivated polio)
The term "polyvalent" is applied to vaccines (e.g., polio,
influenza vaccines) which are prepared from two or more strains of
the same species. The term "auto" or "autogenous" vaccine is
applied when the organism in the vaccine is obtained from the
same patient.
Some vaccines are presented as plain vaccines, some as
adjuvant vaccines and some as freeze-dried preparations. Plain
vaccines are less efficacious than adjuvant vaccines. Adjuvants are
substances that are added to vaccines with the intent of potentiating
the immune response, so that a greater amount of antibody is
produced, a lesser quantity of antigen is required and fewer doses
to be given (127). The mechanism by which adjuvants (e.g.,
aluminium phosphate, aluminium hydroxide, water-in-oil) enhance
antibody protection is not completely understood. It is partly due to
the formation of a local granuloma which retains the antigen and
from which antigen is slowly released. Freeze-dried vaccines (e.g.,
BCG, yellow fever, measles) are more stable preparations than
liquid vaccines.
Immunoglobulins
The human immunoglobulin system is composed of 5 major
classes (IgG, IgM, IgA, IgD and IgE) and sub-classes within them.
The various classes and sub-classes of immunoglobulins represent
different functional groups that are required to meet different types
of antigenic challenges. All antibodies are immunoglobulins, but it
is still an open question whether all immunoglobulins are
antibodies (115). The WHO recommends that the term "gamma
globulin" should not be used as a synonym for "immunoglobulin"
(128).
IgG : IgG is the major immunoglobulin of serum, comprising
about 85 per cent of the total serum immunoglobulins. Because of
its relatively smaller molecular weight (150,000), IgG can diffuse
into the interstitial fluid. In other words, IgG is largely
extravascular. IgG is the only class of IgGs which is transported
across the placenta. Antibodies to gram-positive pyogenic bacteria,
anti-viral and anti-toxic antibodies are found exclusively among
IgG globulins. IgM : It accounts for about 10 per cent of normal
serum immunoglobulins. It represents antibody that is promptly
formed with exposure to antigen (Fig. 19). Its presence may be
indicative of recent infection. IgM antibody has high agglutinating
and complement-fixing ability. Its half life is about 10 days. IgA :
Constitutes about 15 per cent of the total serum immunoglobulins.
Antibody activity to a wide range of viral and bacterial antigens
has been reported in this class (129). IgA is found relatively in
large quantities in body secretions, e.g., saliva, milk, colostrum,
tears, bronchial secretions, nasal mucosa, prostatic fluid, vaginal
secretions and mucus secretions of the small intestine; it provides
the primary defence mechanism at the mucos membranes against
local infection. The half-life of IgA is approximately 6-8 days. IgD
: Normal serum is estimated to contain 0.3 to 40 mg per 100 ml of
IgD. Its half-life is 2.8 days. Its main function has not yet been
determined. IgE : The serum level of IgE is 10-130 micrograms
per 100 ml. Half-life is 2.3 days. IgE is concentrated in submucous
tissues. It is the major antibody responsible for immediate allergic
anaphylactic reactions.
Immunoglobulin preparations:
Two types of immunoglobulin preparations are available for
passive immunization. These are (a) Normal human
immunoglobulin and (b) Specific (hyper-immune) human
immunoglobulin. These are used in the prophylaxis of viral and
bacterial infections, and in replacement of antibodies in
immunodeficient patients.
a. Normal human Ig :
Normal human Ig is an antibody-rich fraction (Cohn fractic
II), obtained from a pool of at least 1000 donors. The WHO hi
laid down definite standards for its preparation. For exampl the
preparation should contain at least 90 per cent intact IgG; should
be as free as possible from IgG aggregates; all IgG sub classes
should be present; there should be a low Ig concentration; the
level of antibody against at least two bacteri; species and two
viruses should be ascertained etc. (130).
Normal human Ig is used to prevent measles in highl
susceptible individuals and to provide temporary protectio (upto
12 weeks) against hepatitis A infection for travellers fc endemic
areas and to control institutional & householi outbreaks of
hepatitis A infection.
Live vaccines should not normally be given for 12 week: after
an injection of normal human Ig, and if a live vaccine ha: already
been given. NHIg injection should be deferred for i weeks.
b. Specific human Ig
The specific (hyperimmune) human Ig should contain al least 5
times the antibody potential of the standard preparation per unit
volume. These preparations are made from the plasma of patients
who have recently recovered from an infection or are obtained
from individuals who have been immunized against a specific
infection. They therefore have a high antibody content against an
individual infection and provide immediate protection e.g., specific
human Igs are used for chickenpox prophylaxis of highly
susceptible individuals and for post-exposure prophylaxis of
hepatitis B, and rabies and for tetanus prophylaxis in the wounded.
Immunoglobulin is administered by intramuscular injection.
Immunoglobulin suitable for intravenous administration has also
become available (130). The intramuscular injections are painful
for some patients but can be better tolerated if procaine 1 per cent
is mixed at 1 part in 10 with the immunoglobulin (131). Doses
larger than 5 ml must be divided and injected into 4-6 intragluteal
sites through a 18 or 20 gauge needle because the preparation is
viscous.
Peak blood levels are reached in 2 days after intramuscular
injection. The half-life is 20-35 days. Generally, immunoglobulins
should not be given shortly before or after active immunization to
avoid inhibiting the immune response; tetanus and hepatitis B
immunization are exceptions to this rule (130).
The advantages of immunoglobulins are : (a) freedom from
hepatitis B, (b) concentration of the antibodies into a small volume
for intramuscular use, and (c) stable antibody content, if properly
stored.
Adverse reactions to immunoglobulin can be local or systemic.
Local reactions (e.g., pain, sterile abscesses) are relatively
common when large volumes are injected intramuscularly.
Systemic reactions can be rapid or late. Rapid reactions occur
during or within minutes of administration, and are anaphylactic in
type (flushing, flank pain, rigor, dyspnoea, and signs of shock).
Late reactions may occur within hours or days, are usually less
severe, and may include urticaria, arthralgia, pyrexia or diarrhoea.
Systemic reactions are less common occurring once in every 5001000 injections. They are more common with intravenous
administration. Systemic reactions can be prevented by giving
hydrocortisone before the injection (130).
The uses of immunoglobulin are listed in Table 32. Use is
recommended.only where the efficacy has been proved; where
efficacy has not been established conclusively, use is listed as
optional. The target populations listed in the table have been welldefined in controlled studies, and use should be limited to these
individuals (130).
TABLE 32
Appropriate uses for human immunoglobulin in the prevention and treatment of disease
I Aoent/
Target population
Preparationab
Dosec
Status
[ Condition___________________________________________________________________________________________________________________
Hepatitis A
Recommended
for prevention
IG
Optional for
Prevention
Percutaneous or mucosal
exposure
HBIG
Recommended for
prevention
HBIG
Recommended for
prevention
HBIG
Optional for
prevention
Rubella
IG
20 ml
Optional for
prevention
Varicella-zoster
Immuno-suppressed contacts
of acute cases or
newborn contacts
VZIGd
Recommended for
prevention
IG
Recommended for
prevention
RIG
Recommended for
prevention
TIG
Recommended
for prevention
or treatment
RhIG
Recommended for
prevention
Hepatitis
non-A, non-B
Hepatitis B
Measles (rubeola)
Rabies
Tetanus
Rh isoimmunization
Family contacts
Institutional outbreaks
Travellers exposed to
unhygienic conditions in
tropical or developing
countries
Percutaneous or mucosal
exposure
IG
IG
IG = immune globulin (human); HBIG = hepatitis B immune globulin; VZIG = varicella-zoster immune globulin;
RIG = rabies immune globulin; TIG = tetanus immune globulin; RhIG = rhesus factor immune globulin, b
Hyperimmune
immunoglobulins have also been used in prophylaxis of mumps and prophylaxis and treatment of pertussis and
diphtheria; there are no conclusive data available, and no recommendations can be given, c
Dose
based on intramuscular administration of 16.5% solution d
Of limited availability at the present time.
Antisera or antitoxins
\/^^The Cold Chain
The term antiserum is applied to materials prepared i/pj VJ_ne "cold cnain" is a system of storage and transport of animals. Originally passive immunization
was achieved by the^V-Kcines at low temperature from the manufacturer to the actual administration of antisera or antitoxins prepared from nonvaccination site. The cold chain system is necessary because human sources such as horses. Since human immunoglobulin vac,cine failure mav occur due J fa[lure tostdre
and
transport preparations exist only for a small number of diseases,
"ndefr stnct temperature controls. This is of concern in view of
..
_r
_
/ - . . i .
the fairly frequent reports of vaccine-preventable disease
antitoxins
prepared
from
non-human
sources
(agamst
tetanus,
^ccurrence
populations
thought
to
have
been
well
diphtheria, botulism, gas gangrene and snake bite) are still the^mmunize(WLong the vaccines, polio is the most sensitive to
mainstay of passive immunization. Administration of antisera^^heatj requiring storage at minus 20 degree C. Vaccines which
may occasionally give rise to serum sickness and anaphylactic, ^ust be stored in the freezer compartment are : polio and
shock due to abnormal sensitivity of the recipient. The current^ measles. Vaccines which must be stored in the COLD PART but
trend is in favour of using immunoglobulins wherever possible^ ?j never allowed to freeze are : typhoid, DPT, tetanus toxoid, DT,
v
The uses of antisera are listed in Table 33.
BCG and diluents? 132).
OK'%^'
V <2^
K
f^ _r_^
h\
HAZARDS OF IMMUNIZATION 99
TABLE 33
Passive immunization procedures with antisera
Disease
1.
Diphtheria
A dose of 500-1,000 of i.u. of diphtheria antitoxin is given intramuscularly to susceptible contacts immediately
after exposure. Protection does not last more than 2-3 weeks.
2.
Tetanus
The usual prophylactic dose is 1,500 units of horse A.T.S. given subcutaneously or intramuscularly, soon after
injury.
3.
Gas gangrene
A polyvalent antitoxin is used. A patient who has sustained a wound possibly contaminated with spores of gas
gangrene should receive a dose of 10,000 i.u. of CI. perfr'mgens. (CI. welchii) antitoxin, 5,000 units of CI.
septicum antitoxin and 10,000 units of CI. oedematiens antitoxin, intramuscularly, or in urgent cases
intravenously.
4.
Rabies
Antirabies serum in a dose of 40 i.u. per kg. of body weight should be given intramuscularly within 72 hours
and preferably within 24 hours of exposure. A part of the antiserum is applied locally to the wound.
5.
Botulism
When botulism is suspected, 10,000 units of polyvalent antitoxin is recommended every 3 to 4 hours.
Duration of isolation
Chickenpox
1.
Disease
Cholera
2.
Plague
3.
Typhoid fever
4.
Influenza
5.
Yellow fever
TABLE 35
Active Immunization Recommended under Special Circumstances
Immunization
Given subcutaneously in 2 equal doses of 0.5 ml. at an interval of 4 to 6 weeks.
During mass immunization campaigns, a single dose of of 1.0 ml is given. Immunity develops 6 days
after inoculation. Booster doses are recommended every 6 month.
Given subcutaneously or intramuscularly in 2 doses at an interval of 7 to 14 days. Immunity starts 5
to 7 days after inoculation and lasts for about 6 months.
For adults, 2 doses each of 0.5 ml typhoid vaccine are given subcutaneously at an interval of 4-6
weeks. Immunity develops 10 to 21 days after immunization. Persons at risk require a booster dose of 0.5
ml every year.
Inactivated vaccines are widely used. Two adequately spaced doses (1.0 ml each) of an aqueous or
saline vaccine are recommended for primary immunization, although one dose may be given when an
epidemic is threatened. The immunity lasts for about 3 to 6 months. Oil-adjuvanted vaccines give
immunity of longer duration, but they tend to produce unpleasant local reaction.
The dose of the vaccine (17 D vaccine) is 0.5 ml given subcutaneously. Immunity begins 10-12 days
after vaccination, and extends up to 10 years.
those individuals who have escaped vaccination or those who have not
developed satisfactory protection. It is well to bear in mind that
immunizations are not all 100 per cent effective, particularly when an
individual is exposed to a large dose of pathogenic organisms.
Immunization has to be planned according to the needs of the
situation. Every country has its own immunization schedule, so does each
medical society and each paediatric society, adding to confusion. Thus
there is an infinite number of immunization schedules, each having its
merits and demerits. If each vaccine were to be given separately, a
minimum of at least 14 visits would be needed to the immunization clinic.
The current trend is to combine immunizing agents into small packages
and thus reduce the number of injections an individual must receive.
A well thought-out immunization schedule must be
(a)epidemiological^ relevant, that is, vaccinations should be included only
against diseases which are public health problems and against which
an effective vaccine exists
(b)immunologically effective : children must be vaccinated at an age when
they can benefit from it, i.e., when they are capable of forming defences
and when they have lost the antibodies transmitted by the mother. Above
all, children must be vaccinated at the right time, that is before they are
exposed to possible infection. An immunization may not be effective if
given within too short an interval between subsequent doses
(c)operationally feasible : this includes cost and ability to achieve a high
percentage of coverage which is a key factor in an effective immunization
programme. The schedule must minimise the number of visits, by
simultaneous administration of vaccines, and (d) socially acceptable : the
schedule must take into account the local customs, beliefs and practices,
seasonal and climatic factors and daily work pattern of the community.
One important factor is to reduce long waiting time for patients whose
sole purpose in visiting the clinic was to be immunized.
A comprehensive list of vaccinations is given in annex 1
Universal Immunization Programme
In May 1974, the WHO officially launched a global immunization
programme, known as Expanded Programme on Immunization (EPI) to
protect all children of the world against six vaccine-preventable diseases,
namely - diphtheria, whooping cough, tetanus, polio, tuberculosis and
measles by the year 2000. EPI was launched in India in January 1978
(144).
The Programme is now called Universal Child Immunization, 1990that's the name given to a declaration sponsored by UNICEF as part of the
United Nations' 40th anniversary in October 1985. It is aimed at adding
impetus to the global programme of EPI.
VrA V
(TABLE 36^)
\Lrl t /$
/f^National InTmunizatiorfSchedule
KzJ*/
%T
i* H
Vaccine
Birth
6 weeks
10 weeks
14 weeks
9 months
Chemoprophylaxis
Cholera
Conjunctivitis,
bacterial
Diphtheria
Influenza
Malaria
Meningitis,
meningococcal
Plague
.,i.
^^^Gh^pie^S (>k>Js*lU*Y\
Sulphadiazine for 4 days only
if the strain is shown to be nonresistant, for household and close
community contacts; immunization
should be initiated in all cases
(against serogroups A and C).
Tetracycline for contacts of
pneumonic plague.
Types of disinfection
(a) Concurrent disinfection : It is the application of
disinfective measures as soon as possible after the discharge of
infectious material from the body of an infected person, or after the
soiling of articles with such infectious discharges (2). In other
words, the disease agent is destroyed as soon as it is released from
the body, and in this way further spread of the agent is stopped.
Concurrent disinfection consists of usually disinfection of urine,
faeces, vomit, contaminated linen, clothes, hands, dressings,
aprons, gloves, etc throughout the course of an illness (b)
Terminal disinfection : It is the application of disinfective
measures after the patient has been removed by death or to a
hospital or has ceased to be a source of infection or after other
hospital isolation practices have been discontinued (9, 100).
Terminal disinfection is now scarcely practised; terminal cleaning
is considered adequate, along with airing and sunning of rooms,
furniture and bedding (9, 100). (c) Precurrent (prophylactic)
disinfection : Disinfection of water by chlorine, pasteurization of
milk and handwashing may be cited as examples of precurrent
disinfection.
Natural Agents
(1) Sunlight: Direct and continuous exposure to sunlight is
destructive to many disease-producing organisms. The ultraviolet
rays of sunlight (these do not penetrate through glass) are
particularly lethal to bacteria and some viruses. Articles such as
linen, bedding, and furniture may be disinfected by exposure to
direct sunlight for several hours (2) Air : Exposure to open air
(airing) acts by drying or evaporation of moisture which is lethal
to most bacteria. In general, natural agents such as sunlight and air,
because of their vagaries, cannot be totally depended upon for
disinfection.
Physical Agents
(1) Burning : Burning or incineration is an excellent method of
disinfection. Inexpensive articles such as contaminated dressings,
rags and swabs can be disposed off by burning. Addition of
sawdust, paper, kerosene or other combustible material aid in
burning. Faeces can be disposed off by burning. Burning should
not be done in open air; it is best done in an incinerator. (2) Hot
air : Hot air is very useful for sterilizing articles such as glassware,
syringes, swabs, dressings, french chalk, oils, vaseline and sharp
instruments. The drawback of hot air is that it has no penetrating
power, and is therefore not suitable for disinfection of bulky
articles such as mattresses. Hot air sterilization is usually done in a
hot air oven. The temperature of the air in the oven should be
maintained at 160-180 deg C for at least one hour to kill spores.
Unfortunately, such elevated temperatures destroy plastic, rubber
and other delicate substances. (3) Boiling : Boiling is an effective
method of disinfection. It provides an atmosphere of boiling and
steam. Boiling for 5-10 minutes (rolling boil) will kill bacteria, but
not spores or viruses. Boilers provide temperature well above 90
deg C in an atmosphere of steam, which is exposed to open air. To
ensure destruction of spores, temperatures above 100 deg C would
be required which cannot be achieved in boilers. Boiling is
suitable for disinfection of small instruments, tools which are not
used for subcutaneous insertion, linen and rubber goods such as
gloves. Linen stained with faeces, pus or blood should be first
washed in cold water (preferably with a disinfectant such as 2V 2
per cent cresol) and then subjected to boiling, with frequent
stirring because linen and clothes are poor conductors of heat.
Addition of 1 per cent soap and 0.3 per cent of washing soda
enhances the effect of boiling. Boiling for about 30 minutes is
adequate to disinfect linen, utensils and bedpans. The
DISINFECTION 10'
Bleaching powder
Crude phenol
Cresol
Formalin
Per cent
50 g 100
ml 50 ml
100 ml
5 10
5 10
2. Sputum :
This is best received in gauze or paper handkerchiefs and
destroyed by burning. If the amount is considerable (as in TB
hospitals), it may be disinfected by boiling or autoclaving for 20
minutes at 20 lbs pressure. Alternatively, the patient may be asked
to spit in a sputum cup half filled with 5 per cent cresol. When the
cup is full, it is allowed to stand for an hour and the contents may
be emptied and disposed off.
3. Room :
Usually thorough cleaning, airing and exposure to direct
sunlight, when possible, for several hours will be sufficient. If
necessary, floors and hard surfaces in the room should be
prohibited for 48 hours (161). For chemical disinfection, floors and
hard surfaces should be sprayed or mopped with one of the
following disinfectants : chlorine preparations such as chlorinated
lime in concentrations that leave 25 ppm or more of free chlorine;
formaldehyde solution at a concentration of 1 per cent or more;
phenolic disinfectants such as 2V2 per cent cresol. The solution
should remain in contact with the surface for at least 4 hours before
final washing (161).
On rare occasions, when fumigation is required, the gas most
commonly used is formaldehyde. It may be generated by boiling
commercial formalin in 2 volumes of water (500 ml of formalin
plus 1 litre of water per 30 c. metres of space) in a stainless steel
vessel, over an electric hot plate or by adding potassium
permanganate to commercial formalin in large jars (170-200 g to
500 ml of formalin plus 1 litre of water per 30 c. metres) (161).
There is vigorous boiling and liberation of formaldehyde gas. The
room is kept closed for 6-12 hours to allow disinfection.
Formaldehyde disinfection is most effective at a high temperature
and a relative humidity of 80-90 per cent (151).
INVESTIGATION OF AN EPIDEMIC
The occurrence of an epidemic always signals some significant
shift in the existing balance between the agent, host and
environment. It calls for a prompt and thorough investigation of
the cases to uncover the factor (s) responsible and to guide in
advocating control measures to prevent further spread.
Emergencies caused by epidemics remain one of the most
important challenges to national health administrations.
Epidemiology has an important role to play in the investigation of
epidemics. The objectives of an epidemic investigation are
(3,21,162).
a. to define the magnitude of the epidemic outbreak or
involvement in terms of time, place and person.
b. to determine the particular conditions and factors
TABLE 40
Information to be included in the final report on an epidemic
Section
Contents
1. Background
Geographical location
Climatic conditions
Demographic status (population pyramid)
Socioeconomic situation
Organization of health services
Surveillance and early warning systems
Normal disease prevalence
2. Historical data
Previous occurrence of epidemics
-of the same disease,
-locally or elsewhere Occurrence of
related diseases, if any
-in the same area
-in other areas
Discovery of the first cases of the present outbreak
3. Methodology of investigations
Case definition
Questionnaire used in epidemiological
investigation
Survey teams
Household survey
Retrospective survey
Prospective surveillance
Collection of laboratory specimens
Laboratory techniques
4. Analysis of data
Clinical data:
-frequency of signs and symptoms
-course of disease
-differential diagnosis
-death or sequelae rates
Epidemiological data :
-mode of occurrence
-in time
-by place
-by population groups
Modes of transmission :
-source(s) of infection
-route(s) of excretion and portal(s) of entry
- factors influencing transmission
Laboratory data:
-isolation of agent(s)
-serological confirmation
-significance of results
Interpretation of data:
-comprehensive picture of the outbreak
-hypotheses as to cause(s)
-formulation and testing of hypotheses by statistical
analysis
5. Control measures
Definition of strategies and
methodology of implementation
- constraints
-results
Evaluation
:
-significance of results
-cost/effectiveness
Preventive measures
It may be necessary to implement temporary control measures at the
commencement of an epidemic on the basis of known facts of the disease.
These measures may be modified or replaced in the light of new
knowledge acquired by the epidemic investigation. As Frost (163)
observed, an epidemiological investigation is more than the collection of
established facts. It includes their orderly arrangement into chains of
inference, which extend more or less beyond the bounds of direct
observation.
British
Aplastic anaemia in
patients irradiated for ankylosing spondylitis, MRC Spl Res.Ser.No.295, London,
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23.Medical Research Council (1951), Brit. Med. J., 2:1463-71
24.WHO cooperative Trial on Primary Prevention of IHD (1980) Lancet, 2:379.
25.Rose, G. and RJ.S. Hamilton (1978). J. Epi and Community Health, 32:275-81.
26.Terry, T.L. (1942). Am. J. Ophthalmology, 25:203-204; 1409-1423
27.Kinsey, V.E. and F.M. Hemphill (1955). Am. J. Oph, 56:481.
28.Kinsey, V.E. {1956). Archives of Oph, 56,481-543.
29.South-East London Screening Study Group (1911). Inj. J. Epi., 6 (4) 357-63
30.Bennet, A.E. (1978). Recent Advances in Community Medicine, Churchill
Livingstone.
31.Sackett, D.L. et al (1974). Ann. Int. Med., 80 : 137.
32.Trichopoulos, D. etal (1983). Lancet, 1:441-443.
33.Moses, L.E. et al (1984). Annual Rev. P. H., 5:267-92
34.Yudkin, J.Roddy, J. (1964). Lancet, 2:6.
35.Bennet, A.E. etal (1970).Lancet, 1:1012.
36.US Public Health Service (1964). Smoking and Health, PH. Service Pub; No.
1103 Washington, US Govt. Printing Press.
Press.
Brown.
41.White, K.L. (1978). In : Basic Health Care in Developing Countries, An
Epidemiological perspective, Basil S. Hetzel (ed). IEA/WHO Handbook, Oxford
Med. Publications.
42.Mckeown, T and C.R. Lowe (1974). An Introduction to Social Medicine, 2nd
ed., Blackwell.
43.WHO (1980). Early Detection of Handicap in Children, EURO Rep and
Studies, 30 Reg.Office WHO, Copenhagen.
44.Melby. J.C (1975). JAMA, 231 : 399.
1.Finnerty, FA. (1975). JAMA, 231 : 402.
2.WHO (1972). WHO Chr., 26 (1)7-11.
3.Letters to the Eidtor (1980). Lancet, 2:1200
4.Benenson, A.S. ed (1981). Control of Communicable Diseases in Man, 13th ed.
American PH. Association, New York.
5.Council for International Organizations of Medical Sciences (1973).
Communicable Diseases, Provisional International Nomenclature, CIOMS/WHO,
Geneva.
6.WHO (1982). Techn. Rep. Ser., No.682.
7.Nelson, G. (1960). Trans. Roy. Soc. Trap. Med. Hyg., 54 : 301.
8.Last, J.M. (1985). World Health Forum, 6(2)135.
(ed), Oxford.
5.Last, J.M. (1980). Maxcy-Rosenau Public Health and Preventive
Medicine, 11th ed., Appletion-Century-Crofts.
6.Pelczar Jr M.J. et al (1977). Microbiology, Tata McGraw Hill, New
Delhi, p.669.
7.Brachman, PS. (1984). In : Oxford Textbook of Public Health, Vol II.
8.Waterson, A.P. (1979). Brit. Med. J., 2:564.
9.Dudgeon, J.A. (1976). Brit. Med. Bull, 32:77-85.
10.WHO (1978). Techn. Rep. Ser., No.626.
11.Fudenberg, H.H. et al (1976). Basic and Clinical Immunology, Los
Altos, Ca, Lange
12.Gell, P.G.H. et al (1975). Clinical Aspects of Immunology, 3rd ed.,
Blackwell, Oxford.
13.Mims, C.A. (1977). The Pathogenesis of Infectious Disease, London,
Academic Press.
14.Youmans, G.P. et al (1980). The Biological and Clinical Basis of
Infectious Diseases, 2nd ed., Saunders.
15.Turk, J.L. (1975). In : Clinical Aspects of Immunology, RG.H. Cell et al
(eds), 3rd ed., Blackwell, Oxford
16.McConnel, I. et al (1981). The Immune System, a Course on the
moleculer and cellular basis of immunity, 2nd ed. Oxford, Blackwell.
- 121. WHO (1976). Public Health Papers, No.62
1.Critchley, M. (ed) (1978). Butterworth Medical Dictionary, 2nd ed.
London, Butterworths, p.870.
2.Illustrated Stedman's Medical Dictionary (1982). 24th ed. Baltimore,
Williams & Wilkins, p.694.
3.Lancet (1984). 1:226-227.
4.Galazka, A.M. etal (1984). World Health Forum, 5 (3).
5.Galazka A.M. et al (1984). Bull WHO, 62:357
6.WHO U976). Techn. Rep. Ser., No.595.
7.WHO (1983). Bull WHO, 61 (1) Directions to Contributors toBulletin.
8.Rowe, D.S. (1975). In: Clinical Aspects of Immunology, P.G.H. Gellet al
(eds), 3rd ed., Blackwell, Oxford.
9.WHO (1982). Bull WHO, 60 (1) 43-47.
10.WHO (1978) Techn. Rep. Ser. No. 630.
11.PAHO (1981). BullPAHO, 15 (2) 179.
12.MBA & the Pharmaceutical Society of Great Britain (1983). British
National Formulary, No.6.
13.WHO (1984). Health for AH, Sr.No.9.
14.WHO (1978). Health for All, Sr.No.l, pp 24-25.
15.Bagshawe, K.D. et al (1978). Brit.Med.J., 2:879-881
16.WHO (1978). WHO Chronicle, 32:439-447.
17.Clark Duncan, W and B. MacMahon (1981). Preventive and
Community Medicine, 2nd ed., Boston, Little Brown & Co.
"Health should mean a lot more than escape from death or, for that matter, escape from disease."
Iceberg phenomenon of disease
Epidemiologist and others who study disease find that the
pattern of disease in hospitals is quite different from that in a
community. That is, a far larger proportion of disease (e.g.,
diabetes, hypertension) is hidden from view in the community
than is evident to physicians or to the general public. The analogy
of an iceberg, only the tip of which is seen, is widely used to
describe disease in the community.
The concept of the "iceberg phenomenon of disease" (page 33)
gives a better idea of the progress of a disease from its subclinical
stages to overt or apparent disease than the familiar spectrum of
disease. The submerged portion of the iceberg represents the
hidden mass of disease (e.g., subclinical cases, carriers,
undiagnosed cases). The floating tip represents what the physician
sees in his practice. The hidden part of the iceberg thus constitutes
the mass of unrecognized disease in the community, and its
detection and control is a challenge to modern techniques in
preventive medicine.
Concept of screening
The active search for disease among apparently healthy people
is a fundamental aspect of prevention. This is embodied in
screening, which has been defined as "the search for unrecognized
disease or defect by means of rapidly applied tests, examinations
or other procedures in apparently healthy individuals." \
Historically the annual health examinations were meant for the
early detection of "hidden" disease. To bring such examinations
within the reach of large masses of people with minimal
expenditures of time and money, a number of alternative
approaches have come into use. They are based primarily on
conserving the physician-time for diagnosis and treatment and
having technicians to administer simple, inexpensive laboratory
tests and operate other measuring devices. This is the genesis of
screening programmes. The original screening programmes were
for individual diseases such as tuberculosis, syphilis or selected
groups such as antenatal mothers, school children and
occupational groups. Over the years, the screening tests have
steadily grown in number (Table 8). Today screening is considered
a preventive care function, and some consider it a logical
extension of health care.
Screening differs from periodic health examinations in
the following respects (1):
*\
1)capable of wide application
vf.
2)relatively inexpensive, and
3)requires little physician-time. In fact the physician is not required
to administer the test, but only to interpret it.
Diagnostic test
2 Applied to groups
Based on evaluation of a or
number of symptoms, signs
and laboratory findings
2Less accurate
More accurate
3Less expensive
More expensive
Source (2)
However, the criteria in Table 1 are not hard and fast. There are
some tests which are used both for screening and diagnosis, e.g.,
test for anaemia and glucose tolerance test. Screening and
diagnosis are not competing, and different criteria apply to each.
Concept of "lead time"
Fig. 1 shows the possible outcomes for a given disease process
.{There is nothing to be gained in screening for diseases whose
oftset is quite obvious. Detection programmes should be restricted
to those conditions in which there is considerable time lag between
disease onset and the usual time of diagnosisjln this period, there
are usually a number of critical points which determine both the
severity of the disease and the success of any treatment in
reversing the disease process. There is clearly little value in
detecting disease in advance of
First
possible
point
Final
critical
diagnosis
Usual
time of
diagnosis
i
"~~~~1
Screening time
OUTC
----- B
OA
Lead time
FIG.l Model for early
detection programmes
"Lead time" is the advantage gained by screening, i.e., the
period between diagnosis by early detection and diagnosis by other
means. In Fig.l, A is the usual outcome of the disease, and B is the
outcome to be expected when the disease is detected at the earliest
possible moment. The benefits of the programme are therefore BA. The benefits of the programme must be seen in terms of its
outcomes. It is also necessary for the complexities and costs of any
detection programme to be viewed against the benefits accruing
therefrom (3).
Aims and objectives
/ The basic purpose of screening is to sort out from a large group of
apparently healthy persons those likely to have the disease or at
increased risk of the disease under study, to bring those who are
"apparently abnormal" under medical supervision and treatment
(Fig.2). Screening is carried out in the hope that earlier diagnosis
and subsequent treatment favourably alters the natural history of
the disease in a significant proportion of those who are identified
as "positive" (4).
Apparently Healthy
(Screening Tests)
Apparently Normal
(Periodic rescreening)
1
Apparently Abnormal
(a) Normal - Periodic
rescreening
(b) Intermediate
-Surveillance
(c) Abnormal
-Treatment
. - '.'
Disease
The disease to be screened should fulfil the following criteria
before it is considered suitable for screening:
1.the condition sought should be an important health problem
(in general, prevalence should be high);
2.there should be a recognizable latent or early asymptomatic
stage;
3.the natural history of the condition, including development
from latent to declared disease, should be adequately understood
(so that we can know at what stage the process ceases to be
reversible);
4.there is a test that can detect the disease prior to the onset of
signs and symptoms;
5.facilities should be available for confirmation of the diagnosis;
6.there is an effective treatment.
7.there should be an agreed-on policy concerning whom to treat
as patients (e.g., lower ranges of blood pressure; border-line
diabetes);
8.there is good evidence that early detection and treatment
reduces morbidity and mortality;
9.the expected benefits (e.g., the number of lives saved) of early
detection exceed the risks and costs.
When the above criteria are satisfied, then only, it would be
appropriate to consider a suitable screening test.
Screening test
The test must satisfy the criteria of acceptability, repeatability
and validity, besides others such as yield, simplicity, safety,
rapidity, ease of administration and cost. Tests most likely to fulfil
one condition may however, be least likely to fulfil another - for
example, tests with greater accuracy may be more expensive and
time consuming. The choice of the test must therefore often be
based on compromise.
1. Acceptability
Since a high rate of cooperation is necessary, it is important that
the test should be acceptable to the people at whom it is aimed. In
general, tests that are painful, discomforting or embarrassing (e.g.,
rectal or vaginal examinations) are not likely to be acceptable to
the population in mass campaigns.
2. Repeatability
An attribute of an ideal screening test or any measurement (e.g.,
height, weight) is its repeatability (sometimes called reliability,
precision or reproducibility). That is, the test must give consistent
results when repeated more than once on the same individual or
material, under the same conditions. The repeatability of the test
depends upon three major factors, namely observer variation,
biological (or subject) variation and errors relating to technical
methods. For example, the measurement of blood pressure is
poorly reproducible because it is subjected to all these three major
factors.
A Observer variation
All observations are subjected to variation (or error). These
may be of two types:
ar-Intra-observer variation:
If a single observer takes two measurements (e.g., blood
No. of films
13,560
877
168
66
42
28
23
39
64
14,867
Per cent
91.21
5.90
1.13
.44
.28
.19
\
.16
.26
.43
100.00
Source (16)
The results shown in Table 2 are sobering and instructive. There
was concurrence of all 8 readers that 91.21 per cent of the films
had one or more positive readings.
Observational errors are common in the interpretation of Xrays, ECG tracings, readings of blood pressure and studies of
histopathological specimens. Observer errors can be minimised by
(a) standardization of procedures for obtaining measurements and
classifications (b) intensive training of all the observers (c) making
use of two or more observers for independent assessment, etc. It is
probable that these errors can never be eliminated absolutely.
B Biological (subject) variation
There is a biological variability associated with many
physiological variables such as blood pressure, blood sugar, serum
cholesterol, etc. The fluctuation in the variate measured in the same
individual may be due to (a) Changes in the parameters observed:
This is a frequent phenomena in clinical presentation. For example,
cervical smears taken from the same woman may be normal one day,
and abnormal on another day. Myocardial infarction may occur
without pain. Subject variation of blood pressure is a common
phenomenon, (b) Variations in the way patients perceive their
symptoms and answer: This is a common subject variation. There
may be errors in recollection of past events when a questionnaire is
administered. When the subject is aware that he is being probed, he
may not give correct replies. In short, subject variation can be a
potential source of error in epidemiological studies, (c) Regression
to the mean: An important example of N biological variability is
regression to the mean. There is a tendency for values at the
extremes of a distribution, either very high or low, to regress toward
the mean or average on repeat measurement. Many features of
disease states vary-,? considerably over time, for example, the pain
of rheumatoid *
Diseased
Diagnosis
Not diseased
a(True positive)
cfFalse negative)
a+c
Total
b(False positive)
a+b + d
d(True negative)
c+d
b+d
a+b+c
TABLE 4
Diagnosis of brain tumours by EEG
EEG results
TABLE 3-B
Screening test result by diagnosis
Screening
test results
Positive
Negative
9840
(d)
9860
(b + d)
Positive
Negative
Total
60
(a+b)
54,000 4
306,000
360,000
40
9940 (c
+ d)
TABLE 5
Diagnosis of brain tumours by computer assisted axial tomography
10,000
(a + b + c + d)
CAT results
Brain
tumour
Absent
(a)Sensitivity
= (40/140) x 100 = 28.57%
A^p
Present
(true positive)
^s
Positive
18,000
39
Negative
(b)Specificity
= (9840/9860) x 100 = 99.79% ^3 (true
342,000
1
negative)
360,000
40
Sensitivity = 39/40 x 100 = 97.5 per cent Specificity =
(c)False negative = (100/140) x 100 = 71.4%
342,000/360,000 x 100 = 95 per cent
(d)False positive
= (20/9860) x 100 = 0.20%
(e)Predictive value = (40/60) x 100 = 66.66% of a
TABLE 6
positive test
Sensitivity and specificity of a 2-hour
(f)Predictive value = (9840/9940) x 100 = 98.9% of a
postprandial blood test for glucose for
negative test
\6*k
70 true diabetics and 510 true non-diabetics
at different levels of blood glucose
^Sensitivity J^<ft (g)
\^ \ ^V^J
The term sensitivity was introduced by Yerushalmy (17) in @ Blood glucose
Sensitivity
Specificity
1940s as a statistical index of diagnostic accuracyf It has beery
level (mg/100 ml)
defined as the ability of a test to identify correctly all those who
d 80
100.0
1.2
have the disease, that is "true positive". A 90 per cent sensitivity M aXJ
98.6
7.3
means that 90 per cent of the diseased people screened by the test
90
will give a "true positive" result and the remaining 10 per cent a . /
97.1
25.3
r) ioo
"false negative" result.
92.9
48.4
</ no
120
130
140
150
160
170
180
190
200
Source (18)
88.6
81.4
74.3
64.3
55.7
52.9
50.0
44.3
37.1
68.2
82.4
91.2
96.1
98.6
99.6
99.8
99.8
100.0
\ v y Jt<3 Predictive
accuracy Y*" v <_/
In addition to sensitivity and specificity, the performance of a
screening test is measured by its "predictive value" which reflects
the diagnostic power of the test/ The predictive accuracy depends
upon sensitivity, specificity and disease prevalence. The "predictive
value of a positive test" indicates 1 the probability that a patient with
a positive test result has, in fact, the disease in question. The more
prevalent a disease is in a given population, the more accurate will
be the predictive value of a positive screening test) The predictive
value of a positive result falls as disease prevalence declines.
Table 7 shows the predictive value of positive Gram-stained
cervical smear test to detect gonorrhoea at prevalences of 5,15 and
25 per cent. In this example, the predictive value of a positive test
was calculated to be 21, 47 and 63 per cent respectively. Thus in
female populations in which the gonorrhoea is low (5 per cent
prevalence), only 21 per cent of patients with positive results really
have gonorrhoea; the remaining 79 per cent have false-positive
results. Furthermore, as the sensitivity of this test is only 50 per
cent, half of the cases are not detected, which greatly reduces the
impact of the detection programme on disease transmission.
Smear
Total
Positive
predictive
value
Prevalence 15%
Culture
Total
+ 25
-25
95
855
120
880
50
950
1000
25
120
Culture
+
xif = 21%
Prevalence 25%
Total
Smear + 75
75
765
85 -
160
840
Total
850
1000
150
Positive
predictive -ry^ X = 47%
160
1 value
Culture
Total
Smear + 125
-125
75
800
200 675
Total
750
1000
Positive125
A- v
predictive
value
250
^QO
xM=63%
FIG. 3 Distribution of a
variable in a population
cancer, breast cancer) and early detection markedly improves
prognosis, a greater degree of sensitivity, even at the expense of
specificity, is desired. In these cases, subsequent diagnostic workup can be relied on to rule out the disease in the false-positives.
That is, a proportion of false-positives is tolerable but not falsenegatives. On the other hand, in a prevalent disease like diabetes
for which treatment does not markedly alter outcome, specificity
must be high and early cases may be missed, but false-positives
should be limited; otherwise the health system will be
overburdened with diagnostic demands on the positives, both true
and false. That is, high specificity is necessary when false-positive
errors must be avoided. A useful index in making this decision is
the predictive value of a positive test. This index measures the
percentage of positive results that are true positives; it is a function
of the sensitivity and specificity as well as the frequency of the
disease.
There are various other points which must also be taken into
account in screening. First, people v;ho participate in the screening
programme may not be those who have most to gain from it, as for
example, those at greatest risk of cancer of the cervix uteri are
least likely to attend for cervical cytology. Therefore screening
must be applied selectively to those people most likely to benefit.
Selection might be based on a person's age, sex, medical history,
occupation, family history or other factors. Secondly, tests with
greater accuracy may be more expensive and time-consuming, and
the choice of the test therefore often be based on compromise.
Thirdly, screening should not be developed in isolation; it should
be integrated into the existing health services. Lastly, the risks as
well as the expected benefits must be explained to the people to be
screened. These risks include any possible complications of the
examination procedures, and the possibility of false-positive and
false-negative test results.
Regardless of the approach taken to screening tests, regular
patient follow-up visits are important (not to leave the patients
high and dry) if effective health and medical care are to result
from the effort. Garfield (21) has stressed the need to meet
Infancy
LCB
Congenital dislocation of hip
Congenital heart disease
Spina bifida
Cerebral palsy
Hearing defects
Visual defects
Hypothyroidism
Developmental screening test
Haemoglobinopathies
Middle-aged men and women
Sickle cell anaemia
Hypertension
Undescended testis
Cancer
Elderly
Diabetes mellitus
Nutritional disorders
Serum cholesterol
Cancer
Obesity
Tuberculosis
Chronic bronchitis
Glaucoma
Cataract
Epidemiology of
Communicable Diseases
risk are those entering wildlife habitats, and those in contact with
pets or wild animals in urban environments. We have to know
more about this disease.
Certain unanswered questions
Finally, there still remain certain unanswered questions which
have been recently raised (14) :
a. Are there hitherto unknown animal reservoirs of
smallpox or smallpox-like viruses ?
b. Can another orthopoxvirus be transferred to smallpox
virus ?
c. Are we absolutely certain that laboratory infections
such as that which occurred in Birmingham, England
will not occur ?
d. Will animal poxviruses (e.g., monkeypox) eventually
replace the eradicated smallpox virus as widespread
pathogens ?
e. Lastly, could biological warfare with smallpox virus be
waged in the future ?
Providing definitive answers to all of the above questions is
impossible at this time. In this connection, however, it should be
kept in mind that vigilance is continuously .exercised by WHO in
regard to animal poxviruses. Moreover, as a protective measure
against some of the above possibilities, vaccine stocks and
bifurcated needles for vaccination of about 300 million people are
maintained indefinitely by WHO in Geneva, Toronto and New
Delhi (14).
References
1.WHO (1980). The Global Eradication of Smallpox, Final Report,
Geneva
2.WHO (1977). WHO Chronicle, 31:3
3.Basu, R.N. et al (1979). The Eradication of Smallpox from India, WHO,
SEARO, New Delhi
4.WHO (1981). Wkly Epid.Rec, 49:380
5.Arita, I and A. Gromyco (1982). Bull WHO, 60 (3) 367
6 WHO (2000), Weekly Epidemiological Record, No. 6, 11th Feb. 2000
1.WHO (1984). World Health, April 1984
2.Foege, W.H. (1979) N.Eng.J.Med., 300 : 670
3.WHO (1984). Bull WHO, 62(5)703
4.WHO (1984). WHO Chronicle, 38 (5) 227
5.WHO (1982). WHO Chronicle, 36 (3) 87 - 91
6.Benenson, A.S.ed (1980). Control of Communicable Diseases in Man,
13th ed., American Public Health Association, Washington.
7.WHO (1982). Techn. Rep. Ser.,No.682
8.Abbas, M.B. (1983). Microbiological Reviews, 47 (4) 1155
__________________________________________CHICKENPOX 123
(B) ERUPTIVE STAGE : In children the rash is often the first ign. It
comes on the day the fever starts. The distinctive eatures of the rash are :
high
QfJ |>!^>t?
TABLE 1 ^_ 95 @
1.
Incubation :
About 12 days
(range: 7-17 days)
About 15 days
(range 7-21 days)
2.
Environmental factors :
<'
Chickenpox shows a seasonal trend in India, the disease
occurring mostly during the first six months of the year.
Overcrowding favours its transmission. In temperate climates,
there is little evidence of any seasonal trend (3).
Prodromal symptoms:
Severe
Usually mild
3.
Incubation period
Usually 14 to 16 days, although extremes as wide as 7 to 21
days have been reported.*""!
Clinical features
The clinical spectrum of chickenpox may vary from a mild
illness with only a few scattered lesions to a severe febrile illness
with widespread rash. Inapparent infection is estimated to occur in
no more than 5 per cent of susceptible children (5). In the majority
of cases, the disease tends to be mild and typical (3). The clinical
course of chickenpox may be divided into two stages :
(A) PRE-ERUPTIVE STAGE : Onset is sudden with mild or
moderate fever, pain in the back, shivering and malaise. This stage
is very brief, lasting about 24 hours. In adults, the prodromal
illness is usually more severe and may last for 2-3 days before the
rash comes out (3).
shows
Smallpox
Transmission
Chickenpox is transmitted from person to person by droplet
infection and by droplet nuclei. Most patients are infected by
"face-to-face" (personal) contact. The portal of entry of the virus is
the respiratory tract. Since the virus is extremely labile, it is
unlikely that fomites play a significant role in its transmission (6).
Contact infection undoubtedly plays a role when an individual
with herpes zoster is an index case. The * virus can cross the
placental barrier and infect the foetus, a condition known as
congenital varicella.
but
4.
5.
Distribution of rash :
(a)deep-seated
(b)vesicles multilocular and
(a) superficial
(b) unilocular; dew-drop like
umbilicated
appearance
(c)only one stage of rash may
(c) rash pleomorphic, i.e.,
be seen at one time
different stages of the rash
evident at one given time,
because rash appears in
successive crops
(d) No area of inflammation is (d) an area of inflammation is
seen around the vesicles
seen around the vesicles
Evolution of rash :
(a) evolution of rash is slow,
(a) evolution of rash very rapid
deliberate and majestic,
passing through definite
stages of macule, papule,
vesicle and pustule
(b) scabs begin to form 10-14 (b) scabs begin to form 4-7
days after the rash appears
days after the rash appears
6.
Fever :
Fever subsides with the
Temperature rises with each
appearance of rash, but
fresh crop of rash
may rise again in the
pustular stage (secondary
rise of fever)
References
A>
and Control, Evans Alfred, S. et al (eds), 2nd ed., Plenum Medical, New
York
3.Christie, A.B. (1980). Infectious Diseases: Epidemiology and Clinical
Practice, 3rd ed., Churchil Livingstone.
4.Ross, A.H. (1962). NEJM267 : 369
5.Stephen, R Preblud and A.R. Hinman (1980), Maxcy-Rosenau : Public
Health and Preventive Medicine, Last, J.M. (ed), 11th ed, Appleton
-Century - Crofts.
6.Brunell, PA. (1979) Principles and Practice of Infectious Disease,
Mandell, G. etal (eds), John Wiley, New York.
7.Bres, P. (1986) Public Health Action in Emergencies caused by
Epidemics. Geneva, WHO
8.WHO (1985) Techn. Rep. Ser., No.725
9.WHO (1982) Bull WHO 60 (1)43-47
10.Wood, Martin J. (1988) Med Int 53 : 2167 (May) 1988
11.WHO (1983) WHO Tech.Rep. Ser. No. 693
12.Takashasi, M. et al (1979) Lancet, 2 : 1288
13.Brunell, PA. (1978). JAMA239: 1034
/Crtfl
\IVA5
-----------..---------- -----------p"^ig:----- ^^--------------- '-------------------------------
MEASLES!
UBUBEOL^JI
MEASLES 125
measles vaccine among infants to reduce measles morbidity and
mortality; (b) Outbreak prevention i.e. aggressive immunization
strategies have prevented forcasted measles outbreak; and (c)
Elimination i.e. reduction of incidence to zero as a result of
deliberate efforts requiring continued control measures (5).
WHO's measles elimination strategy comprises a three part
vaccination strategy, i.e., catch-up, keep-up and follow-up, two of
which are supplementary vaccinations. Catch-up is defined as a
one-time, nation wide vaccination campaign targeting usually all
children aged 9 months to 14 years regardless of history of measles
disease or vaccination status. Keep-up is defined as routine services
aimed at vaccinating more than 95 per cent of each successive birth
cohort. Follow-up is defined as subsequent nation wide vaccination
campaign conducted every 2-4 years targeting usually all children
born after the catch-up campaign (6). Supplementary vaccination
campaigns have been conducted in several countries targeting^
either measles elimination or morbidity and mortality reduction.
Although measles immunization is an effective strategy to
prevent cases, outbreaks can continue to occur, especially in
densely populated areas such as urban slums, even with good
coverage. This is because vaccine efficacy is only 85 per cent and
because there are pockets of poorly immunized children. As the
coverage increases, the time in between outbreaks increases, and a
shift towards older age group may be seen as in Thailand and Sri
Lanka (7). Brazil also had outbreak of measles in unvaccinated
adults during 1997.
The priorities of countries pursuing measles control include :
(1) improve routine vaccination coverage level to at least 90 per
cent; (2) active coverage of more than 90 per cent in catch-up and
follow-up campaigns or active coverage of more than 90 per cent
with routine second dose of measles vaccine; (3) establish casebased surveillance with laboratory confirmation of suspected cases
and virus isolation from all chains of transmission and (4) conduct
supplementary vaccination campaign together with administration
of vitamin A in high risk areas (6).
The WHO estimates of the mortality and burden of disease in
terms of disability-adjusted life years lost, by WHO Regions for
the year 2002 is as shown in Table 1.
TABLE 1
Estimated measles mortality and DALYs in
WHO Regions' 2002
...
WHO Region
Mortality
(000)
DALYs
(000)
Africa
311
10915
Americas
Eastern Mediterranian
Europe
Western Pacific
0
70
6
196
28
0
2479
198
6883
988
Total
611
21475
Source : (8)
In India, measles is a major cause of morbidity and a significant
contributor to childhood mortality. Prior to the immunization
programme, cyclical increase in the incidence of measles were
recorded every third year. With the increase in immunization
coverage levels, the intervals between cyclical peaks has increased
and the intensity of the peak minimized. However, several
outbreaks are reported in tribal and remote areas. The case fatality
rate in hospitalized cases of measles,
according to line list from 7 states during 1991 was 4 per cent with
a range of 1.8 to 7.6%. The retrospective data indicate a declining
trend of measles in the country. During 1987 about 2.47 lakh cases
were reported, whereas, after implementation of UIP, the number
of cases has come down to 51,700 during the year 2001 (9).
However, the estimates are much higher as large number of cases
go unreported.
Epidemiological determinants
0)A
Agent factors
i | \^-r
(a) AGENT : Measles is caused by an RNA paramyxovirus. So
far as is known, there is only one serotype. The virus cannot
survive outside the human body for any length of time!, bul retains
infectivity when stored at sub-zero temperature. The virus has been
grown in cejybcultures. (b) SOURCE OF ^INFECTIOI^The
only^ffuW^firhfection is a case of measles. Carriers are not known
to occurTjThere is some evidence tc Nsuggest that subclinical
measles occurs more often thar 'previously thought, (c)
INFECTIVE MATERIAL : Secretions o: the nose, throat and
respiratory tract of a case of measles during the prodromal period
and the early stages of the rash (d) COMMUNICABILITY :
Measles is highly infectious durinc the prodromal period and at the
time of eruption Communicability declines rapidly after the
appearance of th< rash (The period of communicability is
approximately 4 day: before and 5 days after the appearance of the
rasjplsolation o the patient for a week from the onset of rash m6re
than cover: the period of communicability (10). (e) SECONDARY
ATTACI RATE : There is only one antigenic type of measles virus
Infection confers life long immunity. Most so-called secondar;
attacks represent errors in diagnosis either in initial or secon<
illness (11).
Host factors
(a) AGE : Affects virtually everyone in infancy or childhooi
- between 6 months and 3 years of age in developing countrie
where environmental conditions are generally poor, and olde
children usually over 5 years in developed countries (12,
Following the use of measles vaccine, the disease is now see
in somewhat older age-groups (13). In 1980 children 10 year
old or more accounted for 50 per cent of cases in som
European countries (14). This highlights the importance c
periodic serological checking of the immunity status of th
susceptible population, (b) SEX
Incidence equa
(c) IMMUNITY : No age is immune if there was no previot
immunity. One attack of measles generally confers life-Ion
immunity. Second attacks are rare. Infants are protected b
maternal antibodies up to 6 months of age; in some, materni
immunity may persist beyond 9 months. Immunity aft<
vaccination is quite solid and long-lasting, (d) NUTRITION
Measles tends to be very severe in the malnourished chik
carrying a mortality upto 400 times higher than in well nourished
children having measles (15). This may possibly b related to poor
cell-mediated immunity response, secondary 1 malnutrition (16).
Additionally, severely malnourished childre have been shown to
excrete measles virus for longer perioc than better nourished
children indicating prolonged risk 1 themselves and of intensity
of spread to other (17). Even in healthy child, an attack of severe
measles may be followed t weight loss, precipitating the child
into malnutrition.
Environmental factors
Given a chance, the virus can spread in any season (11).
temperate climates, measles is a winter disease, probab because
people crowd together indoors. Epidemics of measl are common
in India during winter and early spring (Janua to April).
Population density and movement do affe epidemicity (18). In
general, the less favourable the prevailii
MEASLES 125
measles vaccine among infants to reduce measles morbidity and
mortality; (b) Outbreak prevention i.e. aggressive immunization
strategies have prevented forcasted measles outbreak; and (c)
Elimination i.e. reduction of incidence to zero as a result of
deliberate efforts requiring continued control measures (5).
WHO's measles elimination strategy comprises a three part
vaccination strategy, i.e., catch-up, keep-up and follow-up, two of
which are supplementary vaccinations. Catch-up is defined as a onetime, nation wide vaccination campaign targeting usually all
children aged 9 months to 14 years regardless of history of measles
disease or vaccination status. Keep-up is defined as routine services
aimed at vaccinating more than 95 per cent of each successive birth
cohort. Follow-up is defined as subsequent nation wide vaccination
campaign conducted every 2-4 years targeting usually all children
born after the catch-up campaign (6). Supplementary vaccination ,
campaigns have been conducted in several countries targeting^,
either measles elimination or morbidity and mortality reduction.
Although measles immunization is an effective strategy to
prevent cases, outbreaks can continue to occur, especially in
densely populated areas such as urban slums, even with good
coverage. This is because vaccine efficacy is only 85 per cent and
because there are pockets of poorly immunized children. As the
coverage increases, the time in between outbreaks increases, and a
shift towards older age group may be seen as in Thailand and Sri
Lanka (7). Brazil also had outbreak of measles in unvaccinated
adults during 1997.
The priorities of countries pursuing measles control include :
(1) improve routine vaccination coverage level to at least 90 per
cent; (2) active coverage of more than 90 per cent in catch-up and
follow-up campaigns or active coverage of more than 90 per cent
with routine second dose of measles vaccine; (3) establish casebased surveillance with laboratory confirmation of suspected cases
and virus isolation from all chains of transmission and (4) conduct
supplementary vaccination campaign together with administration
of vitamin A in high risk areas (6).
The WHO estimates of the mortality and burden of disease in
terms of disability-adjusted life years lost, by WHO Regions for
the year 2002 is as shown in Table 1.
TABLE 1
Estimated measles mortality and DALYs in
WHO Regions' 2002
WHO Region
Mortality
(000)
DALYs
(000)
Africa
311
10915
Americas
Eastern Mediterranian
Europe
South-East Asia
Western Pacific
Total
0
70
6
196
28
611
0
2479
198
6883
988
21475
Source : (8)
In India, measles is a major cause of morbidity and a significant
contributor to childhood mortality. Prior to the immunization
programme, cyclical increase in the incidence of measles were
recorded every third year. With the increase in immunization
coverage levels, the intervals between cyclical peaks has increased
and the intensity of the peak minimized. However, several
outbreaks are reported in tribal and remote areas. The case fatality
rate in hospitalized cases of measles,
according to line list from 7 states during 1991 was 4 per cent with
a range of 1.8 to 7.6%. The retrospective data indicate a declining
trend of measles in the country. During 1987 about 2.47 lakh cases
were reported, whereas, after implementation of UIP, the number
of cases has come down to 51,700 during the year 2001 (9).
However, the estimates are much higher as large number of cases
go unreported.
Epidemiological determinants
0) A
Agent factors
I \
*^V
(a) AGENT : Measles is caused by an RNA paramyxovirus. So
far as is known, there is only one serotype. The virus cannot
survive outside the human body for any length of time, bul retains
infectivity when stored at sub-zero temperature. The virus has been
grown in ceifevcultures. (b) SOURCE OF ^INFECTION|*The
onlyWiir^dOhfection is a case of measles. Carriers are not known
to occuTTThere is some evidence tc jsuggest that subclinical
measles occurs more often thar ^previously thought, (c)
INFECTIVE MATERIAL : Secretions o; the nose, throat and
respiratory tract of a case of measles during the prodromal period
and the early stages of the rash (d) COMMUNICABILITY :
Measles is highly infectious durinc the prodromal period and at the
time of eruption Communicability declines rapidly after the
appearance of th< rashHThe period of communicability is
approximately 4 day: before and 5 days after the appearance of the
raslpIsolation o the patient for a week from the onset of rash m6re
than cover: the period of communicability (10). (e) SECONDARY
ATTACI RATE : There is only one antigenic type of measles virus
Infection confers life long immunity. Most so-called secondan
attacks represent errors in diagnosis either in initial or seconc
illness (11).
Host factors
(a) AGE : Affects virtually everyone in infancy or childhooi between 6 months and 3 years of age in developing countrie
where environmental conditions are generally poor, and olde
children usually over 5 years in developed countries (12,
Following the use of measles vaccine, the disease is now see in
somewhat older age-groups (13). In 1980 children 10 yeai old or
more accounted for 50 per cent of cases in som European
countries (14). This highlights the importance c periodic
serological checking of the immunity status of th susceptible
population, (b) SEX : Incidence equa (c) IMMUNITY : No age is
immune if there was no previoi. immunity. One attack of measles
generally confers life-Ion immunity. Second attacks are rare.
Infants are protected b maternal antibodies up to 6 months of age;
in some, materni immunity may persist beyond 9 months.
Immunity aft< vaccination is quite solid and long-lasting, (d)
NUTRITION Measles tends to be very severe in the
malnourished chile carrying a mortality upto 400 times higher
than in well nourished children having measles (15). This may
possibly b related to poor cell-mediated immunity response,
secondary i malnutrition (16). Additionally, severely
malnourished childre have been shown to excrete measles virus
for longer perioc than better nourished children indicating
prolonged risk 1 themselves and of intensity of spread to other
(17). Even in healthy child, an attack of severe measles may be
followed I weight loss, precipitating the child into malnutrition.
Environmental factors
Given a chance, the virus can spread in any season (11).
temperate climates, measles is a winter disease, probab because
people crowd together indoors. Epidemics of measl are common
in India during winter and early spring (Janua to April).
Population density and movement do affe epidemicity (18). In
general, the less favourable the prevailii
____________________________MEASLES 127
immunization (26). This recommendation has been adopted in
India. But experts opine that this should not prevent health
workers from administering measles vaccine to 6-8 month-old
malnourished children who are at high risk of complications from
natural measles and who may not return at 9 months of age (27). If
these children do return, they should receive a second dose of
measles vaccine as soon as possible after 9 months of age.
The poorer sero-conversion rate can be circumvented by giving
the first dose at age 8-9 months, and the second a year later (28). In
fact, several countries (Czechoslovakia, the USSR, Sweden)
currently administer a second dose of measles vaccine as a routine
(14). Recent observations have suggested that the/HDCEdmonston-Zagreb strain vaccine may protect I children trom 4 to
6 months of age) This would be a boon to all countries, and field
trials to confirm these observations are already under way (29).
(1)ADMINISTRATION : The reconstituted vaccine is
administered in a single subcutaneous dose of 0.5 ml. The
diluting fluid for reconstituting the vaccine must be kept cold at
4-8 deg C. The reconstituted vaccine should be kept on ice and
used within one hour. Measles vaccine has recently been
adapted for aerosol administration.
(2)REACTIONS : When injected into the body, the attenuated
virus multiplies and induces a mild "measles" illness (fever and
rash) 5 to 10 days after immunization, but in reduced frequency
and severity. This may occur in 15 to 20 per cent of vaccinees.
The fever may last for 1 -2 days and the rash for 1-3 days.
There is no cause for alarm. The vaccines now given rarely
cause severe reaction (11). There is no spread of the virus from
the vaccinees to contacts.
(5) IMMUNITY : The vaccine has convincingly
demonstrated to provide immunity to even severely
malnourished children. Immunity develops 11 to 12 days after
vaccination (30) and appears to be of long duration, probably
for life. One dose of the vaccine appears to give 95 per cent
protection.
(6) CONTACTS : Susceptible contacts over the age of 9-12
months may be protected against measles with measles
vaccine, provided that this is given within 3 days of exposure.
This is because, the incubation period of measles induced by
the vaccine is about 7 days, compared with 10 days for the
naturally acquired measles.
>V^(7) CONTRAINDICATIONS pregnancy is a positive
contraindication. Others include acute illnesses, deficient cellmediated immunity, and use of steroids or other immunosuppressive drugs/! f\W -OS Qjj)
(8) ADVERSE EFFECTS OF VACCINE : .Toxic shock
\syndrome (TSS) occurs when measles vaccine is contaminated
or the same vial is used for more than one session on the same day
or FieXt day. The vaccine should not be used after 4 hours of
opening the vial. TSS is totally preventable and reflects poor
quality of immunization services. The symptoms of TSS are
typical. Severe watery diarrhoea, vomiting and high fever are
reported within few hours of measles vaccination. There are
usually a cluster of cases as all infants vaccinated from
contaminated vial will be affected. This may cause death within 48
hours. Case fatality rates are high (31).
(9) COMBINED VACCINE : Measles vaccine can be
combined with other live attenuated vaccines such as mumps,
and rubella vaccines (MMR vaccine) and such combinations
are also highly effective (32).
2. Immunoglobulin
Measles may be prevented by administration
immunoglobulin (human) early in the incubation period. The
of
RUBELLA
(GERMAN MEASLES)
Rubella or german measles is an acute childhood infection,
usually mild, of short duration (approximately 3 days) and
accompanied by low-grade fever, lymphadenopathy and a
maculopapular rash. Infection in early pregnancy may result in
serious congenital defects, including death of the foetus. The
disease is world-wide in distribution and tends to occur in
epidemics, in non-immunized populations, every 6 to 8 years (1).
History
Rubella was considered a mild and benign disease until 1941
when Norman Gregg, an ophthalmologist reported an epidemic of
congenital cataracts associated with other congenital defects in
children born to mothers who had rubella during their pregnancies
(2). This discovery changed the concept that rubella is not merely
a benign disease of childhood but also one with teratogenic
potential. In 1962, the virus was isolated; in 1967, an attenuated
vaccine was developed.
Epidemiological determinants Agent
factors :
(a) AGENT : Rubella is caused by an RNA virus of the
togavirus family. Only one antigenic type of the virus seems to
exist. The virus has been recovered from the naso-pharynx, throat,
blood, CSF and urine. It can be propagated in cell culture, (b)
SOURCE OF INFECTION : Clinical or Sub-clinical cases of
rubella. A large number of rubella infections are, in fact,
subclinical. This represents one of the major differences between
measles and rubella. There is no known carrier state for postnatally
acquired rubella. Infants born with congenital rubella may shed the
virus for many months. The vaccine virus is not communicable, (c)
PERIOD OF COMMUNICABILITY: Rubella is much less
communicable than measles probably because of the absence of
coughing in rubella. It is difficult to state the exact period of
infectivity. It probably extends from a week before symptoms to
about a week after rash appears. Infectivity is greatest when the
rash is erupting (3).
Host factors :
(a) AGE: Mainly a disease of childhood particularly in the age
group 3 to 10 years. Persons older than 15 years now account for
over 70 per cent cases in developed countries -this is similar to the
changing epidemiological pattern with measles, following
widespread immunization campaigns against the disease (b)
IMMUNITY : One attack results in lifelong immunity; second
attacks are rare. Infants of immune mothers are protected for 4 to 6
months. It is estimated that 10 to 40 per cent of the population could
reach adulthood without experiencing rubella infection in the
absence of immunization (4). Thus many women of child-bearing
age may remain rubella-susceptible. Studies in India indicate that
approximately 40 per cent of women of child-bearing age are
susceptible to rubella (5). 1 Environmental factors :
Disease usually occurs in a seasonal pattern i.e. in temperate
zones during the later winter and spring, with epidemics every 4-9
years.
Transmission
The virus is transmitted directly from person to person by
droplets from nose and throat, and droplet nuclei (aerosols), from
one week before onset of rash to one week after it has
faded. The portal of entry is via the respiratory route. The virus is
maintained in human population by chain transmission. The virus
can cross the placenta (vertical transmission) and infect the foetus
in utero, leading to congenital rubella in the newborn.
Incubation period
2 to 3 weeks; average 18 days
Clinical features
A large percentage of infections (50 to 65 per cent) are
asymptomatic (1). In a typical case, the clinical features comprise
the following: (a) PRODROMAL : The prodromal symptoms
(coryza, sore throat, low-grade fever) herald the onset of viraemia.
They are generally mild and insignificant, and less frequent in
children, (b) LYMPHADENOPATHY : In susceptible individuals,
the enlargement of the post-auricular and posterior cervical lymph
nodes appears as early as 7 days before the appearance of the rash.
This, however, is not pathognomonic since cases of clinical rubella
without enlargement of lymph nodes have been documented (6).
The glands may be found enlarged for 10 to 14 days after the rash,
(a)RASH: The rash is often the first indication of the disease in
children. It appears first on the face, usually within 24 hours of the
onset of prodromal symptoms. It is a minute, discrete, pinkish,
macular rash and not confluent as the rash of measles.
Conjunctivitis may occur. The rash spreads rapidly to the trunk
and extremities, by which time it is often no longer apparent on the
face. The rash spreads much faster and clears more rapidly than
the rash of measles. It disappears altogether by the third day. The
rash is an inconstant feature of the disease; it is absent in
subclinical cases. The incidence of rubella infection without rash
may be up to 25 per cent (7).
(b)COMPLICATIONS : In rare instances arthralgia may occur in
several joints in adults, especially young women. Encephalitis is
very rare. Thrombocytopenic purpura has also been observed as a
complication. Mention has been made already about the congenital
malformations.
Diagnosis
Because of its mildness and variability of symptoms, the
disease can go unrecognized unless it is an epidemic. A definitive
diagnosis of rubella is possible only through virus isolation and
serology. Throat swabs should be cultured for virus isolation; it
takes longer than serological diagnosis. The most widely used
serological test is the haemagglutination inhibition test (HAI)
developed in 1966. Two blood samples are taken, the first sample
within 5 days after onset of illness, and the second 2 weeks later. A
4-fold rise in HI antibody titre in paired sera or presence of IgM in
a single serum sample obtained 2 weeks after the rash is diagnostic
of recent rubella infection. More sensitive serological tests include
the ELISA test and radio-immune assay.
CONGENITAL RUBELLA
Congenital rubella syndrome (CRS) refers to infants born with
defects secondary to intrauterine infection or who manifest
symptoms or signs of intrauterine infection sometime after birth
(8). Congenital infection is considered to have occurred if the
infant has IgM rubella antibodies shortly after birth or if IgG
antibodies persist for more than 6 months, by which time
maternally derived antibodies would have disappeared.
Rubella infection inhibits cell division, and this is probably the
reason for congenital malformations and low birth weight (9). The
most common congenital defects are deafness, cardiac
malformations and cataracts. Other resulting defects include
glaucoma, retinopathy, microcephalus, cerebral palsy,
__________________________________________________RUBELLA 129
intrauterine growth retardation, hepato-splenomegaly, mental and motor
retardation. These defects occurring singly or in combination have
become known as "congenital rubella syndrome".
Congenital rubella is a chronic infection while acquired rubella is an
acute infection. The foetus remains infected throughout gestation and for
months and sometimes years postnatally. The gestational age at which
maternal infection occurs is a major determinant for the extent of foetal
infection as well as the effects on the foetus (10).
The first trimester of pregnancy is the most disastrous time for the
foetus as the organs are developing. If the infection is serious,
spontaneous abortion and stillbirth may occur, or the infant may develop
multiple defects such as the classical triad of patent ductus arteriosus,
cataract and deafness. Infection in the second trimester may cause
deafness, but those infected after week 16 suffer no major abnormalities
(Table 1).
TABLE 1
Risks of damage to foetus by maternal rubella
during pregnancy
Stage of gestation
Percentage of
I (weeks) when mother
foetuses
infected (symptomatic infected
plus asymptomatic)
<11
11-16
17-26
27-36
Source: (11)
Prevention
90
55
33
53
Percentage of
infected
foetuses
damaged
100
37
0
0
Overall risk of
damages to
foetus
(per cent)
90
20
0
0
rjr A
["MUMPS^)
pAn acute infectious disease caused by a specific virus which
\, has a prediliction for glandular and nervous tissues. Clinically,
the disease is recognised by non-suppurative enlargement and
^tenderness of one or both the parotid glands. Other organs
S Vnay also be involvecl) Constitutional symptoms vary, or may
~^be inapparent. Thedisease occurs throughout the world.
Although morbidity rate tends to be high, mortality rate is
negligible.
- _.
Agent factors
^
(a) AGENT : The causative agent, Mixovirus parotiditis is a RNA
virus of the myxovirus family. The virus can be grown readily in chick
embryo or tissue culture. There is only one serotype" (b) SOURCE OF
INFECTION : Both clinical and subclinical cases. Subclinical cases which
account for 30-40 per cent of all cases (1) appear to be responsible for
maintaining the cycle of infection. The virus can be isolated from the
saliva or from swabs taken from the surface of Stenson's duct. Virus has
also been found in the blood, urine, human milk and on occasion in the
CSF. (c) PERIOD OF COMMUNICABILITY : Usually 4-6 days before
the onset of symptoms and a week or more thereafter. The period of
maximum infectivity is just before and at the onset of parotitis. Once the
swelling of the glands has subsided, the case may be regarded as no longer
infectious, (d) SECONDARY ATTACK RATE : Estimated to be about 86
per cent (2).
Host factors
(a) AGE AND SEX : Mumps is the most frequent cause of parotitis in
children in the age group 5-15 years. The average age of incidence of
mumps is higher than with measles, chickenpox or whooping cough.
However, no age is exempt if there is no previous immunity. The disease
tends to be more severe in adults than in children, (b) IMMUNITY : One
attack,
^j^ Pcj
Q^ "N
Clinical features
Mumps is a generalised virus infection. In 30-40 per cent of
cases mumps infection is clinically non-apparent. In clinically
apparent cases, it is characterised by pain and swelling in either
one or both the parotid glands but may also involve the sublingual
and submandibular glands. Often the child complains of "ear ache"
on the affected side prior to the onset of swelling. There may be
pain and stiffness on opening the mouth before the swelling of the
gland is evident. Mumps may also affect the testes, pancreas, CNS,
ovaries, prostate, etc. In severe cases, there may be fever, headache
and other constitutional symptoms which may last from 3-5 days.
The swelling subsides slowly over 1-2 weeks.
COMPLICATIONS : Though frequent are not serious. These
include orchitis, ovaritis, pancreatitis, meningo-encephalitis and
myocarditis. Bilateral orchitis is rare and the assumption that
mumps orchitis may lead to sterility is ill-founded (5). While some
instances of diabetes have occurred in children following mumps
infection, a causal relationship has yet to be demonstrated (3).
Rarer complications include nerve deafness, polyarthritis and
hydrocephalus (6,7).
Prevention
(a) VACCINATION : A highly effective live attenuated
vaccine is now available for the prevention of mumps (8). A
single dose (0.5 ml) intramuscularly produces detectable
antibodies in 95 per cent of vaccinees. The duration of longterm immunity is not known. The vaccine is also available as
combined vaccine, viz. combined measles-mumps-rubella
vaccine/rubella-mumps vaccine.
The use of mumps vaccine is an unsettled question although it
has been recommended for children over one year of age. Some
argue that there is no good reason for trying to interfere with
natural exposure during childhood (1). Its use may be considered
primarily in susceptible adults, especially males who have not had
mumps, inasmuch as the disease tends to be severe should it occur
in adults.
~$y\ As with most other live virus vaccines, mumps vaccine should
not be administered to pregnant women, patients receiving
immunosuppressive therapy or those who are severely ill (9) J
APP$-o @
(b) IMMUNOGLOBULIN: A specific immunoglobulin (Mlg) is
available, but its protective effect has not been established, as
antibody studies have not been carried out on recipients (10).
Control
The control of mumps is difficult because the disease is
infectious, before a diagnosis can be made. The long and variable
incubation period, and the occurrence of subclinical cases make
the control of spread difficult. However, cases
INFLUENZA
Influenza is an acute respiratory tract infection caused by
influenza virus, of which there are 3 types - A, B and C. All
known pandemics were caused by influenza A strains. The disease
is characterised by sudden onset of chills, malaise, fever, muscular
pains and cough.
Problem statement
Influenza is truly an international disease. It occurs in all
countries and affects millions of people every year. Its behaviour is
unpredictable (1). It may occur in several forms. It may smoulder
in a community without clinical recognition, being manifest only
by serological surveys (1). It may occur in pandemics every 10-15
years due to major antigenic changes, as occurred in 1957 and
1968. In between pandemics, epidemics tend to occur at intervals
of 2-3 years in case of influenza A and 4-7 years in the case of
influenza B- but the periodicity is not regular as in the case of
measles or whooping cough because several strains of the virus
may be in simultaneous circulation which means that there may be
outbreaks of influenza practically every year, and sometimes even
twice a year (2,3).
Once an epidemic begins, the picture is quite characteristic.
Preceded by a few early cases, there is a sudden outburst of the
disease. This may be indicated by reports of increased febrile
respiratory illness in children, followed by the same in adults. The
next event is increased hospitalization of cases and sicknessabsenteeism in schools and places of work. Attack rates tend to be
high, varying from 10-50 per cent. The peak of the epidemic is
reached in 3-4 weeks, before tending to decline. The time scale is
compressed for smaller geographic areas (1). The unique features
of influenza epidemics are the suddenness with which they arise,
and the speed and ease with which they spread. The short
incubation period, large number of subclinical cases, high
proportion of susceptible population, short duration of immunity,
and absence of cross-immunity, all contribute to its rapid spread.
The fate of the virus during inter-epidemic periods is also not
known (7). Possible explanations include transmission of virus to
extra-human reservoirs (pigs, horses, birds), latent infection in
humans or continuous transfer from one human to another. This
explains the occurrence of sporadic cases.
At present three types of influenza viruses are circulating in the
world : A (H: HJ, A (H3N2) and B viruses (5). WHO global
surveillance activities have identified human infection with a
INFLUENZA 131
new influenza virus called A (H5 Nj) in Hong Kong in mid 1997.
However, the possibility that the outbreak heralded a global
influenza pandemic did not materialize. The threat of a virus more
easily transmitted between humans remains (5).
Agent factors
(a) AGENT : Influenza viruses are classified within the family
Orthomyxoviridae. There are three viral subtypes, namely
influenza type A, type B and type C. These three viruses are
antigenically distinct. There is no cross immunity between them.
Of importance are the influenza A and B viruses which are
responsible for epidemics of disease throughout the world (6).
Both influenza A and B viruses have 2 distinct surface antigens the haemagglutinin (H) and the neuraminidase (N) antigens. The
H antigen initiates infection following attachment of the virus to
susceptible cells. The N antigen is responsible for the release of
the virus from the infected cell.
The influenza A virus is unique among the viruses because it is
frequently subject to antigenic variation, both major and minor.
When there is a sudden complete or major change, it is called a
shift, and when the antigenic change is gradual over a period of
time, it is called a drift. Antigenic shift appears to result from
genetic recombination of human with animal or avian virus,
providing a major antigenic change. This can cause a major
epidemic or pandemic involving most or all age groups. Antigenic
drift involves "point mutation" in the gene owing to selection
pressure by immunity in the host population. Antigenic changes
occur to a lesser degree in the B group influenza viruses.
Influenza C appears to be antigenically stable.
Since the isolation of the virus A in 1933, major antigenic
changes have occurred twice - once in 1957 (H2N2) and again in
1968 (H3N2). Strains occurring between 1946 and 1957 have been
called HJNJ strains. The shift in 1968 involved only the H antigen.
(b) RESERVOIR OF INFECTION : It has become
increasingly evident that a major reservoir of influenza virus
exists in animals and birds. Many influenza viruses have been
isolated from a wide variety of animals and birds (e.g., swine,
horses, dogs, cats, domestic poultry, wild birds, etc). Some of
these include the major H and N antigens related to human
strains. It is hypothesized. There is increasing evidence that the
animal reservoirs provide new strains of influenza virus by
recombination between the influenza viruses of man, animals
and birds.
(c) SOURCE OF INFECTION : Usually a case or subclinical
case. During epidemics, a large number of mild and
asymptomatic infections occur, which play an important role in
the spread of infection. The secretions of the respiratory tract
are infective.
(d) PERIOD OF INFECTIVITY : Virus is present in the
nasopharynx from 1 to 2 days before and 1 to 2 days after
onset of symptoms.
Host factors
(a) AGE AND SEX : Influenza affects all ages and both sexes.
In general, the attack rate is lower among adults. Children
constitute an important link in the transmission chain. The highest
mortality rate during an epidemic occurs among certain high-risk
groups in the population such as old people (generally over 65
years of age), children under 18 months, and persons with
diabetes or chronic heart disease, kidney and respiratory ailments
(7). (b) HUMAN MOBILITY : This is an important factor in the
spread of infection (c) IMMUNITY : Antibodies are important
in immunity against influenza.
________DIPHTHERIA 133
DIPHTHERIA
Diphtheria is an acute infectious disease caused by toxigenic
strains of Corynebacterium diphtheriae. Three major clinical
types have been described : anterior nasal, faucial and laryngeal;
however, the skin, conjunctiva, vulva and other parts of the body
may be affected. The bacilli multiply locally, usually in the throat,
and elaborate a powerful exotoxin which is responsible for :
(a)the formation of a greyish or yellowish membrane ("false
membrane") commonly over the tonsils, pharynx or larynx (or
at the site of implantation), with well-defined edges and the
membrane cannot be wiped away;
(b)marked congestion, oedema or local tissue destruction
(c)enlargement of the regional lymph nodes; and
(d)signs and symptoms of toxaemia.
Fatality rate on the average is about 10 per cent which has
changed little in the past 50 years in untreated cases, and about 5
per cent in treated cases (1).
Problem statement
WORLD : Diphtheria is a rare disease in most developed
countries owing to routine children vaccination. In countries
where satisfactory vaccination schemes have been instituted the
disease has so declined that it is no longer regarded as a public
health problem. However the disease is seen occasionally among
non-immunized children in developed countries.
Improved socio-economic conditions are changing the
epidemiology of diphtheria. Changes in lifestyle allow far less
opportunity to maintain natural immunity, such as through
frequent skin infection with C. diphtheriae. An example of
waning immunity is the outbreak of diphtheria reported in
Russian Federation, Ukraine in 1990 and Thailand and Laos in
1996. Thailand reported 31 cases, most of whom were between 312 years of age. Approximately 300 cases were reported by Laos
and majority of cases were between 3-15 years (2). These
epidemics are largely due to decreasing immunization coverage
among infants and children, waning immunity to diphtheria in
adults, movement of large groups of population in the last few
years, and an irregular supply of vaccine (3). These outbreaks
highlight the need for booster vaccinations. Recent diphtheria
outbreaks in a number of countries have demonstrated a shift in
the age distribution of cases to older children and adults (4). In
developing countries, the disease continues to be endemic due to
lack of adequate widespread immunization. The true numbers of
diphtheria cases and deaths are unknown because of incomplete
reporting from most countries where the disease occurs. WHO
estimates for the global burden of disease in terms of healthy life
lost attributable to diphtheria is about 185,000 DALYs for the
year 2002. About 5000 persons died due to diphtheria in the same
year (5).
INDIA : Diphtheria is an endemic disease. The available
retrospective data indicate a declining trend of diphtheria in the
country. It is due to increasing coverage of child population by
immunization. The reported incidence of the disease in the
country during 1987 (before wide coverage of immunization) was
about 12952, whereas during the year 2000 there were only 265
cases showing a decline of about 99.06 per cent (6).
Agent factors
(a) AGENT : The causative agent, C. diphtheriae is a grampositive, non-motile organism. It has no invasive power, but
produces a powerful exotoxin. Three types of diphtheria bacilli
DIPHTHERIA 135
{ Current prophylactics
These may be grouped as below :
a. Combined or mixed uaccines
b. Single vaccines
-FT (formal-toxoid)
-APT (alum-precipitated toxoid)
-PTAP (purified toxoid aluminium phosphate)
-PTAH (purified toxoid aluminium hydroxide)
-TAF (toxoid-antitoxin floccules)
c. Antisera
- Diphtheria anti-toxin
a. COMBINED VACCINES
DPT Vaccine
For immunizing infants, the preparation of choice is DPT.
Firstly because, the infant can be immunized simultaneously
against three diseases, viz., diphtheria, pertussis and tetanus
which is a great gain administratively. Secondly the pertussis
component in DPT vaccine enhances the potency of the
diphtheria toxoid.
n"here are two types of DPT vaccine - plain and adsorbed.
Adsorption is usually carried out on a mineral carrier like
aluminium phosphate or hydroxide. Studies have shown that
'adsorption increases the immunological effectiveness of the
vaccine. 'Jhe WHO recommends that only adjuvant DPT
preparations be utilized in immunization programmes (16). The
composition of DPT vaccines in India is shown in Table 3. The
contents per dose vary according to the manufacturer. The
plain (DPT) vaccine can be used as a booster.
TABLE 3
Glaxo (per
0.5 ml)
25 Lf
5Lf
20,000
2.5 mg
0.01%
Kasauli
30 Lf
10 Lf
32,000
3.0 mg
0.01%
3. PASSIVE IMMUNIZATION
The merit of hyperimmune globulin in pertussis prophylaxis
has yet to be established. So far, there is no evidence of its
efficacy in well-controlled trials (10).
The control of pertussis by immunization is still an unsolved
problem. Even if the level of immunization reaches 100 per cent, it
is possible that the disease would not be entirely eliminated
because whooping cough vaccines have never been claimed to be
more than 90 per cent effective.
Epidemiological features
(a) AGENT : The causative agent, N. meningitidis is a gramnegative diplococci. Several serotypes have been identified, viz.
Groups A,B,C,D,X,Y, 29 E, W135, etc. Groups A and C, and to a
lesser extent Group B meningococcal are capable of causing major
epidemics. The incidence of infections by Groups Y and W135
strains are increasing in some countries (3). N. meningitidis is a
delicate organism; it dies rapidly on exposure to heat and cold, (b)
SOURCE OF INFECTION : The organism is found in the
nasopharynx of cases and carriers. Clinical cases present only a
negligible source of infection. More often the infection causes mild
or even unnoticeable symptoms of naso-pharyngitis. 5 to 30 per
cent of the normal population may harbour the organism in the
nasopharynx during inter-epidemic periods. Carriers are the most
important source of infection. The mean duration of temporary
carriers is about 10 months (4). During epidemics, the carrier rate
may go up to 70-80 per cent, (c) PERIOD OF
COMMUNICABILITY : Until meningococci are no longer
present in discharges from nose and throat. Cases rapidly lose their
infectiousness within 24 hours of specific treatment, (d) AGE
AND SEX : This is predominantly a disease of children and young
adults of both sexes, (e) IMMUNITY : All ages are susceptible.
Younger age groups are more susceptible than older groups as
their antibodies are lower. Immunity . is acquired by subclinical
infection (mostly), clinical disease or vaccination. Infants derive
passive immunity from the mother, (f) ENVIRONMENTAL
FACTORS : The seasonal variation of the disease is well
established; outbreaks occur more frequently in the dry and cold
months of the year. Overcrowding, as occurs in schools, barracks,
refugee and other camps, is an important predisposing factor. The
incidence is also greater in the low socio-economic groups living
under poor housing conditions.
References
1.Morley, David
1994-1997,
Regional office for SEAR, New Delhi.
5.WHO (2004), World Health Report 2004, Report of the Director General WHO.
6.Govt, of India, (2002), Annual Report 2001 -2002, Ministry of Health and
Family Welfare, New Delhi.
7.Christie, A.B. (1980). Infectious Diseases : Epidemiology and Clinical Practice,
3rd ed., Churchill Livingstone
8.Fraser, D.W. (1980). in Maxcy-Rosenau: Public Health and Preventive
Medicine, John M. Last (ed.), Appletone-Century-Crofts, New York
9.Gray, James A (1981). Medicine International, 3, 112
10.Manclark, C.R. (1981). Bull WHO, 59: 9-15
11.Y.Sato, etal (1984), Lancet, 1:122
12.MRC Whooping Cough Immunization Committee (1959). Brit. Med. J., 1:994
MENINGOCOCCAL MENINGITIS
Meningococcal meningitis or cerebro-spinal fever is an acute
communicable disease caused by N. meningitidis. It usually begins
with intense headache, vomiting and stiff neck and progresses to
comma within a few hours. The meningitis is part of a septicaemic
process. The fatality of typical untreated cases is about 80 per cent.
With early diagnosis and treatment, case fatality rates have
declined to less than 10 per cent.
Problem statement
Distribution world-wide, occurring sporadically and in small
outbreaks in most parts of the world. The zone lying between 5
and 15 degree N of the equator in tropical Africa is called the
"meningitic belt" because of the frequent epidemic waves that
have been occurring in that region (1). During recent years,
Mode of transmission
The disease spreads mainly by droplet infection. The portal of
entry is the nasopharynx.
Incubation period
Usually 3 to 4 days, but may vary from 2 to 10 days.
Prevention and control
(a)CASES : Treatment with antibiotics can save the lives of 95
per cent of patients provided that it is started during the first 2
days of illness. Penicillin is the drug of choice. In penicillinallergic patients, chloramphenicol should be substituted.
Treatment of cases has practically no effect on the
epidemiological pattern of the disease because it only reduces
the fatality rate of the disease according to the treatment
efficiency (4). Isolation of cases is of limited usefulness in
controlling epidemics because the carriers outnumber cases.
(b)CARRIERS : Treatment with penicillin does not eradicate
the carrier state; more powerful antibiotics such as rifampicin
are needed to eradicate the carrier state.
Mortality
(000)
1118
DALYs lost
(000)
35595
Americas
226
3318
354
10819
Europe
288
3115
South-East-Asia Region
1474
33026
498
8654
3963
94603
Total
Source : (3)
In India, in the states and districts with high infant and chile
mortality rates, ARI is one of the major causes of death. ARI is
also one of the major reasons for which children are brought tc the
hospitals and health facilities. Hospital records from state; with
high infant mortality rates show that upto 13% of inpatien deaths
in paediatric wards are due to ARI. The proportion o death due to
ARI in the community is much higher as mam children die at
home (3). The reason for high case fatality mai be that children
are either not brought to the hospitals o: brought too late.
According to WHO estimates, respiratory infections causec
about 987000 deaths in India of which 969000 were due tc acute
lower respiratory infections (ALRI), 10,000 due to acute upper
respiratory infections (AURI) and about 9000 due tc otitis media.
The burden of disease in terms of DALYs lost wa:
indicator
Percentage
65
19
22
48
Source : (1)
H The agents causing ARI, age group affected and clinical features
Agent
Bacteria
Bordetella pertussis
Corynebacterium diphtheriae
Haemophilus influenzae
Klebsiell pneumonia
Legionella pneumophila
Staphylococcus pyogenes
\'
'""
Streptococcus pneumoniae
___
_ _ _ _ _
Streptococcus pyogenes
All ages
Virus
Adenoviruses - endemic types (1,2,5)
Young children
- epidemic types (3,4,7)
Older children and young adults
Enteroviruses (ECHO and Coxsackie)
All ages
Influenza A
All ages
~n
B
School children _J
C
Measles
Parainfluenza 1
2
3
Respiratory syncytial virus
Rhinoviruses (multiple serotypes)
Coronavirus
J
Other agents
Chlamydia type B (Psittacosis)
Coxiella burntti (Q fever)
Mycoplasma pneumoniae
Source (4)
Rare
Young children
i
J Youn9 children
Infants
Infants and young children
All ages
Adults exposed to infected birds
Adults exposed to sheep and cattle
School children and young adults
Paroxysmal .cough
Nasal/tonsillar/pharyngeal membranous exudate
severe toxaemia
Acute exacerbations of chronic bronchitis pneumonia
Acute epiglottitis (H. influenzae type B)
Lobar pneumonia lung abscess
Pneumonia
Lobar and broncho-pneumonia (esp. secondary to
influenza) + lung abscess
Pneumonia (lobar or multilobular) Acute exacerbations of
chronic bronchitis
Acute pharyngitis and tonsillitis
Lower respiratory
Febrile pharyngitis and influenza-like illness
Variable respiratory
~ Fever, aching, malaise, variable respiratory
Occasional primary pneumonia
__ Secondary bacterial pneumonia in elderly
Mild upper respiratory
Variable respiratory with characteristic rash
i
i re-infection in later life :
J Croup
J mild upper respjratory
Bronchiolitis and pneumonia
Severe bronchiolitis and pneumonia
Common cold
Influenza-like illness and atypical pneumonia
Atypical pneumonia
Febrile bronchitis and atypical pneumonia
J
the child is able to drink (if the child is aged 2 months upto 5
years), has the young infant stopped feeding well (child less than 2
months), has there been any antecedent illness such as measles,
does the child have fever, is the child excessively drowsy or
difficult to wake (if yes, for how long), did the child have
convulsions, is there irregular breathing, short periods of not
breathing or the child turning blue, any history of treatment during
the illness.
Physical examination
Look and listen for the following :
(1) COUNT THE BREATHS IN ONE MINUTE : As the
children get older, their breathing rate slows down. Therefore,
the cut-off point used to determine if a child has fast breathing
will depend on the age of the child. Count the respiratory rate
for full one minute using the second's hand of the watch
looking at the abdominal movement or lower chest when the
child is calm. The chest and abdomen must be exposed for
counting. Increased respiratory rate is of significance only if it
persists.
j Fast breathing is present when the respiratory rate is :
- 60 breaths per minute or more in a child less than 2
months of age
TCA\ ~
50 breaths per minute or more in a child aged 2 fy J
months upto 12 months
- 40 breaths per minute or more in a child aged 12
months upto 5 years. ~\
However, repeat the count for a young infant (age less than 2
months) if the count is 60 breaths per minute or more. This is
important because the breathing rate of young infant is often
erratic. Occasionally young infants stop breathing for a few
seconds, and then breath very rapidly for a short period.
(1)LOOK FOR CHEST INDRAWING : Look for chest
indrawing when the child breaths IN. The child has indrawing
if the lower chest wall goes in when the child breaths in. Chest
indrawing occurs when the effort required to breath in, is much
greater than normal.
(2)LOOK AND LISTEN FOR STRIDOR : A child with stridor
makes a harsh noise when breathing IN. Stridor occurs when
there is narrowing of the larynx, trachea or epiglottis which
interferes with air entering the lungs. These conditions are often
called croup.
(3)LOOK FOR WHEEZE : A child with wheezing makes a soft
whistling noise or shows signs that breathing OUT is difficult,
wheezing is caused by narrowing of the air passage in the
lungs. The breathing-out phase takes longer than normal and
requires effort.
If the child is wheezing, ask the mother if her child has had a
previous episode of wheezing within the past year. If so, the child
should be classified as having recurrent wheeze.
(1)See if the child is abnormally sleepy or difficult to wake. An
abnormally sleepy child is drowsy most of the time when he or
she should be awake and alert.
(2)Feel for fever or low body temperature.
(3)CHECK FOR SEVERE MALNUTRITION : Malnutrition
when present is a high risk factor and case fatality rates are
higher in such children. In severely malnourished children with
pneumonia, fast breathing and chest indrawing may not be as
evident as in other children. A severely malnourished child may
have an impaired or absent response to hypoxia and a weak or
absent Cough reflex. These children need careful evaluation for
pneumonia as well as careful management.
(4)Cyanosis is a sign of hypoxia. Cyanosis must be checked in
good light.
child classified as having severe pneumonia also has other signs such as :
-nasal flaring, when the nose widens as the child breaths in;
Classifying the illness means making decisions about the ype and
severity of disease. The sick child should be put into >ne of the four
classifications :
-grunting, the short sounds made with the voice when the child has
difficulty in breathing; and
I.
II
I.Severe pneumonia
II.Pneumonia (not severe)
III.No pneumonia : cough or cold
Each disease classification has a corresponding treatment )lan which
should be followed. The following guidelines are lsed to manage a child
who is 2 months upto 5 years of age.
. Very severe disease
The danger signs and possible causes are :
a. Not able to drink : A child who is not able to drink could
have severe pneumonia or bronchiolitis, septicaemia,
throat abscess, meningitis or cerebral malaria.
b. Convulsions, abnormally sleepy or difficult to wake : A
child with these signs may have severe pneumonia
resulting
in
hypoxia,
sepsis,
cerebral
malaria
or
meningitis. Meningitis can develop as a complication of
pneumonia or it can occur on its own.
c. Stridor in calm child : If a child has stridor when calm,
the
child
may
be
in
danger
of
life-threatening
obstruction of the air-way from swelling of larynx,
trachea or epiglottis.
d. Severe malnutrition : A severely malnourished child is at
high risk of developing and dying from pneumonia. In
addition, the child may not show typical signs of the
illness.
A child who is classified as having severe disease is very ill and
should be referred urgently to a hospital. Management of a :hild having
very severe disease is summarized in Table 4.
TABLE 4
Management of very severe disease
SIGNS:
(e.g.
Chest indrawing
(if also recurrent wheezing,
go directly to treat wheezing)
CLASSIFY AS
SEVERE PNEUMONIA
PNEUMONIA
TREATMENT
WORSE
Not able to drink Has
chest indrawing Has other
danger signs
THE SAME
IMPROVING
Breathing slower
Less fever Eating
better
TREATMENT
Source: (5)
TABLE 6
Classification and management of illness in young infants
SIGNS
should be
CLASSIFY AS
VERY SEVERE DISEASE
TDCA-rLcM-r
ot ,,nrv, u *
TREATMENT
Refer URGENTLY to hospital
KeeD o
' f nt
Give first dose of an antibiotic
Severe chest indrawing,' No severe chest indrawing
SIGNS
or Fast breathing
and No fast breathing
(60 per minute or more) (less than 60 per minute)
TREATMENT
CLASSIFY AS SEVERE PNEUMONIA NO PNEUMOM^
5 YEARS
Refer URGENTLY to
TREATMENT hospital. Keep young
infant warm.
Give first dose of an
antibiotic(If referral
is not feasible,treat
AGE/WEIGHT
Paediatric tablet:
Paediatric syrup
Sulphamethoxazole 100 mg Each spoon (5 ml): I
and Trimethoprim 20 mg
Sulphamethoxazole |
200 mg and
Trimethoprim 40 mg
< 2 months
(Wt. 3-5 kg)
2-12 months
(Wt. 6-9 kg)
1 -5 years
Three tablets twice a day
One and half spoon
(Wt. 10-19 kg)_____________________________(7.5 ml) twice a day.
In children less than two months, cotrimoxazole is not routinely
recommended. These children are to be treated as for severe pneumonia.
However, in case of delay in referral, cotrimoxazole may be initiated.
Cotrimoxazole should not be given to premature babies and cases of
neonatal jaundice. Such children when seen by a health worker must be
referred to a health facility.
The condition of the child should be assessed after 48 hours.
Cotrimoxazole should be continued for another 3 days in children who
show improvement in clinical condition. If there is no significant change
in condition (neither improvement nor worsening), cotrimoxazole should
be continued for another 48 hours and condition reassessed. If at 48 hours
or earlier the condition worsens, the child should be hospitalized
immediately.
SEVERE fNEUMOMA (CHEST INDRAW1NG)
Children with severe pneumonia should be treated as inpatients with
intramuscular injections of benzyl penicillin (after test dose), ampicillin or
chloramphenicol. The condition of the child must be monitored every day
and reviewed after 48 hours for antibiotic therapy as detailed in Table 8.
Antibiotic therapy must be given for a minimum of 5 days and continued
for at least 3 days after the child gets well.
TABLE 8
Treatment of severe pneumonia (2 Months - 5 Years)
Antibiotics
A. First 48 hours
Benzyl penicillin
or
Ampicillin
or
Chloramphenicol
Dose*
50000IU
per kg/dose
50 mg/kg/dose
25 mg/kg/dose
Interval
Mode i
6 hourly
IM
6 hourly
IM
6 hourly
IM
{TABLED l^<ft()
Treatment of pneumonia in children aged less than 2 months
ANTIBIOTIC
DOSE
FREQUENCY
Age
Age 7 days < 7
days to 2 months
12 hourly
6 hourly 12
hourly
8 hourly 12
hourly
8 hourly
Oral
Oral
IM
______________________________________________SARS 145
Acute Respiratory Disease Control Programme in India
The Acute Respiratory Disease Control Programme was taken
up as a pilot project in the country in the year 1990. Since 199293, the programme is being implemented as part of the CSSM
programme. For details please refer to chapter 7.
References
1.WHO (1999), Health Situation in the South -East Asia Region 1994-
Mode of transmission
The mode of transmission is through close contact with the
patient and infected material via the eyes, nose and mouth, with
infectious respiratory droplets. There was no evidence that SARS
is an airborne disease. The findings that each patient infected on
an average 3 others is consistent with a disease spread by direct
contacts (3). In Hong Kong, sewage, faeces and cockroaches
were suspected transmitters. The SARS virus can survive for
hours on common surfaces outside the human body, and up to
four days in human waste. The virus can survive at least for 24
hours on a plastic surface at room temperature, and can live for
extended periods in the cold.
Epidemiological aspect
Health care workers, especially those involved in procedures
generating aerosols, accounted for 21 per cent of all cases.
Maximum virus excretion from the respiratory tract occurs on
about day 10 of illness and then declines. The efficiency of
transmission appears to be greatest following exposure to severely
ill patients or those experiencing rapid clinical deterioration,
usually during the second week of illness. When symptomatic
cases were isolated within 5 days of the onset of illness, few cases
of secondary transmission occurred. There was no evidence that
patient transmits infection 10 days after fever has resolved.
Children are rarely affected by SARS. To date, there have been
two reported cases of transmission from children to adults and no
report of transmission from child to child. Three separate
epidemiological investigations have not found any evidence of
SARS transmission in schools. Furthermore, no evidence of SARS
has been found in infants of mothers who were infected during
pregnancy.
International flights have been associated with the transmission
of SARS from symptomatic probable cases to passengers or crew.
WHO recommends exit screening and other measures to reduce
opportunities for further international spread associated with air
travel during the epidemic period.
Prevention
The preventive measures for SARS control are appropriate
detection and protective measures which include :
Problem statement
The earliest case was traced to a health care worker in China,
in late 2002, with rapid spread to Hong Kong, Singapore,
Vietnam, Taiwan and Toranto. As of early August 2003, about
8422 cases were reported to the WHO from 30 countries with 916
fatalities (2).
Incubation period
The incubation period has been estimated to be 2 to 7 days,
commonly 3 to 5 days (1).
TUBERCULOSIS
Tuberculosis is a specific infectious disease caused byV
M. tuberculosis. The disease primarily affects lungs and causes;r
pulmonary tuberculosis. It can also affect intestine, meninges,
bones and joints, lymph glands, skin and other tissues of the
body. The disease is usually chronic with varying clinical
manifestations. The disease also affects animals like cattle; this
is known as "bovine tuberculosis", which may sometimes be,
communicated to man. Pulmonary tuberculosis, the most*
important form of tuberculosis which affects man, will bff
considered here.
V_
Problem statement
WORLD
Tuberculosis remains a world-wide public health problem
despite the fact that the causative organism was discovered more
than 100 years ago and highly effective drugs and vaccine are
available making tuberculosis a preventable and curable disease.
Technologically advanced countries have achieved spectacular
results in the control of tuberculosis (1). For example, from 1900
to 1980 tuberculosis death rate declined from 199 to 0.5 per
100,000 in the United States. This decline started long before the
advent of BCG or chemotherapy and has been attributed to
changes in the "non-specific" determinants of the disease such as
improvements in the standard of living and the quality of life of
the people coupled with the application of available technical
knowledge and health resources.
Using the trends in case notification, it is estimated that there
were 8.8 million new cases of tuberculosis in 2002 of which 3.9
million were smear positive. The global incidence rate of
tuberculosis (per capita) is growing at approximately 1.1 per cent
per year and the number of cases at 2.4 per cent per year (2).
During 2002, about 1.56 million people died of this disease, and
the global burden of disease in terms of DALYs lost was about
34.73 million (3). According to WHO estimates there were 16-20
million cases of tuberculosis worldwide in
2001. The global incidence rate for tuberculosis being 119 pei
lakh population with low income countries carrying most of the
burden with the incidence rate of 197 per lakh population Middle
income countries are having the rate of about 85 pei lakh
population, and high income countries about 9 per lakr population
(4). Similarly the mortality rate for tuberculosis is about 26 per
lakh population worldwide. It is about 45 per lakr population for
low income countries, 18 per lakh populatior for middle income
countries and about 2 per lakh populatior for high income
countries (4).
It is estimated that about one-third of the current globa
population is infected asymptomatically with tuberculosis, o
whom 5-10 per cent will develop clinical disease during theii
lifetime. Most new cases and deaths occur in developing countries
where infection is often acquired in childhood. The annual risk of
tuberculosis infection in high burden countries i; estimated to be
0.5-2 per cent. Childhood deaths fron tuberculosis are usually
caused by meningitis or disseminatec disease (5).
The South-East Asia Region countries carry 38 per cent o the
global burden of tuberculosis, with 3 million new cases anc nearly
0.6 million deaths occurring every year. Rising trend ir HIV
infection in some countries, together with the emergence of
multidrug resistant strains of tuberculosis pose additiona threat
(6).
Eight out of ten of all those struck by tuberculosis are ir
economically productive age group of 15-49 years. It kill; more
adujjsjhan any^sther infectious disease.
*jVGlobaRy,jtte> DOTS (Directly Observed Treatment, Short
^course) strategy has been recognized as the best cost-effective
Japproach to tuberculosis control, to reduce the disease burder
and to reduce the spread of infection. DOTS is the only mean;
by which a cure can also be ensured. The challenge is tc
expand the coverage of DOTS so that most patients ge ^effective
treatmenO he target was successful treatment or cun irate of 85
per cefvfof new sputum positive cases, and detectior I of 70 per
cent of such cases by the year 2000 (7). As these
targets were not achieved by the end of the year 2000, the
target year has been reset to 2005 (8).
Globally the countries can be categorized according to the
implementation of DOTS strategy. The categories are as showr in
Table 1.
TABLE 1
Definition
______________________________________TUBERCULOSIS 147
This system of categorization provides a first impression of
each country's progress towards TB control. WHO targets are
expressed more stringently in terms of treatment success and case
detection rate. TB control should ensure high treatment success
before expanding case finding. The reason is that a proportion of
patient given less than a full-curative course of treatment remain
chronically infectious and continue to spread the disease. Thus
DOTS programmes must be shown to achieve high cure rates in
pilot projects before attempting country-wide coverage.
By the year 2002, 180 countries have implemented DOTS
strategy, covering 69 per cent of the world's population. DOTS
programme notified 3 million new cases of tuberculosis of which
1.4 million were smear positive. A total of 13.3 million patients
(6.8 million smear positive) were treated in DOTS programme.
These 1.4 million smear positive cases represent about 37 per cent
of the estimated incidence, just over half way to the 70 per cent
target. The success rate with the DOTS was 2 per cent (2).
In many developing countries particularly in Asia acquired
drug resistance remains high, because national tuberculosis
control programmes in these countries have not been able to
achieve a high cure rate over a very long period of time, even after
the introduction of short-course chemotherapy. Poverty, economic
recession, and malnutrition make populations more vulnerable to
tuberculosis. Recent increase in human migration has rapidly
mixed infected with uninfected communities. To make global
situation worse, tuberculosis has formed a lethal combination with
HIV.
INDIA
India accounts for nearly one-third of global burden of
tuberculosis. Every year, approximately 1.8 million persons
develop tuberculosis of which about 0.8 million are new smear
positive highly infectious cases and about 4.17 lakh people die of
TB every year, one person dies every minute, and about 1000
people die every day (10).
Since 1993, India has successfully implemented Revised
National Tuberculosis Control Programme (RNTCP) using DOTS
strategy. As of March 2004, this programme covers about 76 per
cent of the country's population (more than 851 million persons) in
466 districts and belongs to category 3 of DOTS strategy. Table 2
shows latest tuberculosis estimates in the country.
TABLE 2
The tuberculosis estimates for India (2002)
Population
Global rank
(by estimated number of cases)
Incidence
(all cases/100,000 population)
Incidence
(new smear +ve cases/100,000 population)
Prevalence
(smear +ve/100,000 population)
TB mortality per 100,000 population
Percentage of adult (15 49 years)
TB cases HIV positive
Percentage of new cases multidrug resistant
1049 million
1
168
75
156
37
4.6
3.4
Source : (2)
The 4.4 per cent death rate in RNTCP areas is substantially
lower than the 29 per cent mortality documented among treated
smear positive tuberculosis patients in non-RNTCP areas. The
Indian scenario about DOTS programme has been discussed in
detail in chapter 7.
Infected
(%)
15-24
25-34
35-44
45-54
55+
1.0
6.4
15.4
,<)
31.9
47.3
54.8
60.7
62.1
Total
30.4
"j
2. Frequency of disease :
(a) Prevalence of disease : The prevalence of
bacteriologically confirmed disease was 4 cases per 1,000
population, four times as high as incidence, (b) Incidence of
new cases : The incidence of new cases of tuberculosis
(confirmed by culture) was about 1.5 per 1,000 (excluding
children below the age of 5 years) (19).
v J
3. Age and sex trends :
(a) Age : Prevalence of infection increased with the age up to
the age of 45-54 years in males. Tuberculosis is becoming a
disease of elderly males, (b) Sex : In females, the peak of
tuberculosis prevalence is below 35 years. There was a fall in the
prevalence rates in higher age-groups in women.
4. Time trend:
The trend of tuberculosis appears to be almost constant over the
years except in some cities where better services for diagnosis and
treatment have been available for sometime. Jrj
5. Rural- urban differences :
Tuberculosis infection as well as disease are more or less
uniformly distributed in urban, semi-urban and rural areas. (20).
Thus the vast majority of cases are to be found in rural and semiurban areas, where more than 80 per cent of the country's
population live. In urban areas, tuberculosis is found more
frequently in slum dwellers and lower socio-economic groups than
in well-to-do groups.
6. Non -specific sensitivity :
Non-specific sensitivity is highly prevalent in the entire
country, but it is definitely lower in areas situated at higher
altitudes.
7. Mortality:
Death rates are declining. The rough estimate of mortality from
tuberculosis per 100,000 population was 400 in 1920-1921; 200 in
1950-1951 ; 100 in 1964; 80 in 1970; and 37 in 2002 (21,22). Life
span of tuberculosis patients has increased.
Since death rate is declining and the disease is showing a
decline in younger age groups, epidemiologists are beginning to
think that perhaps we may have crossed the peak of the
______________________________________TUBERCULOSIS 149
patient excreting tubercle bacilli resistant to anti -tuberculosis.,
drugs. This index is directly related to chemotherap^). o\ (<y
\a) Mortality rate : In the past, tuberculosis mortality rate,
i.e./The number of deaths from tuberculosis every year per 1,000 or
100,000 population wasused as an index of the I tuberculosis
problem in a community)Since the introduction of an effective
chemotherapy ana preventive measures, tuberculosis mortality rate
has lost its importance as an epidemiological index for measuring
the magnitude of the tuberculosis problem. However, where
tuberculosis mortality rates are still at a high level, they certainly
indicate the need for an effective treatment programme and
strengthening of the national tuberculosis control programme.
The epidemiological indices mentioned above are all closely
related. They should be considered together in interpreting the
tuberculosis situation in a community.
Some definitions (27) :
Sputum smear examination - Laboratory technique to screen
sputum for tuberculosis, where acid fast bacilli (AFB) are stained
red by the Ziehl Neelsen method, and then identified and counted
using microscopy.
Smear positive tuberculosis - At least two initial sputum smears
positive for AFB or one AFB positive smear and one positive
culture.
Smear negative tuberculosis - At least three negative smears,
but tuberculosis suggestive symptoms and X-ray abnormalities or
positive culture.
Adherence - Person takes appropriate drug regimen for required
time (also known as compliance).
New case - A patient with sputum positive pulmonary
tuberculosis who has never had treatment for tuberculosis or has
taken anti-tuberculosis drugs for less than 4 weeks.
Relapse - A patient who returns smear positive having
previously been treated for tuberculosis and declared cured after
the completion of his treatment.
Failure case - A patient who was initially smear positive, who
began treatment and who remained or became smear positive again
at five months or later during the course of treatment.
Return after default - A patient who returns sputum smear
positive, after having left treatment for at least two months.
Transfer in - A patient recorded in another administrative area
register and transferred into another area to continue treatment
(treatment results should be reported to the district where the
patient was initially registered).
Transfer out - A patient who has been transferred to another
area register.
Cured - Initially smear positive patient who completed
treatment and had negative smear result on at least two occasions
(one at treatment completion).
Treatment completed - Initially smear negative patient who
received full course of treatment, or smear positive who completed
treatment, with negative smear at the end of initial phase, but no or
only one negative smear during continuation and none at treatment
end.
NATURAL HISTORY OF TUBERCULOSIS
Agent Factors
(a) AGENT : M. tuberculosis is a facultative intracellular
parasite, i.e., it is readily ingested by phagocytes and is resistant to
intracellular killing (28). Of importance to man are the human and
bovine strains. The human strain is responsible
for the vast majority of cases. The bovine strain affects mainly
cattle and other animals. Regarding virulence, the Indian tubercle
bacillus is said to be less virulent than the European bacillus. In
recent years, a number of "atypical" mycobacteria have been
isolated from man (29). These have been classified into four
groups - (i) photochromogens (e.g., M. Kansasii); (ii)
scotochromogens (e.g., M. scrofulaceum); (iii) nonphotochromogens (e.g., M. intercellulare) (Battey bacillus); and,
(iv) rapid growers (e.g., M. fortuitum). All these are mainly
saprophytic. Diseases attributed to them have resembled
pulmonary tuberculosis and chronic cervical lymphadenitis. Nonspecific infections have been reported to be widely prevalent in the
southern part of India.
(a)SOURCE OF INFECTION : There are two sources of
infection- human and bovine, (i) Human source : The most
common source of infection is the human case whose sputum is
positive for tubercle bacilli and who has either received no
treatment or not been treated fully. Such sources can discharge
the bacilli in their sputum for years. The tubercle bacilli in a
human case are usually a mixed group - some multiply very
rapidly and some slowly. The more rapidly a bacillary strain
multiplies the more susceptible it is to the bactericidal action of
chemotherapeutic drugs. The slow multipliers are the source of
persister or dormant bacilli; they can remain alive for years
without causing harm to the host, but when conditions are
favourable they may start multiplying again and cause active
disease. That is, they are the seeds of a future relapse (30). (ii)
Bovine source: The bovine source of infection is usually
infected milk. There is no definite evidence that bovine
tuberculosis is a problem in this country because of the practice
of boiling milk before consumption.
(b)COMMUNICABILITY : Patients are infective as long as
they remain untreated. Effective anti-microbial treatment
reduces infectivity by 90 per cent within 48 hours (31).
Host factors
(a) AGE : Tuberculosis affects all ages. Developing countries
show a sharp rise in infection rates from infancy to adolescence. In
India, from an average of 1 per cent in the "under 5 age group", the
infection index climbs to about 30 per cent at age 15 years (Table
3). In the developed countries, the disease is now more common in
the elderly, (b) SEX : More prevalent in males than in females, (c)
HEREDITY : Tuberculosis is not a hereditary disease. However,
twin studies (32) indicate that inherited susceptibility is an
important risk factor, (d) NUTRITION : Malnutrition is widely
believed to predispose to tuberculosis, but the available evidence
on this point is only indirect (33). Pioneering studies in India at the
Tuberculosis Chemotherapy Centre, Chennai showed that diet had
no discernible influence on the recovery of patients in the context
of potent chemotherapeutic drugs (34). (e) IMMUNITY : Man has
no inherited immunity against tuberculosis. It is acquired as a
result of natural infection or BCG vaccination. Past infection with
atypical mycobacteria is also credited with certain amount of
naturally acquired immunity. It is now known that both delayed
hypersensitivity and acquired resistance to tuberculosis are cellmediated responses. In most cases, the cellular immunity proves
adequate to limit further multiplication and spread of bacilli.
In the pre-chemotherapy era, the treatment of tuberculosis was
directed mainly at strengthening the host's resistance to disease by
altering the general host factors (e.g., rest, fresh air, nutrition).
With the advent of chemotherapy host factors are considered to be
less relevant in the epidemiology of tuberculosis (35).
Social factors
Tuberculosis is a social disease with medical aspects. It has
TUBERCULIN TEST
The tuberculin test was discovered by Von Pirquet in 1907. A
positive reaction to the test is generally accepted as evidence of
past or present infection by M. tuberculosis. The tuberculin test is
the only means of estimating the prevalence of infection in a
population.
There are three main tests currently in use : the Mantoux
intradermal test, the Heaf and the Tine multiple puncture tests. The
Heaf test is usually preferred for testing large groups of people
because it is quick and easy to perform, reliable and cheap. The
Mantoux is favoured when a more precise measurement of
tuberculin sensitivity is required. The Tine test is considered by
some authorities as unreliable, and therefore not recommended.
Tuberculin : The test material or antigen is known as
tuberculin. There are two major antigens - the old tuberculin (OT),
and the purified protein derivative (PPD). Since PPD is a purer
preparation, it gives fewer non-specific reactions and is easier to
standardize, it has replaced the OT. PPD is standardized in
terms of its biological reactivity as "tuberculin units" (TU). An
international standard is maintained by WHO against which the
potency of other preparations is measured. This standard PPD
(PPD-S) has been arbitrarily designated as. containing 50,000
tuberculin units per milligram (28)1 One TUt is equal to 0.01 ml of
OT or 0.00002 mg PPD^The WHO' advocates a PPD tuberculin
known as "PPD-RT-23 with Tween80".
Tuberculines for skin testing have also been prepared from
atypical mycobacteria. Thus we have PPD-B from the Battey
mycobacterium; PPD-Y from M. kansasii; scrofulin from M.
scrofulaceum, etc. These antigens are used in epidemiological
surveys; many of them, cross-react (36).
DOSAGE : The dosages of PPD in vogue are : (a) first strength
or 1 TU, (b) intermediate strength or 5 TU, and (c) the second
strength or 250 TU. For routine testing, the vaccinating teams in
India use 1 TU; in some countries, 5 TU are used. Nearly all truly
infected persons react to 1 to 5 tuberculin units. Stroriger doses
elicit a higher proportion of false positive (37). )
(MANTOUX TEST : The Mantoux test is carried out by| tS
injecting intradermally_on the flexor surface of the forearm 1 ./TU of
PPD in 0.1 rmjKhe WHO advocates a preparation
known as "PPD-RT-23 with Jween 80".(The result of the test
is read after 72 hours (3rd day)J
(juberculin reaction consists of erythema and induration.
Since erythema is sometimes difficult to measure, induration
, alone is measured (horizontal transverse diameter of induration
t in millimetres, using a transparent plastic ruler or callipers).
Reactions exceeding 10 mm are considered "positive". Those
: less than 6 mm are considered "negative". Those between 6
and 9 mm are considered "doubtful", i.e., the reaction may be
due to M. tuberculosis or atypical mycobacteria?!
It has been further observed that strong reactors (i.e., those
showing 20 mm or more induration) have greater chances of
developing tuberculosis than those showing 10 mm induration.
Those with less than 5 mm induration have more risk of
______________________________________TUBERCULOSIS 151
Incubation period
The time from receipt of infection to the development of a
positive tuberculin test ranges from 3 to 6 weeks, and thereafter,
the development of disease depends upon the closeness of
contact, extent of the disease and sputum positivity of the source
case (dose of infection) and host-parasite relationship. Thus the
incubation period may be weeks, months or years.
THE CONTROL OF TUBERCULOSIS
Tuberculosis control means reduction in the prevalence and
incidence of disease in the community. The WHO defines that
tuberculosis "control" is said to be achieved when the
prevalence of natural infection in the age group 0-14 years is
of the order of 1 per cent (47). This is about 40 per cent in
India. It means we have to go a long way to reach the goal of
control set by the WHO.
y
a.
b.
c.
d.
problem involved in the long term treatment. It can cause sideeffects which include vestibular damage and nystagmus rather than
deafness. Renal damage may also occur.
Pyrazinamide
This drug is bactericidal and is particularly active against the
slow-multiplying intracellular bacilli which are unaffected by
other drugs. It has been found to increase the sterilizing ability of
rifampicin. Therefore, pyrazinamide has been incorporated in
short-course chemotherapy regimens.
The drug is given orally and the usual dose is 30 mg/kg of body
weight (average 1.5 to 2 g) divided into two or three doses per day;
or 45-50 mg/kg body weight (average 2-3 g) twice weekly.
Complications include hepatotoxicity and hyperuricaemia.
Pyrazinamide achieves high levels in CSF and is, therefore,
recommended in tuberculous meningitis.
BACTERIOSTATIC DRUGS
Ethambutol
Ethambutol is bacteriostatic and is used in combination to
prevent the emergence of resistance to other drugs. It is given
orally. Its major side-effect is retro-bulbar neuritis; this however
does not occur at the usual dosage of 15 mg/kg body weight given
in 2 to 3 doses. Ethambutol has replaced para-aminosalicylic acid
(PAS) almost entirely among adults.
Thioacetazone
It is the only companion drug to INH that is commonly used in
India. The usual adult dose is 2 mg/kg body weight. Side-effects
include gastrointestinal disturbances, blurring of vision,
haemolytic anaemia and urticaria. The incidence of these sideeffects seem to differ in different ethnic groups.
There are other bacteriostatic drugs such as ethionamide,
prothionamide, PAS, cycloserine, kanamycin, viomycin and
capreomycin. The use of bacteriostatic drugs alone gives no
certainty of cure, though they may offer a high possibility of
arresting clinical progress of the disease.
Two-phase chemotherapy :
It is well recognized that there are two phases in the effective
treatment of tuberculosis : (i) the first is a short, aggressive or
intense phase, early in the course of treatment, lasting 1-3 months.
During this intensive phase, three or more drugs are combined to
kill off as many bacilli as possible. The more rapidly the bacilli are
killed initially, the less likely are "persisters" to emerge. The risk
of relapse is also lessened, (ii) the second or "continuation" phase
is aimed at sterilizing the smaller number of dormant or persisting
bacilli. In the standard anti-tuberculous therapy, the duration of
treatment was not less than 18 months to achieve complete
sterilization of the bacilli. With the introduction of rifampicin and
pyrazinamide, this period is now successfully reduced to 6-9
months.
DOMICILIARY TREATMENT:
The self-administration of drugs (generally oral drugs) by the
patients themselves without recourse to hospitalization is called
domiciliary or ambulatory treatment. The classical controlled
clinical trials (53j carried out at the Tuberculosis Chemotherapy
Centre, Chennai showed that the incidence of tuberculosis was no
greater in the contacts of patients treated at home than in the
contacts of patients treated in sanatoria (Table 4). It is now
universally accepted that with good chemotherapy, hospital
treatment has no advantage over domiciliary treatment, and
domiciliary treatment is to be preferred because in the long run, it
is so much cheaper than hospital treatment, and that it can be
managed by the primary
______________________________________TUBERCULOSIS 153
health care system and the general health services of the country. It
may be mentioned that it was this study, the classical Chennai
Study, that prompted a radical departure from the traditional
sanatorium to ambulatory or domiciliary treatment (35).
TABLE 4
Active tuberculosis developing among contacts of
patients treated at home and in hospital, Chennai
Place of treatment of case
No.of contacts
272
256
12 (4.7%)
24 (9.4%)
20 (7.0%)
38 (14.0%)
Source (53)
LONG-COURSE REGIMENS
The classical (long-course) conventional chemotherapeutic
regimens depended upon the use of INH along with one or two
bacteriostatic or "companion" drugs. The main role of the
bacteriostatic drugs was to prevent the emergence of INH-resistant
strains. Sterilization of the lesions thus depended entirely on INH,
and 18 months of treatment was required to avoid relapses. Two
main types of drug regimens were formulated for application in
India (54). These are :
a. daily regimens
b. biweekly or intermittent regimens
a. Daily regimens
In rural areas where medical supervision is not readily at hand,
daily regimens are ideally suited (Table 5).
The most frequently used combination in India is INH (300 mg
for adults) plus a companion drug which is usually thioacetazone
(150 mg) given together in a single daily dose. The combination of
INH plus thioacetazone is inexpensive, easy to administer and
convenient to the patient because he has to swallow only one tablet
a day. Streptomycin is given initially for the first two or three
months. The total duration of treatment is usually 18 months.
Since thioacetazone may have an adverse effect on liver
function, it should be fortified with vitamins of B-complex. In case
of toxicity, thioacetazone may be replaced by PAS or ethambutol.
For treatment of young children, PAS is preferred to ethambutol
because of ocular toxicity.
Observations of the daily regimen showed that in developing
countries, more than 50 per cent of patients defaulted before the
end of this long period of treatment. This is a major cause of
treatment failure. The irregularity of daily drug intake is another
factor leading to the emergence of drug-resistant organisms. Much
research has gone into finding more acceptable regimens.
b. Bi-weekly or intermittent regimens
Studies have shown that instead of daily chemotherapy, biweekly or intermittent regimens can be equally effective. They are
also cheaper, and less toxic to the patient. The standard biweekly
regimen is :
Streptomycin
INH
Pyridoxine
1 g or 0.75 g
600 or 700 mg
10 mg
(B)
Conventional Chemotherapy
1.2SHT + 10 HT
2.2 SH + 10 H2 S2
3.18 HT
4.12 HT
Short-Course Chemotherapy
1.2RHSZ + 4HR
2.2RHSZ + 4H2R2
3.2RHZ + 4HR
4.2 RHSZ + 4 S2 H2 Z2
5.2RHSZ + 6TH
6.6R3H3Z3S3
j-^\
CFOLLOW-UP : Patients on standard re^inren (Rx and R2) are
reviewed after sixth month and again at twelfth month collection.
Patients on short course chemotherapy regimen (RA and RB) are
reviewed at the time of third month collection and at six month
collection. If the patient continues to be smear positive on second
follow-up examination, he is referred to specialised institutions
(55) A
Instructions
Rj
R2
2 STH/10 TH
a) Intensive Phase
(2 months)
S = 0.75 g
H = 300 mg
T = 150 mg
b) Continuation Phase
(10 months) H =
300 mg T = 150
mg
12TH
H = 300 mg
T = 150 mg
12
R.
2 EHRZ/6TH
a) Intensive Phase (2 months)
E = 800 mg
H = 300 mg
R = 450 mg
Z = 1.5 g
b) Continuation Phase
(6 months)
H = 300 mg T =
150 mg
2 SHRZ/4 S2 H2 R2
a) Intensive Phase (2 months)
S = 0.75 g
H = 300 mg
R = 450 mg Z
= 1.5 g
b) Continuation Phase (4 months)
S = 0.75 g
H = 600 mg R =
600 mg
* An additional month is allowed for patients to complete the required treatment compensating for the missed collections. ** E to
replace S & vice versa, depending on availability; E to replace T, wherever not tolerated
S-streptomycin; R-rifampicin; T-thioacetazone; H-isoniazid; Z-pyrazinamide; E-ethambutol
Prefix number to a regimen indicates the number of months of that regimen/phase (e.g., 2 RHZ means RHZ for 2 months in the initial phase)
Number suffixed indicates the frequency of administration (e.g. 4 H2 R2 means INH and Rifampicin given twice weekly for 4 months). No
suffix means daily administration (e.g. 4 HR means INH and Rifampicin once daily for four months).
The dose given are for adults and would need adjustment for children on the basis of their age/weight
Intermittent regimen must be administered under full supervision.
All these regimens are of proven efficiency and anyone of these can be prescribed depending on the circumstance of the patient.
Thioacetazone should not be given to patients known to be HIV positive or at increased risk of HIV infection as severe hypersensitivity
reactions, including fatal exfoliative dermatitis can occur. For this reason thioacetazone should be replaced by ethambutol.
Source :J55) .
\./ft^
,yI DIRECTLY
'- >S-----------------------------------------------------------------OBSERVED TREATMENT, SHORT
medicine for the next week. The drugs are provided in patient-
^\ I
COURSE (DOTS) CHEMOTHERAPY
) r-wX
,
,
,
^ DOTS is a strategy to ensure cure by providing the most
effective medicine and confirming that it is taken. It is the only
strategy which has been documented to be effective worldwide on a programme basis. In DOTS, during the intensive
phase of treatment a health worker or other trained person
watches as the patient swallows the drug in his presence.
During continuation phase, the patient is issued medicine for
one week in a multiblister combipack, of which the first dose is
swallowed by the patient in the presence of health worker or
trained person. The consumption of medicine in the
____t:______i:____~u~.
: -,! l---------------I,1
u.,______t_____ l 4...
_______~iU~A
,;,J
TUBERCULOSIS 155
TABLE 6
Category of patients for treatment
Category
Regimen
Code
Ri
R2
a. Smear negative patients with X-ray evidence of tuberculosis other than those in (Rja).
b. Lost patients, smear negative on reporting back, irrespective of previous history of treatment.
c. Highly irregular patients (e.g. with cumulative default of more than a month in the intensive phase of
any of the regimens or in continuation phase of RB), irrespective of the smear result.
RA
NEW CASES
a. All smear positive cases newly indexed under DTP, irrespective of age and previous treatment outside
the programme.
b. Serious forms of extra-pulmonary tuberculosis (e.g., meningeal, spinal etc.).
RB
RE-TREATMENT CASES
a. Patients remaining smear positive on completion of treatment with Rp R2 & RA or on return after lost.
b. Cured patients returning with smear positive result.
NOTE : Patients requiring retreatment should be referred to DTC for initiation of treatment and sent back to the concerned
PHIs for continuation of prescribed regimen.
.':
.-'
Source : (55)
JT-&BLE7
Type of patient
Category 1
PreTest IF:
treatmen at
result
t
month is
sputum
2(HRZE)3
k THEN
>
Category II
2(HRZES)3
1 (HRZE)3 5
(HRE)3
2 (HRZ)3
4(HR)3
The number before the letters refers to the number of months of treatment. The subscript after the letters refers to the number of doses per
week. H: Isoniazid (600 mg), R: Rifampicin (450 mg), Z: Pyrazinamide (1500 mg), E: Ethambutol (1200 mg), S: Streptomycin (750 mg).
Patients who weigh more than 60 kg receive additional Rifampicin 150 mg. Patients more than 50 years old receive streptomycin 500 mg.
Patients in categories I and II, who have a positive sputum smear at the end of the initial intensive phase, receive an additional month of
intensive phase treatment.
**
Examples of seriously ill extra-pulmonary TB cases are meningitis, disseminated TB, tuberculous pericarditis, peritonitis, bilateral or extensive
pleurisy, spinal TB with neurological complications and intestinal and genito-urinary TB.
*** In rare and exceptional cases, patients who are sputum smear-negative or who have extra-pulmonary disease can have Relapse or Failure. This
diagnosis in all such cases should always be made by an MO and should be supported by culture or histological evidence of current, active
tuberculosis. In these cases, the patient should be categorized as 'Other' and given Category II treatment.
#
Any patient treated with Category I or Category III who has a positive smear at 5, 6 or 7 months of treatment should be considered a Failure
and started on Category II treatment, afresh.
MANAGEMENT OF PATIENTS
WHO INTERRUPT TREATMENT
Table 8, 9 and 10 show the management of patients who terrupt
the treatment under revised national tuberculosis jntrol
programme.
CG vaccination
Ever since Koch discovered M. tuberculosis, attempts have een
made to prepare a prophylactic vaccine against iberculosis using
either attenuated or killed tubercle bacilli.
TABLE 8
Management of patients who were smear-negative at diagnosis and who interrupt treatment
Treatment received
before interruption
Length of
interruption
Do a
sputum smear
examination
Less than 2
months
No
2 months or
more
Yes
Less than 2
months
No
More than 2
months
Yes
Result of sputum
smear
examination
Outcome
Re-registration
Treatment
Negative
Resume treatment
Positive
Negative
Positive
Default
New
Default
Treatment After
Default
Source : (56)
TABLE 9
Management of new smear-positive cases who interrupt treatment (Category I)
Result of sputum
smear
examination
Treatment received
before interruption
Length of
interruption
Do a
sputum smear
examination
Less than 2
weeks
No
2-7 weeks
8 weeks
or more
No
Yes
Positive
Less than 2
weeks
No
2-7 weeks
8 weeks
or more
1-2 months
Less than 2
weeks
2-7 weeks
8 weeks
or more
Outcome
Re-registration
Default
Treatment
Continue CAT I*
New
Negative
Continue CAT I*
Continue CAT I*
Yes
Positive
Negative
Positive
Yes
Continue CAT I*
Start on CAT II**
No
Yes
Yes
Default
Treatment
After Default
Negative
Continue CAT I*
Continue CAT I*
Positive
Default***
Negative
Positive
Negative
Default
Other
Continue CAT I*
Treatment
After Default
Start on CAT II **
Continue CAT I*
* A patient must complete all 24 doses of the initial intensive phase. For example, if a patient has to continue his previous treatment and he
took 1 month of treatment (12 doses) before interrupting, he will have to take 1 more month (12 doses) of the intensive phase treatment.
He will then start the continuation phase of treatment.
** A patient who must 'start again' will restart treatment from the beginning.
*** Although this patient does not strictly fit the definition of default, default most closely describes the outcome of this patient, although at reregistration they should be categorized as 'Other'.
Source : (56)
TUBERCULOSIS 157
TABLE 10
Management or retreatment smear-positive cases who interrupt treatment (Category II)
Treatment received
before interruption
Length of
interruption
Do a
sputum smear
examination
Less than 2
weeks
No
2-7 weeks
8 weeks
or more
No
Yes
Result of sputum
smear
examination
Treatment
After Default
Less than 2
weeks
No
2-7 weeks
Yes
Positive
8 weeks
or more
Yes
Negative
Positive
Less than 2
weeks
2-7 weeks
8 weeks
or more
No
Yes
Yes
Treatment
Positive
Negative
More than 2 months
Re-registration
Negative
1-2 months
Outcome
Default
Default
Positive
Default**
Negative
Positive
Negative
Default
Treatment
After Default
Other
Treatment
After Default
Source : (56)
(1)AIM : The aim of BCG vaccination is to induce a benign,
artificial primary infection which will stimulate an acquired
resistance to possible subsequent infection with virulent
tubercle bacilli, and thus reduce the morbidity and mortality
from primary tuberculosis among those most at risk.
(2)VACCINE : BCG is the only widely used live bacterial
vaccine. It consists of living bacteria derived from an
attenuated bovine strain of tubercle bacilli. The bacilli used for
vaccine production are descendants of the original Calmette
strain of BCG. Due to different methods of maintenance in
various vaccine-production laboratories, many substrains have
evolved during the past few decades. The WHO has
recommended the "Danish 1331" strain for the production of
BCG vaccine. Since January 1967, the BCG Laboratory at
Guindy, Chennai has been using the "Danish 1331" strain for
the production of BCG vaccine (57). Emphasis has been laid on
regular checking of the quality of vaccines at the International
Reference Centre for BCG quality control at Copenhagen.
(3)TYPES OF VACCINE : There are two types of BCG
vaccine - the liquid (fresh) vaccine and the freeze-dried
vaccine. Freeze-dried vaccine is a more stable preparation than
liquid vaccine with vastly superior keeping qualities. Presentday vaccines are distributed in the freeze-dried form.
BCG vaccine is stable for. several weeks at ambient
temperature in a tropical climate, and for up to 1 year jf kepi away
from direct light and stored in a cool environment (preferably
refrigerated at a temperature below 10 deg C (20).
The vaccine must be protected from exposure to light during
TUBERCULOSIS 157
TABLE 10
Management or retreatment smear-positive cases who interrupt treatment (Category II)
Treatment received
before interruption
Length of
interruption
Do a
sputum smear
examination
Less than 2
weeks
No
2-7 weeks
8 weeks
or more
No
Yes
Result of
sputum smear
examination
Positive
Negative
1-2 months
Less than 2
weeks
No
2-7 weeks
Yes
Positive
8 weeks
or more
Yes
Negative
Positive
Negative
More than 2 months
Less than 2
weeks
No
2-7 weeks
Yes
8 weeks
or more
Yes
Outcome
Default
Treatment
After Default
Default**
Negative
Negative
Treatment
After Default
Treatment
Start again on
CAT IP*
Continue CAT II*
Default
Positive
Positive
Re-registration
Default
Other
Treatment
After Default
Start again on
CAT II
Continue CAT II*
___________________________________
TUBERCULOSIS 159
POLIOMYELITIS 161
References
1.WHO (1982), Tech. Rep. Ser, 671.
2.WHO (2004), Global Tuberculosis
20.Snell, N.J.C. (1985). P.G. Doctor Middle East April 1985, 1232
21.Barua, B.N.M. (1978). Souvenir, 33rd National Conference on
p. 73
11.Humphrey, J.H. et al (1970). Immunology for Students of Medicine, Blackwell
12.WHO (1982). Tech. Rep. Ser. No. 652
13.Dam, H.G.T. etal (1976) Bull WHO, 54 (3) 255
14.Galazka, A.M. et al (1984). IV. H. Forum 5 (3) 269
15.Any Questions (1981). Brit. Med.J. 282 : 1305, 18 April 1981
16.Banker, D.D. (1969). Modern Practice in Immunization. Indian Journal of
Medical Sciences, Mumbai.
Tuberculosis
11
1.Pamra, S.R (1976). Ind.J. Chest Dis and allied Sciences, 23 : 152
2.Pamra, S.R (1979). Ind. J. Tuberculosis, 26 (3) 106
3.WHO (1980). WHO Chronicle, 34 : 101
4.Kamat, S.R. (1966). Bull WHO, 34 : 517
5.National Tuberculosis Institute, Bangalore (1974). News Letter, June 1974, p.42
6.Govt of India (1994), Manual for District Tuberculosis Officer, District
POLIOMYELITIS
Poliomyelitis is an acute viral infection caused by an RNA virus. It is primarily
an infection of the human alimentary tract but the virus may infect the central
nervous system in a very small percentage (about 1 per cent) of cases resulting in
varying degrees of paralysis, and possibly death.
Problem statement
In the pre-vaccination era, poliomyelitis was found in all countries of the world
(1). The extensive use of polio vaccines since 1954 has eliminated the disease in
developed countries.
In 1988, the World Health Assembly resolved to eradicate poliomyelitis
globally. Since then, implementation of the eradication strategies has reduced the
number of polio endemic countries from more than 125 in 1988 to 6 in 2003. These
countries are India, Afghanistan, Pakistan, Egypt, Niger
Country
2003
India
225
Pakistan
103
12
Afghanistan
Nigeria
Niger
Egypt
355
40
1
,133
12
1
Source : (2)
Acute flaccid paralysis (AFP) surveillance is conducted to
identify all remaining infected areas, monitor progress towards
eradication and target supplementary immunization appropriately.
Utilizing a network of health facilities throughout each country,
WHO recommends the immediate reporting and investigation of
every case of AFP in children aged less than 15 years, and
collection of 2 stool samples for analysis in a WHO accredited
laboratory. AFP surveillance is evaluated by 2 key indicators : the
sensitivity of reporting (target being non-polio AFP rate of at least
1 case per 100,000 children aged less than 15 years), and the
completeness of specimen collection (target being 2 adequate stool
specimens from at least 80 per cent of all AFP cases). AFP
surveillance in critical countries of the region is being conducted
through a network of surveillance medical officers, who receive
special training and are responsible for a defined catchment area
(3).
Jndia
In South-East Asia Region, India is the only country reporting
polio cases: A total of 225 wild poliovirus cases had been reported
from India during 2003, a marked decrease compared with the 1600
cases reported in 2002. Of the 225 cases, 203 (90%) were due to
wild poliovirus type 1 (PI) and 22 (10%) were wild poliovirus type
3 (P3). The three states with the highest number of cases in 2002
showed a markedly decreased incidence in 2003, with the number
of cases dropping from 1242 to 88 in UP, from 121 to 18 in Bihar,
and from 49 to 28 in West Bengal. In contrast, new foci of disease
erupted in 2003, in three south Indian states that had not> reported
polio cases for at least two years namely Karnataka (36 cases),
Andhra Pradesh (21 cases) and Tamil Nadu (2 cases). Delhi,
Gujarat, Haryana, Rajasthan and Jharkhand reported polio cases in
the early part of 2003. Cases in 2003 were reported from a total of
88 of 587 Indian districts, as compared with 159 districts in 2002.
P3 circulation occurred primarily in UP (16 cases, 73%). Of the 88
virologically confirmed cases in UP, 60 (68%) occurred in minority
populations (4).
All cases reported in India in 2003 were caused by virus
lineages traceable to poliovirus circulating in western UP, which
remains the source of polio that has been reintroduced to areas of
the country which had been polio-free for several months or years.
Although almost half of India's 35 states reported cases during
2003, only UP showed sustained transmission throughout the year.
The elimination of these poliovirus reservoirs will, therefore, be
critical to the success of polio eradication efforts in India and the
world (4).
______________________________________POLIOMYELITIS 163
incidence by dividing the prevalence rate (12.5) by the number of
years at risk (i.e. five), giving an average annual incidence of 2.5
per 1,000 in the age group 0-4 years.
If the 0-4 year population is known (usually 20%) the annual
incidence of polio for the whole population can be determined as
follows :
Annual incidence
per 1,000 in total =
population
POLIOMYELITIS 165
strains in the community and replaces them by attenuated strains
(21). The duration of immunity produced by the OPV is not
known, it may possibly even be lifelong\22j.
Failure of 3- dose regimen :
While 3 doses of OPV have been shown to be highly effective
in inducing immunity in developed countries (23) lower efficacy
has been reported in a number of developing countries (24). This
was amply demonstrated in the Delhi epidemic of 1971. The data
showed that the proportion of children developing antibody after
3 doses of trivalent vaccine can be as low as 30 per cent in
tropical countries, as against the more usual 90 per cent in
temperate climate countries (25, 26). This has been ascribed to
various possible factors, e.g., interference by antibodies in breast
milk, intercurrent enterovirus infections, and the presence of nonspecific inhibitors in saliva of infants etc. None of these
hypotheses has been definitely proved. Further, the frequency of
OPV failure has increased gradually from about 5 per cent in the
late 1960s to about 30 per cent currently (18). This failure
indicates a serious problem. In order to overcome this problem,
the Indian Academy of Paediatricians has recommended 5 doses
of OPV in clinic-based programmes, and 3 doses in community
campaigns. Some have recommended yearly doses up to the age
of 8 years (27). More recently it is recommended that a dose of
OPV is required to be given to all children delivered in health
institutions before their discharge from the hospital. The vaccine
should be given in the maternity wards. The child should not be
taken to regular immunization sessions to avoid risk of infection.
Breast- feeding does not interfere with OPV administration (28).
Advantages :
The advantages of OPV are : (i) since given orally, it is easy to
administer and does not require the use of highly trained
personnel (ii) induces both humoral and intestinal immunity, (iii)
antibody is quickly produced in a large proportion of vaccinees,
even a single dose elicits (except in tropical countries) substantial
immunity (iv) the vaccinee excretes the virus and so infects others
who are also immunized thereby (v) useful in controlling
epidemics (vi) relatively inexpensive (29, 30).
Complications :
OPV is remarkably free from complications. However, being
living viruses, the vaccine viruses, particularly type 3 do mutate
in the course of their multiplication in vaccinated children, and
rare cases of vaccine-associated paralytic polio have occurred in
(a) recipients of the vaccine, and (b) their contacts (13, 31). The
WHO has estimated the risk of vaccine-associated paralysis to be
about 1 case per million vaccinees, and the risk of a close contact
of a vaccinee developing paralytic polio, about 1 case per 5
million doses of vaccine (17).
Contraindications:
The contraindications for the administration of OPV are acute
infectious diseases, fevers, diarrhoea and dysentery. Patients
suffering from leukaemias and malignancy and those receiving
corticosteroids may not be given OPV. There is as yet no
indication that polio immunization may pose any danger to a
pregnant mother or developing foetus. However, OPV should be
delayed until after pregnancy unless immediate protection is
required, when IPV is indicated (9).
Storage:
(a) Stabilized vaccine : Recent oral polio vaccines are heat
stabilised. They can be kept without losing potency for a year at 4
deg. C, and for a month at room temperature (32).
OPV
(Sabin type)
POLIOMYELITIS 165
strains in the community and replaces them by attenuated strains
(21). The duration of immunity produced by the OPV is not
known, it may possibly even be lifelongV22j.
Failure of 3- dose regimen :
While 3 doses of OPV have been shown to be highly effective
in inducing immunity in developed countries (23) lower efficacy
has been reported in a number of developing countries (24). This
was amply demonstrated in the Delhi epidemic of 1971. The data
showed that the proportion of children developing antibody after
3 doses of trivalent vaccine can be as low as 30 per cent in
tropical countries, as against the more usual 90 per cent in
temperate climate countries (25, 26). This has been ascribed to
various possible factors, e.g., interference by antibodies in breast
milk, intercurrent enterovirus infections, and the presence of nonspecific inhibitors in saliva of infants etc. None of these
hypotheses has been definitely proved. Further, the frequency of
OPV failure has increased gradually from about 5 per cent in the
late 1960s to about 30 per cent currently (18). This failure
indicates a serious problem. In order to overcome this problem,
the Indian Academy of Paediatricians has recommended 5 doses
of OPV in clinic-based programmes, and 3 doses in community
campaigns. Some have recommended yearly doses up to the age
of 8 years (27). More recently it is recommended that a dose of
OPV is required to be given to all children delivered in health
institutions before their discharge from the hospital. The vaccine
should be given in the maternity wards. The child should not be
taken to regular immunization sessions to avoid risk of infection.
Breast- feeding does not interfere with OPV administration (28).
Advantages :
The advantages of OPV are : (i) since given orally, it is easy to
administer and does not require the use of highly trained
personnel (ii) induces both humoral and intestinal immunity, (iii)
antibody is quickly produced in a large proportion of vaccinees,
even a single dose elicits (except in tropical countries) substantial
immunity (iv) the vaccinee excretes the virus and so infects others
who are also immunized thereby (v) useful in controlling
epidemics (vi) relatively inexpensive (29, 30).
Complications:
OPV is remarkably free from complications. However, being
living viruses, the vaccine viruses, particularly type 3 do mutate
in the course of their multiplication in vaccinated children, and
rare cases of vaccine-associated paralytic polio have occurred in
(a) recipients of the vaccine, and (b) their contacts (13, 31). The
WHO has estimated the risk of vaccine-associated paralysis to be
about 1 case per million vaccinees, and the risk of a close contact
of a vaccinee developing paralytic polio, about 1 case per 5
million doses of vaccine (17).
Contraindications :
The contraindications for the administration of OPV are acute
infectious diseases, fevers, diarrhoea and dysentery. Patients
suffering from leukaemias and malignancy and those receiving
corticosteroids may not be given OPV. There is as yet no
indication that polio immunization may pose any danger to a
pregnant mother or developing foetus. However, OPV should be
delayed until after pregnancy unless immediate protection is
required, when IPV is indicated (9).
Storage:
(a) Stabilized vaccine : Recent oral polio vaccines are heat
stabilised. They can be kept without losing potency for a year at 4
deg. C, and for a month at room temperature (32).
OPV
(Sabin type)
References
1.WHO (1999), Health Situation in the South - East Asia Region 1994-1997,
Regional office for South East Asia, New Delhi.
2.WHO (2004), Weekly Epidemiological Record No. 25, June 18th 2004
3.WHO (2000), Weekly Epidemiological Record No. 26, 30 June 2000
4.WHO (2004), Weekly Epidemiological Record No. 13, March 26th 2004
5.LaForce, EM. et al (1980). Bull WHO, 58 (4) 609
6.ICMR (1975). ICMR Bulletin, Jan. 1975
7.Ofosu-Amaah Setal (1977). Brit.Med.J., 1 : 1012
__________________VIRAL HEPATITIS___________________
Viral hepatitis may be defined as infection of the liver caused
by any of half dozen viruses. Twenty years ago, hepatitis A virus
(HAV) and hepatitis B virus (HBV) were the only known
aetiological agents of viral hepatitis. Today, in addition to HAV
and HBV hepatitis viruses C, D, E and G have also been identified
and are recognized as aetiological agents of viral hepatitis. It is
known that many other viruses may be implicated in hepatitis such
as cytomegalo-virus, Epstein-Barr virus, yellow fever virus and
rubella virus. Viruses of herpes simplex, varicella and
adenoviruses can also cause severe hepatitis in immunocompromised individuals, but are rare.
HEPATITIS A
Hepatitis A (formerly known as "infectious" hepatitis or
epidemic jaundice) is an acute infectious disease caused by
hepatitis A virus (HAV). The disease is heralded by nonspecific
symptoms such as fever, chills, headache, fatigue, generalised
weakness and aches and pains, followed by anorexia, nausea,
vomiting, dark urine and jaundice. The disease spectrum is
characterised by the occurrence of numerous subclinical or
asymptomatic cases. The disease is
\*(G\
HEPATITIS B 169
Diagnosis
A specific laboratory diagnosis of hepatitis A can be obtained
by (15) :
a. demonstration of HAV particles or specific viral
antigens in the faeces
b. demonstration of a rise in anti-HAV titre
c. Detection of IgM antibody to HAV in the patient's
serum; this antibody appears early in the illness, and
persists for a limited time, usually for 3 to 4 months
after onset; IgG antibody indicates past infection and
immunity.
Prevention and containment
a. Control of reservoir :
Control of reservoir is difficult because of the following
factors: (a) faecal shedding of the virus is at its height during the
incubation period and early phase of illness (b) the occurrence of
large number of subclinical cases (c) absence of specific
treatment, and (d) low socio-economic profile of the population
usually involved. Strict isolation of cases is not a useful control
measure because of (a) and (b). However, attention should be
paid to the usual control measures such as notification, complete
bed rest and disinfection of faeces and fomites. The use of 0.5
per cent sodium hypochlorite has been strongly recommended as
an effective disinfectant (16).
b. Control of transmission :
The best means of reducing the spread of infection is by
promoting simple measures of personal and community hygiene,
e.g., handwashing before eating and after toilet; the sanitary
disposal of excreta which will prevent contamination of water,
food and milk; and purification of community water supplies by
flocculation, filtration and adequate chlorination. A question is
often asked how much chlorine is needed to inactivate the virus.
Studies indicated that 1 mg/L of free residual chlorine can cause
destruction of the virus in 30 minutes at pH values of 8.5 or less
(17). The water treatment and distribution system should be
improved. During epidemics, boiled water should be advocated
for drinking purposes. Several countries of the world have
achieved control of water-borne HAV infection. Other control
measures include proper autoclaving of syringes, needles and
other equipment. If all these measures are properly implemented,
a substantial reduction of HAV infection can be expected.
Problem statement
WORLD
Hepatitis B is endemic throughout the world, especially in
tropical and developing countries and also in some regions of
Europe (11). Its prevalence varies from country to country and
depends upon a complex mix of behavioural, environmental and
host factors. In general, it is lowest in countries or areas with high
standards of living.
The HBV infection is a global problem, with 66 percent of all
the world's population living in areas where there are high levels of
infection.
More than 2 billion people world wide have evidence of past or
current HBV infection and 350 million are chronic carriers of the
virus, which is harboured in the liver, the virus causes 60-80 per
cent of all primary liver cancer, which is one of the three top
causes of cancer death in East and SEAR, the Pacific Basin and
Sub-Saharan Africa (19).
Infection with HBV is a major cause of morbidity and
mortality in the SEAR. More than One-third of the papulation has
been infected with HBV, and it is estimated that there are
Myanmar
1
3.9
U12
Thailand
10
=IT
~Bangladesh
19
Indonesia
Bhutan
]6
"J2.5
(idem
"
Sri Lanka
____Jl.3
Nepa
l
1 Hepatitis B carriers
(2000)
3 Hepatitis C carriers
Maldives
India
16
11.8
1
5
11
~"1 1
31.4
|1
10
HBsAg
HBeAg
...:u.
.= Anti-HBs
___________....un.
Incubation
Acute infection
HEPATITIS B 171
cell-mediated immunity to hepatitis B antigens has also been
Hpmnn<;tratprl /Jfl]
Convalescence
Recovery
Modes of transmission
Symptoms
/\
/ \ /
'^- "
L I,
8
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1!
*$
1 /X\ X.** ^
i
>
i
1
i
2
//
//V
///|y
A
7\
/ / \/ \?
(E
,<***"
a. Parenteral route :
Hepatitis B is essentially a blood-borne infection. It is
transmitted by infected blood and blood products through
transfusions, dialysis, contaminated syringes and needles,
pricks of skin, handling of infected blood, accidental
inoculation of minute quantities of blood such as may occur
during surgical and dental procedures, immunization,
traditional tattooing, ear piercing, nose piercing, ritual
circumcision, accupuncture, etc. Accidental percutaneous
inoculations by shared razors and tooth brushes have been
implicated as occasional causes of hepatitis B (10).
b.
Perinatal transmission :
Spread of infection from HBV carrier mothers to their babies
appears to be an important factor for the high prevalence of
HBV infection in some regions, particularly China and SE Asia
(22). The risk of infection varies from country to country and
may reach 40 per cent. The mechanism of perinatal infection is
uncertain (10). Although HBV can infect the foetus in utero, this
rarely happens and most infections appear to occur at birth, as a
result of a leak of maternal blood into the baby's circulation, or
ingestion or accidental inoculation of blood (15). Infection of the
baby is usually anicteric and is recognized by the appearance of
surface antigen between 60-120 days after birth (10).
c. Sexual transmission :
There is ample evidence for the spread of infection by
intimate contact or by sexual route. The sexually promiscuous,
particularly male homosexuals, are at very high risk of infection
with hepatitis B.
d. Other routes :
Transmission from child-to-child, often called horizontal
transmission, is responsible for a majority of HBV infections
and carriers in parts of the world other than Asia. The
researchers believe that the spread occurs through physical
contact between children with skin conditions such as impetigo
and scabies, or with cuts or grazes. Often transmission occurs
when children play together or share the same bed (23).
Transmission by blood sucking arthropods (e.g., mosquitoes,
bed bugs) is suspected, but there is no convincing evidence to
support this suggestion (15).
In short, transmission occurs in a wide variety of
epidemiological settings. It can spread either from carriers or
from people with no apparent infection, or during the incubation
period, illness or early convalescence.
CIncubation period *f MftpWiC S
^- 45 to 180 days. Lower doses of the virus result often in longer
incubation period. The median incubation period is said
to be lower than 100 days/24j.(^t^^.
/ \l * s -f; . \
Clinical picture
The symptoms and manifestations of hepatitis B are similar
to those of the other types of viral hepatitis. But the picture is
complicated by the carrier state and by chronic liver disease,
which may follow the infection. Chronic liver disease may be
severe, and may progress to primary liver cancer which, in some
parts of the world, is one of the commonest human cancers,
particularly in men (25). The clinical course of hepatitis B in
adults is as shown in Fig. 4.
5-10%
85-90%
0%
0-90% 'nt
ClllUllil . cdiiiei
r
o L: . i.:
10-3
"1
FIG. 4
Clinical course of hepatitis B in adults
Source (26)
There are three distinct antigen antibody systems that relate to HBV
infection and a variety of circulating makers that are useful in diagnosis.
Interpretation of common serological patterns is as shown in Fig. 5.
Anti
HBc
HBsAg
Acute
Persistent
carrier
Recovery/
immunity
Immunity
from
vaccination
FIG. 5
(26)
PREVENTION AND CONTAINMENT
Since there is no specific treatment, prevention has been the major aim
C ^f*---------
af Hepatitis B vaccineN
HT) PLASMA DERIVED VACCINE : This is based on the surface
antigen (HBsAg) which is harvested and purified from the plasma of
human carriers of hepatitis B virus. The final vaccine is a formalin
inactivated sub-unit viral vaccine for intramuscular injection. Each 1.0 ml
dose of the vaccine contains 20 micrograms of hepatitis surface antigen
formulated in an alum adjuvant. The vaccine is given in 3 doses at 0,1 and
6 months (Table 1). An effective antibody response is generally attained
after 3 doses in 95 per cent of vaccinees (27). Immunity continues at
protective levels for approximately 3-5 years. Booster doses may be given
after 3-5 years.
TABLE 1
Hepatitis B vaccine : Immunization schedule
1st dose
2nd dose
3rd dose (booster)
1 ml
1 ml
1 ml
at elected date
1 month later
6 months after the
first dose
Children under 10 years of age should be given half of
above dosage at the same time intervals
____________________________________________HEPATITIS C 173
TABLE 2
Nomenclature and definitions of hepatitis viruses, antigens and antibodies
Component
{ System
Disease
Hepatitis A
HAV
Anti - HAV
IgM class antibody to HAV. Indicates recent infection with hepatitis A; positive up to 4-6 months after
infections
HBV
HBsAg
HBeAg
Hepatitis B e antigen. Soluble antigen ; associated with HBV replication, with high titers of
HBV in serum, and with infectivity of serum.
Hepatitk 15
Definition
passive
HBc
Hepatitis C
Anti - HCV
Hepatitis D
HCV
HDV
Hepatitis D virus. Etiologic agent of delta hepatitis ; causes infection only in presence of
HBV.
Hepatitis E
HDAg
Anti - HDV
HEV
Hepatitis E virus. Enterically transmitted hepatitis virus. Causes large epidemics in Asia and
North Africa ; faecal - oral or waterborne transmission. Perhaps a calicivirus.
Hepatitis G
Immune globulins
HGV
IG
HBIG
Source : (36)
,months
genus
___________CHOLERA 175
have been reported from Borneo, India, Indonesia, Mexico, Nepal,
Pakistan etc. However, Hepatitis E outbreaks or even sporadic cases are
rare in temperate climates. In Central Europe and in North America,
hepatitis E has been diagnosed only in patients returning from countries
with high endemicity for viral hepatitis. But screening of blood donors in
these areas has shown a prevalence of anti-HEV antibodies upto 2.5%.
The findings were similar for blood donors from South Africa (1.4%)
and Thailand (2.8%). Seroprevalence in blood donors from Saudi Arabia
and Egypt were significantly higher (9.5% and 24% respectively).
Diagnosis is made by the level of anti-HEV antibodies in the serum.
No confirmatory assay is currently available. Anti-HEV IgM antibodies
have been determined; however, their usefulness for the diagnosis of
acute hepatitis E infection remains to be confirmed.
Hepatitis E appears to be widespread problem in developing countries
where there are problems in providing safe drinking water and adequate
sewage disposal. General precautions against the infection are as outlined
for hepatitis A. For prevention, travellers to highly endemic areas are
recommended to take the usual elementary food hygiene precautions.
There is no specific treatment for hepatitis E. Only supportive measures
are required. Recovery from hepatitis E is always complete. No vaccine
or specific immunoglobulin prophylaxis is available. Preliminary studies
in primates indicate that protection through vaccination may be
achievable in the foreseeable future.
DELTA HEPATITIS
A new form of hepatitis that is considered to be a widespread threat is
"delta hepatitis" or hepatitis D (14). Delta hepatitis infection always
occurs in association with hepatitis B (carrier state). The mode of
transmission of this infection, its prevention and control are identical to
thosefor hepatitis B. Immunization against hepatitis B also protects
against delta infection (24). Delta hepatitis has not been reported as
significant in India (35).
HEPATITIS G
Hepatitis G virus HGV was discovered recently in 1996. The
prevalence of this infection is still not known. A few publications
provide information on the association of this infection with blood
transfusion in India (1).
The nomenclature and definitions used in the disease are shown in
Table 2.
References
1.WHO (1999), Health Situation in the South - East Asia Region 1994-97, South East Asia Region, New Delhi.
of Humans : Epidemiology
and Control.
TABLE 1
Number of cholera cases, deaths and case fatality rate
worldwide, notified to WHO 1961-2003
Year
1961
1971
1981
1991
1995
1996
1997
2000
2003
Cases (000)
62
176
51
595
208
143
147
137
112
Deaths
30560
26048
2448
19040
5034
6689
6274
4908
1894
TABLE 2
Notified cholera cases, deaths and case fatality rate in India
Year
Cases
Deaths
1950
176,307
86,997
49.34
1965
1975
1985
1994
1995
1996
1997
2000
2001
2003
43,285
21,955
5,808
4,973
3,315
4,396
2,768
3,807
12,947
2,320
155
32
5
34
16
18
6
2
29.9
10.5
2.6
0.64
0.15
0.77
0.58
0.47
0.15
4,081
2,893
0.069
...........................
Epidemiological features
...............................
CHOLERA 177
"epidemic strain" has also been used for these vibrios. Vibrios
that are biochemically similar to the epidemic strains
(V. cholerae 01) but do not agglutinate in V. cholerae 01
antiserum have been referred to in the past as
non-agglutinating (NAG) vibrios or as non-cholera vibrios
(NCV). These are now included in the species V cholerae and
are referred to as non-O Group 1 V. cholerae (non-epidemic
strains). It is now recognized that the NCV/NAG vibrios include
some species that are pathogenic for humans (e.g., Vibrio
parahaemolytlcus) which have caused outbreaks of choleralike diarrhoea. It is, therefore, necessary to identify V cholerae
01 for specific diagnosis of cholera (19). Within the O-Group
1, two biotypes - classical and El Tor, have been differentiated.
It may be mentioned that the El Tor biotype was first isolated at
the El Tor quarantine station in Egypt in 1905. Cholera is now
caused mostly by the El Tor biotype. Classical and El Tor
vibrios are further divided each into 3 serological types namely
Inaba, Ogawa and Hikojima. Most of the El Tor vibrios isolated
in India belong to the Ogawa serotype. The El Tor biotype
which are known for their haemolytic property, lost this
property as the pandemic progressed. They may be
distinguished from classical vibrios by the following tests :
(a)El Tor vibrios agglutinate chicken and sheep erythrocytes
(b)they are resistant to classical phage IV
(c)they are resistant to polymyxin B-50-unit disc
(d)the VP reaction and haemolytic test do not give
consistent results
12
are infectious for 2-3 weeks. The chronic carrier state may last
from a month up to 10 years or more.
Carriers in cholera (23)
A cholera carrier may be defined as an apparently healthy
person who is excreting V cholerae 01 (classical or El Tor) in
stools. Four types of cholera carriers have been described (24) :
(a) PRECLINICAL OR INCUBATORY CARRIER : Since the
incubation period of cholera is short (1-5 days), incubatory
carriage is of short duration. The incubatory carriers are
potential patients, (b) CONVALESCENT CARRIER : The
patient who has recovered from an attack of cholera may
continue to excrete vibrios, during his convalescence for 2-3
weeks. Convalescent state has been found to occur in patients
who have not received effective antibiotic treatment. The
convalescent carriers can often become chronic or long-term
carriers, (c) CONTACT OR HEALTHY CARRIER : This is the
result of subclinical infection contracted through association
with a source of infection, be it a case or infected environment.
The duration of contact carrier state is usually less than 10 days;
the gall bladder is not infected, and the stool culture is
frequently positive for V. cholerae 01. Contact carriers probably
play an important role in the spread of cholera,
(d)/CHRONIC CARRIER : A chronic carrier state occurs
infrequently. The longest carrier state was found to be over 10
years (25). Studies indicate that gall bladder is infected in
chronic carriers. Since carriers excrete fewer vibrios than cases,
selective media and proper enrichment are important for their
diagnosis) In carriers, the antibody titre against V. cholerae 01
rises anet remains positive as long as the person harbours the
organism. This method may be used to detect long-term
carriers along with bacteriological examination of stools.
Host factors
(a) AGE AND SEX : Cholera affects all ages and both sexes.
In endemic areas, attack rate is highest in children
(b) GASTRIC ACIDITY : An effective barrier. The vibrio is
destroyed in an acidity of pH 5 or lower. Conditions that
reduce gastric acidity may influence individual susceptibility
(25). (c) POPULATION MOBILITY : Movement of population
(e.g., pilgrimages, marriages, fairs and festivals) results in
increased risk of exposure to infection. In this jet age, cases and
carriers can easily transfer infection to other countries,
(d) ECONOMIC STATUS : The incidence of cholera tends to be
the highest in the lower socio-economic groups, and this is
attributable mainly to poor hygiene, (e) IMMUNITY : Natural
infection confers quite effective immunity (26). It appears that
immunity to V. cholerae is mediated mainly by the local
intestinal immune system (27). Vaccination gives only
temporary, partial immunity for 3-6 months.
Environmental factors
Vibrio transmission is readily possible in a community with
poor environmental sanitation. The environmental factors of
importance include contaminated water and food. Flies may
carry V. cholerae but not vectors of proven importance.
Numerous social factors have also been responsible for the
endemicity of cholera in India. These comprise certain human
habits favouring water and soil pollution, low standards of
personal hygiene, lack of education and poor quality of life.
Mode of transmission
Transmission occurs from man to man via (a) FAECALLY
CONTAMINATED WATER : Uncontrolled water sources such
as wells, lakes, ponds, streams and rivers pose a great threat.
(b) CONTAMINATED FOOD AND DRINKS : Ingestion of
contaminated food and drinks have been associated with
outbreaks of cholera. Bottle-feeding could be a significant risk
factor for infants. Fruits and vegetables washed with
Incubation period
X, From a few hours up to 5 days, but commonly 1 -2 days.
(Pathogenesis ^W
^ f The main symptom of cholera is diarrhoea. Diarrhoea in
cholera was attributed in the past to such factors as increased
permeability of the intestinal epithelial cells, increased
peristalsis, mucosal damage, an increase in mesenteric blood
flow and failure of the "sodium pump", i.e., interference with
the passage of sodium from the lumen to the plasma. None of
these theories stood the test of timej29).
According to current concepts, the cholera vibrio get
through the mucus which overlies the intestinal epithelium. It
probably secretes mucinase, which helps it move rapidly
through the mucus. Then it gets attached or adhered to the
intestinal epithelial cells, and this it probably does by an
adherence factor on its surface. When the vibrio becomes
adherent to the mucosa, it produces its enterotoxin which
consists of 2 parts - the light or L toxin and the heavy or
H toxin. The L toxin combines with substances in the epithelial
cell membrane called gangliosides and this binds the vibrio to
the cell wall. Binding is irreversible. The mode of action of
H toxin is not fully clear. What we know is that there is a
substance called "adenyl cyclase" in the intestinal epithelial
cells, and H toxin activates this substance. The activated
adenyl cyclase causes a rise in another substance, called 3, 5adenosine monophosphate, better known as cyclic or cAMP
(A physiologist got Noble Prize for describing this substance).
cAMP provides energy which drives fluid and ions into the
lumen of the intestine. This fluid is isotonic and is secreted by
all segments of small intestine. The increase in fluid is the cause
of diarrhoea, and not increased peristalsis. There is no
evidence that V. cholerae invades any tissue, nor the
enterotoxin to have any direct effect on any organ other than
the small intestine (29).
Clinical features
The severity of cholera is dependent on the rapidity and
duration of fluid loss. Epidemiological studies have shown that
more than 90 per cent of El Tor cholera cases are mild and
clinically indistinguishable from other acute diarrhoeas (5).
However, a typical case of cholera shows 3 stages : (a) STAGE
OF EVACUATION : The onset is abrupt with profuse, painless,
watery diarrhoea followed by vomiting. The patient may pass
as many as 40 stools in a day. The stools may have a "rice
water" appearance, (b) STAGE OF COLLAPSE : The patient
soon passes into a stage of collapse because of dehydration.
The classical signs are : sunken eyes, hollow cheeks, scaphoid
abdomen, sub-normal temperature, washerman's hands and
feet, absent pulse, unrecordable blood pressure, loss of skin
elasticity, shallow and quick respirations. The output of urine
decreases and may ultimately cease. The patient becomes
restless, and complains of intense thirst and cramps in legs and
abdomen. Death may occur at this stage, due to dehydration
and acidosis resulting from diarrhoea (c) STAGE OF
RECOVERY : If death does not occur, the patient begins to
Ingredient
Quantity
Sodium chloride
Sodium bicarbonate
Potassium chloride
Glucose (dextrose)
3.5g
2.5 g
1.5 g
20.0 g
Potable water
1 litre
Ingredient
Sodium chloride
Trisodium citrate dehydrate
Potassium chloride
Glucose
Potable water
Quantity
3.5 g
2.9 g
1.5 g
20.0 g
1 litre
TABLE 8
Maintenance therapy
Mild diarrhoea
j (not more than one stool every 2
hours or longer or less than 5 ml
stool per kg per hour)
Severe diarrhoea (more than
one stool every 2 hours, or more
than 5 ml of stool per kg per
hour)
Doxycycline
once
Infants
(under 12 months)
hour
5 hours
Older
30 minutes
2V2 hours
/~
TABLE 9
TABLE 7
First give 30 ml/kg in
6. Adjuncts to therapy
Antibiotics should be given as soon as vomiting has
stopped, which is usually after 3 to 4 hours of oral rehydration.
Injectable antibiotics have no special advantages. No other
medication should be given to treat cholera, like
antidiarrhoeals, antiemetics, antispasmodics, cardiotonics and
corticosteroids. Table 9 shows the antibiotics commonly
prescribed in severe cases of cholera. In regions where cholera
is present, it is important to identify those antibiotics to which
the vibrio cholerae 01 is resistant. If diarrhoea persists after 48
hours of treatment, resistance to antibiotic should be
suspected.
Age
Amount of diarrhoea
Tetracycline
4 times a day for 3 days
Trimethroprim (TMP)
sulfamethoxazole (SMX)
twice a day for 3 days
Furazolidone
4 times a day for 3 days
Children
Adults
300 mg(b) 500
12.5 mg/kg
TMP 5 mg/kg and
SMX 25 mg/kg (c)
1.25 mg/kg
mg
TMP 160 mg
SMX 800 mg
100 mg(d)
7. Epidemiological investigations
General sanitation measures must be applied at the onset of
an outbreak (see under sanitation measures). At the same time,
epidemiological studies must be undertaken to define the
extent of the outbreak and identify the modes of transmission
so that more effective and specific control measures can be
applied. The epidemiologist must maintain contact with all
health and civic units in his area to ensure detection of new
foci of disease.
There are certain institutions which are able to assist in
investigating outbreaks. These include the National Institute of
Communicable Diseases, Delhi and the All India Institute of
Hygiene and Public Health, Kolkata where epidemiological
teams are available for investigating epidemics. In addition,
stools for phage typing may be sent to the National Institute of
Mortality (000)
Africa
Americas
Eastern Mediterranean Region
Europe
South - East Asia
Western Pacific
Total
DALYs lost(000)
707
.57
259
16
605
154
1798
23237
2350
8661
692
20299
6687
61966
Source : (7)
As far as South - East Asia Region is concerned, the household
surveys carried out during 1994-1995 show that in under five year
children diarrhoea episodes ranged from 0.7 to 3.9 episodes per child per
year (Table 2).
Bangladesh
Bhutan
DPR Korea
India
Indonesia
Maldives
Myanmar
Nepal
Sri Lanka
Thailand
Estimated number of
episodes (000)
65,715
386
3,442
192,943
18,589
80
8207
11,171
1261
7253
Agent factors
In developing countries, diarrhoea is almost universally infectious in
origin. A wide assortment of organisms cause acute diarrhoea, and many
of them have been discovered only in recent years such as rotaviruses and
Campylobacters (Table 3).
TABLE 3
( 1. Viruses :
Rotaviruses
Astroviruses
I^^^J^, <
Adenoviruses
Calciviruses
Coronaviruses
Norwalk group viruses
Enteroviruses
2. Bacteria :
Campylobacter jejuni
Escherichia coli
Shigella
Salmonella
Vibrio cholerae
Vibrio parahaemolyticus
Bacillus cereus
3. Others
E. histolytica Giardia
intestinalis Trichuriasis
Cryptosporidium SPP
Intestinal worms \
Source (5)
TABLE 2
Country
Morbidity rate
(episodes per year per child
under five years)
3.5
3.9
1.3
1.7
0.8
2.0
1.7
3.3
0.7
1.3
Until recent years, the identification of pathogens in the stool was only
feasible in about 25 per cent of patients with acute diarrhoea. At present,
new techniques enable competent laboratories to identify these pathogens
in about 75 per cent of cases. The infectious agents most often connected
with diarrhoea in young children, in developing countries, are as shown in
Table 4.
TABLE 4
Pathogens frequently identified in children with acute diarrhoea
in treatment centres in developing countries
Pathogen
Viruses
Rotavirus
15-25
Bacteria
Enterotoxigenic
Escherichia coli
Shigella
Campylobacter jeijuni
Vibrio cholerae 01
Salmonella (non typhoid)
Enteropathogenic
Escherichia coli
10-20
5-15
10-15
5-10
1-5
1-5
Source : (6)
In India diarrhoeal disease is a major public health problem among
children under the age of 5 years. In health institutions, up to a third of
total paediatric admissions are due to diarrhoeal diseases and up to 17 per
cent of all deaths in indoor paediatric patients are diarrhoea related (8).
The household survey conducted during 1994 shows that the morbidity
rate in terms of diarrhoea episodes per year per child under five years is
about 1.7 (Table 2). The National Diarrhoeal Disease Control Programme
has made a significant
% of cases
Protozoans
No pathogen found
Cryptosporidium
-
Source (9)
(a) VIRUSES :
A great many diarrhoeal diseases are caused by viruses
5-15
20-30
that diarrhoea may be caused by a parenteral infection (nondigestive origin) and particularly so in younger children. These
include ENT infections, respiratory or urinary infections, malaria,
bacterial meningitis, or even simple teething (9).
Besides the above causes, malnutrition may lead to certain
nutritional diseases such as kwashiorkor, sprue, coeliac disease
and pellagra which are all associated with diarrhoea. In the
developed countries, the causes of diarrhoea may be slightly
different. Diarrhoea in the newborn is unusual and may be due to
inborn errors of metabolism such as congenital enzyme
deficiencies. It may also be associated with severe infections like
septicaemia or necrotizing enterocolitis (16).
Persistent diarrhoea is one of the main clinical signs of AIDS in
the tropics (an episode of diarrhoea lasting more than 30 days,
according to the WHO definition of AlDS in children). This is
associated with one or several other signs of the disease. Children
with measles or who have had measles recently, run a high risk of
developing severe or fatal diarrhoea (9).
Reservoir of infection
For some enteric pathogens, man is the principal reservoir and
thus most transmission originates from human factors ; examples
are enterotoxigenic E. coli, shigella spp., V. cholerae, Giardia
lamblia and E. histolytica. For other enteric pathogens, animals are
important reservoirs and transmission originates from both human
and animal faeces; examples are Campylobacter jejuni,
Salmonella spp and Y. enterocolitica. For viral agents of
diarrhoea, the role of animal reservoirs in human disease remains
uncertain.
Host factors
Diarrhoea is most common in children especially those
between 6 months and 2 years. Incidence is highest in the age
group 6-11 months, when weaning occurs. It reflects the
combined effects of declining levels of maternally acquired
antibodies, the lack of active immunity in the infant, the
introduction of contaminated food, and direct contact with
human or animal faeces when the infant starts to crawl. It is
also common in babies under 6 months of age fed on cow's
milk or infant feeding formulas (3). Diarrhoea is more common
in persons with malnutrition. Malnutrition leads to infection
and infection to diarrhoea which is a well known vicious circle.
Poverty,
prematurity,
reduced
gastric
acidity,
immunodeficiency, lack of personal and domestic hygiene and
incorrect feeding practices are all contributory factors.
Environmental factors
Distinct seasonal patterns of diarrhoea occur in many
geographical areas. In temperature climates, bacterial diarrhoea
occur more frequently during the warm season, whereas viral
diarrhoea, particularly diarrhoea caused by rotavirus peak during
the winter. In tropical areas, rotavirus diarrhoea occurs throughout
the year, increasing in frequency during the drier, cool months,
whereas bacterial diarrhoeas peak during the warmer, rainy season.
The incidence of persistent diarrhoea follows the same seasonal
patterns as that of acute watery diarrhoea (11).
Mode of transmission
Most of the pathogenic organisms that cause diarrhoea and all the
pathogens that are known to be major causes of diarrhoea in many
countries, are transmitted primarily or exclusively by the faecal-oral
route. Faecal-oral transmission may be water-borne; food-borne, or
direct transmission which implies an array of other faecal-oral routes
such as via fingers, or fomites, or dirt which may be ingested by /
young children (17).
Agent factors
(a)AGENT : S. typhi is the major cause of enteric fever. S.
para A and S. para B are relatively infrequent (6). S. typhi has
three main antigens - O, H and Vi and a number of phage types
1.Mata, L. (1986) World Health April 1986.
(at least 80). Phage typing has proved a useful epidemiological
2.WHO (1999), Health Situation in the South-East Asia Region 1994-1997,
tool in tracing the source of epidemics. S. typhi survives
Regional office of SEAR, New Delhi.
intracellularly in the tissues of various organs. It is readily
3.WHO (2004), World Health Report 2004, Report of the Director General,
killed by drying, pasteurization, and common disinfectants. The
WHO.
factors which influence the onset of typhoid fever in man are
4.Govt of India (1994), National Child Survival and Safe Motherhood
the infecting dose and virulence of the organism. - Y~~
Programme, MCH Division, Department of Family Welfare, Ministry of Health
4
StyC"T f%. h\ 9 h*' ^
and Family Welfare, New Delhi.
(b)RESERVOIR OF INFECTION': Man'is the only known
5.Fricker, J., Children in the Tropics 1993 - No.204
6.Bull WHO (1993) 61 : 252
reservoir of infection, viz cases and carriersN (i) CASES : The
7.WHO (1992) Readings on diarrhoea, Student Manual
case may be mild, missed or severe. A -case (or carrier) is
8.Steinhoff, M.C. and John T.J. (1980). Int. J. Paediat 47 : 317
infectious as long as bacilli appear in stools or urine. (ii)
9.Christie, A.B. (1980) Infectious Diseases : Epidemiology and Clinical Practice
CARRIERS Jflne carriers may be temporary (incubatory,
(3rd Ed), Churchill Livingstone.
convalescent) oT*T!hronic, Convalescent carriers excrete the
10.Pal, S.C. (1986) World Health April P. 14
bacilli for 6 to 8 weeks, after which their numbers diminish
rapidly. By the end of three months, not more than 4 per cent of
11.WHO (1980) Bull WHO, 58 (6) 819-830
cases are still excreting the organisms; and by the end of one
12.Pizzarro, D. (1985). Dialogue on Diarrhoea, Issue No.22 Sept.1985,
year, the average carrier rate is around 3 per cent (7). Persons
AHRTAG, 85 Marylebone High Street, London
who excrete the bacilli for more than a year after a clinical
13.R.G. Feachem (1984) Bull WHO 62 (3) 467-476
attack are called chronic carriers. In most chronic carriers, the
organisms persist in the gall bladder and in the biliary tract. A
C\
TYPHOID FEVER
chronic carrier sjate may be expected to develop in 2 to 5 per
csct of cases.fA^ chronic carrier may excrete the bacilli for
^several years (may be as long as 50 years) either continuously ;'^br
[Typhoid fever is the result,of systemic infection mainly by intermittently. The famous case of "Typhoid Mary" who
S^TQphi found only in manj The disease is clinically characterised v.j/gave rise to more than 1300 cases in her life time is a good
example of a chronic carrier. Faecal carriers are more frequent
by a typical continuous fever for 3 to 4 weeks,/ relative
than urinary carriers. Chronic urinary carrier state., is often
bradycardia with involvement of lymphoid tissues and
assocfateu1 wrtfr some abnormality &f the urinary Jxaat \ J^ _>
considerable constitutional symptoms. The term "enteric fever"
(c) SOURCE OF INFECTION : The primary source's of
includes both typhoid and paratyphoid fevers. The disease may
infection are faeces and urine of cases or carriers; the
occur sporadically, epidemicafity or encfemrcaA'y'.
secondary sources contaminated water, food, fingers and flies.
Problem statement
There is no evidence that typhoid bacilli are excreted in sputum
or milk.
WORLD
diarrhoeal diseases. EURO
Reports. Ser.No.44 Copenhagan, WHO
4 WHO (2004), Strengthening the Foundation of Health in South-East Asia, Vol.
Ill, 2001-2004
?B^----------
--------------- '
Host factors
\<A Q %^ %
(a) Age : Typhoid fever may occur at any age; Highest
incidence of this disease occurs in the 5-19 years of age groupj
After the age of 20 years, the incidence falls probably due t<5
acquisition of immunity from clinical or subclinical infection. (b)
Sex : More cases are reported among males than females, probably
as a result of increased exposure to infection. But carrier rate is
more in females, (c) Immunity: All ages are susceptible to
infection. Antibody may be stimulated by the infection or by
immunization; however, the antibody to the somatic antigen (O) is
usually higher in the patient with the disease, and the antibody to
the flagellar antigen (H) is usually higher in immunized
individuals. Serum antibodies are not the primary defences against
infection; S. typhi being an intracellular organism, cell-mediated
immunity plays a major role in combating the infection. Natural
typhoid fever does not always confer solid immunity; second
attacks may occur when challenged with a large oral dose. Among
the host factors that contribute to resistance to S. typhi are gastric
acidity and local intestinal immunity.
Environmental and social factors
Enteric fevers are observed all through the year. The peak
incidence is reported during July-September (8). This period
coincides with the rainy season and an increase in fly population.
Outside the human body, the bacilli are found in water, ice,
food, milk and soil for varying periods of time. Typhoid bacilli do
not multiply in water; many of them perish within 48 hours, but
some may survive for about 7 days. They may survive for over a
month in ice and icecream. They may survive for up to 70 days in
soil irrigated with sewage under moist winter conditions, and for
half that period under drier summer conditions (9). Food being a
bad conductor of heat, provides shelter to the bacilli which may
multiply and survive for sometime in food. Typhoid bacilli grow
rapidly in milk without altering its taste or appearance in anyway.
Vegetables grown in sewage farms or washed in contaminated
water are a positive health hazard. These factors are compounded
by such social factors as pollution of drinking water supplies, open
air defecation and urination, low standards of food and personal
hygiene and health ignorance. Typhoid fever may therefore be
regarded as an index of general sanitation in any country.
Incubation period
Usually 10-14 days. But it may be as short as 3 days or as long
as three weeks depending upon the dose of the bacilli ingested.
Modes of transmission
{Typhoid fever, js transmitted via the faecal-oral route or urineoral routesTjhis may take place directly through soiled
SOCIAL FACTORS
CULTURAL FACTORS
188
M
Faeces /
and
urine
----- >|
from
cases
or
carriers
Water
4^ Foods
Soil
raw
or
cooked
------------------------\
/*
~*|
Fingers
QUALITY OF LIFE
FIG.l Dynamics of
Typhoid Fever Transmission
Mouths
of
well
persons
C FACTORS
FOOD POISONING
Food poisoning is an acute gastro-enteritis caused by ingestion of food
or drink contaminated with either living bacteria or their toxins or
inorganic chemical substances and poisons derived from plants and
animals. The condition is characterised by (a) history of ingestion of a
common food (b) attack of many persons at the same time and (c)
similarity of signs and symptoms in the majority of cases.
Types of Food Poisoning
Food poisoning may be of two types : non-bacterial and bacterial, (a)
Non-bacterial : Caused by chemicals such as arsenic, certain plant and sea
foods. In recent years, there has been a growing concern about
contamination of food by chemicals, e.g., fertilisers, pesticides, cadmium,
mercury. (b) Bacterial: Caused by the ingestion of foods contaminated by
living bacteria or their toxins. The conventional classification of bacterial
food poisoning into toxic and infective types is becoming increasingly
blurred with the knowledge that in some types, both multiplication and
toxin production are involved (1). Bacterial food poisoning may be of the
following types :
Salmonella Food Poisoning
An extremely common form of food poisoning. Five reasons have been
given for its increase in recent years : (a) an increase in communal feeding
(b) increase in international trade in human food (c) a higher incidence of
salmonellosis in farm animals (d) widespread use of house-hold detergents
interfering with sewage treatment, and (e) wide distribution of "prepared
foods" (2).
(a) AGENT(S): The species most often incriminated in human
outbreaks are S. typhimurium, S. cholera -suis and S. enteritidis, besides
many others, (b) SOURCE : Salmonellosis is primarily a disease of
animals. Man gets the infection from/arm animals and poultry - through
contaminated meat, milk and milk products, sausages, custards, egg and
egg products. Rats and mice are another source; they are often heavily
infected and contaminate foodstuffs by their urine and faeces. Temporary
human carriers can also contribute to the problem, (c) INCUBATION
PERIOD : 12 to 24 hours commonly (d) MECHANISM OF FOOD
POISONING : The causative organisms, on ingestion, multiply in the
intestine and give rise to acute enteritis and colitis. The onset is generally
sudden with chills, fever, nausea, vomiting, and a profuse watery
diarrhoea which usually lasts 2 -3 days. Mortality is about 1 per cent. A
convalescent carrier state lasting for several weeks may occur (1).
Salmonellosis is described in detail separately.
Staphylococcal Food Poisoning
It is about as common as salmonella food poisoning, (a) AGENT :
Enterotoxins of certain strains of coagulase-positive Staphylococcus aureus.
At least 5 different enterotoxins have been identified, and a sixth may exist
(3). Toxins can be formed at optimum temperatures of 35 deg. to 37 deg. C. These
toxins are relatively heat stable and resist boiling for 30 minutes or more (b)
SOURCE : Staphylococci are ubiquitous in nature, and are found on the skin and in
the nose and throat of men and animals. They are a common agent of boils and
pyogenic infections of man and animals. Cows suffering from mastitis have
been responsible for /v^J outbreaks of food poisoning involving milk and milk
products, ty _ The foods involved are salads, custards, milk ad milk products /J,lwhich get contaminated by staphylococci, (c) INCUBATION PERIOD : 1-6 hours.
The incubation period is short because of ^preformed" toxin, (cf) MECHANISM
OF FOOD POISONING : >\Fbod poisoning results from ingestion of toxins
preformed in VtEe food in which bacteria have grown ("intradietetic" toxins). 51
organism has been found in faeces of humans and animals, and in soil,
water and air. The majority of outbreaks have been associated with the
ingestion of meat, meat dishes and poultry. The usual story is that the food
has been prepared and cooked 24 hours or more before consumption, and
allowed to cool slowly at room temperature and then heated immediately
prior to serving, (c) INCUBATION PERIOD : 6 to 24 hours, with a peak
from 10 to 14 hours (d) MECHANISM OF FOOD POISONING : The
spores are able to survive cooking, and if the cooked meat and poultry are
not cooled enough, they will germinate. The organisms multiply between
30 deg. and 50 deg. C and produce a variety of toxins, e.g., alpha toxin,
theta toxin, etc. Prevention consists either by cooking food just prior to its
consumption or, if it has to be stored, by rapid and adequate cooling (10).
(e) CLINICAL SYMPTOMS : The most common symptoms are
diarrhoea, abdominal cramps and little or no fever, occurring 8 to 24 hours
after consumption of the food. Nausea and vomiting are rare. Illness is
usually of short duration, usually 1 day or less. Recovery is rapid and no
deaths have been reported.
B. cereus Food Poisoning
Bacillus cereus is an aerobic, spore-bearing, motile, gram positive rod.
It is ubiquitous in soil, and in raw, dried and processed foods. The spores
can survive cooking and germinate and multiply rapidly when the food is
held at favourable temperatures. B. cereus has been recognised as a cause
of food poisoning, with increasing frequency in recent years.
Recent work has shown that B. cereus produces at least 2 distinct
enterotoxins, causing 2 distinct forms of food poisoning. One, the emetic
form with a short incubation period (1-6 hours) characterised by
predominantly upper gastrointestinal tract symptoms, rather like
staphylococcal food poisoning. The other, the diarrhoeal form, with a
longer incubation period (12-24 hours) characterised by predominantly
lower intestinal tract symptoms like CI perfringens food poisoning
(diarrhoea, abdominal pain, nausea with little or no vomiting and no fever.
Recovery within 24 hours is usual). The toxins are preformed and stable.
Diagnosis can be confirmed by isolation of 10 5 or more B. cereus
organisms per gram of epidemiologically incriminated food. Treatment is
symptomatic.
Differential diagnosis
Food poisoning may be mistaken for cholera, acute bacillary dysentery
and chemical (arsenic) poisoning. The differentiating points between
cholera and food poisoning are given in Table 1.
Cholera
Food poisoning
day" is a golden rule. When foods are held between 10 deg. C (50
deg. F) and 49 deg. C (120 deg.F) they are in the danger zone for
bacterial growth. Cold is bacteriostatic at temperature below 4 deg.
C (40 deg.F), and refrigeration temperature should not exceed this
level.
SURVEILLANCE : Food samples must be obtained from the
food establishments periodically and subjected to laboratory
analysis if they were unsatisfactory. Continuing surveillance is
necessary to avoid outbreaks of food-borne diseases.
References
1.Mandal, B.K. (1981). Medicine International, 2 : 56
2.Beveridge, W.I.B. (1967). in Health of Mankind, 100th Symposium,
AMOEBIASIS
The term "amoebiasis" has been defined by WHO (1) as the
condition of harbouring the protozoan parasite Entamoeba
histolytica with or without clinical manifestations. The
symptomatic disease occurs in less than 10 per cent of infected
individuals (2). The symptomatic group has been further
subdivided into intestinal and extraintestinal amoebiasis. Only a
small percentage of those having intestinal infection will develop
invasive amoebiasis. The intestinal disease varies from mild
abdominal discomfort and diarrhoea to acute fulminating
dysentery. Extraintestinal amoebiasis includes involvement of liver
(liver abscess), lungs, brain, spleen, skin, etc. Amoebiasis is a
potentially lethal disease. It carries substantial morbidity and
mortality.
Problem statement
WORLD : Amoebiasis is a common infection of the human
gastro-intestinal tract. It has a world-wide distribution. It is a major
health problem in the whole of China, South East and West Asia
and Latin America, especially Mexico. Globally it is estimated
that, in 1997, 45 million people carried E. histolytica in their
intestinal tract and approximately one-tenth of infected people,
suffered from invasive amoebiasis. It is probable that invasive
amoebiasis, accounted for about 70,000 deaths in the world (3).
Prevalence rates vary from as low as 2 per cent to 60 per cent or
more in areas devoid of sanitation (4). In areas of high prevalence,
amoebiasis occurs in endemic forms as a result of high levels of
transmission and constant reinfection. Epidemic water-borne
infections can occur if there is heavy contamination of drinking
water supply.
INDIA: It is generally agreed that amoebiasis affects about 15
per cent of the Indian population (5). Amoebiasis has been
reported throughout India : the prevalence rate is about 15%
ranging from 3.6 to 47.4 per cent in different areas (4). The
reported variations in prevalence are attributed to variations in
clinical diagnostic criteria (6) and to technical difficulties in
establishing a correct diagnosis and lack of sampling criteria (7).
AMOEBIASIS 193
Agent factors
(a) AGENT : Amoebiasis is caused by potentially pathogenic
strains of E. histolytica. Recent studies (8) have shown that
E. histolytica can be differentiated into at least 18 zymodemes
(a zymodeme is a population of organisms differing from
similar population in the electrophoretic mobilities of one or
more enzymes). It has furthermore been shown that pathogenic
strains are all from particular zymodemes; that non-invasive
strains are from quite distinct zymodemes; that invasive strains
can give rise to faecal cysts, and the organisms breed true (8).
The iso-enzyme characteristics do not, however, determine
why a particular zymodeme is able to invade. Isoenzyme
electrophoretic mobility analysis have so far identified 7
potentially pathogenic and 11 non-pathogenic zymodems (9).
E. histolytica exists in two forms - vegetative (trophozoite) and
cystic forms. Trophozoites dwell in the colon where they multiply
and encyst. The cysts are excreted in stool. Ingested cysts release
trophozoites which colonize the large intestine. Some trophozoites
invade the bowel and cause ulceration, mainly in the caecum and
ascending colon; then in the rectum and sigmoid. Some may enter
a vein and reach the liver and other organs.
The trophozoites are short-lived outside the human body; they
are not important in the transmission of the disease. In contrast the
cysts are infective to man and remain viable and infective for
several days in faeces, water, sewage and soil in the presence of
moisture and low temperature. The cysts are not affected by
chlorine in the amounts normally used in water purification, but
they are readily killed if dried, heated (to about 55 deg C) or
frozen.
(a)RESERVOIR OF INFECTION : Man is the only reservoir of
infection. The immediate source of infection is the faeces
containing the cysts. Most individuals infected with E.
Histolytica remain symptom free and are healthy carriers of the
parasite (12). The carriers can discharge up to 1.5 x 107 cysts
daily (6). The greatest risk is associated with carriers engaged
in the preparation and handling of food (6).
(b)PERIOD OF COMMUNICABILITY : As long as cysts are
excreted; the period may be several years, if cases are
unrecognized and untreated.
Host factors
Amoebiasis may occur at any age. There is no sex or racial
difference in the occurrence of the disease. Amoebiasis is
frequently a household infection. When an individual in a family is
infected, others in the family may also be affected. Specific
antiamoebic antibodies are produced when tissue invasion takes
place. There is strong evidence that cell-mediated immunity plays
an important part in controlling the recurrence of invasive
amoebiasis (10).
Environmental factors
Amoebiasis is more closely related to poor sanitation and socioeconomic status than to climate. The use of nightsoil for
agricultural purposes favours the spread of the disease. In countries
with marked wet-dry seasons, infection rates are higher during
rains, presumably since cysts may survive longer and the potential
for transmission is thereby increased. Epidemic outbreaks are
usually associated with sewage seepage into the water supply.
Mode of transmission
(i) Faecal-oral route : This may readily take place through
intake of contaminated water or food. Epidemic water-borne
infections can occur if there is heavy contamination of drinking
water supply. Vegetables, especially those eaten raw, from fields
irrigated with sewage polluted
water can readily convey infection. Viable cysts have been found
on the hands and under finger nails. This may lead to direct hand
to mouth transmission. (ii) Sexual transmission: by oral-rectal
contact is also recognized, especially among male homosexuals,
(iii) Vectors : such as flies, cockroaches and rodents are capable
of carrying cysts and contaminating food and drink.
Incubation period
About 2 to 4 weeks or longer.
PREVENTION AND CONTROL
1. Primary prevention
The measures aimed at primary prevention centre round
preventing contamination of water, food, vegetables and fruits with
human faeces, (a) Sanitation : Safe disposal of human excreta
coupled with the elementary sanitary practice of washing hands
after defecation and before eating is a crucial factor in the
prevention and control of amoebiasis. But there are too many
hurdles (both social and economic) in enforcing it in many
developing countries. With the cooperation of the local
community, the sanitary systems should be selected and
constructed (14) taking into consideration the customs and
practices of the population and the available resources.
(a)Water supply : The protection of water supplies against faecal
contamination is equally important because amoebic cysts may
survive for several days and weeks in water. The cysts are not
killed by chlorine in amounts used for water disinfection. Sand
filters are quite effective in removing amoebic cysts. Therefore
water filtration and boiling are more effective than chemical
treatment of water against amoebiasis.
(b)Food hygiene : Environmental measures should also include the
protection of food and drink against faecal contamination.
Uncooked vegetables and fruits can be disinfected with aqueous
solution of acetic acid (5-10 per cent) or full strength vinegar (1).
In most instances, thorough washing with detergents in running
water will remove amoebic cysts from fruits and vegetables. Since
food handlers are major transmitters of amoebiasis, they should be
periodically examined, treated and educated in food hygiene
practices such as hand-washing, (d) Health education : In the long
term, a great deal can be accomplished through health education of
the public.
2. Secondary prevention
(a)Early diagnosis : Demonstration of trophozoites containing
red cells is diagnostic. They are most readily seen in fresh
mucus passed per rectum. Microscopy should be performed
immediately before its cooling results. The absence of pus cells
in the stool may be helpful in the differential diagnosis with
shigellosis. Serological tests are often negative in intestinal
amoebiasis, but if positive, they provide a clue to extraintestinal
amoebiasis. Indirect haemagglutination test (IHA) is regarded
as the most sensitive serological test. Newer techniques include
counter immuno-electrophoresis (CIE) and ELISA technique
(11).
(b)Treatment : (i) Symptomatic cases : At the health centre
level, symptomatic cases can be treated effectively with
metronidazole orally and the clinical response in 48 hours may
confirm the suspected diagnosis. The dose is 30 mg/kg of body
weight/day, divided into 3 doses after meals, for 8-10 days.
Tinidazole can be used instead of metronidazole. Suspected
cases of liver abscess should be referred to the nearest hospital.
(ii) Asymptomatic infections : In an endemic area, the
consensus is not to treat such persons because the probability of
reinfection is very high (10). They may, however, be treated, if
the carrier is a food handler. In non-endemic areas they are
ASCARIASIS
An infection of the intestinal tract caused by the adult, Ascaris
Iumbricoides and clinically manifested by vague symptoms of
nausea, abdominal pain and cough. Live worms are passed in the
stool or vomited. Occasionally, they may produce intestinal
obstruction or may migrate into the peritoneal cavity (1).
Geographic distribution and prevalence
Ascaris is cosmopolitan in distribution. It is the most common
helminthic infestation. It is estimated that about 1.3 billion people
were infected worldwide and the prevalence of the infestation was
about 250 million during 1997 (2).
Epidemiological features
(a) AGENT : Ascaris Iumbricoides lives in the lumen of small
intestine, where it moves freely. Sexes are separate. The female
measures 20-35 cm in length, and the male 12-30 cm. Egg
production is very heavy - an estimated 2,40,000 eggs per day by
each female, which counterbalances the heavy losses in the
environment. The eggs are excreted in the faeces. They become
embryonated in the external environment and become infective in
2-3 weeks. On ingestion by man, the embryonated eggs hatch in
the small intestine. The resulting larvae penetrate the gut wall and
are carried to the liver and then to the lungs via the blood stream.
In the lungs, they moult twice. They break through the alveolar
walls and migrate into the bronchioles. They are coughed up
through the trachea and then swallowed by the human host. On
reaching the intestine, they become mature into adults in 60-80
days. The life span of an adult is between 6-12 months, maximum
reported being 1.5 years, (b) RESERVOIR OF INFECTION : Man
is the only reservoir, (c) INFECTIVE MATERIAL : Faeces
containing the fertilized eggs, (d) HOST : Infection rates are high
in children; they are the most important disseminators of infection.
Adults seem to acquire some resistance. There is a high degree of
host-parasite tolerance. Roundworms rob man of his food.
Mode of transmissiorj^^ ^
f By the FAECAL-ORAL route, i.e., by ingestion of infective egs
with food or drink. Foods that are eaten raw such as salads and
vegetables readily convey the infection, and so is polluted water.
Other means of spread are by fingers contaminated with soil or by
ingestion of contaminated soil (pica) as usually happens in the
case of children playing with soil. There is increasing evidence
that dust may play an important role in the dissemination of ascaris
in arid areas (3).
Incubation period
About 2 months.
PREVENTION AND CONTROL
Primary prevention
Methods based on primary prevention are the most effective in
interrupting transmission. These are : sanitary disposal of human
excreta to prevent or reduce faecal contamination of the soil,
provision of safe drinking water, food hygiene habits, and health
education of the community in the use of sanitary latrines,
personal hygiene and changing behavioural patterns. Prevention,
to be effective, must take into consideration the life cycle of the
parasite and the peculiar ecological, social and cultural
circumstances that prevail in a community.
Secondary prevention
Effective drugs are available for the treatment of the human
reservoir. These are piperazine, mebendazole, levamisole and
pyrantel; the last two drugs are effective in a single dose. (a)
Piperazine : More than 20 years of experience world-wide has
confirmed the safety record of this drug (4). The most widely used
preparations are piperazine citrate prepared as a flavoured syrup
and piperazine phosphate as tablets. An accepted and safe schedule
is an oral dose of 75 mg/kg of body weight with a maximum
individual dose of 3.5 g for 2 days (5). The drug paralyses the
worms, which can then be expelled by a purgative, (b)
Mebendazole : The usual dose is 100 mg twice daily for 3 days
irrespective of the patient's age (3). (c) Levamisole ; It is the
levorotatary form of tetramisole and is more active than the parent
compound. For many it is now the drug of choice. A single oral
dose of 2.5 mg/kg of body weight (maximum 150 mg) has been
recommended. There are usually no side effects. It has been used
successfully in the mass treatment of ascariasis.(d) Pyrantel:
Effective in a single dose of 10 mg/kg of body weight (3) with a
maximum of lg.
of Pediatrics, Saunders,
Philadelphia
HOOKWORM INFECTION
Hookworm infection is defined as "any infection caused by
Ancylostoma duodenale or Necator americanus" (1). They may
occur as single or mixed infections in the same person.
Problem statement
Ancylostoma duodenale and Necator americanus are the main
nematodes causing hookworm infection in man. Almost eradicated
from Europe and the USA (2), hookworm infection is still seen in
warm, moist climates in tropical and subtropical regions between
45N and 30S of the equator (e.g., Asia, Africa, Central and
South America and the South Pacific). The geographic distribution
of these two hookworms used to be regarded as relatively distinct,
the former being more prevalent in Europe and South-western
Asia, and the latter in tropical Africa and in the Americas.
However, over the past decades both parasites have become
widely distributed throughout the tropics and subtropics, and rigid
demarcations are no longer tenable (2).
It is estimated that during 1997 the global prevalence of
hookworm infection was about 151 million cases. The annual
number of deaths were approximately 65,000 as a result of
hookworm anaemia (3).
INDIA : Hookworm infection is widely prevalent in India
(4,5,6,7,8). Necator americanus is predominant in South India, and
Ancylostoma duodenale in North India. Recently another species,
A. ceylanicum has been reported from a village near Kolkata^.
The heavily infected areas are found in Assam (tea gardens),
West Bengal, Bihar, Orissa, Andhra Pradesh, Tamil Nadu, Kerala
and Maharashtra. More than 200 million people are estimated to be
infected in India. It is believed that 60 to 80 per cent of population
of certain areas of West Bengal, U.P., Bihar, Orissa, Punjab and
eastern coast of Tamil Nadu and AnfUtra Pradesh are infected with
hookworms (10).
r
EniJemic index
" /-N [Morbidity and mortality from hookworm infection depends
^Anuch on the worm load. Chandler (11) worked out an index
on the basis of average number of hookworm eggs per gram of
TABLE 1
Recommended anthelminthics for hookworm infection
Single dose
Albendazole
Mebendazole
400 mg
(all ages above 2 years)
500 mg
(all ages above 2 years)
OR
100 mg twice daily
for 3 days
+++
N, americanus
Divided doses
Efficacy
Species sensitivity
+++
A. duodenale
Side-effects
Contraindications
Broad-spectrum,
effective against
Source : (12)
Levamisole
Pyrantel
50-150 mg
(3 mg/kg) body wt)
+
A. duodenale
DRACUNCULIASIS 197
3. Treatment of anaemia
When anaemia is severe it should be treated. A cheap and
effective treatment is ferrous sulphate 200 mg three times a day
orally, and continued for 3 months after the haemoglobin has risen
to 12 g/100 ml. Patients with severe hypoalbuinaemia should be
adequately and quickly dewormed (2). If concomitant folic acid
deficiency exists, it should be treated.
4. Health education
Community involvement through health education is an
important aspect in the control of hookworm infection. Health
education should be aimed at promoting the use of sanitary latrines,
prevention of soil pollution and measures of personal prophylaxis
such as wearing of protective footwear and making use of health
facilities for diagnosis and treatment.
What is needed is an integrated approach incorporating the
above principles of prevention and control. Such a programme
must be comprehensive and cover the fundamental aspects of
sanitation and personal prophylaxis. Since the incidence of
ancylostomisis reflects the quality of life of the people and its
on
cultural habits, its reduction is directly dependent on improvement
of economic and social conditions.
References
1.
WHO (1987) Tech. Rep. Ser. 749
2.WHO (1981) Tech. Rep. Ser. 666
3.WHO (1998), World Health Report 1998, Report of the Director
General WHO
4.Patel, J.C. (1954). Indian J. Med. Res., 42 : 279-304
5.Arora, D.D. et al (1971). J. Cow. Dis., 3 (3-4) 146-158
6.Saxena,P.C. and Prasad, B.G. (1971). Ind. J. Pub. Health, 15(1)31-37
7.Rao, C.K. et al (1973). J. Com. Dis., 5 (2) 80-86.
8.Arora, R.R. et al (1976). J. Com.Dis., 8 (1) 66-76
9.Chowdhury, A.B. and Sehad, G.A. (1972). Am. J. Trop.MedandHyg.,
21:300-301
10.Dutta, PR. (1962). Rural Health Surveys in India, PH. centres CHEB,
DGHS, New Delhi
11.Chandler, A.C. (1927). Indian J. Med., Res., 15 : 695-743
12.Powlowski, Z.S. Schad, G.A., Stott, G.J., Hookworm Infection and
Anaemia, Approaches to Prevention & Control, WHO Publication
DRACUNCULIASIS
Natural history
(a) AGENT : The adult parasite inhabits the subcutaneous
tissue mainly of the legs but also of other parts of the body,
including the head and neck. The female grows to a length of
55 to 120 cm, and the male is very short (2-3 cm). The gravid
female makes her way down to the infected person's lower
limbs near the skin surface. There she penetrates into the
dermis and induces an inflammatory reaction and subsequent
blister formation. Upon contact with water, the blister soon
ruptures and the parasite releases up to one million,
microscopic, free-swimming larvae into water. The larvae may
remain active in water for 3-6 days. They are picked up by
small fresh-water crustaceans called cyclops. The larvae
require a period of about 15 days for development in cyclops,
which is the intermediate host.
Man acquires infection by drinking water containing infected
cyclops. In the human body, digested by gastric juice, the parasites
are released. They penetrate the duodenal wall. Subsequently they
migrate through the viscera to the subcutaneous tissues of various
parts of the body. They grow into adults in 9-12 months.
(a)RESERVOIR OF INFECTION : An infected person
harbouring the gravid female. The possibility of an animal
reservoir exists but not proved (4).
(b)HOST FACTORS : Host susceptibility is universal. Multiple
and repeated infections may occur in the same individual. The
habit of washing and bathing in surface water and using stepwells is important.
(c)ENVIRONMENTAL FACTORS : The main link in the
transmission of guineaworm disease is water infested with
cyclops. The risk of transmission exists where such cyclopsinfested water-sources are frequented by infected persons.
Season : The seasonal variations in the incidence of the disease
are marked. Where the step-wells are the source of water
supply, peak transmission occurs during the dry season (MarchMay) when the contact between open cases of gunieaworm
disease and the drinking water is the greatest; and there is little
transmission when the wells are full during and after rains.
Where the ponds are used, transmission appears to be confined
to June-September, when the ponds contain water (5,6).
Temperature : The larvae develop best between 25 and 30 deg
C, and will not develop below 19 deg C. Therefore, the disease
is limited to tropical and subtropical regions (7).
Eradication
f Guineaworm disease is amenable to eradication. The
eradication strategy comprises the following elements :
i) Provision of safe drinking water (e.g., piped water, installation
of hand pumps)
ii) Control of cyclops (see. Chap. 12)
iii) Health education of the public in matters relating to boiling or
sieving drinking water through a double-thickness cotton cloth
for personal protection, and prevention of water contamination
by infected persons.
iv) Surveillance : Active search for new cases
v) Treatment of cases : The drugs available for this purpose are
Niridazole, Mebendazole and Metronidazole. None of these
drugs have any effect in preventing transmission of the disease
(5). No drug is suitable for effective mass treatment (8).
Problem statement
Of all the arthropod-borne viral diseases, dengue fever is the most
common. Dengue fever is one of the most important emerging disease of
the tropical and sub-tropical regions, affecting urban and periurban areas.
The geographical distribution of the disease has greatly expanded and the
number of cases has increased dramatically in the past 30 years. Some 2.53 billion people live in areas where dengue viruses can be transmitted. A
pandemic in 1998, in which 1.2 million cases of dengue fever and dengue
haemorrhagic fever were reported from 56 countries, was unprecedented.
Preliminary data for 2001, indicates a situation of comparable magnitude.
However, only a small proportion of cases were reported to WHO; it is
estimated that each year 50 million infections occur, with 5,00,000 cases
of dengue haemorrhagic fever and at least 12000 deaths, mainly among
children, although fatalities could be twice as high (3). The increase of
dengue and DHF is due to uncontrolled population growth and
urbanization without appropriate water management, to the global spread
of dengue via travel and trade, and to erosion of vector control programme
(4).
By 1997 most of the countries of SEAR have experienced large
outbreaks of the disease. Currently, DF/DHF is endemic in Bangladesh,
India, Indonesia, Maldives, Myanmar, Sri Lanka and Thailand and
approximately 1.3 billion people are living in the endemic areas. Dengue
is notifiable disease in Indonesia, Myanmar, Sri Lanka and Thailand in the
Region. During the last 15 years, all four dengue subtypes have been
isolated in India, Indonesia, Myanmar and Sri Lanka and DEN-2 and
DEN-3 have been reported in Maldives and Bangladesh (5).
Over the past 10-15 years, next to diarrhoeal disease and acute
respiratory infections, dengue has become a leading cause of
hospitalization and deaths, among children in the South East Asia Region.
In addition, DHF is increasing and spreading to new areas. The estimated
number of annual dengue cases in the Region is between 20-30 million
and DHF cases about 2,00,000 (5). However, the number of DHF cases
reported by endemic countries is substantially lower. The case
I------------- '------------ 1
Asymptomatic
Symptomatic
|------------------------ '--------------- 1
Undiffrentiated
(viral syndrome)
Dengue haemorrhagic
fever
Dengue fever
(syndrome)
,__________(plasma
_____________I___________
Without
haemorrhage
With unusual
haemorrhage
Dengue fever
I----------------------------------- (DF) --------------------------------------- 1
FIG. 1 Manifestations of the dengue syndrome Source : (1)
leakage)
No shock
Dengue shock
syndrome (DSS)
Dengue haemorrhagic
I------------------------------- fever(DHF)----------------------------------- '
Cases
Deaths
95
0
2882
14
249
95
1226
3546
772
0
848
685
1600
738
12750
5
0
35
2
9
6
7
68
45
0
13
11
8
8
217
Source : (6)
Since 1996, NAMP has been monitoring dengue situation in the
country. Government of India has issued certain guidelines on
prevention and control of dengue.
Refer to chapter 7 for details.
1. Classical Dengue Fever
Classical Dengue or "break-bone fever" has been known in
India for a very long time. It is an acute viral infection, caused by
at least 4 serotypes (1, 2, 3 and 4) of dengue virus. Dengue fever
can occur epidemically or endemically. Epidemics may be
explosive and often start during the rainy season when the breeding
of the vector mosquitoes (e.g., Aedes aegypti) is generally
abundant. Temperature also plays an important role in the
transmission of dengue virus by mosquitoes. Mosquitoes kept at
26C fail to transmit DEN-2 virus (2), Hence, the low incidence of
DHF in certain seasons could be explained by this observation.
The reservoir of infection is both man and mosquito. The
transmission cycle is "Man-mosquito-Man". Aedes aegypti is the
main vector. Dengue outbreaks have also been attributed to Aedes
albopictus, Aedes polynesiensis, and several species of the Aedes
scutellaris complex.
The Aedes mosquito becomes infective by feeding on a
patient from the day before onset to the 5th day (viraemia stage) of
illness. After an extrinsic incubation period of 8 to 10 days, the
mosquito becomes infective, and is able to transmit the infection.
Once the mosquito becomes infective, it remains so for life.
Transovarian transmission of dengue virus has been demonstrated
in the laboratory.
All ages and both sexes are susceptible to dengue fever.
Children usually have a milder disease than adults. The illness is
characterised by an incubation period of 3 to 10 days (commonly
5-6 days). The onset is sudden with chills and high fever, intense
headache, muscle and joint pains, which prevent all movement.
Within 24 hours retro-orbital pain, particularly on eye movements
or eye pressure and photophobia develops. Other common
symptoms include extreme weakness, anorexia, constipation,
altered taste sensation, colicky pain and abdominal tenderness,
dragging pain in inguinal region, sore throat and general
depression. Fever is usually between 39 C and 40C. Fever is
typically but not inevitably followed by a remission of a few hours
to 2 days (biphasic curve). The skin eruptions appear in 80 per cent
of cases during the remission or during second febrile phase, which
lasts for 1-2 days. The rash is accompanied by similar but milder
symptoms. The rash may be diffuse flushing, mottling or fleeting
pin-point eruptions on the face, neck and chest during the first half
of the febrile period and a conspicuous rash, that may be
maculopapular or scarlatiniform on 3rd or 4th day. It starts on the
chest and trunk and may spread to the extremities and rarely to the
face. It may be accompanied by itching and hyperaesthesia. The
rash lasts for 2 hours to several days and may be followed by
desquamation (2). Fever lasts for about 5 days, rarely more than 7
days after which recovery is usually complete although
convalescence may be protracted (7). The case fatality is
exceedingly low. Infection with one dengue serotype gives
immunity against that particular serotype and partial protection
against others.
2. Dengue Haemorrhagic Fever
Dengue haemorrhagic fever (DHF) is a severe form of dengue
fever, caused by infection with more than one dengue virus. The
severe illness is thought to be due to double infection with dengue
viruses - the first infection probably sensitizes the patient, while the
second appears to produce an immunological catastrophe (8). DHF
is transmitted by A. aegypti.
Following an incubation period of four to six days, the illness
commonly begins abruptly with high fever accompanied by facial
flushing and headache. Anorexia, vomiting, epigastric discomfort,
tenderness at the right costal margin and generalized abdominal
pain are common. During the first few days the illness usually
resembles classical DF, but maculopapular rash usually rubelliform
type, is less common. It may appear early or late in the course of
the illness. Occasionally, the temperature may be 40C to 41 C
and febrile convulsions may occur particularly in infants {2).
The major pathophysiologic changes that determine the severity
of disease in DHF and differentiate it from DF are plasma leakage
and abnormal haemostasis, as manifested by a rising haematocrit
value and moderate to marked thrombocytopenia. These two
clinical laboratory changes are distinctive and constant findings.
CRITERIA FOR CLINICAL DIAGNOSIS OF DHF
The following clinical manifestations have been selected as
indicating a clinical diagnosis of DHF without shock (9).
Clinical diagnosis
(a) Fever - acute onset, high, continuous, and lasting 2 to 7
days.
MALARIA 201
CONTROL MEASURES
1. Mosquito control
The vectors of DF and DHF (e.g., A. aegypti) breed in and around
houses and, in principle can be controlled by individual and community
action, using antiadult and antilarval measures. These measures are
outlined in chapter 12.
2. Vaccines
So far, there is no satisfactory vaccine and no immediate prospect of
preventing the disease by immunization.
3. Other measures
Isolation under bed nets during the first few days; individual protection
against mosquitoes.
References
1.WHO (1986). Dengue HaemorrhagicFever, P.7
2.WHO (1993), Monograph on Dengue/Dengue Haemorrhagic Fever,
Compiled by Prasert Thongchroen, Regional Publication, SEARO No.22
3.WHO (2002), Weekly Epidemiological Record, No. 6, 8th Feb. 2002.
4.WHO (1999), World Health Report 1999, Making a Difference, Report of
the Director - General WHO.
5.WHO (1999), Health Situation in the South East Asia Region 1994
-1997, Regional office for SEAR, New Delhi.
6.Govt, of India 2004, Annual Report 2003 -2004 Ministry of Health and
Family Welfare, New Delhi.
7.Simpson, D.I.H. (1978). Bull WHO, 56 (6) 819-832
8.Editorial (1975). Brit. Med. J. 4 : 67
9.WHO (1986) DHE : Diagnosis treatment and Control
MALARIA
History
For details, please refer to the 15th edition of this book.
Problem Statement
WORLD
At present, about 100 countries in the world are considered malarious,
almost half of which are in sub-Saharan Africa. Although this number is
considerably less than it was in the mid - 1950s, more than 2.4 billion of
the world's population are still at risk.
The incidence of malaria worldwide is estimated to be 300-500 million
clinical cases each year, with about 90 per cent of these occurring in SubSaharan Africa, and mostly caused by P. falciparum. Malaria is thought to
kill between 1.1 and 2.7 million people world wide each year, of whom
about 1 million are children under the age of 5 years in these areas. These
childhood deaths resulting mainly from cerebral malaria and
1136
40855
Americas
East Mediterranean
Europe
1
59
0
111
1196
21
SEAR
Western Pacific
65
11
2777
371
1272
46481
Total
Malaria is a protozoal disease caused by infection with parasites of the
genus Plasmodium and transmitted to man by certain species of infected
female Anopheline mosquito. A typical attack comprises three distinct
stages : cold stage, hot stage and sweating stage. The clinical features of
malaria vary from, mild to severe, and complicated, according to the
species of parasite present, the patient's state of immunity, the intensity of
the infection and also the presence of concomitant conditions such as
malnutrition or other diseases. The febrile paroxysms occur with definite
intermittent periodicity repeating every third or fourth day depending upon
the species of the parasite involved.
Mortality (000)
(The figures are rounded up and may not add up to the numbers
quoted)
Source : (2)
The predominant causal organisms in the South East Asia Region
(SEAR) are Plasmodium uiuax followed by Plasmodium falciparum. P.
falciparum causes almost all the deaths due to malaria. Malaria cases in
SEAR have remained static and about 2.6 million cases were reported
during 2000, although the estimates fluctuate between 20-23 million. There
were 4927 deaths reported due to malaria (estimates are about 27712
deaths). The percentage of P. falciparum cases was about 49.3 (3).
All countries of the Region, except Maldives have indigenous malaria
transmission. DPR Korea reported malaria in 1997 after a lapse of many
years. An estimated 1.3 billion people, or 85 per cent of the total
population of SEAR, are at risk of malaria, 30 per cent of this population
lives in areas with moderate to high risk of malaria, mainly in India,
Myanmar and Thailand.
The Region is under threat of drug-resistant P. falciparum, a problem
that has progressed from mono to multi-drug resistance. An estimated 400
million population is at risk of acquiring drug resistant malaria. Drug
resistance enhances malaria morbidity and mortality and increases the
treatment cost.
The overall situation in SEAR is as shown in Table 2.
TABLE 2
Malaria incidence and mortality in SEAR countries (2000)
Country
population)
Malaria cases
(per 100,000
India
40
Bhutan
285
Indonesia
920
Myanmar
224
20
Bangladesh
Nepal
Sri Lanka
Thailand
33
11
1110
130
Source : (4)
By mid 1995 all malaria endemic countries in the Region had
adopted the revised malaria control strategy to reduce morbidity and
mortality and to reduce its area okdistribution, particularly of
multidrug resistant malaria, fjhe use of stratification approach by the
majority of anti-malaria programmes in the Region has led to more
cost-effective ^interventions. Vector resistance to insecticides has
necessitated the use of more expensive pyrethroid, thereby limiting
the coverage. Malaria control added impetus as Roll Back Malaria
initiative was launched by WHO, UNICEF UNDP and the World
Bank in 1998jThe main strategies of this initiative are (5) :
(a)Strengthen health system to ensure better delivery of health
care, especially at district and community level.
(b)Ensure the proper and expanded use of insecticide treated
mosquito nets.
(c)Ensure adequate access to basic health care and training of
health care workers.
(d)Encourage the development of simpler and more effective
means of administering medicines, such as training of village
health workers and mothers on early and appropriate treatment
of malaria, especially in children.
(e)Encourage the development of more effective and new antimalaria drugs and vaccines.
In partnership with SAARC (South Asian Association for
Regional Cooperation) and the Environmental Health Project,
WHO has initiated cross-border control of HIV/AIDS, TB, malaria
and kala-azar in 11 border districts of Bangladesh, Bhutan, India
and Nepal.
INDIA
In India, with the implementation of Modified Plan of
Operation (MPO) in 1977, the upsurge of malaria cases dropped
down from 6.74 million cases in 1976 to 2.1 million cases in 1984.
Since then, the epidemiological situation did not show any great
improvement. It seemed to have reached a plateau which was
causing concern.
Since 1997, there is a consistently declining trend in the annual
malaria incidence in the country. During 2003 about 1.65 million
cases were reported with 943 deaths. There were 0.7 million cases
of P. falciparum malaria (3). Table 3 shows year-wise reported
number of cases and deaths. The disease is grossly under-reported.
TABLE 3
Malaria situation in Indie
Year
1996
1997
1998
1999
2000
2001
2002
2003
2.66
2.22
2.28
2.03
2.09
1.84
1.64
1.04
1.03
1.14
1.05
1.01
0.89
0.70
Deaths
API
1010
3.48
879
664
1048
932
1005
973
943
2.86
2.44
2.41
2.09
2.06
1.80
1.62
MALARIA 203
TABLE 4
Statewise malaria situation in India 2002 and 2003
2002
Positive cases
State
Andhra Pradesh
Arunachal Pradesh
Assam
Bihar
Chhattisgarh
Goa
Gujarat
Haryana
Jharkhand
Karnataka
Kerala
Madhya Pradesh
Maharashtra
Manipur
Meghalaya
Mizoram
Nagaland
Orissa
Punjab
Rajasthan
Tamil Nadu
Tripura
Uttar Pradesh
West Bengal
Total
Deaths
2003
Positive cases
Deaths
38053
35090
46431
89601
3683
235434
16818
82966
936
126589
132584
3360
108818
45568
1268
17918
7859
3945
473223
250
68627
34523
13319
90199
194421
1842019
0
72
2
3
15
17
0
31
33
8
30
43
9
41
35
0
465
0
11
0
5
0
152
973
33366
55375
2550
53093
11370
113372
4336
112740
99889
2380
93780
62969
2589
16503
7293
3370
417276
377
142738
43382
13577
81853
232846
1647378
0
38
1
0
1
34
0
13
22
4
22
85
17
38
49
0
333
1
66
0
9
0
207
943
Source : (6)
fftts CRURAL MALAR1M. These include irrigated areas of arid and
Sjeniicfrid plains of Haryana, Punjab, Western Uttar Pradesh,
parts of Rajasthan and Madhya Pradesh, plain desert areas and
'plain costal areas of Orissa, Andhra Pradesh and Tamil Nadu.
Malaria is of moderate to low endemicity.Mn. culicifacies is the
main vector and P.vivax is predominant during lean period and P.
falciparum during periodic exacerbatiorT^In these the health
infrastructure is moderately developed.
^R J URBAN MALARIA^ : 15 major cities including 4
^'metropolitans account for nearly 80 per cent of malaria cases
s')covered under urban malaria control scheme. The cities are Delhi,
Mumbai, Chennai, Kolkata, Hyderabad, Bangalore, Ahmedabad,
Bhopal,
Jaipur,
Lucknow,
Chandigarh,
Vadodara,
Vishakhapatnam, Vijaywadjj and Kanpur. This covers about 42.39
million population|_Jmportant features of malaria are moderate to
low endemicity with P. uivax predominance and focal P.
falciparum transmission. An.culicifaiies is the main vectorjhe
health infrastructure is well developed. In peri-urban areas malaria
situation is influenced by poor sanitary conditions and low socioeconomic groups living in unplanned settlements prone to
periodical epidemics.
MALARIA IN PROJECT AREAS : Project areas are those areas
where construction and developmental activities are taken up and
temporary tropical aggregation of labour takes place bringing in
different strains of malaria parasite and nonimmune population.
This results in disturbance in eco-system, prolific increase in
vector breeding places and increased man-mosquito contact
favouring high malaria transmission. These pockets contribute a
large number of malaria cases which are highly disproportionate to
the relatively small population groups inhabitating the area. One
or more major vectors are involved in malaria transmission.
Limited health facilities for prompt treatment is invariably
associated with chloroquin resistant malaria parasite. Hence
specific control strategy is required for such areas.
Agent factors
(a) AGENT
Malaria in man is caused by four distinct species of the malaria
parasite - P. vivax, P. falciparum, P. malariae and P. ovale.
Plasmodium vivax has the widest geographic distribution
throughout the world. In India, about 70 per cent of the infections
are reported to be due to P.vivax; 25 to 30 per cent due to P.
falciparum and 4-8 per cent due to mixed infection. P. malariae
has a restricted distribution and is said to be responsible for less
than 1 per cent of the infections in India. The largest focus of P.
malariae in India is reported to be in Tumkur and Hassan districts
in Karnataka (9). P. ovale is a very rare parasite of man, mostly
confined to tropical Africa. It has also been reported in Viet-Nam
(10). The severity of malaria is related to the species of the
parasite.
L histor :
fV^Thev malaria'
^ |f\)parasite-undergoes 2 cycles of development -
the human cycle (asexual cycle) and the mosquito cycle (sexual
cycle). Man is the intermediate host and mosquito the
definitive hos) (Fig. 1).
i^..0|Cf f-jjp^
(i) Asexual cycle: The asexual cycle begins(when anj infected
mosquito bites a person and injects sporozoiteTjA cons!cTerable
amount of new knowledge about the parasite's life-cycle has become
available in recent years, concerning almost all phases of the cycle
(11). A brief description is as follows - four phases are described in
the human cycle: (a) HEPATIC PHASE: The sporozoites disappear
within 60 minutes from the peripheral circulation (12). Many of them
are destroyed by phagocytes, but some reach the liver cells. After 1-2
weeks of development (depending upon the species), they become
hepatic schizonts, which eventually burst releasing a shower of
merozoites. The number of merozoites produced from a single
sporozoite varies considerably with the infecting species. A single P.
falciparum sporozoite may form as many as 40,000 merozoites,
whereas sporozoites from other species of plasmodia produce only
2,000 to 15,000 merozoites (12)$JnJhe case of P. falciparum^,, the
intrahepatic schizonts rupture almost simultaneously andry there is no
persistent tissue phase""! (the so-called exo- \ erythrocytic phase). On
the contrary,-tfTe intrahepatic schizonts of the other plasmodia do not
burst all at the same time. Some hepatic forms persist and remain
dormant in the hepatocytes for considerable periods before they begin
to grow and undergo pre-erythrocytic schizogony, thus liberating
merozoites into the blood stream causing relapses of these infections.
P. vivax and P. ovale may continue to relapse for 2 to 3 years and P.
malariae may persist for 10 to 20 years or more. Once the parasites
enter the RBC, they do not reinvade the liver, (b) ERYTHROCYTIC
PHASE: Many of the merozoites are quickly destroyed, but a
significant number attach to specific receptor sites on the RBC. The
merozoites then penetrate the RBC and pass through the stages of
trophozoite and schizont. The erythrocytic phase ends with the
liberation of merozoites, which infect fresh red blood cells. The cycle
is repeated over and over again until it is slowed down by the immune
response of the host (13). The duration of the erythrocytic cycle is
constant for each species of malaria parasite- 48 hours for P
falciparum, P. vivax and P. ovale; and 72 hours for P. malariae. (c)
GAMETOGANY In all species of malaria some erythrocytic forms
do not divide but become male and female gametocytes. These are the
sexual forms of the parasite which are infective to mosquito.
(ii) Sexual cycle: The mosquito cycle (sporogony) begins
Sporozoites
---------------------------------- in saliva from mosquito
injected into human host
Exoerythrocytic multiplication
------------------------------ in liver parenchymal cells
y
Oocyst grows (multiple
division stage: cyst bursts
to release sporozoites)
SPOROGONY
SCHIZOGONY
4J* Merozoites s.
Mature schizont
(Segmentes)
..
, ,
(Enter red cells)
IT
Erythrocytic cycle
CLINICAL MALARIA
Immature schizont
Ookinete (motile zygote)
N.
GAMETOGENY
^______- Microgamete
Zygote iCT"
(fertilization) 4---------------------Macrogamete
Source : (14)
Ring trophozoite
,.
..
mosquito
I------------------
^s^
Mature Trophozoite
Microgametocyte
i._______________
4-------------------- (differentiation)
.__------""'"::=""^
Macroqametocyte
*c~~
FIG. 1
Life cycle of the malaria parasite.
^ \0)
MALARIA 205
Relapses: It is usual for vivax and ovale malaria to relapse
more than 3 years after the patient's first attack. Recurrences of
falciparum malaria usually disappear within 1-2 years. P. malariae
has a tendency to cause prolonged low-level, asymptomatic
parasitaemia (15). The infection is known to persist for 40 years or
more. It is probable that persons harbouring such infections are at
least occasionally infective to mosquitoes.
It is now considered more likely that vivax and ovale relapses
are derived from original, sporozoite-induced, liver schizonts
which have lain latent long before bursting. In P falciparum and P.
malariae infections latent liver schizonts do not appear to occur.
Relapses in these species, most authorities maintain, are due to a
chronic blood infection, i.e., erythrocytic schizogony persisting at
a low level.
Host factors
The main variables of the human element that have an
influence on malaria epidemiology include the following :
(a) AGE : Malaria affects all ages. Newborn infants have
considerable resistance to infection with P. falciparum. This has
been attributed to the high concentration of foetal haemoglobin
during the first few months of life, which suppresses the
development of P. falciparum (16). (b) SEX : Males are more
frequently exposed to the risk of acquiring malaria than females
because of the out-door life they lead. Further, females in India are
usually better clothed than males, (c) RACE : Individuals with AS
haemoglobin (sickle-cell trait) have a milder illness with
falciparum infection than do those with normal (AA) haemoglobin
(12). Persons whose red blood cells are "Duffy negative" (a genetic
trait) are resistant to P vivax infection, (d) PREGNANCY :
Pregnancy increases the risk of malaria in women. Malaria during
pregnancy may cause intrauterine death of the foetus; it may also
cause premature labour or abortion. Primigravid women are at
greatest risk (17). (e) SOCIO-ECONOMIC DEVELOPMENT :
Malaria has demonstrated the relationship between health and
socio-economic development. It is generally accepted that malaria
has disappeared from most developed countries as a result of
socio-economic development (17). (f) HOUSING: Housing plays
an important role in the epidemiology of malaria. The ill-ventilated
and ill-lighted houses provide ideal indoor resting places for
mosquitoes. Malaria is acquired in most instances by mosquitobites within the houses. The site, type of construction, nature of the
walls, etc. influence the selection of control measures (18). (g)
POPULATION MOBILITY : People migrate for one reason or
other from one country to another or from one part of a country to
another. Labourers connected with various engineering, irrigation,
agricultural and other projects and periodic migration of nomads
and wandering tribes are outstanding examples of internal
migration. Some of them may import malaria parasites in their
blood and reintroduce malaria into areas where malaria has been
controlled or eliminated. Imported malaria has become quite a
public health problem in Europe, North America, and other
temperate parts of the world, owing to the rising tide of air travel,
tourism and migration (12). (h) OCCUPATION : Malaria is
predominantly a rural disease and is closely related to agriculture
practices, (i) HUMAN HABITS : Habits such as sleeping out of
doors, nomadism, refusal to accept spraying of houses, replastering
of walls after spraying and not using measures of personal
protection (e.g. bed nets) influence man-vector contact, and
obviously the choice of control measures, (j) IMMUNITY: The
epidemic of malaria is influenced by the immune status of the
population. Immunity to malaria in humans is acquired only after
repeated exposure over several years. Thus in endemic malarious
areas a state of collective immunity becomes established slowly, so
that infants, young children, migrants and travellers from non-
endemic areas suffer most from the disease. Those, however, who
survive to the adult age show less evidence of adverse effects to
the attenuated infection. Infants born of immune mothers are
generally protected during the first 3-5 months by maternal Ig G
antibody; infants born of semi-immune mothers are only partially
protected. Active immunity is species -specific, that is, immunity
against one strain does not protect against another. People living in
endemic areas exposed continually to malaria develop considerable
degree of resistance to clinical disease, but their partial immunity
to malaria declines with time after they leave their endemic
countries. Semi-immune individuals may harbour malaria parasites
without presenting any symptoms of disease. Both humoral and
cellular factors play a role in this protection.
Environmental factors
India's geographic position and climatic conditions had been,
for long, favourable to the transmission of malaria.
(a)SEASON : Malaria is a seasonal disease. In most parts of India,
the maximum prevalence is from July to November.
(b)TEMPERATURE: Temperature affects the life cycle of the
malaria parasite. The optimum temperature for the development of
the malaria parasite in the insect vector is between 20 deg. to 30
deg.C (68 deg. to 86 deg.F). The parasite ceases to undergo
development in the mosquito if the mean temperature is below 16
deg.C (60.8 deg.F). Temperatures higher than 30 deg.C are lethal
to the parasite.
(c)HUMIDITY: The atmospheric humidity has a direct effect on
the length of life of the mosquito, although it has no effect on the
parasite. A relative humidity of 60 per cent is considered necessary
for mosquitoes to live their normal span of life. When the relative
humidity is high, mosquitoes are more active and they feed more
voraciously. If the humidity is low, mosquitoes do not live long,
(d) RAINFALL : Rain in general provides opportunities for the
breeding of mosquitoes and may give rise to epidemics of malaria.
Rain increases the atmospheric humidity which is necessary for the
survival of mosquitoes. However, heavy rain may have an adverse
affect in flushing out the breeding places. Paradoxically in some
areas, (e.g., Sri Lanka) severe epidemics of malaria followed years
of drought. It was because, the lessor monsoon rains led to the
formation of small pools of water in river beds, which served as
active breeding places for malaria vectors. The relationship
between rainfall (total and its distribution) and mosquito-breeding
is of fundamental importance (19). (e) ALTITUDE: As a rule,
Anophelines are not found at altitudes above 2000-2500 metres,
due to unfavourable climatic conditions, (f) MAN-MADE
MALARIA: Burrow pits, garden pools, irrigation channels and
engineering projects have led to the breeding of mosquitoes and an
increase in malaria. Malaria consequent on such human
undertakings is called "man-made malaria".
Vector of Malaria
Out of about 45 species of anopheline mosquitoes in India, only
a few are regarded as vectors of primary importance. These are:
An. culicifacies, An. fluviatilis, An. Stephens!, An. minimus, An.
philippinensis, An. sundaicus, and An. maculatus. The vectors of
major importance are An culicifacies in rural areas and An.
stephensi in urban areas.
In the absence of a vaccine, vector control is the only practical
approach to malaria control. A knowledge of anopheline biology is
essential for understanding the epidemiology of malaria and its
prevention. The main factors which determine the vectorial
importance of mosquitoes are: (a) DENSITY : To be an effective
vector, a species must be present in adequate density in or near
human habitations. A sudden increase in density of vectors, may be
a cause of epidemic outbreaks. For each vector, there is what is
known as
___________________________________________MALARIA 207
Diagnosis
The diagnosis of malaria depends on demonstration of the
parasite in the blood. Suspicion of the diagnosis is aroused by
epidemiological and clinical evidence.
Two types of blood films are useful in searching for and
identification of malaria parasite. The "thin film" and the "thick
film". It is recommended that both types of film be prepared on a
single microscope glass slide. The thick film is more reliable in
searching for parasite, as large volume of blood is examined under
each microscope field. When scanty, parasite may be found about
20 times more rapidly in thick slide than in thin slide. The thin
slide is more valuable for identifying the species of the parasite
present. In it they are seen more clearly.
The malarial fluorescent antibody test usually becomes positive
two weeks or more after primary infection, by which time the
infection may have been cured. A positive test is therefore, not
necessarily an indication of current infection. The test is of the
greatest value in epidemiological studies and in determining
whether a person has had malaria in the past (26). The latest
simple and rapid diagnostic technique is a dipstick (antigen
capture) assay for detection of P. falciparum, evaluated in field
trials and compared favourably with microscopy (27).
Measurement of malaria
PRE-ERADICATION ERA :
In the pre-eradication era, the magnitude of the malaria
problem in a country used to be determined mostly from the
reports of the clinically diagnosed malaria cases. The classical
malariometric measures are spleen rate, average enlarged spleen,
parasite rate etc. In a control programme, the case detection
machinery is weak. Therefore, the classical malariometric
measures may provide the needed information, i.e. the trend of the
disease.
(a) SPLEEN RATE : it is defined as the percentage of children
between 2 and 10 years of age showing enlargement of spleen.
Adults are excluded from spleen surveys, because causes other
than malaria frequently operate in causing splenic enlargement in
them. The spleen rate is widely used for measuring
the
endemicity of malaria in a community.
(b) AVERAGE ENLARGED SPLEEN : This is a further
refinement of spleen rate, denoting the average size of the
enlarged spleen (28). It is a useful malariometric index.
(c) PARASITE RATE : It is defined as the percentage of children
between the ages 2 and 10 years showing malaria parasites in
their blood films, (d) PARASITE DENSITY INDEX : It indicates
the average degree of parasitaemia in a sample of well-defined
group of the population. Only the positive slides are included
in the denominator (12). (e) INFANT PARASITE RATE : It is
defined as the percentage of infants below the age of one year
showing malaria parasites in their blood films. It is regarded as
the most sensitive index of recent transmission of malaria in a
locality. If the infant parasite rate is zero for 3 consecutive years
in a locality, it is regarded as absence of malaria transmission
even though, the Anopheline vectors responsible for previous
transmission may remain, (f) PROPORTIONAL CASE RATE :
Since the morbidity rate is difficult to determine, except in
conditions when the diagnosis and reporting of each case is
carried to perfection, proportional case rate is used (12). It is
defined as the number of cases diagnosed as clinical malaria
for every 100 patients attending the hospitals and dispensaries.
This is a crude index because the cases are not related to their
time/space distribution.
ERADICATION ERA (current incidence levels) :
During the eradication era, the microscopic diagnosis of
malaria cases became the main method of diagnosis. The
TABLE 4
Drug regimens for prophylaxis and treatment of malaria
Drugs
Generic name
Adult dose
For prophylaxis
Chloroquineb
Aralen
Avlochlor
Nivaquine
Resochin
100 or 150 mg
(base)
Proguanilc
Paludrine
100 mg
Sulfadoxine+
pyrimethamine
Sulfalene+
pyrimethamine
Mefloquined
Fansidar
500mg + 25mg
Metakelfin
500 mg + 25 mg
Lariam Eloquin
Mephaquin
Doxycycline8
bf
Halofantrine '
a.
b.
c.
d.
e.
f.
Not applicable
Not applicable
250 mg
300 mg
Not applicable
Vibramycin
100 mg
Half an
250 mg
Not applicable
Quinine
14
tablet or capsule
For treatment3
600 mg (base) on the first and
second days, and 300 mg
(base) on the third day (total 10
tablets of 150 mg or 15 of
100 mg)
Not applicable
1500 mg + 75 mg = 3 tablets in
one dose
1500 mg + 75 mg = 3 tablets in
one dose
1000 mg (4 tablets) or 15
mg/kg of body weight,
whichever is lower, in one dose
OR 1000 mg (4
tablets) initially, followed by 500
mg (2 tablets) 6-8 hours later
600 mg (2 tablets) 3 times a
day for 7 days (total 42 tablets)
Not applicable
500 mg (2 tablets) in one dose
+500 mg after 6 hours +500 mg
after 6 more hours (total 6 tablets
in 12 hours)
This does not cover all aspects of treatment, the same regimens can be used for stand-by treatment.
Also available as suspension.
Recommended only in association with chloroquine.
The use of the higher treatment dose regimen is recommended for infections acquired in areas on the Thailand/Cambodia and Thailand /
Myanmar borders only.
There is relatively little experience with this drug, and knowledge of its efficacy and toxicity is limited.
Must not be administered with food. The manufacturer advises that a second treatment course be taken one week later. Not recommended
for stand-by treatment.
Source: (37)
References
1.WHO (2000), Tech. Rept. Ser., No. 892
2.WHO (2004), World Health Report - 2004, Report of the Director
General WHO
3.WHO (2002), Health Situation in the South - East Asia Region 1998-
LYMPHATIC FILARIASIS
Problem statement
Filariasis is a global problem. It is a major social and
economic scourage in the tropics and subtropics of Africa,
Asia, Western Pacific and parts of the Americas, affecting over
120 million people in 80 countries. More than 1.1 billion
people live in areas where there is a risk of infection (2).
It is estimated that about 600 million people are living in
areas endemic for lymphatic filariasis in SEAR. There are about
60 million people infected in the Region and about 31 million
people have clinical manifestation of the disease (3). In the
Region all three types of parasites are present.
Lymphatic filariasis is a major public health problem in India.
The problem is increasing every year due to gross
mismanagement of the environment. The disease is endemic all
over India, except in Jammu and Kashmir, Himachal Pradesh,
Punjab, Haryana, Delhi, Chandigarh, Rajasthan, Nagaland,
Manipur, Tripura, Meghalaya, Sikkim, Arunachal Pradesh,
Mizoram and Dadra and Nagar Haveli. However, surveys
carried out during the past two decades indicate that areas
previously known to be free from filariasis are showing evidence
of low degrees of transmission (4). Heavily infected areas are
found in Uttar Pradesh, Bihar, Jharkhand, Andhra Pradesh,
Orissa, Tamil Nadu, Kerala and Gujarat.
Present estimates indicate that about 467 million people are
living in zones where lymphatic filariasis is endemic - of which
109 million are living in urban areas and the rest in rural
areas (5). There are estimated to be at least 6 million attacks of
acute filarial disease per year, and at least 20 million persons
currently have one or more chronic filarial lesions (6).
Agent factors
There are at least 8 species of filarial parasites that are
specific to man (7). These are shown in Table 1. The first three
worms are responsible for lymphatic filariasis; and the rest for
"non-lymphatic filariasis". The parasites causing nonlymphatic filariasis will not be described as they are not found
in India. Table 2 shows the differences between the
microfilariae (Mf) of W. bancrofti and B. ma/ayi.
Vectors
Disease produced
6. Nuclear column
Mf. W. bancrofti
Mf. B. malayi
Graceful, sweeping
Crinkled, secondary
curves
244 to 296 u
curves
177 to 230 fi,
Nearly twice as long as
broad
As long as broad
Not prominent
Uniformly tapering
to a delicate point,
No terminal nuclei
present
Nuclei discrete
Prominent
Kinkled and two
terminal nuclei present
Smudged
PERIODICITY:
The Mf of W. bancrofti and B.malayi occurring in India display
a nocturnal periodicity, i.e., they appear in large numbers at night
and retreat from the blood stream during the day. This is a
biological adaptation to the nocturnal biting habits of the vector
mosquitoes. The maximum density of Mf in blood is reported
between 10 pm and 2 am. When the sleeping habits of the host are
altered, a reversal in periodicity has been observed.
In most parts of the world, Mf axe nocturnally periodic but in
the South Pacific islands and in limited foci in the Nicobar islands,
Thailand and Vietnam W. bancrofti Mf are non-periodic (subperiodic), being detectable throughout the 24 hours with a slight
peak during day or night. Sub-periodic B.malayi is found in parts
of Malaysia and Indonesia.
LIFE CYCLE:
Man is the definitive host and mosquito the intermediate host of
Bancroftian and Brugian filariasis. The adult worms are usually
found in the lymphatic system of man. The males are about 40 mm
long and the females 50 to 100 mm long. The females are
viviparous. They give birth to as many as 50,000 Mf per day (8)
which find their way into blood circulation via the lymphatics. The
life span of. the Mf is not exactly known, probably up to a year or
more. The adult worms may survive for 15 years or more (8).
There is a case on record of a woman, in whom live Mf were
present 40 years after she left an endemic area (9).
The mosquito cycle begins when the Mf are picked up by the
vector mosquito during feeding. The following stages of
Mode of transmission
2. OCCULT FILARIASIS
CONTROL MEASURES
The current strategy of filariasis control is based on :
a. Chemotherapy
b. Vector control
Many years of experience with DEC chemotherapy has
shown that, even after the full regimen of treatment, some
microfilariae still persist in the body. Due to this and other
reasons (e.g., toxic effects), it has not been possible to prevent
the spread of filariasis by the administration of DEC alone.
Chemotherapy must, therefore, be supplemented by an
effective vector control programme, if the disease transmission
has to be effectively prevented.
1. Chemotherapy
a. Diethylcarbamazine:
Diethylcarbamazine (DEC) is both safe and effective. The
dose of DEC that is most generally accepted for the treatment
of Bancroftian filariasis is 6 mg/kg body weight per day orally
for 12 days, given preferably in divided doses after meals. This
amounts to a total of 72 mg of DEC per kg of body weight. For
Brugian filariasis, recommended doses range from 3 to 6 mg of
DEC/kg body weight per day, up to a total dose of 18-72 mg
DEC/kg body weight (14).
DEC is rapidly absorbed after oral administration, reaching
peak blood levels in 1-2 hours. It is also rapidly excreted - the
blood half-life is only 2-3 hours in alkaline urine and about
10-20 hours in acid urine.
DEC causes rapid disappearance of M/from the circulation.
It is effective in killing Mf. The effect of the drug on the adult
worm is uncertain. It has probably no effect on the infective
stage larvae.
Toxic reactions : DEC may produce severe side reactions.
The reactions may be of two kinds : (a) those due to the drug
itself, e.g., headache, nausea, vomiting, dizziness, etc, These
reactions are observed a few hours after the first dose of DEC
and generally do not last for more than 3 days, and (b) those
which are allergic reactions due to destruction of microfilariae
and adult worms, e.g., fever, local inflammations around dead
worms, orchitis, lymphadenitis, transient lymphoedema and
hydrocele. The local reactions tend to occur later in the course
of treatment and to last longer. If the drug is given in spaced
doses, systemic reactions are much less frequent and less
intense after the second dose and are rare after subsequent
doses. These reactions disappear spontaneously and
interruption of treatment is not necessary.
b. Filaria control in the community :
There are three reasons why filariasis never causes explosive
epidemics : (a) the parasite does not multiply in the insect
vector, (b)the infective larvae do not multiply in the human
host, and (c) the life cycle of the parasite is relatively long, 15
years or more. These factors favour the success of control
programme (14).
DEC is still the only drug available for chemotherapeutic
control of filariasis. The administration of DEC can be carried
out in various ways :
(i) Mass therapy :
In this approach, DEC is given to almost everyone in the
community irrespective of whether they have microfilaraemia,
disease manifestations or no signs of infection. It is generally
accepted that mass therapy is indicated in highly endemic
areas (14).
Mass treatment control projects using DEC have markedly
reduced prevalence of W.bancrofti in many of the Pacific
2. Vector control
Where mass treatment with DEC is impracticable, the
control of filariasis must depend upon vector control. Vector
control may also be beneficial when used in conjunction with
mass treatment. The most important element in vector control
is the reduction of the target mosquito population in order to
stop or reduce transmission quickly. The techniques for
controlling mosquitoes are given in chapter 12. Briefly they
are:
/ Antilarval measures :
The ideal method of vector control would be elimination of
breeding places by providing adequate sanitation and
underground waste-water disposal system. This involves
considerable expenditure amounting to several crores of
rupees. Because of financial constraints, this may not be
feasible in developing countries such as India in the near
future. For the time being, therefore, vector control must be
based on temporary or recurrent methods.
The current approach in India is to restrict the antilarval
measures to urban areas, because it is operationally difficult
and very costly to cover the vast rural areas of the country. The
urban areas include an extra 3-km peripheral belt because the
flight range of Culex quinquefasciatus (C. fatigans) is about
(iiij DEC medicated salt:
3 km.
The use of DEC-medicated salt is a special form of mass
The anti-larval activities comprise the following (4).
treatment using very low doses of the drug over a long period
(1)CHEMICAL CONTROL : faj Mosquito larvicidal oil :
of time. Common salt medicated with 1-4 g of DEC per kg has
Mosquito larvicidal oil (MLO) is active against all
been used for filariasis control in some endemic areas of
preadult stages. It has been the main chemical used
W. bancrofti and B. ma/ayi, particularly after an initial
to control C. quinquefasciatus for some time. Since it has
reduction in prevalence has been achieved by mass or selective
proved to be less efficient under field conditions and more
treatment of Mf-carriers. Treatment should be continued for afV
expensive than other chemical preparations^ it is being
least 6 to 9 months. In the Lakshadweep islands, this regimen^
replaced by pyrethrum oil, temephos and fenthiory (b)
has been shown to be safe, cheap and effective (14).
Pyrosene oil - E : This is a pyrethrum-based
The combination of the long life of the adult parasite for
emulsinable larvicide. The emulsion concentrate
several years and infectiousness of a patient with low
contains 0.1 to 0.2 per cent pyrethrins by weight and is
parasitaemia represents a serious obstacle to control
required to be diluted with water before use. The
programmes based on chemotherapy alone (20).
emulsion is diluted in the ratio of 1:4, (c)
Organophosphorus larvicides : During the past 10
b. Ivermectin
years, Organophosphorus larvicides (e.g., temephos,
Ivermectin is a semisynthetic macrolide antibiotic with a
fenthion) have been widely used with successful results.
broad spectrum of activity against a variety of nematooles and
However, the vector mosquito has developed resistance
ectoparasites.
to many of these chemicals. The frequency of
application is once weekly on all breeding places.
Studies carried out in Brazil, French Polynesia, Haiti, India
(2 sites), Kenya, Papua New Guinea and Sri Lanka for
(2)REMOVAL OF PISTIA PLANT : In the case of Mansonia
W. Bancrofti showed that ivermectin in single oral dose of 20mosquitoes, breeding is best controlled by removing
400 ng/kg of body weight were effective in completely clearing
the supporting aquatic vegetation such as the pistia plant
blood microfilaria in all treated cases within weeks, but by 3
from all water collections and converting the ponds to
months microfilaraemia recurred in most patients, and by 6
fish or lotus culture. Alternatively, certain herbicides such
months reached geometric mean level of approximately 5-40
as phenoxylene 30 or Shell Weed Killer D may be used
per cent of pretreatment values. The variability in results at 6
for destroying the aquatic vegetation.
months generally occurred at lower doses of ivermectin (21).
(3) MINOR ENVIRONMENTAL MEASURES : Larvicidal
Trials for B. ma/ayi carried out in India, Indonesia and
operations are complemented by minor engineering operations
Malaysia indicated that the microfilaricidal response to
such as filling up of ditches and cesspools, drainage of stagnant
ivermectin was qualitatively different from that of W.Bancrofti
water, adequate maintenance of septic tanks and soakage pits,
infections. Rather than causing rapid and complete clearance
etc. Environmental management is the most efficient approach
of blood microfilariae ivermectin caused a gradual decrease in
to the problem of controlling mosquito breeding.
microfilaria levels over 2-4 weeks to approximately 15-20 per
cent of the pretreatment values. However, these low levels were
//. Anti -adult measures :
sustained for at least 6 months after treatment. Maximum
effectiveness was seen at the higher dosage of 200 and 400 |ag/
The vector mosquitoes of filariasis have become resistant to
kg body weight (21).
DDT, HCH and dieldrin. The use of these compounds for
indoor residual spraying, tried earlier, has been discontinued.
There is no drug toxicity in normal volunteers. However, in
Pyrethrum, as a space spray, still holds promise. It is useful as a
microfilaraemic patients there may be a variety of reactions as
temporary means of personal protection, but has no practical
value in present-day vector control programmes.
. Personal prophylaxis :
The most effective preventive measure is avoidance of
Dsquito bites (reduction of man-mosquito contact) by using
Dsquito nets. Screening of houses can substantially reduce
insmission, but it is expensive.
tegrated vector control
None of the above vector control measures applied alone is
:ely to bring about sustained control of filariasis vectors. An
tegrated or combined approach is needed to control filariasis
ing all the above strategies and approaches in optimum
'inbination.
imary health care
Since the vertical approach to the control of filariasis has
id very limited success in India in terms of coverage of the
>pulation at risk, it is now recognized that a horizontal
iproach making use of the primary health care system is
sential, in the context of the WHO's goal of "Health for All",
le Village Health Guide is the key person who should be
lined and involved in anti-filaria activities, with community
pport, at the village level.
In filariasis four major breakthroughs have occurred. The
st of these is the development of safe, single-dose, annual
ug treatment. Trials have proved that a single dose of DEC is
iry effective even two years after treatment. A single dose of
ermectin has proved to be equally effective. A combination
single dose of both drugs reduced microfilaraemia more than
i per cent, 2 years after treatment. Secondly, intensive local
/giene on the affected limb, with or without the use of
itibiotic and antifungal creams, has been shown to have
amatic effects by halting the progression of, or even reversing
sphantiasis and lymphoedema. Thirdly, DEC-medicated
ble or cooking salt has been introduced in India. The
irefully controlled addition of very low concentration of DEC
is long been recognized as an effective means of eliminating
mphatic filariasis infections in communities. However, the
Idition increases the price of the salt. During 1994, the first
immercially prepared DEC salt went on sale in India, at about
'ice the price of ordinary salt. Finally, there has been the
jvelopment of insecticide sprays and polystyrene beads to
al latrines and roof-top water-storage tanks, to eliminate or
duce populations of urban Culex mosquitoes (22).
ational Filaria Control Programme
See chapter 7 for details.
eferences
Lancet (1985), i: 1135
WHO (1998), World Health Report 1998, Life in the 21st century, A
vision for all, Report of the Director General WHO.
WHO (1999), Health Situation in the South - East Asia Region 19941997, Regional office for SEAR, New Delhi.
National Institute of Communicable Diseases (1979). Operation
Manua/NFCP, Delhi
Govt of India (1996), Annual Report 1995-96, DGHS, Ministry of
Health and Family Welfare, New Delhi
7 5 :8 3 5
6.WHO (1992), Tech.Rep.Ser., No.821
7.WHO (1996), World Health Report 1996, Fighting disease Fostering
development, Report of the Director General WHO
IV. ZOONOSES
Zoonotic diseases have been known since antiquity.
Bubonic plague and rabies were known since biblical times.
The discovery of causative agents during the "golden era" of
microbiology called attention principally to diseases exclusively
pathogenic to man. Zoonotic diseases were overshadowed by
diseases peculiar to man alone. Only as human infections came
under better control was attention drawn to zoonotic diseases.
More than 150 zoonqses have been recognized. In recent
years, several new zoonotic diseases have emerged e.g. KFD,
Monkey Pox etc., Quite apart from the morbidity and mortality
they cause, zoonoses are responsible for great economic losses,
particularly in animals, meat, milk and other foods and
products of animal origin. The developing countries suffer
much more severe losses than do the industrialized countries,
partly because they have less well-developed public health
and veterinary services and partly because of their
unfavourable climatic and environmental conditions.
Zoonoses and human health are matters of particular
concern in India - because nearly 80% of India's population is
rural and live in close contact with domestic animals, and often
not far from wild ones. r~2\
RABIES 217
Definition
(jRabies, also known as hydrophobia is an acute, highly fatal
viral disease of the central nervous system, caused by
Lyssavirus type 1. It is primarily a zoonotic disease of warmblooded animals, particularly carnivorous such as dogs, cats,
jackals and wolvesylt is transmitted to man usually by bites or
licks of rabid animals. Classical hydrophobia is clinically
characterized by a long and variable incubation period, a short
period of illness due to encephalomyelitis ending in death,
despite intensive care. It is the only communicable disease of
man that is always fatal.
Problem statement
Diagnosis
A clinical diagnosis of hydrophobia can be made on the basis
of history of bite by a rabid animal and characteristic signs and
symptoms.
Rabies can be confirmed in patients early in the illness by
antigen detection using immunofluorescence of skin biopsy, and
by virus isolation from saliva and other secretions.
Immunofluorescence of corneal impression smears has proved
unreliable. Neutralising antibodies are not usually detectable in
serum or CSF before the eighth day (7).
Treatment :
There is no specific treatment for rabies. Case management
includes the following procedure :
(a) The patient should be isolated in a quiet room protected as
far as possible from external stimuli such as bright light, noise or
cold draughts which may precipitate spasms or convulsions, (b)
Relieve anxiety and pain by liberal use of sedatives. Morphia in
doses of 30-45 mg may be given repeatedly. The drug is well
tolerated and once the diagnosis is established there appears to be
no reason to restrict the administration of a drug which does so
much to allay acute suffering, (c) If spastic muscular contractions
are present use drugs with curare-like action, (d) Ensure hydration
and diuresis, (e) Intensive therapy in the form of respiratory and
cardiac support may be given.
Patients with rabies are potentially infectious because the virus
may be present in the saliva, vomits, tears, urine or other body
fluids. Nursing personnel attending rabid patients should be
warned against possible risk of contamination and should wear
face masks, gloves, goggles and aprons to protect themselves.
Persons having bruises, cuts or open wounds should not be
entrusted to look after the patient. Where human cases of rabies
are encountered frequently pre-exposure prophylaxis with 2-3
doses of HDC vaccine is recommended.
VACCINES FOR IMMUNIZATION OF MAN
Vaccine :
(^Rabies vaccine is defined as a fluid or dried preparation of
rabies "fixed" virus grown in the neural tissues of rabbits, sheep,
goats, mice or rats or in embryonated duck eggs, or in cell
cultures, and inactivated by a suitable method (18). Inactivation is
commonly done by treatment with phenol or betapropiolactone'All vaccines are tested in accordance with the
control procedures laid down by WHO (18).
I Following Pasteur's initial development of rabies vaccine, a
variety of rabies vaccines have been developed. The vaccines
currently or recently in use are of 3 types :
1. Nervous tissue vaccines (NTV)
(a)derived from adult animal nervous tissue (e.g., sheep)
(b)derived from suckling mouse brain
1.Duck embryo vaccine (DEV)
2.Cell-culture vaccines
(a)Human diploid cell (HDC) vaccine
(b)"second generation" tissue culture (animal cell) vaccines )
1. NERVOUS TISSUE VACCINES :
BPL inactivated vaccine (nervous tissue origin) is used in much
of the world. It is prepared from fixed virus grown in the brains of
adult sheep (Semple type) or other animals. The final vaccine is a
5% emulsion of the infected sheep's brain containing the
inactivated virus. Nervous tissue vaccines are crude products
capable of causing severe and even fatal
TABLE 1
Guidelines for post - exposure treatment
Category
Recommendations
III
a.
b.
c.
Exposure to rodents, rabbits and hares seldom, if ever, requires specific anti-rabies treatment.
If an apparently healthy dog or cat, in or from a low risk area is placed under observation, the situation may warrant delaying
initiation of treatment.
This observation period applies only to dogs and cats. Except in the case of threatened or endangered species, other domestic and
wild animals suspected as rabid should be killed humanely and their tissues examined using appropriate laboratory techniques.
Source : (20)
3. Immunization
In 1883, Pasteur performed the first successful human antirabies vaccination. In recent years, great progress has been made in
developing vaccines and immunoglobulins for the prevention of
rabies in man, before and after exposure. Very potent vaccines
have been developed in tissue culture, which offer improved safety
over earlier types. The aim of vaccination is to produce an immune
status as quickly as possible so that the virus will not become
established in the peripheral nerve along which it will travel to the
central nervous system. Serum antibodies appear approximately 7
days after vaccination. Immunity is less effective after a nerve
infection has been established. Immunity is not absolute and
treatment failures do occur, especially in instances whgje the
incubation period is short or exposure is very severe /TTabies
vaccine is unique because it is the only vaccine that is given after
exposure to infection""!
^ o ^ v >J^K^~^
TABLE 3
Dosage Schedule of BPL inactivated vaccine
(Recommended by the Pasteur Institute, Coonoor)
Class of
treatment
Class I
Class II
Class III
1 ml
3 ml
3 ml
Duration of
treatment
7 days 10
days 10
days
TABLE 2
Dosage schedule of BPL inactivated vaccine per day
(Recommended by the Central Research Institute, Kasauli)
Class
of treatment
Adults
Children (weighing 30
kg. or below)
Class I
2 ml
Class II
5 ml
Class III
5 ml
2 ml
2 ml
2 ml
Duration of treatment
Booster
7 days
Nil
10 days
10 days
Source : (21)
Duration of immunity
The development of immunity after anti-rabies immunization is
rather slow. Though serum antibodies appear approximately 7 days
after vaccination (7), it takes at least 30 days to achieve a
maximum level of immunity (22). The protection afforded lasts
about 6 months from the date of completion of the course. A study
at the Pasteur Institute, Coonoor showed that the mortality rate in
the completely treated (where the animals were known to be rabid)
was 7% as compared to 56% in a comparable group which did not
take the treatment (23).
Anti rabies serum
Combined vaccine and immunoglobulin/serum treatment offers
the best prophylaxis of rabies in exposed persons. Antirabies serum
prevents replication of the virus at the site of the bite (24). It
should be given as promptly as possible after a sensitivity test,
irrespective of the interval between exposure and beginning of the
treatment (3). ARS has been shown to prolong the incubation
period of the disease if administered soon after exposure to rabies.
Complete protection from rabies can, however, be ensured only if
sero-therapy is followed by a complete course of vaccine including
specified booster doses of vaccine. Passive immunity is
particularly important in situations where the incubation period is
likely to be short as in class III bites; cases of vaccine failure have
been described when passive immunity was omitted.
Two preparations of anti rabies serum are available for passive
immunization : (i) HORSE ANTI RABIES SERUM : Potent
antirabies serum has been produced in horse and other animals
(mules, donkeys, rabbits). It should be given on day 0 in a single
dose of 40 International Unit per Kg of body weight subject to a
maximum of 3000 Units. Half of the serum is infiltrated around the
bite wound and the rest is given intramuscularly. This should be
followed by a course of vaccine, (it) HUMAN RABIES
IMMUNOGLOBULIN : Human rabies Ig. (HRIG) has now
replaced equine anti-rabies serum in many countries. It is now
commercially available. The dose recommended is a single
administration of 20 IU per kg of body weight. The recommended
procedure is to inject part of the dose around the wound and to
administer the rest by IM in the gluteal region. This should be
followed by a course of vaccine and additional booster doses of
vaccine as indicated. It does not require any prior sensitivity
testing. However, there have been a few isolated reports of
angioneurotic oedema, nephrotic syndrome and anaphylactic shock
after injection. A* slight rise in temperature may be noted.
Sensitization to, repeated injections of HRIG is rare (3).
up the infection, (b) undue physical and mental strain and late
nights should be avoided, (c) cortico-steroids and other
immunosuppressive agents should not be used (21). (d) rabies-may
develop following inadequate immunization^ sr ^^ (^
The current trend is to limit or abandon completely the
production of nervous tissue vaccines and replace them by safer
and more effective inactivated cell-culture vaccines in both
developed and developing countries.
(ii) ANTIRABIES SERUM:
Administration of anti rabies serum of heterologous origin
(e.g., horse serum) induces anaphylactic reaction and serum
sickness. Serum sickness occurs in approximately 15% - 45% of
persons receiving the horse serum; it is less frequent in persons
below 15 years of age (3). The incidence can be reduced by the
administration of a large dose of an anti-histaminic drug
simultaneously with the serum and further sustaining doses on the
following days. Therefore it is absolutely necessary to make sure
that the patient is not sensitive to horse serum. If the sensitivity
test is positive, if possible, serum produced in another species
should be used.
2. CELL CULTURE AND PURIFIED DUCK EMBRYO
VACCINES
The use of modern, inactivated, purified cell-culture and
purified duck embryo vaccine should, where economically and
technically feasible, replace those produced on brain tissue in both
developing and developed countries. These vaccines with a
potency at least 2.5 IU per single intramuscular dose should be
applied according to one of the following schedules.
A. Intramuscular Schedules : The vaccination schedule
recommended consists of 6 doses (1 ml each) on days 0, 3, 7, 14
and 28 and a booster dose on day 90 (3). Injections are given
intramuscularly (deltoid) and must not be given in to the buttock
(7).
The major advantages of cell-culture vaccines over
conventional vaccines are their efficacy and safety. Results
indicated that 3 to 4 injections of cell-culture vaccines produce
antibody levels comparable with those induced by 10 injections of
a nervous tissue vaccine (25). The disadvantage of cell-culture
vaccines is their cost.
The standard WHO intramuscular regimen is as shown below
(26):
Dose one im dose (1.0 or 0.5 ml) into deltoid
0
,:____,,_______.,
14
28
______J.___________,,__5 vials
5 visits
Rabies immunoglobulin
21
XI
XI
Rabies immunoglobulin
4 vials 3
visits
Sites
X2
X2
X2
28
90
XI
XI
'
A
< 2 vials
5 visits
Rabies immunoglobulin
28
xi
.. ________.,____________________4''
Rabies immunoglobulin
90
xi
_________:' <2 vials
4 visits
PRE-EXPOSURE PROPHYLAXIS
Persons who run a high risk of repeated exposures such as
laboratory staff working with rabies virus, veterinarians, animal
handlers and wild-life officers should be protected by preexposure
immunization.
Such immunization should preferably consist of a dose of cellculture vaccine, given either as 1 ml intramuscularly or 0.1 ml
intradermally on days 0, 7 and 28. The presence of virus
-neutralizing antibodies in vaccinated individuals should be as
contained where feasible, on serum samples drawn one month after
the third injection. If titres are less than 0.5 IU/ml, booster doses of
1 ml IM or 0.1 ml intradermally, should be administered until
antibodies become demonstrable. Further booster injections should
be administered at intervals of 2 years as long as exposed person
remains at risk (7).
1C
Iv
forest mosquitoes. In urban areas, the reservoir is man (subclinical and clinical cases) besides Aedes aegypti mosquitoes, (c) PERIOD OF
COMMUNICABILITY : (i) MAN : Blood of patients is infective during the first 3 to 4 days of illness, (ii) MOSQUITOES : After an "extrinsic
incubation period" of 8 to 12 days, the mosquito becomes infective. The virus multiplies in the insect vector. After becoming infective, the
mosquito remains so for life. Transovarian transmission of the virus in mosquitoes has been shown to occur in adverse conditions (e.g., during
extended dry seasons), in the absence of susceptible hosts (1).
Host factors
(a) AGE AND SEX : All ages and both sexes are susceptible to yellow fever in the absence of immunity (b) OCCUPATION : Persons
whose occupation brings them in contact with forests (wood cutters, hunters) where yellow fever is endemic are exposed to the risk of
infection (c) IMMUNITY : One attack of yellow fever gives life-long immunity; second attacks are unknown. Infants born of immune mothers
have antibodies up to 6 months of life.
Environmental factors
(a) CLIMATE : A temperature of 24 deg.C or over is required for the multiplication of the virus in the mosquito. It should be accompanied
by a relative humidity of over 60 per cent for the mosquitoes to live long enough to convey the disease, (b) SOCIAL FACTORS : In Africa,
urbanization is leading to the extension of yellow fever. In addition, the expanding population is encroaching on areas that were previously
sparsely populated, thereby bringing man closer to the jungle cycles of yellow fever. The increasing number of people who travel and the
greater speed with which they are transported from endemic areas to receptive areas, also gives a cause for concern (4).
Modes of transmission
There are two known cycles of transmission, the jungle and the urban cycles.
(a) THE JUNGLE (OR SYLVAN) CYCLE : The jungle cycle which was discovered in 1930s involves transmission of the disease between
monkeys by various mosquitoes. In the Americas, mosquitoes of the genus Haemagogus are the primary vectors. In Africa, the jungle cycle is
maintained chiefly by Aedes mosquitoes, such as Aedes ctfricanus and Aedes simpsoni, but mosquitoes of other genera may also be involved.
Transmission from monkey to man is accidental and is the result of human penetration into an infected focus.
(b) THE URBAN CYCLE : The urban cycle involves person-to-person transmission by Aedes aegypti and is now virtually abolished in the
Americas owing to efforts to eradicate the vector. The urban yellow fever is often traced to persons who had been infected in forested areas,
and had brought the disease into the city, and less frequently by an infected monkey which has strayed into human settlements and is bitten by
an Aedes mosquito.
Incubation period
3 to 6 days (6 days recognized under International Health Regulations).
CONTROL OF YELLOW FEVER Jungle yellow fever
Jungle yellow fever continues to be an uncontrollable disease. The virus maintains itself in the animal kingdom. Mosquito control is
difficult and can be considered only in restricted areas. Vaccination of humans with 17D vaccine is the only control measure.
Urban yellow fever
(1) VACCINATION : Rapid immunization of the population at risk is the most effective control strategy for yellow fever. For international
use, the approved vaccine is the 17D vaccine. It is a live attenuated vaccine prepared from a non-virulent strain (17D strain), which is grown in
chick embryo and subsequently freeze-dried.
The sensitivity of the lyophilized 17D vaccine to heat is a major drawback to the use of this vaccine, in mass campaigns in tropical
countries. It has to be stored between +5 and -30 deg.C, preferably below zero deg. C until reconstituted with the sterile, cold physiological
saline diluent provided. Reconstituted vaccine should be kept on ice, away from sunlight, and discarded if not used within half an hour.
The vaccine is administered subcutaneously at the insertion of deltoid in a single dose of 0.5 ml irrespective of age. Immunity begins to
appear on the 7th day and lasts for more than 35 years, and possibly for life (2). However, WHO recommends revaccination after 10 years for
international travel.
Although no teratogenic effects have been ascribed to yellow fever vaccine, immunization should be avoided during pregnancy if there is
no risk of exposure. Similarly, immunization may be postponed until the child is one year, if there is no risk of exposure to yellow fever virus
(3).
Mild post-vaccinial reactions (e.g., myalgia, headache,
OTHERS
(Alphauiruses)
Sindbis
Chikungunya
Umbre
Sathuperi
Chandipura
Chittor
Ganjam
Minnal
Venkatapuram
Dhori
Kaisodi
Sandfly fever
African Horse sickness
Vellore
Group B
(Ftaviviruses)
Dengue
KFD
JE
West Nile
CLINICAL SYNDROMES
Although arboviruses are many, only a small number of them are
known to be capable of infecting man, and a much smaller number
capable of producing disease. A high proportion of the infections is
inapparent. For convenience, three clinical syndromes have been
described : (a) FEBRILE GROUP : This is the most common group
which comprises a large number of relatively undifferentiated
fevers, generally benign with or without rashes and joint pains.
Viruses responsible for this group of illness in India are the sindbis,
chikungunya and dengue viruses, (b) HAEMORRHAGIC FEVERS
: The second group is that of haemorrhagic fevers, generally
associated with moderate or high mortality. Viruses responsible for
haemorrhagic fevers in India are the dengue, chikungunya and KFD
viruses, (c) ENCEPHALITIDIS : TheN third group is that of
encephalitidis or meningo-encephalitis which is associated with a
considerable and sometimes high mortality. The disease reported
now frequently in some parts of India is the Japanese encephalitis.
0
1.The Dengue Syndrome
Vj^r
This is detailed separately at page 199.
2.Japanese Encephalitis
(Japanese encephalitis (JE) is a mosquito-borne encephalitis
caused by a group B arbovirus (Flavivirus) and transmitted by
culicine mosquitoes. It is a zoonotic disease, i.e., infecting mainly
animals and incidentally man\ Twenty-five years ago, JE was
known as an endemic diseasein East Asia, especially in Japan,
China and Korea (4). In recent years, it has spread widely in SE
Asia, and outbreaks of considerable magnitude have occurred in
Thailand, Indonesia, Vietnam, India, Myanmar and Sri Lanka (4).
An estimated 43,000 cases of JE occur globally each year, with
11,000 deaths and nearly 9000 disabled. The vast majority of cases
(about 85 per cent), occur among children less than 15 years of
age. Nearly 10 per cent of the cases are among those over 60 years,
perhaps reflecting waning protective immunity. About threequarters of the cases occur in the Western Pacific countries,
primarily China and adjacent countries, with the remainder
occurring in South-East Asia,
especially India. The disease is rare in other parts of the world, and
when seen, is generally associated with travellers returning from
endemic areas (5).
PROBLEM IN INDIA
Recognition of JE, based on serological surveys, was first made
in 1955 in Tamil Nadu (6). Subsequent surveys carried out by the
National Institute of Virology, Pune indicated that about half the
population in South India had neutralising antibodies to this virus
(7). In the year 2003, there has been a major upsurge of JE in
Assam, Andhra Pradesh, Bihar, Karnataka, Haryana, Maharashtra,
Tamil Nadu and Uttar Pradesh. JE incidence during the past few
years is as given in Table 2 :
TABLE 2
Incidence of Japanese Encephalitis in India
Year
Cases
1998
1999
2000
2001
2002
2003
2004 (upto March)
2120
3428
2593
2061
1765
2241
67
Deaths
507
680
556
479
460
670
0
Source : (8)
Epidemiological Features
Unlike the dengue viruses, JE virus infects several extrahuman
hosts, e.g., animals and birds. Available evidence indicates that the
basic cycles of transmission are :
(a)Pig > Mosquito > Pig
(b)The Ardeid bird > Mosquito > Ardeid bird
The disease is transmitted to man by the bite of infected
mosquitoes.Q^an is an incidental "dead-end" host. Man to ejpan
transmission has not so farbeen recorded^ y; - "OV f7^""\
nfyua) Animal hosts
(jMWanimal
hosts, pigs have been
TncrTfnTnated as the major vertebrate hosts for JE virus'Mn some
places, up to 100 per cent of pigs may be infectlfeeUwith JE virus.
Infected pigs do not manifest any overt symptoms of
; illness but circulate the virus so that mosquitoes get infected and
can transmit the virus toWa*/The pigs are thus considered
\ as "amplifiers" of the virus (SQ^tpttle and buffaloes may also be
infected with the JE virus; altKough they may not be natural hosts
of JE virus, they act as "mosquito attractantsVJ Horses are the only
domestic animals so far known which now signs of encephalitis
due to JE virus infection, (b) Birds : Some species of birds such as
pond herons; cattle egrets and perhaps poultry and ducks appear to
be involved in the natural history of JE
MOSQUITO VECTORS Y^'0 \x
2,Jj/Culicine mosquitoes, notably C. tritaeniorhynchus, C. vishnui
and C. gelidus along with some anophelines have been
incriminated as the vectors of JE. Among these, C.
tritaeniorhynchus has been implicated as the most important vector
in South India/ (10). These mosquitoes generally breed in irrigated
rice fields, shallow ditches and pools. The rice fields are probably
the most important breeding places. These mosquitoes are
zoophilic, feeding primarily on vertebrate hosts. Female
mosquitoes get infected after feeding on a viraem|c host, and after
9-12 days incubation period, they can trarrernit the virus to other
hosts/)
J
800 sq.km. Newer foci have since been recognized. The disease is
now restricted to four districts (Shimoga, North Kannada, South
Kannada and Chikamagaloor) in Karnataka State in India covering
over 6000 sq.km. (11). Serological surveys in different parts of India
revealed antibodies to KFD or a closely related virus in human and
animals, particularly in cattle in Kutch and Saurashtra (12).
According to the reports, the disease continues to be active in its
endemic foci. The outbreak during 1983-1984 seems to be the largest
with 2167 cases and 69 deaths, as against 571 cases and 15 deaths
during 81. The Karnataka Government has established a surveillance
system which monitors the occurrence of KFD in humans and
mortality in monkeys in known epidemic areas, as well as
neighbouring areas. Deaths of monkeys are considered as heralders
of this disease in endemic areas.
The reported number of cases and deaths due to Kyasanur forest
Disease from Karnataka state in 1991-97 is as shown in Table 3.
TABLE 3
Reported cases and deaths due to KFD from Karnataka State
Year
Cases
1991
1992
1993
1994
1995
1996
1997
940
1171
699
110
174 .
140
75
Deaths
15
5
3
0
3
3
4
CONTROL:
(a) VECTOR CONTROL : The Aedes aegypti mosquito should
be the main target of control activities. It requires active
community involvement to keep water storage containers free of
mosquitoes and to eliminate the other breeding places of
mosquitoes in and around houses and dwellings (19). The
organophosphorus insecticide, Abate is increasingly being used as
a larvicide. It can prevent breeding for up to 3 months when
applied on sand granules; does not harm man and does not affect
the taste of water. Antilarval measures can prevent an epidemic,
but do not give immediate results when an epidemic has already
broken out. In such cases, antiadult measures alone can bring about
a rapid interruption of transmission. A new technique consisting of
aerosol spray of ultra low-volume (ULV) quantities of malathion
or sumithion (250 ml/hectare) has been found to be effective in
interrupting transmission and stopping epidemics of DHF. The tiny
droplets kill the mosquitoes in the air as well as on water. By
making 2 ULV treatments at about 10 days apart, the Aedes
Research Unit in Bangkok was able to reduce adult mosquito
densities by more than 98 per cent for several weeks (20, 21). (b)
VACCINE: No vaccine has yet been developed that is considered
suitable for use.
5. West Nile Fever
An acute febrile illness caused by a group B arbovirus. The
disease is endemic in Africa, the Middle East, South-West Asia
and India, and transmitted by certain species of Culex mosquitoes.
Clinically, it is manifested by a sudden onset of fever, severe
headache and malaise lasting several days. In children, a
maculopapular rash of short duration may appear. In the aged, a
fatal meningo-encephalitis may be produced (16).
6. Sandfly Fever
Sandfly fever is known to occur in the arid regions of West
Pakistan and Middle East. Its occurrence in India was thought to be
doubtful. However, in 1967, the Sandfly fever virus was isolated in
Aurangabad (Maharashtra) from febrile cases. The virus was also
isolated from sandflies (22). The control of sandfly fever is based
on the control of insect vector.
References
1.WHO (1967). Tech. Rep. Ser., No.369
2.ICMR (1975). Permanent Institutes, New Delhi
3.Jawetz, E. et al (1980). Review of Medical Microbiology, 14th ed, Lange Medical
Publications, California
______________________________________BRUCELLOSIS 231
19.WHO (1979). WHO Chronicle, 33 : 107
20.WHO (1972). World Health, Aug-Sept, 1972
21.WHO (1972). WHO Chronicle, 26, 463
22.WHO (1975). WklyEpidRec, No. 23, 6 June 1975
BRUCELLOSIS
Brucellosis is one of the major bacterial zoonoses, and in
humans is also known as Undulent fever, Malta fever or
Mediterranean fever. It is occasionally transmitted to man by direct
or indirect contact with infected animals. It is caused by different
species of the brucella group of organisms and characterised by
intermittent or irregular febrile attacks, with profuse sweating,
arthritis and an enlarged spleen. The disease may last for several
days, months or occasionally years. Brucellosis is both a severe
human disease and a disease of animals with serious economic
consequences.
Problem statement
Brucellosis is a recognized public health problem with worldwide distribution. It is endemic wherever cattle, pigs, goats and
sheep are raised in large numbers. Important endemic areas for
brucellosis exist in Mediterranean zones, Europe, Central Asia,
Mexico and South America. Eastern Mediterranean countries have
experienced an increase in the number of cases in last 10 years.
The disease is now rare in most European countries and in North
America and Australia. Majority of cases (about 90,000 cases a
year) are reported from Middle East countries (1).
Animal brucellosis is reported from practically every State in
India. However, no statistical information is available about the
extent of infection in man in various parts of the country (2).
The prevalence of human brucellosis is difficult to estimate.
Many cases remain undiagnosed either because they are inapparent
or because physicians in many countries are unfamiliar with the
disease.
Agent factors
(a) AGENT : The agents are small, Gram negative rod-shaped,
non-motile, non-sporing and intracellular coccobacilli of the genus
Brucella. Four species infect man : B. melitensis, B. abortus, B.
suis, and B. canis. B. melitensis is the most virulent and invasive
species; it usually infects goats and occasionally sheep. B. abortus
is less virulent and is primarily a disease of cattle. B. suis is of
intermediate virulence and chiefly infects pigs. B. canis is a
parasite of dogs, (b) RESERVOIR OF INFECTION : Main
reservoirs of human infection are cattle, sheep, goats, swine,
buffaloes, horses and dogs. In animals the disease can cause
abortion, premature expulsion of the foetus or death. Cross
infections can often occur between animal species. The infected
animals excrete Brucella in the urine, milk, placenta, uterine and
vaginal discharges particularly during a birth or abortion. The
animals may remain infected for life.
Host factors
Human brucellosis is predominantly a disease of adult males.
Farmers, shepherds, butchers, and abattoir workers, veterinarians
and laboratory workers are particularly at special risk because of
occupational exposure. Immunity follows infection.
Environmental factors
Brucellosis is most prevalent under conditions of advanced
domestication of animals in the absence of correspondingly
advanced standards of hygiene. Overcrowding of herds, high
rainfall, lack of exposure to sunlight, unhygienic practices in milk
and meat production, all favour the spread of brucellosis.
The infection can travel long distances in milk and dust. The
environment of a cowshed may be heavily infected. The organism
can survive for weeks, or months in favourable conditions of
water, urine, faeces, damp soil and manure.
Mode of transmission MtM"C3'k(lM.
Transmission is usually from infected animals to man. There is
no evidence of transmission from man to man (3). The routes of
spread are :
(a) Contact infection : Most commonly, infection occurs by
direct contact with infected tissues, blood, urine, vaginal
discharge, aborted foetuses and especially placentay Infection
takes place through abraded skin, mucosa or Conjunctiva
(mucocutaneous route). This type of spread is largely occupational
and occurs in persons involved in handling livestock and slaughter
house workers.
(^ (b) Food-borne infection ): Infection may take place indirectly
by the ingestion or raw milk or dairy products (cheese) from
infected animals. Fresh raw vegetables can also carry infection if
grown on soil containing manure from infected farms. Water
contaminated with the excreta of infected animals may also serve
as a source of infection.
(J C(c) Air-borne infection y The environment of a cowshed imay
be heavily infected." Few people living in such an
environment can escape inhalation of infected dust or aerosols.
Brucellae may be inhaled in aerosol form in slaughter houses
and laboratories, so these infections are notified as
occupational.
Incubation period
Highly variable. Usually 1-3 weeks, but may be as long as 6
months or more.
Pattern of disease
Brucella infection in man can vary ffom an acute febrile disease
to a chronic low-grade ill-defined disease, lasting for several days,
months or occasionally years.
The acute phase is characterised by a sudden or insidious onset
of illness with (i) swinging pyrexia (up to 40-41 deg C), rigors and
sweating (ii) arthralgia/arthritis (usually monoarticular) involving
larger joints such as hip, knee, shoulder and ankle, (iii) low back
pain (iv)headache, insomnia (v) small firm splenomegaly and
hepatomegaly (vi) leucopenia with relative lymphocytosis (4). The
most striking aspect of the clinical picture is the severity of the
illness and the absence of clinical signs. The acute phase subsides
within 2-3 weeks. If the patient is treated with tetracycline, the
symptoms may disappear quickly, but the infection, being
intracellular, may persist giving rise to subacute or relapsing
disease.
In a few patients (up to 20 per cent), symptoms recur for
prolonged periods. Diagnosis is established by isolation of the
organism from cultures of blood, bone marrow, exudates and
biopsy specimens during the acute phase of the disease; and by
serological tests.
Control of brucellosis
(a) IN THE ANIMALS :
The most rational approach for preventing human brucellosis is
the control and eradication of the infection from animal reservoirs
which is based on the combination of the following measures : (a)
Test and slaughter : Case finding is done by mass surveys. Skin
tests are available. The complement fixation test is also
recommended. Those animals infected with brucellosis are
slaughtered, with full compensation paid to farmers! This is the
only satisfactory solution aimed at eradication of the disease (b)
Vaccination : Vaccine of B. abortus strain 19 is commonly used
for young
General WHO
2.DGHS, NICD (1985) Manual on Zoonoses
3.WHO (1976) Techn. Rep. Ser., No.598
4.J.V. Zammit Maempel (1984). Medlnt 2 : 85 Feb 1984 Middle Eastern
edition
5.T. Fujlkuva (1985) World Health July, 1985 P. 13
LEPTOSPIROSIS
Leptospirosis is essentially animal infection by several
serotypes of Leptospira (Spirocheates) and transmitted to man
under certain environmental conditions. The disease manifestations
are many and varied, ranging in severity from a mild febrile illness
to severe, and sometimes fatal disease with liver and kidney
involvement. Weils disease is one of the many manifestations of
human leptospirosis.
Problem Statement
Leptospirosis is considered to be the most widespread of the
disease transmissible from animal to man (1). It has high
prevalence in warm humid tropical countries. Out breaks mostly
occur as a result of heavy rainfall and consequent floodings (3). It
has been known to occur in India since long. Reports indicate that
it is fairly widespread throughout India (2). Recently there was
outbreak of leptospirosis in Orissa after the super cyclone of 29th
Oct. 1999. Later on in the month of August 2000 there were cases
of leptospirosis in Gujarat, Kerala, Maharashtra and Andaman and
Nicobar (3).
Agent factors
(a) Agent: Leptospira are thin and light motile spirocheates
0.1 - 0.2 ^m wide and 5-15 um long with hooked ends. Only the
strains of L. interrogans are pathogenic. The organisms are visible
by dark-field illumination and silver staining. At present, 23
serogroups and 200 serovers have been recognized from various
parts of the world. They are serologically related with cross
reactivity, (b) SOURCE OF INFECTION : Leptospira are excreted
in the urine of infected animals for a long time, often for an entire
life time in cases of rodents (c) ANIMAL RESERVOIRS :
Leptospirosis affects wild and domestic animals worldwide
especially rodents such as rats, mice and voles. Most domestic
animals including cattle, sheep, goats, water buffalo, pigs and
horses may be infected through grazing in areas contaminated by
the urine of the carrier host. Pet animals, particularly dogs may
also be infected. Infection may spread from wild animals to
domestic livestock, and thence to humans. Rats and small rodents particularly R. norvegicus and Mus musculus are the most
important reservoirs.
Host factors
(a) AGE : Children acquire the infection from dogs more
frequently than do adujts. Human infection is only accidental
(a)OCCUPATION :|_Human infections are usually due to occupational
exposure to the urine of infected animals, e.g,
$J agricultural and
livestock farmers, workers in rice fields, VC-*> sugarcane fields, and
underground sewers, abattoir workers,
/ meat and animal handlers,
veterinarians etc. (2). Leisure time activities such as swimming and
fishing may also carry risks J
(b)IMMUNITY : A solid serovar specific immunity follows
infection.
Environmental factors
Leptospirosis infection is unique in that it is acquired through
contact with an environment contaminated by urine and faeces
from carrier (reservoir) animal or other infected animals.
Leptospira shed in the urine can survive for weeks in soil and
water, so environmental contamination may reach high levels in
areas where carrier animals frequently urinate (4). The association
of poor housing, limited water supply, inadequate method of waste
disposal, all combine to make the disease a significant risk for the
poor population in both urban and rural areas.
Mode of transmission
(a) DIRECT CONTACT : Leptospira can enter the body
through skin abrasions or through intact mucous membrane by
direct contact with urine or tissue of infected animal (b)
INDIRECT CONTACT : Through the contact of the broken skin
with soil, water or vegetation contaminated by urine of infected
animals or through ingestion of food or water contaminated with
leptospirae (c) DROPLET INFECTION : Infection may also occur
through inhalation as when milking infected cows or goats by
breathing air polluted with droplets of urine (5).
Direct man to man infection is rare.
Incubation period
Usually 10 days with a range of 4-20 days.
Diagnosis
It is not possible to diagnose leptospirosis with certainty on
clinical grounds alone. Because of the wide spectrum of signs and
symptoms, the diagnosis is made by isolation of leptospires from
blood during the acute illness and from urine after the first week
(5). Early in the disease, the organism may be identified by darkfield examination of the patient's blood or by culture on a semisolid
medium. Culture takes 1-6 weeks to become positive. The
organism may also be grown from the urine from 10th day to 6
weeks. Diagnosis is usually made by means of serological tests, of
which several are available. Agglutination
____________________________________________PLAGUE 233
tests (microscopic using live organism, and macroscopic using
killed antigen) become positive after 7-10 days of illness and peak
at 3-4 weeks and may persist at high level for many years. Indirect
haemagglutination, immunoflourescent antibody and ELISA tests
are also available. The IgM ELISA is particularly useful in making
an early diagnosis, as it is positive as early as 2 days into illness
(6). Now Lepto - Dipstick test is also available.
Control
(a)ANTIBIOTICS : Penicillin is the drug of choice but other
antibiotics (tetracycline or doxycycline) are also effective. The
dosage of penicillin is 6 million units daily intravenously.
(b)ENVIRONMENTAL MEASURES: This includes preventing
exposure to potentially contaminated water, reducing
contamination by rodent control and protection of workers in
hazardous occupation. Measures should be taken to control
rodents, proper disposal of wastes and health education etc.
Vaccination
Immunization of farmers and pets prevent disease. In some
countries for instance Italy, USSR and China, where certain
occupations carry a high risk of infection, vaccines are available. It
is important that they should incorporate strains of the serotypes
that predominate in the particular area since immunity to one type
of Leptospira may not protect against infection by another (5).
References
1.WHO (1978), World Health, Oct. 1978
2.Pedro N, Acha and B Szybres, Zoonoses and Communicable Diseases
Common to Man and Animals, 2nd Ed., Pan America, Health organization.
3.WHO (2000), Weekly Epidemiological Record, No. 27, 7th July 2000
4.WHO (1985), World Health, July 1985
5.Coghlan, J.D., Post graduate Doctor, May 1983
6.Lawrence M. Tierney, Jr. et al. Current Medical Diagnosis and
Treatment, 38th Ed. 1999, International edition.
PLAGUE
Plague is primarily and basically a zoonoses, caused by Y.
pestis, involving rodents and fleas. It exists in natural foci, and is
transmitted by infected flea bites to humans living or intruding into
the same ecological environment. Plague occurs in many forms enzootically, epizootically, sporadically and in epidemics of all
types including anthroponotic and primary pneumonic forms.
Despite the enormous body of knowledge regarding plague, this
communicable disease continues to pose a threat in many areas.
History
Epidemics of plague are mentioned in the Bible. The
association of plague with rats was known to the ancients. It is
mentioned in Bhagwat Puran (an ancient Indian text written about
1500-800 B.C.) that as soon as the dead rats are seen, the residence
should be immediately abandoned. Down the ages, plague was
known as "Mahamari", the great death.
Since the dawn of Christian era, there have been three great
pandemics : the first began in the year 542 (Justinian plague) and is
estimated to have caused 100 million deaths; the second began in
the year 1346, lasted for three centuries and claimed 25 million
lives; and the last began in 1894 and continued until 1930s (1). As
a result of the last pandemic, "natural foci" of infection outside man
were established in many countries e.g., Central Asia, Iranian
Kurdistan, Arabia, Central and South Africa, Myanmar, Vietnam,
Indonesia, South America and the Western United States of
America. The danger still exists that
plague may spill over into the human population as has happened
in India where plague has reappeared in 1994 after a silent period
of 28 years.
Problem statement
WORLD :
From time immemorial, plague has dogged man's footsteps, and
at various periods in history it has taken a heavy toll of human lives
(2, 3). It has declined considerably in the second half of the 20th
century - from 40,484 cases recorded in 1950, to 3037 cases
between 1980-1984 (4, 5). Over the last 10 years, the mean annual
global plague case fatality rate has been 7 per cent, ranging from
just over 14 per cent in Africa to just under 4 per cent in the
Americas. During 2001 about 2671 cases were reported worldwide with 175 deaths. There were 2557 cases in the region of
Africa with about 165 deaths (6) .The high rate persists despite the
availability of highly effective drugs against the disease.
In SEAR, natural foci of plague exists in India, Indonesia,
Myanmar and possibly in Nepal. Hence there is a need to be
vigilant about this disease. There are no reports of plague in the
recent past from any country. The last case of human plague was
recorded in Sri Lanka in 1938, Thailand in 1952, Nepal in 1968
and India in 2002, and Myanmar in 1994.
In the early years of this century, plague constituted a serious
problem in India. The annual mortality was over 500,000 deaths
between 1898 and 1908. The disease continued to be major public
health problem until the mid-1940s. Thereafter it began to decline
speedily as a result of the large-scale application of DDT for the
purpose of malaria control. Uttar Pradesh, which was one of the
plague-active states in India, became free of plague in 1959, and
Madhya Pradesh in 1960.
The last PHA-positive sera specimen from rodents were
observed in 1976 in Maharashtra where suspected human cases
were reported in Beed district and in 1979 in Kolar (7,8).
Return of plague : Since the last reported cases in 1966, there
have been no laboratory confirmed case of human plague in India,
till its reappearance in Sept 1994, when 4 persons tested positive
for bubonic plague in Beed (Maharashtra), followed by an
outbreak of pneumonic plague in Surat (Gujarat). Cases were also
reported from Delhi, Mumbai, Kolkata and some other places.
4780 suspected cases were reported, out of which 167 tested
positive for plague and 53 deaths were reported (9). More recently
as of 19th Feb. 2002, the Ministry of Health reported a total of 16
cases of pneumonic plague (including 4 deaths) in Hat Koti village,
Shimla Dist. Himachal Pradesh since the onset of the outbreak on
4th Feb. 2002. The disease was confirmed byNICD{10;.
Agent factors
(a)AGENT : The causative agent, Y. pestis is a Gram-negative,
non-motile, cocco-bacillus that exhibits bipolar staining with
special stains (e.g., Wayson's stain). The bacilli occur in great
abundance in the buboes, blood, spleen, liver and other viscera
of infected persons, and in the sputum of cases of pneumonic
plague. The virulence of the organism is related to its ability to
produce exotoxin, endotoxin, Fraction 1 and many other
antigens and toxins. It has been shown that plague bacilli can
survive, and indeed multiply in the soil of rodent burrows
where micro-climate and other conditions are favourable (11).
(b)RESERVOIR OF INFECTION : Wild rodents (e.g., field
mice, gerbils, skunks and other small animals) are the natural
reservoirs of plague. These are found in mountains, deserts,
cultivated areas and forests in temperate and tropical regions.
2. Epizootiology
Plague is epizootic and enzootic in wild rodents. Two
ecological cycles have been described :
a. WILD PLAGUE : Wild plague is defined as "plague existing
in nature, independent of human populations and their activities"
(11). The disease spreads among wild rodents by wild rodent fleas.
The epizootic wipes out the susceptible
should not be handled with naked hands. The neck of the bag
should be tied to avoid escape of ectoparasites. The bag should
then be placed in a wooden box or tin. The empty space left in the
box or tin should be filled with absorbent cotton or sawdust to
eliminate chances of leakage of effluents outside the box. The box
is labelled giving details of collection and sent to the nearest
laboratory. (2) AUTOPSY AND COLLECTION OF SMEARS :
The rat is held with a pair of tongs, and dipped in a solution of 5
per cent cresol. The animal is laid on its dorsum, stretched and the
limbs nailed on a wooden board. The abdomen is swabbed with
lysol or spirit. The skin is lifted and cut up to the chest. The
instruments used are then put back into boiling water. Using
another set of instruments, small portions of the viscera (spleen,
liver, lungs, bubo) are cut and the freshly cut surface is first blotted
on a blotting paper so as to remove excess of blood or plasma.
Then the same surface of the tissue is gently pressed on the glass
slides so as to make thin impressions (never rub the tissue on the
slides). If the rat is completely decomposed and no tissue is left,
smears should be obtained from the bone marrow. The smears are
dried, treated with alcohol for three minutes and fixed by exposure
to open flame. The fixed smears may be sent for examination.
Persons handling infected rats are exposed to the risk of pneumonic
plague and this danger should be borne in mind. (3) ANIMAL
INOCULATION : It may be difficult to isolate the plague bacilli
by cultural methods owing to gross contamination of the carcass. In
such cases, small portions of liver or spleen are taken, ground in a
mortar with a little saline and inoculated into a guinea pig or a
white mouse. If there is plague infection, the guinea pig will die in
7 days and the white mouse in 48 hours. (4) PATHOLOGICAL
CHANGES : The pathological changes in an animal infected with
plague are as follows: (a) there is oedema and necrosis at the site of
injection, (b)the lymph nodes are enlarged, (c) the spleen is
enlarged and congested and shows necrotic patches, (d) liver shows
mottling, (e) lungs also show necrotic lesions, (f) there is
subcutaneous congestion and haemorrhages.
HUMAN PLAGUE
Mode of transmission
Human plague is most frequently contracted from : (a) the bite
of an infected flea, (b) occasionally by direct contact with the
tissues of the infected animal or (c) by droplet infection from cases
of pneumonic plague. The dissemination of plague by plague
patients (by the bite of the human flea, Pulex irritans) is a rare and
exceptional occurrence.
There are at least 5 basic types of transmission cycles in plague.
These cycles are as follows (17) :
1. Commensal rats > rat fleas -^man
This is the basic cycle in epidemic bubonic plague
2. Wild rodents-^ wild rodent fleas or direct contact > man
The disease is transmitted from rodent to rodent via
wild rodent fleas or contaminated soil. Man contracts
the infection from infectious wild rodent fleas or by
direct contact with infected rodents
3. Wild rodents, peridomestic rodents, commensal rodents
> wild rodent fleas, peridomestic rodent fleas,
commensal rodent fleas >man
;.
Plague foci impinge upon the habitats of peridomestic
or commensal rodents. Interaction of the rodents and
their fleas convey the infection to man
4. Man > human flea (Pulex irritans) -^man
This variety may be encountered in certain areas
2 to 7 days
2 to 7 days
1 to 3 days
Disease in man
There are three main clinical forms : (a) Bubonic plague :
This is the most common type of the disease. The infected rat fleas
usually bite on the lower extremities and inoculate the bacilli. The
bacilli are intercepted by the regional lymphatic glands where they
proliferate. Typically the patient develops sudden fever, chills,
headache, prostration and painful lymphadenitis. Usually within a few
days greatly enlarged tender lymph nodes (buboes) develop in the groin
and less often in the axilla or neck, depending upon the site of the bite
by the flea. When suppuration takes place it is considered a favourable
sign. Bubonic plague cannot spread from person to person as the bacilli
are locked up in the buboes and do not find a way or easy exit.Qb)
Pneumonic plague : Primary pneumonic plague is rare; it generally
follows as a complication p of bubonic-septicaemic plague. The
incidence of pneumonic I plague is usually below 1 per cent (14).
Pneumonic plague is KU highly infectious and spreads from man to man
by droplet infection. The plague bacilli are present in the sputum^ (c)
Septicaemic plague : Primary septicaemic plague is rare except for
accidental laboratory infections. However, bubonic plague may develop
into septicaemic plague in the face of an overwhelming infection.
Laboratory investigations
The absolute confirmation of plague infection in human beings,
rodents or fleas requires the isolation and identification of the
plague bacillus. The important laboratory methods of diagnosis
include the following : (a) Staining : It is important to prepare
smears of the clinical material (e.g., bubo fluid, sputum) which
should be fixed with alcohol and then stained with Giemsa's or
Wayson's stain to demonstrate bipolar bacilli in the specimen, (b)
Culture ; Blood for culture should be collected from all patients.
Under ideal circumstances, appropriate culture media should be
inoculated on the spot with blood, bubo fluid or sputum to ensure
speedy isolation of the plague bacilli. When this is not possible, the
specimen must be transported to the laboratory in Cary-Blair
transport medium. (c)Serology : Acute and convalescent specimens
of blood sera should be collected for antibody studies (d) Other
methods : These include inoculation of guinea pigs or mice or
immunofluorescent microscopic test.
PREVENTION AND CONTROL
1. Control of cases
(a) EARLY DIAGNOSIS : During epidemic situations, diagnosis
of plague can be made readily on clinical grounds, e.g., acute fever
and painful lymph node enlargement developing into buboes in the
inguinal and other regions of the body. In other situations, "rat
falls" (dead rats) provide a useful warning of a possible outbreak.
It is essential that plague-suspected humans and rodents be
examined bacteriologically to confirm the presence of plague. It is
often possible to arrive at a prima facie diagnosis by the
examination of smears that show the characteristic bipolar stained
plague bacilli (17). (b) NOTIFICATION : If a human or rodent
case is diagnosed, health authorities must be notified promptly.
Case notification
Booster Dose
six-monthly
Adult males
Adult females
Children
1-4 years 5-10 years 1116 years Infants under 6
months are not
immunized.
1.0 ml
0.75 ml
1.5 ml
1.0 ml
1.0 ml
0.75ml
0.2 ml 0.3
ml \ 0.4 ml
J
double the
first dose
Same as the
first dose
Source : (22).
^jfLv^fhemoprophylaxis
P Chemoprophylaxis is a valuable preventive measure, highly
^recommended. It should be offered to all plague contacts,
' medical, nursing and public health personnel exposed to the
yisk of infection. The drug of choice is tetracycline. For adults,
the dose is 500 mg 6-hourly for 5 days (23). A cheaper
alternative is sulfonamide, 2 to 3 g daily for 5 to 7 daysM
6. Surveillance
Plague has a potential for spread into susceptible areas. Therefore, in
areas where natural plague foci exist or where there is a history of past
infection, surveillance is essential. Surveillance should cover all aspects of
rodent and human plague, e.g., microbiology, serology, entomology,
mammalogy, epidemiology and ecology. On the basis of information
provided by surveillance, effective control measures must be established
(21). Surveillance of plague in its natural foci should, therefore, replace
quarantine measures which have been shown to be ineffective (11).
7. Health education
Health education is an essential part of any plague control programme.
Education should aim at providing the public with the facts about plague
and at enlisting their cooperation. Emphasis must be placed on the need for
the prompt reporting of dead rats and suspected human cases so that
preventive measures can be taken. Medical practitioners should keep
plague in mind in differential diagnosis of any cases of fever with
lymphadenopathy, or when multiple cases of pneumonia occur (11).
Epidemiological investigations (24)
The determination of the source of infection and the distribution,
prevalence, and potential spread of plague in human population is the main
objective of epidemiological surveillance. This means that those engaged
in surveillance must evaluate human plague in its relationship with
epizootic factors and that the investigations must be based on direct
contact with villages and other communities affected by plague. While the
collection of demographic data and information on such subjects as
population movements and local occupations, customs, and habits is
important, special attention must be given to the factors bringing man into
contact with the vertebrate reservoirs and vectors of y. pestis
Some of the responsibilities of the surveillance team are as follows :
(1)to make a detailed study of all cases of human plague, giving
special attention to dwellings where cases have occurred, in order to
establish the rodent/ vector source of the infection or the occurrence
of man-to-man transmission;
(2)to keep complete and uniform records of each case of plague,
using standardized forms, and to issue questionnaires to the
population at risk;
(3)to isolate strains of y. pestis and subject them to detailed
biochemical analysis, samples being lyophilized for later study;
(4)to make a serological survey of the target population; such
surveys are of value in investigation of possible cases of subclinical
plague, of recovered untreated infections, and of asymptomatic
pharyngeal infection in "carriers";
(5)to investigate changes in the human population, social or
economic activities, and other features of natural foci where there is
close contact between human populations and commensal rodents;
(6)to keep a watch on containerized cargoes of grain and other food
crops originating in areas with natural plague foci and destined for
national or international trade;
(7)to undertake surveillance in cooperation with adjacent countries
when natural foci are common to two or more countries;
(8)to give special attention, in the case of sea-ports or airports, to the
proximity of natural foci where there is contact between wild and
commensal rodents, the proximity of epidemics, and the transport of
cargo from enzootic areas.
The surveillance team should also be prepared to assist the national or
community health service in organizing and carrying out the treatment of
human cases and measures for the control and prevention of plague. An
organizational basis should be established for rapid emergency services in
the event of an epidemic.
Reporting of cases and outbreaks of plague (24)
The WHO should be informed promptly of the occurrence of any
epidemic or isolated case of plague. The report should include details
about the administrative area and exact locality involved. This preliminary
notification should be followed up as soon as possible by a more detailed
report containing the following information :
(a)The locality and administrative area, shown on a map if possible
(b)The date, the first case was noticed
(c)The period during which field investigations were made
(d)The number and types of cases of plague detected :
clinical diagnosis only (presumptive)
laboratory diagnosis (confirmed)
recovered and confirmed serologically
types of cases - bubonic, pneumonic, etc.
age of patient with a confirmed diagnosis of plague
number of deaths
Agent factors
AGENT : Salmonellae comprise a large and important group of
bacteria. This group is now known to comprise more than 2200 serotypes
capable of infecting humans (2), but in most countries only a small
number of them (usually about 10) are endemic at any one time (4).
Compared with other gram-negative rods, salmonellae are relatively
resistant to various environmental factors. They have been shown to be
resistant to drying, salting, smoking and freezing even for years. This
explains why these organisms survive in many kinds of food. As a result,
salmonellae have been isolated from divergent foods such as chocolates,
biscuits, coconuts and spices. The bacterium is sensitive to heat and will
not survive temperatures above 70 deg C.
From an epidemiological point of view, salmonellae can be classified
into three main groups (2).
(i) those which infect only man - e.g., S. typhi, S. paratyphi A and
C.
(ii) those that-are host-adapted for particular species of animals,
e.g., S. cholera-suis in swine, S. dublin in cattle, S. abortus
equi in horses, S. gallinarum in poultry, etc. Some of these
are also pathogenic for man, e.g., S. cholera-suis, S. dublin.
(iii) those with no particular host preference and can infect both
man and animals - e.g., S. typhimurium, S.enteritidis. In this
group (approximately 2200 serovars) are the principal agents
of salmonellosis that occurs today (2). They can be
transmitted from animals to man and vice versa. S.
typhimurium is responsible for up to 50 per cent or more of all
human salmonella infections all over the world. S. enteritidis
has also emerged as an important pathogen.
RESERVOIR AND SOURCES OF INFECTION : The main reservoir
of Salmonella is the intestinal tract of man and animals. The source of the
infecting agent could be contaminated food, animals, man or the
environment.
(a) Foods:
Foods of animal origin, particularly commercially prepared foods such
as meat, poultry and egg products are considered to be the primary sources
of salmonellosis. Most of these foods, e.g., meat and poultry become
contaminated during slaughter. Every food that is produced or processed
(including chocolates, spices, coconut) in a contaminated environment
may become contaminated. Cross-contamination of cooked foods from
raw ingredients, kitchen utensils or surfaces has been described frequently
as a cause of salmonellosis (4). Eggs may be infected directly through
shell-cracks. Recent investigations suggest that salmonellae may penetrate
the ovaries of egg-laying chickens. What food will ultimately become the
vehicle varies from country to country (5). For example, in the USA, beef
is the main source of salmonella infection, while in England and Wales
poultry accounts for more than 50 per cent of Salmonellosis outbreaks (2).
(b) Animals :
Animals are the hosts and the principal vectors of zoonotic
salmonellosis. Many animals including cattle, swine, rodents and fowl are
naturally infected with a variety of salmonellae and have the bacilli in
their tissues (meat), eggs or excreta. Carriers occur among both man and
animals.
(c) Environment:
Salmonellae are widely distributed in the environment - in dust, water,
manure, sewage, sludge, vegetables, insects, birds, fish, rodents and other
mammals. They can survive in soil for
Incubation period
6 to 72 hours (usually)
Clinical features
The disease arises from the ingestion of the living organisms. Recent
studies indicate that Salmonella spp possess both invasive and cholera-like
enterotoxic properties (5). Clinically, the disease may be manifest by one
of three syndromes :
(i) Enteric fever : S. typhi, S. paratyphi A and C are human pathogens,
and are not considered zoonotic agents (2). S. paratyphi B, while
predominantly found in man has also been isolated from turkeys, chickens,
cattle, sheep, swine, mice and monkeys. This syndrome (enteric fever) is
dealt with separately (see page 187).
fiij Salmonella entero-colitis (gastroenteritis) : This is the most
common manifestation of Salmonella infection. 6 to 48 hours after
ingestion of Salmonellae there is nausea, headache, vomiting and
diarrhoea. Low grade fever is common. Most infections are mild with
diarrhoea as the only symptom. In severe cases there may be dehydration
requiring replacement of fluids and electrolytes. The episode usually
resolves in 2 to 3 days, but the stools often remain loose for several weeks.
The excretion of salmonella may be prolonged by antimicrobial therapy.
Blood cultures are usually negative but stool cultures are positive for
salmonella and may remain positive for several weeks after clinical
recovery. Death is rare and occurs primarily in neonates, infants and
elderly.
(in) Septicemia with focal lesions : Non-typhoid salmonellae (e.g., S.
cholera -suis) may occasionally invade the blood stream leading to
generalized or localised infection presenting itself as pyrexia of unknown
origin. Focal infection may result in osteomyelitis, pyelonephritis, arthritis,
meningitis, cholecystitis and endocarditis. Stool cultures are negative but
blood cultures are positive.
Prevention and control
Since salmonellosis is zoonotic in origin, preventive measures should
begin at the farm and embrace all the elements of the food chain through
live animals, animal products, processing, final food preparation to
consumption. Approaches indicated at the farm level are : (i) disease
control, e.g., immunization of farm animals against salmonellosis (ii) the
use of hygienic animal feed, and (iii) ensuring a sanitary environment for
the animals. The aim is to raise "salmonella -free" animals.
The other approaches include : hygienic slaughtering and milking,
pasteurization of milk and eggs; proper disposal of liquid and solid wastes,
cold storage facilities, and health education and training.
Since the health sector alone cannot solve the problem of
salmonellosis, responsibility for prevention and control
Rickettsial
. agent
Insect
vectors
Mammalian
reservoirs
R. prowazekii
R. typhi
R. tsutsugamushi
Louse
Flea
mite*
Humans
Rodents
Rodents
R. conorii
Tick*
Rodents, dogs
R. rickettsii
Tick*
Rodents, dogs
R. akari
Mite*
Mice
C. burnetii
nil
Rochalimaea
quintana
Louse
Cattle, sheep,
goats
Humans
1.Typhus group
a. Epidemic typhus
b. Murine typhus
c. Scrub typhus
2. Spotted fever group
a. Indian tick
typhus
b. Rocky Mountain
spotted fever
c. Rickettsial pox
3. Others
a. Q fever
b. Trench fever
Man
which indicates the location of the mite bite. The pyrexia falls by
lysis in the 3rd week in untreated cases. The Weil Felix reaction is
strongly positive with the Proteus strain OXK.
Control measures
(a) TREATMENT : Tetracycline is the drug of choice. With
proper therapy the mortality is nil (b) VECTOR CONTROL :
clearing the vegetation where rats and mice live; application of
insecticides such as lindane or chlordane to ground and vegetation
(c) PERSONAL PROPHYLAXIS : Impregnating clothes and
blankets with miticial chemicals (benzyl benzoate) and application
of mite repellents (diethyltoluamide) to exposed skin surfaces (6).
No vaccine exists at present.
Y
(MURINE TYPHUS
vVjf cA i (Endemic or Flea-borne typhus) )
K
Distribution
Murine typhus (MT) is a zoonoses. It is world-wide in
distribution especially in areas of high rat infestation. It appears to
be more prevalent in South-East Asian and Western Pacific
countries than previously recognized (1). In USA, fewer than 80
cases are reported annually. Cases tend to be scattered. Successful
isolation of the causative agent from rats, fleas and bandicoots was
made at many places in India, viz Shimla hills, Mumbai, Jabalpur,
Kashmir, Lucknow, Pune, etc (5). The percentage of sero-positive
individuals in the general population in South East Asian countries
ranged from 6 to 22 per cent (1). Focal infections are often
associated with docks and shipping places where rats abound.
/Agent factors
^V0*^
V (a) AGENT : Rickettsia typhi (R. mooseri). (b) RESERVOIR OF
INFECTION : Rats are the reservoir (Rattus rattus and R.
norvegicus). Infection in rats is inapparent, long-lasting and nonfatal. "^
Mode of transmission
The infection spreads from rat to rat (X. cheopis) and possibly
by the rat louse (7). The actual mode of transmission is not by the
bite of the rat flea, but by (i) inoculation into skin of faeces of
infected fleas, and (ii) possibly by inhalation of dried infective
faeces. There is no direct man to man transmission. Once infected
the flea remains so for life. The flea cannot transmit the rickettsiae
transovarially. The transmission cycle may be shown as below :
Rat - Rat flea >
Rat -
Rat flea
> Rat
Man
Incubation period
1 to 2 weeks, commonly 12 days
Incubation period
Usually 10 to 12 days; varies from 6 to 21 days
Clinical features
The clinical features resemble that of louse-borne typhus, but
milder and rarely fatal. The Weil Felix reaction with Proteus OX19 becomes positive in the 2nd week.
Clinical features
Scrub typhus resembles epidemic typhus clinically. The onset is
acute with chills and fever (104-105 F), headache, malaise,
prostration and a macular rash appearing around the 5th day of
illness. Generalized lymphadenopathy and lymphocytosis are
common. One typical feature is the punched-out ulcer covered with
a blackened scab (eschar)
Control measures
(a) TREATMENT : Tetracycline is the only drug of choice.
Since rickettsial growth is enhanced in the presence of
sulfonamides, these drugs should not be given (b) CONTROL OF
FLEAS : Residual insecticides (e.g., BHC, malathion) are effective
against rat fleas. Rodent control measures should be implemented
in the affected areas. No Murine Typhus vaccine is currently
available.
- Tick
Dog
Man
I
Tick
> Man
Incubation period
Usually 3-7 days
Clinical features
The patient usually gives history of a recent tick-bite and a
careful examination will reveal a lesion or eschar at the site of
the bite. After an interval of 3 to 7 days, there is an acute onset
I
of fever, which may persist for 2 to 3 weeks, malaise and
headache. A maculopapular rash appears on the third day. Unlike
the rash in other rickettsial diseases, the rash appears first on the
extremities (ankles and wrist), moves centripetally and involves the
rest of the body. The clinical syndrome may be confused with
atypical measles.
Control measures
(a) TREATMENT : Broad spectrum antibiotics have proved to
be effective (b) PERSONAL PROPHYLAXIS : Known tickinfested areas should be avoided. Daily inspection of the body for
ticks is particularly important for those who are exposed to the risk
of infection. Disinfection of dogs will minimise the tick population.
Health education of the people in the mode of transmission by
ticks, and the means of personal protection is equally important.
Q FEVER
Distribution
Q fever is a highly infectious zoonotic disease with world-16
wide distribution. It occurs mainly in persons associated with
Hosts of infection
T. saginata and T solium pass their life cycles in two hosts. In man, the
adult parasites live in the small intestine. The adult T. saginata measures 5
to 12 metres in length, and may be up to 24 metres; T. solium measures 2
to 6 metres.
TABLE 1 Hosts of
infection
1.
2.
Parasite
Definitive
Intermediate host
T saginata
T. solium
Man
Man
The larval stage of T. saginata (C. bovis) mainly occurs in cattle. The
pig is the main host for the larval stage of T. solium (C. cellulosae) but
man may also be infected. This may lead to muscular, ocular and cerebral
cysticercosis.
The adult stages of T saginata and T solium may persist for several
years in infected humans. Mixed infections of both the parasites can occur.
Although the life span of C. cellulosae in man is not known, it is suspected
to be some years.
Mode of transmission ftf
7#nife- '
HYDATID DISEASE
I
______________________________________________________
I
Hydatid Disease is a zoonoses - a group of cestode infections
which are important zoonotic diseases of man. The disease in man
is caused by the metacystode stage (infective larva) of the canine
intestinal tapeworm Echinococcus; the adult worms are found in
dogs and other carnivores.
Geographic distribution
In recent years, hydatidosis has been recognized as a public
health problem of nearly global dimensions (1). It is found in all
sheep-raising countries, e.g., Australia, New Zealand, Tasmania,
Middle East countries, Turkey, Greece, USSR, Cyprus, Latin
America and the Far East etc. It is believed that there are relatively
few countries in which cestodes of the genus Echinococcus are
entirely absent (2). Foci are also known to exist in India where the
highest prevalence is reported in Andhra Pradesh and Tamil Nadu
than in other parts of the country (3).
LEISHMANIASIS
Leishmaniasis are a group of protozoal diseases caused by
parasites of the genus Leishmania, and transmitted to man by the
bite of female phlebotomine sandfly. They are responsible for
various syndromes in humans - kala-azar or visceral leishmaniasis
(VL), cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis
(MCL), anthroponotic cutaneous leishmaniasis (ACL), zoonotic
cutaneous
leishmaniasis
(ZCL),
post-kala-azar
dermal
leishmaniasis (PKDL), etc (1). The visceral type of disease, kalaazar, is still an important disease in India. The majority of the
leishmaniasis are zoonoses involving wild or domestic mammals
(rodents, canines). Some forms (e.g., Indian kala-azar) are
considered to be nonzoonotic infections (2).
Problem statement
WORLD
(a) Visceral leishmaniasis : Occurs widely throughout the
world, viz South America, South Africa, the Mediterranean
countries, India, Bangladesh and China. Nine out of ten cases
occur in Bangladesh, Brazil, India and Sudan (4). (b) Cutaneous
leishmaniasis : Occurs in the dry, semi-desert rural areas of
Central Asia, Middle East, North and West Africa, and the
highlands of Ethiopia and Kenya. Endemic foci are also found in
Central and South America. Nine out of ten cases occur in
Afghanistan, Brazil, Islamic Republic of Iran, Peru, Saudi Arabia
and Syrian Arab Republic, (c) Muco-cutaneous leishmaniasis :
The main concentration of this form of leishmaniasis is in Brazil,
Bolivia and Peru. It is rarely found outside the New World (3).
Currently, the leishmaniasis is endemic in 88 countries. The
large number of endemic countries illustrates the global
importance of the problem. The overall prevalence is 13 million
cases and the estimated population at risk is about 350 million. A
common estimate of the incidence per year is 1.8 million newly
reported clinical cases (4). Worldwide there is an increasing
number of cases and a more widespread geographical distribution,
the disease being reported from previously non-endemic areas.
Economic and demographic circumstances that contribute to
increased prevalence include : new agro- industrial projects, largescale migration of populations, unplanned urbanization, and manmade environmental changes (5).
Co-infection of VL and AIDS is emerging due to spread of the
AIDS pandemic particularly in southern Europe, where 25 to 70
per cent of adult VL cases are related to HIV infection, and 1.5 to 9
per cent of AIDS patients suffer from newly acquired or
reactivated VL (4).
INDIA
(a) Kala-azar : Kala-azar has its home in the plains of the
Ganges and Brahmaputra. It has been known to occur
epidemically, and endemically in well-defined areas in the eastern
sector of the country, viz Assam, West Bengal, Bihar, eastern
districts of Uttar Pradesh, foothills of Sikkim, and to a lesser extent
in Tamil Nadu and Orissa(3j.
As a result of the massive insecticide spraying campaign for
malaria eradication between 1958 and 1964, kala-azar and
cutaneous leishmaniasis declined to a point of extremely low
endemicity. During this period, some patients with PKDL
apparently acted as a reservoir of infection, since periodically, new
cases of kala-azar were seen, especially in children (1).
After its resurgence in Bihar in the early seventies, the disease
spread from the four northern districts to adjoining areas. Currently
about 33 districts of Bihar and 10 districts of West Bengal and 2
districts of Uttar Pradesh are affected by
LEISHMANIASIS 245
Kala-azar. The increasing trend of the disease was evident from
the fact that the total number of cases which were 17,806 with 72
deaths in 1986 rose to total of 77,102 cases with 1419 deaths in
1992. The present situation is as shown in Table 1.
TABLE 1
Kala-azar incidence and mortality in India
Year
Cases
1986
17806
Deaths
72
1992
1993
1994
1999
2000
2001
2002
2003
2004 (end of Feb.)
77102
45459
25652
12886
14753
12239
12140
17321
1702
1419
720
384
297
150
213
168
210
7
Source : (6,7)
(b) Cutaneous leishmaniasis (CL) : Cutaneous leishmaniasis
used to occur in the dry, north-western states of India, bordering
Pakistan, extending from Amritsar to Kutch and Gujarat plains. In
recent years, one focus of zoonotic cutaneous leishmaniasis (ZCL)
has been discovered in the Rajasthan area; in the peak year of
1971, 828 cases of ZCL were reported. Cases of anthroponotic
cutaneous leishmaniasis (ACL) have been reported from Bikaner
city (8,9) where unexpectedly, several dogs were also found to be
infected with L. tropica (1).
While both cutaneous (ZCL, ACL) and visceral (VL) diseases
occur in India, kala-azar is by far the most important leishmaniasis
in India.
Agent factors
(a) AGENTS : The leishmania are intracellular parasites. They
infect and divide within macrophages. At least nineteen different
leishmania parasites have been associated with human infection.
Further, the majority of these offer no cross immunity of one
against the other (10). Leishmania donovani is the causative agent
of kala-azar (VL); L. tropica is the causative agent of cutaneous
leishmaniasis (oriental sore); and, L. brazi/iensis is the causative
agent of muco-cutaneous leishmaniasis. But this distinction is not
absolute; visceral forms may produce cutaneous lesions, and
cutaneous forms may visceralize (11). The life cycle is completed
in two different hosts- a vertebrate and an insect; in the former, it
occurs in an amastigote form (called "leishmaina bodies") and in
the latter as a flagellated promastigote. (b) RESERVOIRS OF
INFECTION : There is a variety of animal reservoirs, e.g., dogs,
jackals, foxes, rodents and other mammals. Indian kala azar is
considered to be a non-zoonotic infection with man as the sole
reservoir. This assumption is based largely on the absence of
evidence (12).
Host factors
(a) AGE : Kala-azar can occur in all age groups including
infants below the age of one year. In India, the peak age is 5 to 9
years (1). (b) SEX : Males are affected twice as often as females,
(c) POPULATION MOVEMENT : Movement of population
(migrants, labourers, tourists) between endemic and non-endemic
areas can result in the spread of infection. The recent resurgence of
kala azar in West Bengal which is an extension of the epidemic
outbreak of the disease in Bihar in 1977 was due to movement of
infected persons with either kala-azar or PKDL. (d) SOCIOECONOMIC STATUS : Kala-
CONTROL MEASURES
In the absence of an effective vaccine, the control measures
comprise the following :
1. Control of reservoir
Since man is the only reservoir of kala azar in India, active and
passive case detection and treatment of those found to be infected
(including PKDL) may be sufficient to abolish the human reservoir
and control the disease. House-to-house visits and mass surveys
may be undertaken in endemic areas for early detection of cases.
TREATMENT : Pentavalent antimony compounds are the sheet
anchor of treatment. The recommended schedule is a daily
injection (IV or IM) of sodium stibogluconate, 10 mg/kg body
weight (to a maximum of 850 mg) for 20 days for adults, and 20
mg/kg of body weight for children. With this dosage and duration,
the relapse rate is stated to be virtually negligible (0.05 per cent),
as compared to standard 10-day treatment (15 per cent) (1). PKDL
responds well to this treatment.
Those who do not respond to the above treatment are given the
"second line" drug, pentamidine isethionate (3 mg/kg of body
weight, IV) for 10 days. Since this drug is toxic, the patient should
be hospitalized, while the drug is being administered.
The patient, in either case should be examined 3 and 12 months
after the treatment course to detect any relapse.
Animal reservoirs :
If animal reservoirs (e.g., dogs) are involved, appropriate
control measures against them should be undertaken. In many
endemic countries, extensive dog and rodent control programmes
have contributed greatly to the reduction in the number of human
cases.
2. Sandfly control
The application of residual insecticides has proved effective in
the control of sandflies. DDT is the first choice since the vector of
kala azar, P. argentipes is susceptible to DDT. (P. papatasi in
north Bihar has been shown to be resistant to DDT, but fortunately,
it is not the vector of kala azar in India). Insecticide spraying
should be undertaken in human dwellings, animal shelters and all
other resting places up to a height of 6 feet (2 metres) from floor
level. DDT (two rounds per year) at the rate of 1-2 g per sq. metre
is considered sufficient to control transmission. Spraying should be
preceded and followed by an assessment of susceptibility. Any
sign of resistance in vector should lead to an immediate change in
insecticide. BHC should be kept as a second line of defence.
Spraying should be repeated at regular intervals to keep down
the density of sandflies. For long-lasting results, insecticidal
spraying should be combined with sanitation measures, viz
elimination of breeding places (e.g., cracks in mud or stone walls,
rodent burrows, removal of firewood, bricks or rubbish around
houses), location of cattle sheds and poultry at a fair distance from
human dwellings, and improvement of housing and general
sanitation.
3. Personal prophylaxis
The risk of infection can be reduced through health education
and by the use of individual protective measures such as avoiding
sleeping on floor, using fine-mesh nets around the bed. Insect
repellants (in the form of lotions, creams, or sticks) for temporary
protection and keeping the environment clean. There are no drugs
for personal prophylaxis.
References
1.WHO (1984). Tech. Rep. Ser., No. 701
2.WHO (1979). Tech. Rep. Ser., No.637, P.41
Strategy for Health for All by the year 2000, Second evaluation, Vol. 1, Global
review, 1993.
6.Govt, of India (1998), Health Information of India 1995 and 1996, Ministry of
Health and Family Welfare, New Delhi.
7.Govt, of India (2004), Annual Report 2003-2004, Ministry of Health and Family
Welfare, New Delhi.
8.Govt, of India (1985). Swasth Hind, 29 (8) 186. Central Health Education
Bureau, New Delhi
Workshop on
TRACHOMA
Trachoma is a chronic infectious disease of the conjunctiva and
cornea, caused by Chlamydia trachomatis, but other pathogenic
microorganisms often contribute to the disease. Trachoma
inflammation may undergo spontaneous resolution or may
progress to conjunctival scarring which can cause inward deviation
of eyelashes (trichiasis) or of the lid margin (entropion). The
abrasion of the cornea by eyelashes frequently result in corneal
ulceration, followed by scarring and visual loss.
From the public health point of view, trachoma is classified as
blinding and non-blinding (1). A community with blinding
trachoma can be recognized by the presence of persons with
lesions such as entropion, trichiasis and corneal ulcers. It is the
blinding trachoma that requires urgent control measures. Nonblinding trachoma often becomes blinding trachoma when other
ocular pathogens interact synergistically and enhance the risk of
damage to eye sight (2).
Diagnosis
In epidemiological studies, more stress is now put on the upper
tarsal conjunctiva as a convenient index of trachomatous
inflammation in the eye as a whole (2). For the purpose of
diagnosis in the field, cases must have at least 2 of the following
diagnostic criteria (3).
a. follicles on the upper tarsal conjunctiva
b. limbal follicles or their sequelae, Herbert's pits
c. typical conjunctival scarring (trichiasis, entropion)
d. vascular pannus, most marked at the superior limbus
Problem statement
Trachoma is a major preventable cause of blindness in
developing countries. According to recent estimates, about 6
million people currently suffer from irreversible blindness due to
trachoma in Africa and Asia. Another 152 million suffer from the
disease and need treatment (4) and about 540 million are at risk of
infection (5).
The incidence and prevalence of trachoma has shown a
significant decrease in many endemic countries of SEAR during
the past few decades. This decrease has been mainly due to
improved sanitation, water and housing, and implementation of
control measures. However, trachoma, particularly in its active
form, still remains a public health concern in some parts of
Myanmar, in the western region of Nepal and in a few rural areas
in India (6). It is estimated to be responsible for 0.2 percent of
visual impairment and blindness in India (7).
_________________________________________TRACHOMA
247
Agent factors
(a) AGENT : The classical endemic trachoma of developing
countries is caused by C. trachomatis of immune types A, B, or C.
The sexually-transmitted C. trachomatis (serotypes D,E,F,G,H,I,J
or K) may also infect, causing an eye disease difficult to
differentiate from endemic trachoma. Milder cases of this are
usually called "inclusion conjunctivitis". These strains rarely
produce permanent visual loss - but they cause respiratory
infections (pneumonia) in infants and genital tract infections in
adults (2). Other pathogenic organisms (e.g., Morax-Axenfeld
diplobacillus, the Koch-Weeks bacillus, the gonococcus) often
contribute to the disease process. The Morax-Axenfeld
diplobacillus is the most innocuos; the Koch-Weeks bacillus is the
most widespread, and the gonococcus the most dangerous (8). C.
trachomatis, originally believed to be a virus, is an obligatory
intracellular bacteria, now classified as Chlamydia, (b)
RESERVOIR : Children with active disease, chronically infected
older children and adults, (c) SOURCE OF INFECTION : Ocular
discharges
of
infected
persons
and
fomites
(d)
COMMUNICABILITY: Trachoma is a disease of low infectivity.
It is infective as long as active lesions are present in the
conjunctiva, but not after complete cicatrization.
Host factors
(a) AGE : In endemic areas, children may show signs of the
disease at the age of only a few months. But typically, children
from the age of two to five years are the most infected, and this
contributes not only to the high rate of blindness but also to the
rate of occurrence among children, (b) SEX : Prevalence equal in
younger age groups. In older age groups, females have been found
to be affected more than males. The explanation for this may be
that women remain more in contact with children who infect
them. Further, females are more exposed to irritating factors such
as smoke than males (c) PREDISPOSING FACTORS : Direct
sunlight, dust, smoke and irritants such as kajal or surma may
predispose to infection.
Environmental factors
(a) SEASON : Seasonal epidemics are associated with vastly
increased number of eye-seeking flies. The incidence of active
trachoma is found generally high in India during April-May and
again during July-September. The higher temperature and rainfall
favours the increase in fly population, (b) QUALITY OF LIFE :
Trachoma is associated with poor quality of life. The disease
thrives in conditions of poverty, ignorance, poor personal hygiene,
squalor, illiteracy and poor housing. As living conditions improve
the disease tends to regress, (c) CUSTOMS : The custom of
applying kajal or surma to the eyes is a positive risk factor.
Mode of transmission
In communities where trachoma is endemic, eye-to-eye
transmission can be considered as a rule (8). This may occur by
direct or indirect contact with ocular discharges of infected
persons or fomites, e.g., infected fingers, towels, kajal or surma.
Eye-seeking flies (e.g., Musca spp., Hippelatus spp) play some
role in spreading the infection by mechanical transmission. In
countries where only sporadic cases of trachoma occur, genital
localisation of C. trachomatis (urethral, cervical) may lead to
venereal transmission (8).
It has been shown that trachoma is a familial disease. When
one case is detected, others will almost certainly be found in
the family group. There is a continuous feedback of infection,
partly as a result of grandfathers or sisters and brothers tending
small children (9).
Incubation period
5 to 12 days.
5. Health education
In the long run, most of the antibiotic treatment must be carried
out by the affected population itself. To do this, the population
needs to be educated. The mothers of young children should be the
target for health education. Measures of personal and community
hygiene should also be incorporated in programmes of health
education. Thus real primary prevention could only come through
health education for the total elimination of transmission. This
would require a permanent change in the behaviour patterns and in
environmental factors. The final solution would be the
improvement of living conditions and quality of life of the people
(9).
6. Evaluation
Lastly evaluation. Trachoma control programme must be
evaluated at frequent intervals. The effect of intervention can be
judged by the changes in the age-specific rates of active trachoma
and in the prevention of trichiasis and entropion.
The 28th World Health Assembly in 1975, in a resolution
requested the Director-General of WHO "to encourage Member
countries to develop national programmes for the prevention of
blindness especially aimed at the control of trachoma,
xerophthalmia, onchocerciasis and other causes". With this came
the reorientation of strategies away from single cause prevention,
to the adoption of the concept of integrated delivery of eye care as
part of primary health care. In this context, many countries have
now integrated their trachoma control programmes into National
Programmes for the Prevention of Blindness, to give simultaneous
introduction of other specific measures for dealing with all causes
of avoidable blindness.
The trachoma control programme in India which was launched
in 1963 has now been integrated with the National Programme for
Control of Blindness (see Chapter 7). The "Health for All by 2000"
had set a target of reducing the prevalence of blindness to 0.3 per
cent (12).
References
1.Dawson, C.R. et al (1975). Bull WHO, 52 : 279
2.WHO (1984). Strategies for the prevention of blindness in National Programmes.
TETANUS
An acute disease induced by the exotoxin of Clostridium tetani
and clinically characterised by muscular rigidity which persists
throughout illness punctuated by painful paroxysmal spasms of the
voluntary muscles, especially the masseters (trismus or "lockjaw"), the facial muscles (risus sardonicus), the muscles of the
back and neck (opisthotonus), and those of the lower limbs and
abdomen (1). The mortality tends to be very high, varying from 40
to 80 per cent.
___________________________________________TETANUS 249
Problem statement
WORLD
Tetanus is now comparatively rare disease in the developed
countries. Until recently, most reporting forms did not list neonatal
tetanus separately from tetanus contracted at older ages. Neonatal
tetanus (NT) is a killer disease, second only to measles among the
six target diseases of the EPI. Even with treatment, the casefatality rate can be as high as 80-90 per cent. It tends to occur in
areas with poor access to health care, hence it often remains hidden
within the community. Neonatal tetanus is one of the most underreported notifiable disease.
Community surveys have consistently shown that only a small
proportion of NT cases are routinely reported to notifiable disease
reporting system in most developing countries; and under-reporting
is often highest in areas at highest risk for NT. Because of this low
notification efficiency, WHO makes estimates of annual neonatal
tetanus morbidity and mortality. Estimation methods previously
used the number of live births, the estimated number of infants
protected at birth by routine vaccination strategies and
prevaccination mortality rates based on community surveys.
Estimation methods were recently updated to account also for the
number of infants protected through supplementary vaccination
and as a result of skilled deliveries.
The estimated global number of NT cases decreased from
510,000 in 1990 to 355,000 in 1997, indicating a notification
efficiency of only 3 percent in 1997. The estimated global number
of NT deaths decreased from 408,000 in 1990 to 248,000 in 1997,
representing a 39 percent decline (2). Table 1 shows reduction of
NT mortality in some countries.
TABLE 1
Estimated NT mortality and reduction of mortality rates in some
countries (1990-1997)
1990
Country
Estimated
number of
deaths
1997
Mortality Estimated
rate per number of
1000 live deaths
births
3.0
55,200
Mortality -"ercentage
rate per
change
1000 live n mortality
i
rate
births
2.3
-23
India
77,700
China
75,700
3.2
12,800
0.6
-81
Bangladesh
Pakistan
Indonesia
Nepal
38,600
36,300
22,800
6,700
9.9
7.0
4.7
8.8
16,300
26,400
6,400
5,800
5.0
5.0
1.4
7.0
-49
-29
-70
-20
4,400
3.2
1.500
1.1
Myanmar
66
Source : (2)
The decline was mainly the result of a significant increase in
immunization coverage of pregnant women with a protective dose
of tetanus toxoid. The greatest decrease in NT mortality in SEAR
was observed in Indonesia (-70%), Myanmar (-66%), Bangladesh
(-49%) and India (-23%), which together accounted for 95 percent
of all estimated NT deaths in the region in 1990 (2). Five countries
in the region, namely Bhutan, DPR Korea, Maldives, Sri Lanka
and Thailand have declared NT elimination.
In the year 1989, in recognition of the magnitude of neonatal
tetanus incidence, as well as the preventable nature, the World
Health Assembly resolved to eliminate neonatal tetanus by 1995,
by aiming to reduce the incidence to less than 1 case per 1000 live
births for each health block. This goal was reaffirmed in 1999 and
a new target date was set for elimination of NT by the year 2005
(3).
INDIA
Tetanus is an important endemic infection in India. Behaviours
such as hand-washing, delivery practices, traditional birth customs
and interest in immunization, are all important factors affecting the
disease incidence. Medically under-served areas and livestock
raising regions are two environments particularly associated with
behaviour conducive to neonatal tetanus.
Prior to the national immunization programme, an estimated
3.5 lakh children died annually due to neonatal tetanus. According
to estimates for the year 1993-94, at least 2.8 lakh neonatal tetanus
cases were averted. An estimated 70,000 cases continue to occur,
largely in Uttar Pradesh, Madhya Pradesh, Rajasthan, Orissa,
Bihar and Assam where the baseline rates for neonatal tetanus are
high, TT immunization coverage levels are below the national
average and over 70 per cent of the deliveries are conducted by
untrained personnel (4).
The preventive measures in the areas of high risk are being
accelerated to reduce the number of cases. In areas considered at
low risk, the surveillance system is being sensitized to ensure that
no case is missed. A district classification has, therefore, been
suggested, so that area-specific action oriented measures, could be
taken and the progress monitored.
Districts are being classified into three categories depending on
NT incidence rates, immunization coverage levels in pregnant
women with two doses or a booster dose of tetanus toxoid vaccine,
and proportion of clean deliveries by trained personnel (5).
Neonatal tetanus elimination (Classification of districts)
NT high risk :
Rate > 1/1000 live births
or
TT2 coverage < 70%
or
Attended deliveries < 50%
NT control:
Rate < 1/1000 live births
and
TT2 coverage > 70%
and
Attended deliveries > 50%
NT elimination :
Rate < 0.1/1000 live births
and
TT2 coverage > 90%
and
attended deliveries > 75%
Hospital records show a major male preponderance of cases.
Since there is no biological reason why male infants should be
more susceptible, it is in all likelihood, due to the male children
being brought to the health facilities more frequently. For purpose
of classification of districts with NT risk, the male bias is taken
into account. The total number of cases of NT for a district is
considered to be two times the number of reported male cases (5).
NT has a marked seasonal incidence in India. More than 50 per
cent of the total annual cases of NT occur in the month of July,
August and September.
Reporting of NT cases by hospitals and other treatment facilities
has been made mandatory. A monthly "nil" report is required to be
submitted by all hospitals, if no NT case is seen. The cases are
reported to the chief medical officer of the concerned district. Line
lists of the cases are submitted to enable identification of high risk
pockets of areas for specific interventions.
Agent factors
(a) AGENT : CI. tetani is a gram-positive, anaerobic, sporebearing organism. The spores are terminal and give the organism a
drum-stick appearance. The spores are highly resistant to a number
of injurious agents, including boiling, phenol, cresol and
autoclaving for 15 minutes at 120 deg. Centigrade (6). They
germinate under anaerobic conditions and produce a potent
exotoxin ("tetanospasmin"). The spores are best destroyed by
steam under pressure at 120 deg. C for 20 minutes or by gamma
irradiation, (b) RESERVOIR OF INFECTION : The natural
habitat of the organism is soil and dust. The bacilli are found in
b. Monovalent vaccines
Purified tetanus toxoid (adsorbed) has largely supplanted plain
toxoid because it stimulates a higher and longer-lasting immunity
response than plain toxoid (15). However, the latter
_____________________________________________________________TETANUS 251
I----------------------------------- '-------------------------------1
Wounds less than 6 hours old, clean, non-penetrating
and with negligible tissue damage.
Other wounds
I--------- '-------------1
Immunity category
A
B
C
D
I---------- '----------- 1
Treatment
Immunity category
A
B
C
D
Treatment
Nothing more required
Toxoid 1 dose
Toxoid 1 dose + Human Tet. Ig.
Toxoid complete Course +
Human Tet. Ig A =
Has had a complete course of toxoid or a booster dose within the past 5 years.
B = Has had a complete course of toxoid or a booster dose more than 5 years ago and less than 10 years ago. C = Has
had a complete course of toxoid or a booster dose more than 10 years ago. D = Has not had a complete course of toxoid
or immunity status is unknown^ TVdft ^ \j *-Q %,
r F I G . I ")^P^ *-^
Recommendations for prevention of tetanus in the wounded
LEPROSY
Leprosy (Hansen's disease) is a chronic infectious disease caused by
M. leprae. It affects mainly the peripheral nerves. It also affects the skin,
muscles, the eye, bones, testes and internal organs. The disease manifests
itself in two polar forms, namely the lepromatous leprosy and tuberculoid
leprosy, lying at the two ends of a long spectrum of the disease. Between
these two polar types occur the borderline and indeterminate forms
depending upon the host response to infection.
Leprosy is clinically characterised by one or more of the following
cardinal features :
a. hypopigmented patches
b. partial or total loss of cutaneous sensation in the
affected areas (the earliest sensation to be affected is
usually light touch)
c. presence of thickened nerves, and
d. presence of acid-fast bacilli in the skin or nasal smears
The signs of advanced disease are striking : presence of nodules or
lumps especially in the skin of the face and ears; plantar ulcers; loss of
fingers or toes, nasal depression, foot-drop, claw toes and other
deformities.
The case definition includes patients who started MDT but who have
not received treatment for 12 consecutive months (defaulters) and
subsequently present with signs of active disease, as well as patients who
relapse after completing a full course of treatment. It does not include
cured persons with late reactions or residual disability (1).
History
Leprosy is probably the oldest disease known to mankind. The word
leper comes from a Greek word meaning scaly. For a long time, the
disease was confused with psoriasis, elephantiasis and pellagra. In India,
leprosy is known since ancient times as kustha roga and attributed to
punishment or curse from God. During the middle ages, leprosy was
widespread in almost all countries of the world. Thereafter, it declined
slowly in many European countries, partly due to strict isolation and partly
due to improvements in the standard
___________________________________________LEPROSY 253
less than one case per 1000 patients per year. No drug resistance to
MDT was reported (4). Among 122 countries considered endemic
in 1985, 112 countries have reached elimination at the country
level. At the end of 2000 leprosy was a public health problem only
in 10 counrties (prevalence rate more than 1 per 10,000), mainly in
Africa, Asia and Latin America. Today, the highest burden is
concentrated in 6 countries, in diminishing order of disease burden
in India, Brazil, Myanmar, Madgascar, Nepal and Mozambique.
The global trend of detection increased between 1995 and 1998
partly because of leprosy elimination campaigns (5).
The South-East Asia Region accounts for 80 per cent of the
global leprosy case load. India alone represents 64 per cent of
prevalence and 78 per cent of new case detection world wide (5).
While Bangladesh, Indonesia, Maldives, Sri Lanka and Thailand
have already achieved the elimination goal, Myanmar (prevalence
rate 2.37 per 10,000) and Nepal (prevalence rate 3.6 per 10,000)
are likely to reach the goal by the year 2003. India with prevalence
rate of 3.73 per 10,000 is expected to achieve elimination by the
end of year 2005 (6).
Special action projects for the elimination of leprosv,
(SAPELs) were initiated in major endemic countries with the aim
of providing MDT services to patients living in difficult tc access
areas or situations, and to those belonging to neglectec population
groups. In SEAR such projects were implemented ir India,
Bangladesh, Indonesia, Myanmar and Nepal in 1996 Another
initiative is to conduct leprosy elimination campaign: (LECs).
These campaigns seek to detect leprosy cases particularly "cases
of consequence" i.e., patients either witl five or more skin lesions
who are smear positive which remaii undetected due to lack of
awareness about the disease o because leprosy services are
inadequate. In SEAR countrie LEG projects are being
implemented in Bangladesh, Indie Indonesia, Myanmar and Nepal
(7).
INDIA
Leprosy is widely prevalent in India. Although the disease :
present throughout the country, the distribution is uneven. As c
March 2004, the prevalence rate is 2.3 cases per 10,00
population, reduced from 57 per 10,000 in 1981. Th elimination
level i.e., prevalence rate less than 1 case for 10,00 population has
been achieved in 16 states, and seven states ai very near to this
goal (8). As shown in Table 1,12 endemic stat< contribute 93 per
cent of the country's leprosy case load.
Table 1
Leprosy situation in highly endemic states in India (April 2002-March 2003)
State
Andhra Pradesh
Bihar
Chhattisgarh
Jharkhand
Karnataka
Madhya Pradesh
'Maharashtra
'lamu .Xad'u
Uttar Pradesh
Uttaranchal
West Bengal
Total
Total no.
of cases
37258
93561
18468
28982
13079
16570
48548
. S2 ^"'
90586 ' 2246
32018
473558
,'
32.01
40.77
37.62
35.62
44.06
28.30
SJ.^J?
28.85
44.10
35.08
41.01
35.26
40.0834.78
35.31
41.44
33.38
44.30
&/%?
38.50'
34.02
29.88
25.87
33.98
16.11
11.28
16.42
21.28
770
19.78
JS.P
17.84
8.33
5.37
12.89
14.91
1.48
2.65
1.83
1.01
3.77
1.53
J.Z?
1.78
1.51
2.00
2.44
1.80
-------
Detection rate
per 100,000
population
Prevalence rate
per 10,000
population
47.85
108.60
85.93
103.34
24.02
26.28
48.19
Sl(Z7 -'
39.04
52.13
25.58
38.63 44
37
2.53
8.60^
7.20V
6.43^
1.90
1.91
2.95
7 2? ty
2.34
4.12
1.88
2.71
areas where leprosy is rare, the first contact may not take place early in life and consequently, the disease may appear late. However, the presence
of leprosy in child population is of considerable epidemiological importance. A high prevalence of infection among children means that the
disease is active and spreading.
(a)SEX : Both the incidence and prevalence of leprosy appear to be higher in males than in females in most regions of the world. Sex
difference is found least in children below 15 years, and more marked among adults; more marked among lepromatous cases than among nonIepromatous cases. The excess of cases in males has sometimes been attributed to their greater mobility and increased opportunities for contact
in many populations.
(b)MIGRATION : In India leprosy was considered to be mostly a rural problem. However, because of the movement of population from rural
to urban areas, leprosy is creating a serious problem in the urban areas also (17).
(c)IMMUNITY : It is a well-established fact that only a few persons exposed to infection develop the disease. A large proportion of early
lesions that occur in leprosy heal spontaneously. Such abortive and self-healing lesions suggest immunity acquired through such lesions.
Subclinical infections are far more common than was thought earlier; they are also believed to contribute to active immunity. A certain degree
of immunity is also probable through infections with other related mycobacteria (18).
It is now recognized that cell-mediated immunity (CMI) is responsible for resistance to infection with M. leprae. In lepromatous leprosy, there
is a complete breakdown of CMI; in these cases the lepromin test is negative. CMI does not however, exclude the participation of humoral
response. Antibodies have been demonstrated throughout the spectrum of leprosy; they are more pronounced at the lepromatous end. Similarly an
increase of immunoglobulins of IgG and IgM classes is noted towards the lepromatous end (19). Leprosy workers have recently found that the
anergy of lepromatous leprosy is due to suppression of T cell production of interleukin-2 (T-cell growth factor). This is normally secreted by
activated T cells to make other T cells proliferate. If exogenous interleukin-2 is added, the process may be reversed. However, further studies are
needed to find out whether administration of IL-2 would benefit the lepromatous patient (19).
(e) GENETIC
FACTORS
:
There
is
now
evidence
that
HLAlinked
genes
influence
the
type
of
immune
response
that
develops (10).
Environmental factors
The risk of transmission is predominantly controlled by environmental factors (14) : (a) the presence of infectious cases in that environment.
There is evidence that humidity favours the survival of M. leprae in the environment. M. leprae can remain viable in dried nasal secretions for at
least 9 days and in moist soil at room temperature for 46 days (10), (b) overcrowding and lack of ventilation'within households, and (c) social
factors governing closte.contact.
Social pathology
Leprosy is often called a "social disease". There are numerous social factors which favour the spread of leprosy in the community -such as
poverty and poverty related circumstances (e.g., overcrowding, poor housing, lack of education, lack of personal hygiene) and above all, fear, guilt
and unfounded prejudices regarding the disease. The social stigma of leprosy is due to the deformities it can cause. Over the centuries, a "legend"
has grown round leprosy that it is
___________________________________________LEPROSY 255
highly contagious and that it is incurable. Even today, in spite of scientific information available about leprosy, this legend is deeply rooted in the
minds of most people at all levels of society with the result that social ostracism is apparent everywhere. This has led patients to hide their early
lesions and thereby delay treatment just at the period when they could be most speedily cured. The deep-rooted psychosocial factors cannot be
banished overnight, much less by legislation. In most leprosy control programmes, these important psychosocial factors are overlooked, and
emphasis is laid only on early detection and treatment. Failure to appreciate the importance of the social and psychological factors has resulted in
the failure of otherwise well conceived programmes.
Mode of transmission
The mode of transmission of leprosy has not been established with certainty. The following theories are frequently debated :
(a) Droplet
infection
:
There
is
more
and
more
evidence
leprosy
may
be
transmitted
via
aerosols
containing
M.
(droplet
infection).
With
the
realization
of
the
importance
the
nose
as
a
portal
of
exit,
there
has
been
increased
on the respiratory tract as the portal of entry.
that
leprae
of
emphasis
(b) Contact
transmission
:
Numerous
studies
indicate
that
leprosy
is
transmitted
from
person-to-person
by
close
contact
between
an
infectious
patient
and
a
healthy
but
susceptible
person.
This
contact
may
be
direct
(e.g.,
skin-to-skin)
or
indirect
(e.g.,
contact
with
soil,
and
fomites
such
as
contaminated clothes and linen).
Now that it is known that leprosy bacilli can survive for long periods of time in the soil under favourable environmental conditions, the
hypothesis that leprosy can be transmitted by indirect contact has been strengthened (20). In epidemiological studies, the first lesions were found
in feet and legs of patients from hilly areas in India, where injury to the skin is common. In the Philippines 91 per cent of the first lesions were
seen in extremities open to injury (17). These observations lend support to indirect transmission. Although contact transmission has been a longfavoured hypothesis, leprologists opine that skin-to-skin contact is really not necessary to acquire infection, and that the disease is transmissible
with far less than intimate contact (11, 13).
(c) Other
routes
:
Bacilli
may
also
be
transmitted
via
breast
milk
from
lepromatous
mothers,
by
insect
vectors,
or
by
tattooing
needles.
These
transmission
channels
cannot
be
ruled
out
(20).
However,
there
is
no
evidence
that
any
of
these
transmission routes is important in nature (10).
Incubation period
Leprosy has a long incubation period, an average of 3 to 5 years or more for lepromatous cases. The tuberculoid leprosy is thought to have a
shorter incubation period (10). Failure to recognize early symptoms or signs may contribute to an assumed prolonged incubation period in some
patients. Some leprologists prefer the term "latent period" to incubation period because of the long duration of the incubation period.
Knowledge of incubation period of relapses is also essential, as this will define the duration of surveillance after treatment has been stopped.
Classification
Leprosy is a disease bedevilled by classifications, e.g., the Madrid classification (21). Ridley-Jopling classification (22), the Indian
classification (23), etc. These classifications are based on clinical, bacteriological, immunological and histological status of patients.
'____________________________________LEPROSY 257
of skin smears and of microscopy is probably the weakest link in
most leprosy elimination programmes. In view of this situation,
and since it is possible to classify leprosy without skin smear
results, it should not be a pre-requisite for implementing the MDT
(1).
A brief account of method of skin smear and nasal smear
examination is as follows :
(i) Skin smears : Material from the skin is obtained from an
active lesion, and also from both the ear lobes by the "slit and
scrape" method. Conventionally, six sites are examined. The skin
is cleaned with ether or spirit and allowed to dry. A fold of the skin
is nipped between the thumb and forefinger (of left hand in an
operator). Enough pressure should be applied to stop or minimise
bleeding. Holding the point of knife vertical to the apex of the skin
fold, it is pushed into the skin to a depth of about 2 mm or so, to
reach the dermis. A tiny incision is made 5 mm or so in length. If
blood exudes, it should be wiped off with a small dry cotton-wool
swab. The knife blade is rotated transversely to the line of the cut
and the knife point is used to scrape first on one side and then on
the other side of the incision 2 or 3 times to obtain a tissue pulp
from below the epidermis. This material is transferred on to a glass
slide and spread over an area of 5 to 7 mm diameter. The wound is
dressed and closed with a piece of sticking tape applied over the
site.
(ii) Nasal smears or blows : Nasal smears can be best prepared
from early morning mucus material. The patient blows his nose
into a clean dry sheet of cellophane or plastic. The smear should
be made straightaway and fixed. This should be done in the early
morning from the first blowing of the nose. Nose-blowing smears
are used for assessing the patient's infectivity. In patients with
untreated lepromatous leprosy, nose-blow smears may show a
higher percentage of solid -staining bacilli than skin smears.
(in) Nasal scrapings : An alternative is to use a nasal mucosal
scrapper. After going in 4.5 cm, the blade is rotated towards the
septum and scraped a few times and withdrawn. A small ball of
cotton is introduced into the nostril to absorb any blood that may
ooze out. Nasal scrapings are not recommended as a routine,
because they are painful, and nonpathogenic atypical mycobacteria
may be present in the nose of healthy persons. Leprosy bacilli are
not found in nasal mucosa if they are absent in skin lesions.
During treatment, M leprae may disappear from the nasal mucosa
before they disappear from the skin lesions (29).
The skin or nasal smear is immediately fixed by lightly *"
passing the underslide of the slide over the spirit lamp flame and
transported to the laboratory for staining with Ziehl-Neelsen
method.
The glass slides used should be absolutely clefan. They should
not be reused for making smears a second time as organisms from
a previous examination may give a false positive result (23).
Before a smear is declared negative, at least 200 fields should be
examined (11).
Bacterial index (13)
Bacterial index (BI) is the only objective way of monitoring
the benefit of treatment. The WHO grading of smears for BI is as
follows (13) :
Negative
No bacilli found in 100 fields
One plus ( + )
One or less than one bacillus in each
microscopic field
Two plus (+ + )
Bacilli found in all fields
Three plus (+ + +) Many bacilli found in all fields
Add G to the entry if globi are present
Bacterial index is calculated by- totalling the number of
" + " given to each smear and dividing this number by the smears
collected. A minimum of 7 sites should be examined; smears from
4 skin lesions, one nasal swab, and smears from both ear lobes,
e.g.,
Right ear
+++
Left ear
+++
Nasal smear
+ + -f
First skin lesion
+++
Second skin lesion
++
Third skin lesion
+++
Fourth skin lesion
++
19
Bacterial index (BI) = ------------------------------7 sites of examination
In paucibacillary leprosy the bacterial index is less than 2; in
multibacillary leprosy, it is greater than 2.
Two other types of grading are also in use for reporting
bacterial index, e.g., Dharmendra's scale (13) and Ridley's scale
(30).
Morphological index
During the course of microscopic examination of smears, it is
possible to distinguish and count the number of solid staining
organisms (organisms that stain completely) and irregularly
staining bacilli. The percentage of solid staining bacilli in a stained
smear is referred to as morphological index (MI). The total of the
Mis for all sites divided by the number of sites gives the average
MI for the body. The criteria for calling the bacilli solid-rods are
(23) :
a. uniform staining of the entire organism
b. parallel sides
'
c. rounded ends, and
d. length 5 times that of the width
It has been widely believed that only solid-staining organisms
are viable. Recently, however, doubts have been raised about this
notion (10).
3, FOOT-PAD CULTURE :
Vjhe only certain way to identify M. leprae is to inoculate the
material into the foot-pads of mice and demonstrate its
multiplication. Mouse foot-pad inoculation is 10 times more
sensitive at detecting M. leprae than are slit-skin smearsTfiBlJ.
The drawback of this technique is that it is time consuming and
requires 6 to 9 months before the results are obtained. Newer in
vitro methods such as macrophage culture have been evolved,
which take only 3 to 4 weeks to obtain results.
Mouse foot-pad technique has been successfully used for
(i)detecting drug resistance (ii) evaluating the potency of antileprosy drugs, and (iii) detecting the viability of the bacilli during
treatment.
4. HISTAMINE TEST:
The histamine test is a very reliable method for detecting at an
early stage peripheral nerve damage due to leprosy. The test is
carried out by injecting intradermally 0.1 ml of a 1:1000 solution
of histamine phosphate or chlorohydrate into hypopigmented
patches or in areas of anaesthesia. In normal persons, it gives rise
to a wheel surrounded by an erythematous flare within a few
minutes (Lewis triple response). In cases of leprosy where the
nerve supply is destroyed, flare response is lost. Histamine test is
recommended when difficulty is experienced in the diagnosis, as
for example, indeterminate leprosy (27).
5. BIOPSY:
When the examinations detailed above do not yield diagnosis,
histopathological examination may be necessary. It allows a more
accurate classification of the disease. It also gives information
about the bacterial content of the skin.
6. IMMUNOLOGICAL TESTS :
There are now available different kinds of immunological tests.
These may be classified as (32) :
a. tests for detecting cell mediated immunity (CMI)
b. tests for humoral antibodies (serological tests)
a. TESTS FOR DETECTING CMI:
(i) LEPROMIN TEST
The test is performed by injecting intradermally 0.1 ml of
lepromin into the inner aspect of the forearm of the individual. As
a routine, the reaction is read at 48 hours and 21 days (11). Two
types of positive reactions have been described :
(a) EARLY REACTION : The early reaction is also known as
Fernandez reaction. An inflammatory response develops within
24 to 48 hours and this tends to disappear after 3 to 4 days. It
is evidenced by redness and induration at the site of
inoculation. If the diameter of the red area is more than 10 mm
at the end of 48 hours, the test is considered positive.
The early positive reaction indicates whether or not a person
has been previously sensitized by exposure to and infection by the
leprosy bacilli. In this sense, the early reaction is much superior to
the late reaction. The early reaction has been described as delayed
hypersensitivity reaction to "soluble" constituents of the leprosy
bacilli. The reaction corresponds to the Mantoux reaction in
tuberculosis, caused by the soluble antigens (PPD) of the tubercle
bacilli.
(b) LATE REACTION : This is the classicalMitsuda reaction.
The reaction develops late, becomes apparent-in 7-10 days
following the injection and reaching its maximum in 3 or 4
weeks. The test is read at 21 days. At the end of 21 days, if
there is a nodule more than 5 mm in diameter at the site of
inoculation, the reaction is said to be positive. The nodule may
even ulcerate and heal with scarring if the antigen is crude.
It may be noted that the diameter of the red area in the early
reaction, and the diameter of the nodule in the late reaction are
measured. The early reaction is induced by the soluble constituents
of the leprosy bacilli; and the late reaction by the bacillary
component of the antigen. It indicates cell-mediated immunity.
^\In the first 6 months of life, most children are lepromin
\ negative; some may become positive by the end of first year)
( Data obtained from different parts of the world indicate that m
endemic areas, lepromin reaction is already positive in 20 per
cent of children under 5 years of age, and this proportion
increases to around 60 per cent or more in the 10-14 years age
group, and to 80 per cent or more in persons over 19 years of
age (16) (BCG vaccination is capable of converting the lepra
reaction trom negative to positive in a large proportion of
^individuals.}
Value of the lepromin test:
|L(Lepromin test is not a diagnostic test. The two drawbacks that
stand in the way of this test being used for diagnosis are : (i)
positive results in non-cases, and (ii) negative results in
lepromatous and near-lepromatous casesY17).
\ U"he test has been generally accepted as a useful tool in /
evaluating the immune status (CMI) of leprosy patients. It is of ;
considerable value in confirming the results of classification of
other words, the test is widely used as an aid to classify the type of
disease^
The test is'also of great value in estimating the prognosis in
cases of leprosy of all types. The test is usually strongly positive in
the typical tuberculoid cases and the positivity getting weaker as
one passes through the spectrum to the lepromatous end, the
typical lepromatous cases being lepromin negative indicating a
failure of CMI. It is known that lepromin negative individuals are
at a higher risk of developing progressive multibacillary leprosy,
but those who are lepromin positive either escape the clinical
disease (the majority) or develop paucibacillary disease (the
minority).
(ii) LTT and LMIT
In recent years, newer in vitro tests such as lymphocyte
transformation test (LTT) and leucocyte migration inhibition test
(LMIT) have been developed. They give a measure of the cell
mediated immunity. These tests have been used to detect
subclinical infection. A disadvantage of these highly sophisticated
tests is that they cannot be applied on a mass scale under field
conditions (33).
b. TESTS FOR HUMORAL RESPONSES TO M. LEPRAE :
Probably the most important recent advance in the study of the
epidemiology of leprosy is the development of serological tests.
These tests are expected to have value in detecting subclinical
infections, preclinical manifestations and follow-up efficacy of
drug treatment. These tests include :
(i) FLA-ABS test
The Fluorescent Leprosy Antibody Absorption Test is now
widely used for identification of subclinical infection. Studies
revealed that FLA-ABS test is 92.3 per cent sensitive and 100 per
cent specific in detecting M. leprae specific antibodies in all types
of leprosy irrespective of the type and duration of the disease (34).
(ii) Monoclonal antibodies
Monoclonal antibodies against M. leprae antigens have been
produced. It has been shown that these antibodies recognise
specific and non-specific epitopes of M. leprae antigens. If
antibodies against specific antigens are found, they will become
reagents of choice for identifying M. leprae. An antibody
competition test (SACT) based on this approach has been found to
be quite sensitive for detection of M. leprae antibody (35).
(iii) Others
There are numerous other sensitive tests which include the
radio-immune assay and ELISA tests. The ELISA test is based on
a phenolic glycolipid (PGL) antigen.
For the present, the only practical approach is to use FLA-ABS
test till some other more sensitive and specific tests are available
for use on a large scale (36).
^C^TA)
LEPROSY CONTROL
Candidate Vaccines
Category II
(based on cultivable
mycobacteria)
1. Killed M. leprae
2. Killed M. leprae + BCG
3. Acetoacetylated M. leprae
1.
2.
3.
BCG
BCG + M. Vaccae
Killed ICRC bacillus
Source : (44)
All the reported "candidate" vaccines have shown a similar degree of
lepromin conversions in lepromatous patients (50-70 per cent) and
lepromin negative healthy individuals (90 per cent). Maximum work has
been done with BCG + heat-killed M. leprae. However, none of the
candidate vaccines have attained as yet "vaccinehood" (45).
VI. Chemoprophylaxis
The value of chemoprophylaxis especially among contacts of leprosy,
has been the subject of study in India since 1963 (46, 47, 48). These
studies, established that dapsone prophylaxis (at a dose of 1 -4 mg per kg
body weight per week) gave a protection among child contacts ranging
between 35 to
TABLE 2
Differences between reversal reaction and relapse
Reversal Reaction
Time interval
Relapse
Hands
: (29)
Other deformities
VIII. Rehabilitation
Feet
Eyes
X. Others
(a) Protection of people at risk : This includes protection of
healthy contacts, particularly children. Preventing contact with
infectious cases and fomites is an accepted method for controlling
the spread of any communicable disease, and leprosy is no
exception (b) Socio-economic conditions : It is difficult to envisage
effective leprosy control without significant improvement in the
socio-economic conditions of the affected communities.
2. SOCIAL SUPPORT
Chemotherapy alone is not likely to solve the whole problem of
leprosy. The economic and social problems of the patient and his
family should be identified and met. This may include social
assistance and social support. This may take various forms
depending upon the local situation, e.g., assistance to the patient to
travel to and from the clinic; help to the needy families in terms of
foodgrains, clothes, care of children and their education, and job
placement; abolishing the social evil of beggary; programmes such
as slum improvement, etc. Such care should be provided through
voluntary agencies and Departments of Social Welfare.
3. PROGRAMME MANAGEMENT
Leprosy control is a long-term activity. Therefore planning and
programme management are essential ingredients. It is generally
assumed that with existing tools, we can achieve rapid control of
leprosy, provided the "operational performance" is stepped up to
the maximum level required. This is the responsibility of
programme managers. These issues are discussed under evaluation
(see operational indicators and epidemiological indicators). Among
the resources that are needed are adequate infrastructure, trained
health personnel, adequate supply of drugs and vehicles, and
financial allocation. The National Leprosy Eradication Programme
incorporates all these elements (see chapter 7).
4. EVALUATION
An important aspect of leprosy control is to assess the impact of
the control operations on the endemicity of the disease, and to
compare results between different times and places. Indicators are
required for such an evaluation. It is important that these indicators
can be easily used and satisfy the criteria of repeatability and
validity. Ideally they should be conceived and treated as signals for
action by programme managers (10). There are two main types of
indicators in leprosy control.
(a) Operational indicators
These are primarily managerial in character, that is, to monitoi
the functioning of ongoing-control activities in the field. These are
related to case-finding, treatment, relapses and disabilities (12). For
example, the relapse rate is one of the best indicators of the
efficacy of the drug regimen. Others include case detection ratio
(that is the number of cases registered to estimated number of
cases), proportion of children (0-14 years) among newly detected
cases, proportion of multibacillary cases on regular treatment
during the year, etc (for details see reference 10).
1999 -30 June 2001, Biennial Report of the Regional Director WHO
7.WHO (1999), Health Situation in the South -East Asia Region 19941997, Regional office for SEAR, New Delhi
8.Govt, of India (2004), Annual Report 2003 - 2004, Ministry of Health
and Family Welfare, New Delhi.
9.Dharmendra (1985), Leprosy Vol III Samant and Company, Bombay
10.WHO (1988). Techn. Rep. Ser., No. 768
11.Job, C.K. et al (1975). Leprosy : Diagnosis and Management, Hind
Kusht Nivaran Sangh, New Delhi
B.
C.
D.
E.
Bacterial agents
Neisseria gonorrhoeae
Chlamydia trachomatis
Treponema pallidum
Haemophilus ducreyi
Mycoplasma hominis
Ureaplasma urealyticum
Calymmatobacterium granulomatis
Shigella spp.
Campylobacter spp.
Group B streptococcus
Bacterial vaginosis-associated organisms
Viral agents
Human (alpha) herpesvirus 1 or 2 (herpes simplex virus)
Human (beta) herpesvirus 5 (formerly cytomegalovirus)
Hepatitis virus B Human papilloma viruses Molluscum
contagiosum virus Human immunodeficiency virus
Protozoal agents
Entamoeba histolytica
Ciardia lamblia
Trichomonas vaginalis
Fungal agents
Candida albicans
Ectoparasites
Phthirus pubis
Sarcoptes scabiei
TABLE 2
Common syndromes and sequelae for which sexual
transmission is of epidemiological importance
Male urethritis
Lower genital syndromes in women : vaginitis/cervicitis/urethritis
Genital ulceration
Proctitis/colitis
Salpingitis
Epididymitis/orchitis
Infertility!ectopic pregnancy
Postnatal and perinatal morbidity
Hepatitis/hepatic carcinoma
Genital carcinoma
Acquired Immuno Deficiency Syndrome (AIDS)
Source : (1) Extent of the
problem
WORLD
The true incidence of STDs will never be known not only because of
inadequate reporting but because of the secrecy that surrounds them. Most
of them are not even notifiable. All available data, however, indicate a
very high prevalence of STD (from 1 per cent to 14 per cent) in the
vulnerable population groups (3). The trend in gonorrhoea and primary
20 million
30 million
Agent factors
Over 20 pathogens have been found to be spread by sexual
contact. A classification of these agents and the diseases caused by
them are as shown in Table 3.
TABLE 3
Important sexually transmitted pathogens and
the diseases caused by them
Pathogen
Disease or syndrome
Neisseria gonorrhoeae
Treponema pallidum
Haemophilus ducreyi
Chlamydia trachomatis
Calymmatobacterium
granulomatis
Herpes simplex virus
Hepatitis B uirus
Human papillomaviruses
Human immunodeficiency virus (HIV)
Molluscum contagiosum
Candida albicans
Trichomonas vaginalis
Sources : (2, 8)
Host factors
(a) Age : For most notifiable STDs, the highest rates of
incidence are observed in 20-24 year-olds, followed by the 25-29
and 15-19 year age groups. The most serious morbidity is observed
during foetal development and in the neonate (2). (b) Sex : For
most STDs, the overall morbidity rate is higher for men than for
women, but the morbidity caused by infection is generally much
more severe in women, as for example, pelvic inflammatory
disease (c) Marital status : The frequency of STD infection is
higher among single, divorced and separated persons than among
married couples (d) Socio-economic status : Individuals from the
lowest socio-economic groups have the highest morbidity rate.
Demographic factors
Certain demographic factors will undoubtedly contribute to
increase in STDs in the developing countries. These include
population explosion and marked increase in the number of young
people, the group at highest risk for STD in the population; rural to
urban migration; increasing educational opportunities for women
delaying their marriage and increasing STD risks.
Social factors
Numerous social and behavioural factors are involved in the
spread of STDs. These include : (a) Prostitution : This is a major
factor in the spread of STDs. The prostitute acts as a reservoir of
infection. In Asia, most STDs are contracted from prostitutes,
whereas in many developed countries, the professional prostitute
has largely been replaced by the "good-time girl". The male
component of prostitution - the prostituant is equally important.
Prostitution supplies a demand; if there were no prostituants, there
would be no prostitutes (9). (b) Broken homes : Social studies
indicate the promiscuous women are usually drawn from broken
homes,
1.Initial planning
2.Intervention strategies
3.Support components
4.Monitoring and Evaluation
INITIAL PLANNING
Control programmes have to be designed to meet the unique
needs of each country and to be in line with that country's health
care system, its resources and priorities. This requires initial
planning which comprises the following steps : (1) PROBLEM
DEFINITION : The disease problem must be defined in terms of
prevalence, psychosocial consequences and other health effects by geographic areas and population groups, with the aid of seroepidemiological surveys and population surveys. This is an
important first step, since such information is usually inadequate or
non-existent in most cases. (2) ESTABLISHING PRIORITIES :
Rational planning requires establishment of priorities. This will
depend upon health problem considerations (e.g., magnitude,
consequences) and feasibility of control (e.g., availability of
adequate resources, social and political commitment). Priority
groups may be categorised on the basis of age, sex, place of
residence, occupation, drug addiction, etc. (3) SETTING
OBJECTIVES : Priorities must be converted into discrete,
achievable and measurable objectives. That is, to reduce the
magnitude of the problem, in a given population and a stated time.
To be most useful, objectives should be unambiguous and
quantifiable. Broad coverage of the population is crucial for
effective STD control (4) CONSIDERING STRATEGIES : A
variety of intervention strategies are available. Planners must
define the mixture of strategies that appears to be most appropriate
to the setting. (The reader is referred to chapter 18 for a broad
discussion of the planning cycle).
INTERVENTION STRATEGIES
1. Case detection
Case detection is an essential part of any control programme.
The usual methods of early detection in a STD control programme
are :
(1)Screening : Screening is the testing of apparently healthy
volunteers from the general population for the early detection
of disease. High priority is given to screening of special groups,
viz. pregnant women, blood donors, industrial workers, army,
police, refugees, prostitutes, convicts, restaurant and hotel staff,
etc. The availability of an appropriate test is critical for
screening purposes. The sensitivity, specificity, and the
predictive value of a test are important considerations (see
Chapter 4).
(2)Contact tracing : Contact tracing is the term used for the
technique by which the sexual partners of diagnosed patients
are identified, located, investigated, and treated (12). This is
one of the best methods of controlling the spread of infection.
Patients are interviewed for their sexual contacts by specially
trained staff. The key to success in contact tracing is the patient
himself who must disclose all sex contacts voluntarily. In some
parts of USA, contacts are sought as quickly as possible using
telephone, telegram and other rapid means of communication.
The contacts are then persuaded to attend a STD clinic for
examination and treatment. Where prevalence is low, contact
tracing is relatively expensive.
(3) Cluster testing : Here the patients are asked to name
other persons of either sex who move in the same socio-sexual
environment. These persons are then screened (e.g., blood
testing). This technique has been shown almost to double the
number of cases found (13).
2. Laboratory services
Adequate laboratory facilities and trained staff are essential for
proper patient management. It provides a basis for correct
aetiological diagnosis and treatment decisions; for contact tracing;
surveillance of morbidity and detection of antimicrobial resistance.
The diagnostic tests that should be available for the important
sexually transmitted pathogens are given in a recent WHO report
(11).
3. Primary health care
The current trend is to integrate STD control activities into
primary health care system. This will imply inclusion of primary
health care workers (e.g., village health guides, multipurpose
workers) in the STD "health team". Then only it will be possible to
provide effective treatment to the greatest number of cases in the
community. Such management limits further disease transmission.
Primary health care which is based on the principles of universal
coverage, community participation, equity and intersectoral
coordination is ideally suited to control STD in the community.
4. Information system
The basis of an effective control programme of any
communicable disease is the existence of an information system. It
is a prerequisite for effective programme planning, coordination,
monitoring and evaluation. Three types of data requirement are
relevant in the control of STDs: these are clinical notification,
laboratory notification, and sentinel and adhoc surveillance.
National notification system, at best, includes only the
"classical" venereal diseases, where existing, reporting systems
suffer from undernotification, inaccurate diagnosis and
concealment of cases owing to social stigma. Without a
notification system, it is not possible to assess the magnitude of the
problem, to allocate resources and to evaluate the impact of control
measures. There is an urgent need to develop an effective and
detailed reporting system of STDs in countries where it does not
exist. Sentinel surveillance systems and/or adhoc surveys can be
used to supplement the routine reporting system. Population-based
sample surveys may also be used to identify the true distribution of
disease in a particular setting. Such surveys are very expensive and
are generally of limited use for sexually transmitted disease
programmes (11).
The information system should be built around a small number
of questions : How many cases were interviewed ? How many
villages were visited ? How many cultures were examined? The
system should provide information on activities, resource
utilization and task accomplishment of programme personnel (11).
5. Legislation
Many countries are still far away in enacting suitable legislation
for the control of STDs (15). Although legislations and regulations
cannot wipe out STDs, they are nonetheless needed, particularly to
establish responsibilities and define standards. The purpose of
legislation should be to encourage patients to seek early treatment
and name their sexual contacts, to screen high risk groups, to
improve notification by general practitioners, health education of
the public, etc. The Immoral Traffic (Prevention) Act, 1986 (which
replaced the earlier Suppression of the Immoral Traffic Act, 1956)
covers all persons, whether male or female, who are exploited
sexually for commercial purposes. It makes punishment for the
offences under the Act more stringent than the previous Act.
6. Social welfare measures
STDs are social problems with medical aspects. It implies
General WHO
5.Upe. G.V. etal (1979). Journal Indian MA. 72 (7) 157-159
6.Nair, B.K.H. et al (1974). Ind. J. Med. Res., 62 : 1826
7.Rama Rao, N.V.S. etal (1966). Ind. J. Der. andVen., May-June, 66:101
8.WHO (1981). Techn. Rep. Ser., No. 660
9.Willcox, R.R. (1961). Brit. J. PSM, 15 : 42
10.Willcox, R.R. (1976). Sexually Transmitted Diseases, R.D. Catterall and
C.S. Nicol (eds). Academic Press.
11.WHO (1985). Control of Sexually Transmitted Diseases, WHO, Geneva
12.WHO (1982). Techn. Rep. Ser., No. 674
13.WHO (1963). Techn. Rep. Ser., No. 262
14.WHO (1978). Techn. Rep. Ser., No. 616
15.WHO (1975). VD Control: A Survey of Recent Legislation, Geneva
_______________________
___________________
.'
________________________________________;___________________
ENDEMIC SYPHILIS
Endemic syphilis (Bejel is a local name for this disease in
Syria) occurs in the arid areas of Syria, Saudi Arabia, Iraq, Iran,
Yugoslavia, northern and southern Africa and Australia. It does not
occur in the Americas. The causative agent is difficult to
differentiate from T. pallidum. The claim that it is the same
microorganism has yet to be substantiated (4). It is transmitted nonvenereally by direct or indirect contact - among children and
adolescents through their play or by drinking vessels and common
eating and other household utensils under primitive, crowded and
substandard conditions of living. It is thought that poor hygiene
rather than climatic conditions is a major factor in the continued
transmission of Bejel. It is thought that 25 per cent of children
acquire the infection before the age of 10 years. The figure is
increased to 60 per cent before the age of 16 years (4). Endemic
syphilis produces highly infectious skin lesions. Late
manifestations include gumatous lesions of the skin, nasopharynx
and bones (5). A single injection of benzathine penicillin G is the
treatment of choice. For patients under 10 years the dose is 0.6
mega units, and for patients age 10 years and over, the dose is 1.2
mega units (3).
YAWS
ENDEMIC TREPONEMATOSES
i_^_____________________________________________________________________..
_______________________________________________AIDS 271
TREATMENT : In meso-endemic communities (5 to 10 per cent
prevalence), treatment is given to all cases and to all children
under 15 years of age and other obvious contacts of infectious
cases (c) SELECTIVE MASS TREATMENT : In hypoendemic or
areas of low prevalence (less than 5 per cent) treatment is confined
to cases, their household and other obvious contacts of infectious
cases.
3. Resurvey and treatment
It is unlikely that a single round of survey and treatment will
cover the entire population. In order to interrupt transmission, it is
necessary to find out and treat the missed cases and new cases.
Resurveys should be undertaken every 6 to 12 months. Several
such follow-ups may be needed before eradication is achieved.
4. Surveillance
With the decline of yaws to very low levels, emphasis has
shifted to "Surveillance and containment" - a technique which has
proved highly successful in the eradication of smallpox. The
surveillance and containment measures would be concentrated on
affected villages, households and other contacts of known yaws
cases. The measures comprise epidemiological investigation of
cases to identify probable source(s) of infection and contacts of
each known case so as to discover previously unknown cases and
prevent new cases; treatment of cases; prophylactic treatment of
contacts with BPG; and, monthly follow-up of households with
confirmed cases for at least 3 to 4 months after treatment of the
last active case to assure interruption of transmission.
5. Environmental Improvement
In a disease like yaws, an attack on social and economic
conditions of life is as important as an attack on the biological
cause. Recrudescence of the disease is apt to occur unless
environmental improvement is promoted, e.g., improvement of
personal and domestic hygiene, adequate water supply, liberal use
of soap, better housing conditions and improvement of the quality
of life.
6. Resurgence of Yaws
Research has shown (3) that treponemes may persist in lymph
glands following treatment and apparent cure. Further, such
treponemes are viable and are capable of infecting laboratory
animals. This has given cause for concern. It indicates the
persistence of infection in the individual and in the population
notwithstanding community-wide penicillin treatment. There has
been a resurgence of yaws especially in West Africa. Small focal
clinical outbreaks (as in Nigeria and Thailand) or wider
recrudescences (as in Haiti) have occurred following mass
campaigns (8). It emphasizes the need for periodic assessment of
the situation by epidemiological and serological studies.
7. Evaluation
To determine whether or not yaws has really been brought
under control, serological studies are needed. Ideally if no yaws
antibodies were found among children born since the yaws mass
campaign was completed, it would mean that the campaign had
been totally successful. The actual sample of the population to be
tested may be as low as 1 or 2 per cent.
Eradication of Yaws ?
Epidemiological^ yaws is not as vulnerable to eradication as is
smallpox (7). The reasons are : (a) cases of yaws (untreated) are
contagious for months or years after onset of symptoms
(b)
latent cases occur frequently, and the
AIDS
AIDS, the acquired immuno -deficiency syndrome (sometimes
called "slim disease") is a fatal illness caused by a retrovirus
known as the human immuno-deficiency virus (HIV) which breaks
down the body's immune system, leaving the victim vulnerable to a
host of life-threatening opportunistic infections, neurological
disorders, or unusual malignancies (1). Among the special features
of HIV infection are that once infected, it is probable that a person
will be infected for life. Strictly speaking, the term AIDS refers
only to the last stage of the HIV infection. AIDS can be called our
modern pandemic, affecting both industrialised and developing
countries.
Problem statement
WORLD
Recognized as an emerging disease only in the early 1980s,
AIDS has rapidly established itself throughout the world, and is
likely to endure and persist well into the 21st century. AIDS has
evolved from a mysterious illness to a global pandemic which has
infected tens of millions in less than 20 years.
Today, an estimated 34-46 million people are living with
HIV/AIDS. Already, more than 20 million people have died from
AIDS, 3 million in 2003 alone (2). Four million children have been
infected since the virus first appeared. Of the 5 million people who
became infected with the virus in 2003, about 0.7 million were
children, almost entirely as a result of transmission during
pregnancy and childbirth or from breast feeding (3). The global
HIV/AIDS epidemic by the end of December 2003 is summarized
in Table 1.
1
as of December 2003
40 million (34-46 million) 37
million (31-43 million) 2.5
million (2.1-2.9 million)
5 mr'llinn (4 9-^ 8 million!
Iii 1984, Thailand was the first country in the SEAR report a case of
AIDS. In most other countries, HIV infecti was not diagnosed till 1986
or later. Since then HIV infecti has spread rapidly and WHO estimates
for SEAR countries c as shown in Table 2.
TARI F 9
Reported AIDS cases and estimated HIV infections in the , ^ SEAR
countries, as of May 2003
1p
.
AIDS cases
4.2 million (3.6-4.8 million)
700 000 (590 000-810 000)
3 million (2.5-3.5 million) 2.5
million (2.1-2.9 million) 500
000 (420 000-580 000)
Source : (2)
The most pxnlnsivp ornurth r>f the enirlemir nrrnrrpd in mirl
Bangladesh
Bhutan
Korea
48933
120000 Maldives
100 Myanmar
Nepal
Lanka
208456
Total
Reported
infections
17
13
0
3970000 Indonesia
9
5623
624
405
670000
267000
Estimated HIV
13000
< 100 DPR
< 100 India
3568
<
420000
58000 Sri
4800 Thailand
4653000
AIDS 211
18
the
in any of the high risk groups is still less than 5% and is less than 1%
country. among antenatal women.
According to the sentinel surveillance data from antenatal clinics in 7
Gro
up
I metro cities in the country, HIV infection has crossed 2 per cent mark in
Mumbai, is more than 1 per cent in Hyderabad, Bangalore, Chennai, and
High
Prevalen is below 1 per cent in Kolkata, Ahmedabad and Delhi. This data clearly
ce States supports the evidence that HIV infection is percolating from various high
risk groups to the general population.
:
includes
states of Estimation of HIV infection among adult population (8)
Maharas
Although the HIV sentinel surveillance data has been primarily used
htra,
for monitoring the trends i.e. to assess how rapidly HIV infection
Tamil
increases or decreases over the time in different groups and areas, it can
Nadu,
also provide an estimate of the total burden of HIV infection in the
Karnatak country.
a,
Such estimates are made by applying the formula :
Andhra
Pradesh,
V = (P/T) x (R)
Manipur
Here V is the total estimate of burden of HIV, P is the number of HIV
and
positives, T is the number of samples tested and R is the estimated size of
Nagalan
the population. As the extent of reliability of HIV estimate will depend
d where
upon the accuracy of the estimation of the size of risk group population,
the HIV
careful assumptions are required in respect of various parameters like
infection
urban rural mix, male female ratio, STD prevalence in urban and rural
has
areas etc. Using consistent methodology, estimates of HIV infections are
crossed 5
worked out. A range of 20% is applied to the point estimate, to provide
per cent
higher and lower values on this estimate.
mark in
HIV/AIDS is spreading rapidly in India. During the year 2003 the
high-risk
number of HIV cases rose to 5.1 million. The estimates from the year
group
and 1% 1981 to 2003 are as shown in Fig. 1.
or more
5.1
in
5
4.58
antenatal
women.
3 )7
Gro
up
II
Moderat
e
Prevalen
ce States
:
includes
states of
Gujarat,
Goa and
Pondich
erry
where
HIV
infection
has
crossed
5% or
more
among
high risk
groups
but the
infection
is below
1%
in
antenatal
women.
Gro
up III
Low
Prevalen
ce States
:
includes
remainin
g states
where
the HIV
infection
4
3
2
1
n
-
3.5 3.7
3 86
FIG. 2
Distribution of reported AIDS cases by states upto August, 2003
Source : (10)
The cumulative number of AIDS cases in the country has risen to
86028 by August 31st 2004. This includes 6205C males and 23978
females, 7799 new cases of AIDS were detected in the month of
August 2004 (5206 males and 259c females). The distribution of
likely source of infection and th< percentage is as shown in Table 3.
y TABLE 3
The royfe of infection in India, 2004
Sexual*
Perinatal transmission
Total
.
.
Nagalan
d
0.6%
Maharashtra less
Mumbai 16.7%
Others
TABLE 4
0 0.2
J-
1 75
2062
18145
37033
4810
1357
10776
10576
1269
3419
28921
47609
6079
Total
62050
23978
86028
Source : (9)
2130
780
1 II [I 75 n * n I.
431
267
e |! y il If I if 21 I
3*
if Si 1
Va
& Is 5
en
to
FIG. 3
Number of People Living with HIV Treated for
different Opportunistic infections - 2003
Source : (9)
The burden of AIDS cases is beginning to be felt in states
affected early in the epidemic. Mumbai in Maharashtra and Imphal
in Manipur, report high hospital bed occupancy rates from HIV associated illness. Home-based care is still in its infancy in most
parts of the country. Today, greater awareness of HIV has triggered
a mixed response from the society. While individual examples of
support and care are increasingly seen, HIV-positive individuals in
general have been poorly received in the society. Assess to health
care is emerging as a critical first point of contact with services for
HIV positive individuals and their families, and is a site of frequent
discrimination.
EPIDEMIOLOGICAL FEATURES
1. Agent factors :
(a) AGENT : When the virus was first identified it was called
"lymphadenopathy-associated virus (LAV)" by the French
scientists. Researchers in USA called it "human T-cell
lymphotropic virus III (HTLV-III)". In May 1986, the International
Committee on the Taxonomy gave it a new name : human
immuno-deficiency virus (HIV).
The virus is 1/10,000th of a millimetre in diameter. It is a protein
capsule containing two short strands of genetic material (RNA) and
enzymes. The virus replicates in actively dividing T4 lymphocytes
and like other retroviruses can remain in lymphoid cells in a latent
state that can be activated. The virus has the unique ability to
destroy human T4 helper cells, a subset of the human Tlymphocytes. The virus is able to spread throughout the body. It
can pass through the blood-brain barrier and can then
destroy some brain cells. This may account for certain of the
neurological and psychomotor abnormalities, observed in AIDS
patients. HIV mutates rapidly, new strains are continually
developing. There are two types of HIV - the most common HIV 1
and a more recently recognized virus (in West Africa) called HIV 2.
The virus is easily killed by heat. It is readily inactivated by
ether, acetone, ethanol (20 per cent) and beta-propiolactone (1:400
dilution), but is relatively resistant to ionizing radiation and
ultraviolet light (11).
(b) RESERVOIR OF INFECTION : These are cases and
carriers. Once a person is infected, the virus remains in the body
life-long. The risk of developing AIDS increases with time. Since
HIV infection can take years to manifest itself, the symptomless
carrier can infect other people for years.
(fc) SOURCE OF INFECTION : The virus has been found irn
greatest concentration in blood, semen and CSF. Lower
concentrations have been detected in tears, saliva, breast milk,
urine, and cervical and vaginal secretions"!)HIV has also been
isolated in brain tissue, lymph nodes, bone marrow cells and skin.
To date, only blood and semen have been conclusively shown to
transmit the virus (12).
2. Host factors
(a)AGE : Most cases have occurred among sexually active
persons aged 20-49 years. This group represents the most
productive members of the society, and those responsible for
child-bearing and child-rearing. Children under 15 make up less
than 3 per cent of the cases.
(b)SEX : In North America, Europe and Australia, about 51 per
cent of cases are homosexual or bisexual men. In Africa, the
picture is very different; the sex ratio is equal. Certain sexual
practices increase the risk of infection more than others, e.g.,
multiple sexual partners, anal intercourse, and male
homosexuality. Higher rate of HIV infection is found in
prostitutes.
(c)HIGH RISK GROUPS : Male homosexuals and bisexuals,
heterosexual partners (including prostitutes), intravenous drug
abusers, transfusion recipients of blood and blood products,
haemophiliacs and clients of STD.
Immunology
The immune system disorders associated with HIV
infection/AIDS are considered to occur primarily from the gradual
depletion in a specialised group of white blood cells (lymphocytes)
called T-helper or T-4 cells. The full name of T-helper cell is CD4
+ T lymphocyte and is also commonly known as CD4 + cell.
These cells play a key role in regulating the immune response.
HIV selectively infects T-helper cells apart from several other
cells in the immune system such as B-cells, microphages and nerve
cells. When the virus reproduces, the infected T-helper cells are
destroyed. Consequently people with AIDS tend to have low
overall white blood cell count (13). Whereas healthy individuals
have twice as many "helper" cells as "suppressor" cells, in the
AIDS patients the ratio is reversed. A decreased ratio of T-helper
to T-suppressor cells may be an indirect indicator of reduced
cellular immunity. One of the most striking features of the immune
system of patients with AIDS is profound lymphopenia, with a
total lymphocyte count often below 500 c. mm. It is the alteration
in T-cell function that is responsible for the development of
neoplasms, the development of opportunistic infections, or the
inability to mount a delayed-type hypersensitivity response. The
lack of an obvious immunological response by the host to the virus
is one of the problems confronting scientists (14). That is, those
with antibodies to HIV, usually will have too few of HIV
antibodies, and these antibodies are also ineffective against the
virus.
_______________________________________________AIDS 275
Mode of transmission
The causative virus is transmitted from person-to-person, most
frequently through sexual activity. The basic modes of
transmission are :
(a) Sexual transmission
AIDS is first and foremost a sexually transmitted disease. Any
vaginal, anal or oral sex can spread AIDS. In the USA, over 51 per
cent of the cases were in homosexual or bisexual men. In contrast,
in equatorial Africa, AIDS is acquired mainly through heterosexual
contact (infected man to woman; infected woman to man). Every
single act of unprotected intercourse with an HIV-infected person
exposes the uninfected partner to the risk of infection. The size of
the risk is affected by a number of factors, including the presence
of STD, the sex and age of the uninfected partner, the type of
sexual act, the stage of illness of the infected partner, and the
virulence of the HIV strain involved. A European study of 563
heterosexual couples in which only one partner was infected at the
start, suggests that chances of transmission of HIV infection from
male to female is twice as likely as from female to male (15).
Generally, women are more vulnerable to HIV infection because a
larger surface is exposed, and semen contains higher concentration
of HIV than vaginal or cervical fluids.
Anal intercourse carries a higher risk of transmission than
vaginal intercourse because it is more likely to injure tissues of the
receptive partner. For all forms of sex, the risk of transmission is
greater where there are abrasions of the skin or mucous membrane.
For vaginal sex the risk is greater when woman is menstruating.
Exposed adolescent girls and women above 45 years of age are
more prone to get HIV infection. In teenagers the cervix is thought
to be less efficient barrier to HIV than in mature genital tract of
adult women. The thinning of mucosa at menopause is believed to
lessen the protective effect. The production of mucus in the genital
tract of adolescent girls and in postmenopausal women is not as
prolific as in women between these life stages and this may also
enhance their susceptibility to HIV infection.
An STD in either the HIV-negative or the HIV-positive partner
facilitates the transmission of HIV. If an STD, such as syphilis,
chancroid or herpes, causes ulceration in the genital or perineal
region of the uninfected partner, it becomes far easier for HIV to
pass into his or her tissues. An STD causes inflammation. T-cells
and monocytes/macrophages, get concentrated in the genital area.
In a person already infected with HIV, some of these key cells of
the immune system will be carrying the virus - which magnifies
the risk of transmission to the uninfected partner.
As for HIV-infected people, they are more infectious to others
in the very early stages, before antibody production i.e. during the
"window period", and when the infection is well advanced,
because levels of virus in the blood at that time is higher than at
other times.
(b) Blood contact
AIDS is also transmitted by contaminated blood -transfusion of
whole blood cells, platelets and factors VIII and IX derived from
human plasma. There is no evidence that transmission ever
occurred through blood products such as albumin,
immunoglobulins or hepatitis vaccines that meet WHO
requirements (11). Contaminated blood is highly infective when
introduced in large quantities directly into the blood stream. The
risk of contracting HIV infection from transfusion of a unit of
infected blood is estimated to be over 95 per cent. Since the
likelihood of HIV transmission through blood depends on the
"dose" of virus injected, the risk of getting infected through a
contaminated needle, syringe or any other skin-piercing instrument
is very much lower than with
8
*->
>>
u J=
200aE
8*
0)
Bacterial infections
Tuberculosis
Herpes simplex
Herpes zoster
Vaginal candidiasis
Hairy leukoplakia
Kaposi's sarcoma
i
Pneumocystosis Toxoplasmosis
*. Cryptococcosis
Coccidioidomycosis
Cryptosporidiosis
r
"3
50 "o
Disseminated MAC
infection
Histoplasmosis
CMV retinitis CNS
lymphoma
c/)
<
r
HIV enzyme-linked
immunosorbent
assay (ELISA)
Significance
Screening test for HIV infection,
Sensitivity > 99.9%; to avoid false-positive
results, repeatedly reactive results must be
confirmed with Western blot.
Western blot
CBC
Anaemia,
neutropenia,
and
thrombocytopenia common with advanced
HIV infection.
Absolute CD4
Most widely used predictor of HIV
lymphocyte count progression. Risk of progression to an AIDS
opportunistic infection or malignancy is high
with CD4 < 200 cells/uL.
CD4 lymphocyte
percentage
HIV viral load tests These tests measure the amount of actively
replicating HIV virus. Correlates with disease
progression and response to antiretroviral
drugs.
B2 - Microglobulin
p24 antigen
Control of AIDS
There are four basic approaches to the control of AIDS :
1. Prevention
(a) EDUCATION
Until a vaccine or cure for AIDS is found, the only means at present
available is health education to enable people to make life-saving choices
(e.g., avoiding indiscriminate sex, using condoms). There is, however, no
guarantee that the use of condoms will give full protection. One should
also avoid the use of shared razors and toothbrushes. Intravenous drug
users should be informed that the sharing of needles and syringes involves
special risk. Women suffering from AIDS or who are at high risk of
infection should avoid becoming pregnant, since infection can be
transmitted to the unborn or newborn. Educational material and guidelines
for prevention should be made widely available. All mass media channels
should be involved in educating the people on AIDS, its nature,
transmission and prevention; this includes international travellers.
(b) PREVENTION OF BLOODBORNE HIV TRANSMISSION
TABLE 5
Test
Dose
Monitoring
Nucleoside analogs
Zidovudine (AZT)
(Retrovir)
Didanosine (ddl)
(Videx)
12-300 mg orally
twice daily (for pill
formulation)
Zalcitabine (ddC)
(Hivid)
Stavudine (d4T)
(Zerit)
No additional monitoring
Abacavir (ziagen)
No specific monitoring
Gastrointestinal distress
Renal function
Nucleotide analog
Tenofovir (Viread)
Protease inhibitors
Saquinavir
(invirase)
No additional monitoring
Ritonavir (Novir)
Indinavir (Crixivan)
Kidney stones
Bimonthly aminotransferases.
bilirubin level
Nelfinavir (Veracept)
Diarrhoea
No additional monitoring
Gastrointestinal, rash
Cholesterol, triglycerides
Diarrhoea
daily
Amprenavir (Agenerase)
Lopinavir / ritonavir
(Kaletra)
month aminotransferases
Rash
No additional monitoring
Rash
No additional monitoring
Neurologic disturbances
No additional monitoring
times daily
Efavirenz (Sustiva)
Source : (22)
load by 2-3 logs and allow suppression of HIV RNA to below the
threshold of detection for longer than 2 years in some individuals. Data
from clinical trials have demonstrated the superiority of regimens that
contain either nonnucleoside or protease inhibitor agents in addition to
nucleoside agents alone. There is a consensus about the desirability of
treating aggressively once a decision to start antiretroviral therapy has been
made rather than adding drugs subsequently over months or years (18).
Fig. 5 outlines the current approaches to first line and salvage antiretroviral
therapy.
Monitoring HIV-infected patients with serial T-helper cell count and
other clinical and laboratory markers is standard practice in the developed
nations.
First-line
treatment
I
1
)
AZT + 3TC or
ddl
or AZT + ddl
or AZT+ddC
Tr
Intolerance to regimen
Change to alternative
First-line treatment
->r
-.r
Saquinavir +
Second - line 1 one or more
treatment
| nucleoside
analogs
analogs
Ritonavir +
one or more
nucleoside
ir
^r
Indinavir +
^r
d4T + 3TC
d4T + ddl
nucleoside
analogs
Progression of disease or
viral load criteria as above
-*r
Sa
Third-line 1 In<
treatment \ n
nu
an
Nucleoside analogs
AZT = zidovudine
ddl = didanosine
Indinavir
= lamivudine
Source : (18)
quinavir +
linavir +
ir
Nevirapine +
AZT + ddl
Nelfinavir +
one or more
nucleoside cleoside
analogs
alogs
Protease inhibitors
Nonnucleoside reverse
Saquinavir
transcriptase inhibitors
Ritonavir
Nevirapine ddC = Zalcitabine
Delaviridine d4T = stavudine
Nelfinavir 3TC
FIG. 5 Approach to
antiretroviral combination therapy
3. Specific prophylaxis
Until more effective antiviral therapy becomes available, the
main aim of existing therapies will be to treat the manifestations of
AIDS. Primary prophylaxis against P. carinii pneumonia should be
offered to patients with CD4 count below 200 cells/uL. The
regimens available are trimethoprim -sulfamethoxazole,
aerosolized pentamidine and dapsone.
Agent
1973 Rotavirus
1Parvovirus B19
2Cryptosporidium parvum
1977 Ebola virus
1977 Legionella pneumophila
1977 Hantaan virus
1977 Campylobacter jejuni
1Human T-lymphotropic virus 1 (HTLV-1)
2Toxin-producing strains of Staphylococcus aureus
1982 Escherichia coli 0157:H7
1982 Borrelia burgdoferi
1982 HTLV-2
1983 Human immunodeficiency virus (HIV)
1983 Helicobacter pylori
1Enterocytozoon bieneusi
2Cyclospara cayetanensis
1986 BSE agent?
1988 Human herpesvirus 6 (HHV-6)
1Hepatitis E virus
2Ehrlichia chaffeensis
1989 Hepatitis C virus
1991 Guanarito virus
1991 Encephalitozoon hellem
1New species of Babesia
2Vibrio cholerae 0139
1Bartonella henselae
2Sin Nambre virus
1Encephalitozoon cuniculi
2Sabia virus
3Human herpesvirus 8
4nvCJD Australian bat lyssavirus
1997 H5N1
1999 Nipah virus
2003 Corona virus
Type
Virus
Virus
Parasite
Virus
Bacterium
Virus
Bacterium
Virus
Bacterium
Bacterium
Bacterium
Virus
Virus
Bacterium
Parasite
Parasite
Non-conventional agent
Virus
Virus
Bacterium
Virus
Virus
Parasite
Parasite
Bacterium
Bacterium
Virus
Parasite
Virus
Virus
Virus
Virus
Virus
Virus
Disease/Comments
Major cause of infantile diarrhoea worldwide
Aplastic crisis in chronic haemolytic anaemia
Acute and chronic diarrhoea
Ebola haemorrhagic fever
Legionnaires'disease
Haemorrhagic fever with renal syndrome (HRFS)
Enteric pathogen distributed globally
T-cell lymphoma-leukaemia
Toxic shock syndrome
Haemorrhagic colitis; haemolytic uraemic syndrome
Lyme disease
Hairy cell leukaemia
Acquired immunodeficiency syndrome (AIDS)
Peptic ulcer disease
Persistent diarrhoea
Persistent diarrhoea
Bovine spongiform encephalopathy in cattle
(Mad cow disease)
Exanthem subitum
Enterically transmitted non-A, non-B hepatitis
Human ehrlichiosis
Parenterally transmitted non-A, non-B liver hepatitis
Venezuelan haemorrhagic fever
Conjunctivitis, disseminated disease
Atypical babesiosis
New strain associated with epidemic cholera
Cat-scratch disease; bacillary angiomatosis
Hantavirus pulmonary syndrome
Disseminated disease
Brazilian haemorrhagic fever
Associated with Kaposi's sarcoma in AIDS patients
Avian flu (Bird flu)
SARS
indicates that this problem will increase in the foreseeable future. Changes
in lifestyle, behaviour (including injecting and non-injecting drug use) and
cultural or social values are behind the emergence of some infectious
diseases such as syphilis. Increases in the number of sexual partners have
been the main factor in the spread of HIV infection and other sexually
transmitted diseases. Travel, including tourism, also plays a role. The
spread of syphilis in the 18th and 19th centuries was related to the
movement of armies. Today, the introduction of HIV in many parts of the
world is due to greatly increased human mobility. Studies show that
whereas only a few generations ago most people in their lifetime travelled
no further than 40 kilometres from their birthplace, many today go up to
1000 times further, travelling the whole world.
Re-emerging diseases
The term re-emerging diseases refers to the diseases which were
previously easily controlled by chemotherapy and antibiotics, but now
they have developed antimicrobial resistance and are often appearing in
epidemic form.
1. Sources
The sources are patients, hospital staff and the environment.
(a)PATIENTS : Patients suffering from infectious diseases are
potential sources of infection. These cases may be certain viral
infections (measles, german measles, influenza, viral hepatitis);
Skin infections (discharging wounds, infected skin lesions,
eczema, psoriasis, boils, bed sores); respiratory infections (sore
throat, pulmonary tuberculosis, chest infection); and urinary tract
infection (B. coli infection). All these are very common sources of
hospital acquired infection
(b)STAFF: The hospital staff (viz doctors, nurses, ward boys) who
come in close contact with patients may often be an important
source of cross infection. For example, staphylococcus aureus is
commonly carried in the nose or on the skin. Haemolytic
streptococci may be carried in the throat and salmonella in the gut.
(c) ENVIRONMENT : The hospital environment (viz. hospital
dust, linen, bed clothes, furniture, sinks, basins, door handles and
even the air) is laden with microorganisms, and is thus an
important source of infection.
2. Routes of spread
The common routes of spread of cross infection are :
(a) Direct contact, i.e. the organism may be transferred directly
from the hands of a nurse or doctor to a susceptible patient;
(b) Droplet infection, e.g. droplets released from nose and
throat through coughing or sneezing : (c) Air-borne particles ;
(d) release of hospital dust into the air; (e) through various
hospital
procedures,
viz,
catheterisation,
intravenous
procedures, infected cat gut, dressings, sputum cups, bed pans,
urinals etc.
3. Recipients
All patients in hospitals are potential recipients of cross
infection. Some patients are more susceptible than others,
especially those who are severely ill and those under corticosteroid
therapy. Cross infection is greater in intensive care units,
urological and geriatric wards and in special baby care units.
Preventive measures
The main preventive measures are : (a) Isolation : Infectious
patients must be isolated. Patients who are susceptible to infection
should not be placed in beds next to patients who are a source of
infection (b) Hospital staff : Those who are suffering from skin
diseases, sore throat, common cold, ear infection, diarrhoea or
dysentery and other infectious ailments should be kept away from
work until completely cured. They should be careful about
personal hygiene and in regular changes of aprons and outer
clothing (c) Hand-washing : The most common route of infection
is via the hands. When dealing with patients, handwashing must be
thorough. Hand-washing with soap and water may not be
sufficient, a suitable disinfectant must be employed for Handwashing, (d) Dust control : Hospital dust contains numerous
bacteria and viruses. The dust is released during sweeping, dusting
and bed making. Suppression of dust by wet dusting and vacuum
cleaning are important control measures
(e) Disinfection : The articles used by the patient as well as
patient's urine, faeces, sputum should be properly disinfected.
Proper sterilization of instruments should be enforced.
(a)Control of droplet infection : Use of face masks, proper bed
spacing, prevention of overcrowding and ensuring adequate
lighting and ventilation are important control measures
(b)Nursing techniques : Barrier nursing and task nursing have also
been recommended to minimise cross infection, (h) Administrative
measures : There should be a hospital "Control of Infection
Committee" to formulate policies regarding admission of
infectious cases, isolation facilities, disinfection procedures and in
fact all matters relating to control of hospital acquired infection.
Epidemiology of
Chronic Non-communicable
Diseases and Conditions
"While there are many diseases, there is, in a sense, only one health"
.
..
.. ....v
The problem
Chronic non-communicable diseases are assuming increasing
importance among the adult population in both developed and
developing countries. Cardiovascular diseases and cancer are at
present the leading causes of death in developed countries (e.g.,
Europe and North America) accounting for 70 to 75 percent of
total deaths. The prevalence of chronic disease is showing an
upward trend in most countries, and for several reasons this trend is
likely to increase. For one reason, life expectancy is increasing in
most countries and a greater number of people are living to older
ages and are at greater risk to chronic diseases of various kinds.
For another, the life-styles and behavioural patterns of people are
changing rapidly, these being favourable to the onset of chronic
diseases. Modern medical care is now enabling many with chronic
diseases to survive. The impact of chronic diseases on the lives of
people is serious when measured in terms of loss of life,
disablement, family hardship and poverty and economic loss to the
country. Developing countries are now warned to take appropriate
steps to avoid the "epidemics" of non-communicable diseases
likely to come with socioeconomic and health developments.
Non-communicable disease risk factors
Most epidemiologists accept that six key sets of "risk factors"
are responsible for a major share of adult non-communicable
disease morbidity and premature mortality (6). These are as
follows:
1.Cigarette use and other forms of smoking
2.Alcohol abuse
3.Failure or inability to obtain preventive health services (e.g.,
for hypertension control, cancer detection, management of
diabetes)
4.Life-style changes (e.g., dietary patterns, physical activity)
5.Environmental risk factors, (e.g., occupational hazards, air and
water pollution, and possession of destructive weapons)
6.Stress factors.
Gaps in natural history
There are many gaps in our knowledge about the natural history
of chronic diseases. These gaps cause difficulties in aetiological
investigations and research (7). These are -
2. Multifactorial causation:
Most chronic diseases are the result of multiple causes -rarely is
there a simple one-to-one cause-effect relationship. In the absence
of a known agent, the term "risk factor(s)" is used to describe
certain factors in a person's background or life-style that make the
likelihood of the chronic condition more probable. Further, chronic
diseases appear to ret It from the cumulative effects of multiple
risk factors. These lactors may be both environmental and
behavioural or constitutional. Epidemiology has contributed
massively in the identification of risk factors of chronic diseases.
Many more are yet to be identified and evaluated.
Integrated approach :
It is now felt that the principles of prevention of CHD can be
applied also to other major non-communicable diseases (NCDs)
because of common risk factors. A broader concept is emerging,
that is, to develop an overall integrated programme for the
Prevention and Control of NCDs as part of primary health care
systems, simultaneously attacking several risk factors known to be
implicated in the development of non-communicable diseases.
Such concerted preventive action should reduce not only
cardiovascular diseases but also other major NCDs, with an overall
improvement in health and length of life (8).
This chapter will consider some of the more important chronic
diseases and conditions.
References
1.Report on a
CARDIOVASCULAR DISEASES
Cardiovascular diseases (CVD) comprise of a group of diseases
of the heart and the vascular system. The major conditions are
ischaemic heart disease (IHD), hypertension, cerebrovascular
disease (stroke) and congenital heart disease. Rheumatic heart
disease (RHD) continues to be an important health problem in
many developing countries.
Problem statement
WORLD
In today's world, most deaths are attributable to noncommunicable diseases (32 million) and just over half of these
(16.7 million) are as a result of CVD; more than one-third of these
deaths occur in middle-aged adults. In developed countries, heart
diseases and stroke are the first and second leading cause of death
for adult men and women. These facts are familiar and hardly
surprising, however, surprisingly in some of the developing
countries, CVD have also become the first and second leading
causes responsible for one-third of all deaths (1).
The four patterns of CVD mortality at four different stages of
epidemiological transition are shown in Table 1. Developing
countries of South East Asia Region are typically in the second
stage of this transition. While some rural population are still in
stage one, many urban populations have entered third stage
characterized by very high CVD mortality.
CVD deaths
(% of total)
5-10
10-35
Predominant
CVD
Affected
SEAR
populations
RHD, infectious
Some
and nutritional
cardiomyopathies
As above plus
hypertensive heart
disease and
haemorrhagic
stroke
All forms of stroke;
IHD at relatively
young ages
rural
areas
SEAR as a
whole-rural
population
Age of
35-55
Urban
degenerative
population
and man made
diseases
3.
Age of delayed
<50
Stroke and IHD
degenerative
at older ages
diseases
4. Source : (2)
Cardiovascular diseases are responsible for about 25 per cent of the
DALYs lost due to non communicable diseases in SEAR countries. Of
these IHD accounts for about 40 per cent of DALYs lost, cerebrovascular
diseases about 19 per cent, Rheumatic heart disease 6 per cent,
inflammatory heart diseases about 6 per cent and other conditions about
29 per cent.
The incidence of CVD is greater in urban areas than in rural areas
reflecting the aquisition of several risk factors such as tobacco
consumption, lack of physical activity, unhealthy diet (today's fast food
habits) and obesity. A peculiar cause of concern is the relative early age of
CVD deaths in the developing countries. Ironically CVDs are now in
decline in the industrialized countries first associated with them. They
seem to have crossed the peak of the epidemic by now. The decline is
largely a result of the success of primary prevention and to a lesser extent,
treatment. The middle and low-income countries are at the mid-point of
the emerging epidemic and will face its full impact in the coming years.
These countries can be benefited from the strategy of primary prevention.
INDIA
In India an estimated 2.27 million people died due to CVD during
1990, and according to projections the number of deaths due to IHD was
to increase from 1.17 million in 1990 to 1.59 million in 2000 and 2.03
million by 2010. There were over 5 million persons suffering from CVD
during 1999. The prevalence of CVD is reported to be 2-3 times higher in
the urban population as compared to the rural population. In one study, the
prevalence of IHD among adults (based on clinical and ECG criteria) was
estimated at 96.7 per 1000 population in the urban and 27.1 per cent in
rural areas (2).
The present mortality rates are the consequence of previous exposure
to behavioural risk factors such as inappropriate nutrition, insufficient
physical activity and increased tobacco consumption. It is called the "lagtime" effect of risk factors for CVD. Overweight, central obesity, high
blood pressure, dyslipidaemia, diabetes and low cardio- respiratory fitness
are among the biological factors contributing principally to increased risk.
It is now well established fact that a persistently high cholesterol level
can almost certainly precipitate a cardiac event such as CHD. Still most
people do not have an idea of nutritional requirements and a balanced diet.
Unhealthy dietary practices include a high consumption of saturated fats,
Decreased risk
Inufficient
Myristic and
palmitic acids
Trans fatty acids
High sodium intake
Overweight
High alcohol intake
(for stroke)
Dietary cholesterol
Unfiltered boiled
coffee
Calcium
Magnesium
I_________ Vitamin C
EPA, eicosapentaenoic acid: DHA, docosahexaenoic acid; NSP,
non-starch polysaccharides.
Source : (3)
The dietary aspect of CVD has been discussed in detail in the chapter
of Nutrition and Health, page 468 and the recommended nutrient intake
goals for prevention of CHD are shown in Annexure 7 of that chapter.
In summary, the major CVD risk factors of tobacco use, inappropriate
diet and physical inactivity explain at least 75-85 per cent of new cases of
coronary health disease. In the absence of elevation of these risk factors,
CHD is a rare cause of death. Unfortunately, the vast majority of the
populations in almost all countries are at risk of developing CVD because
of higher than optimal levels of main risk factors.
References
1.WHO (2003), The World Health Report 2003, Shaping the Future.
2.WHO (2002), Health Situation in the South-East Asia Region
1998-2000, New Delhi.
3.WHO (2003), Tech. Rep. Ser. 916
c-
Male
Scotland (1983)
192.3
283.9
124.0
Finland (1980)
Sweden (1982)
Australia (1981)
England & Wales (1982)
USA (1980)
Denmark (1982)
Canada (1982)
Italy (1980)
France (1981)
Japan(1982)
176.5
158.4
155.9
154.7
154.6
153.4
145.1
79.6
47.3
29.5
283.7
231.5
223.7
231.4
219.7
220.6
205.2
113.8
71.5
39.3
101.7
98.0
100.3
94.9
104.1
99.6
94.7
51.9
28.1
22..0
Source : (17)
Female
30
c
0
is
13 20
"Ho
US O o O
O i-H
a>
o "
TABLE 2
>
(0
10 3
.a
o
Li
Not modifiable
Modifiable
Age
Sex
Family history
Genetic factors
Personality (?)
Cigarette smoking
High blood pressure
Elevated serum cholesterol
Diabetes
Obesity
Sedentary habits
Stress
1. Smoking
Some people commit suicide by drowning, but many by smoking. A
uniquely human habit, smoking has been identified as a major CHD risk
factor (21,22) with several possible mechanisms-carbon monoxide
induced atherogenesis; nicotine stimulation of adrenergic drive raising
both blood pressure and myocardial oxygen demand; lipid metabolism
with fall in "protective" high-density lipoproteins, etc.
It has been calculated that in countries where smoking has been a
widespread habit, it is responsible for 25 per cent of CHD deaths under 65
years of age in men (23). Cigarettes seem to be particularly important in
causing sudden death from CHD especially in men under 50 years of age
(23).
The degree of risk of developing CHD is directly related to the number
of cigarettes smoked per day (24). Filter cigarettes are probably not
protective (25). There is evidence that the influence of smoking is not only
independent of, but also synergistic with other risk factors such as
hypertension and elevated serum cholesterol (Fig. 1). This means that the
effects are more than additive (23).
The risk of death from CHD decreases on cessation of smoking. The
risk declines quite substantially within one year of stopping smoking and
more gradually thereafter until, after 10-20 years, it is the same as that of
non-smokers (23). For those who have had a myocardial infarcation, the
risk of a fatal recurrence may be reduced by 50 per cent after giving up
smoking (23).
a.
120 130 140 150 160 170 180 190 200
(16.0) (17.3) (18.7)(20.0) (21.3) (22.7)(24.0) (25.3) (26.7)
SBP mmHg (kPa)
FIG. 1
The importance of risk-factor combinations, illustrated by the
six-year risk of myocardial infarction at various levels of SBP
and serum cholesterol in smokers and non-smokers
The vertical axis gives the probability of myocardial infarction
occuring in the next 6 years per 1000 men with a given SBP. Curve a
: risk in the absence of smoking and elevated serum
cholesterol. Curve b : risk in smokers. Curve c : risk
with elevated serum cholesterol. Curve d : risk with smoking and
elevated serum cholesterol.
The vertical bars a-d show how the increment in the risk of myocardial
infarction associated with a given SBP elevation depends on the various
"constellations" (combinations) of risk factors. The ratios of the lengths
of the bars provide a measure of the risk due to a particular risk-factor
constellation.
Source : (23 a)
'
2. Hypertension
The blood pressure is the single most useful test for identifying
individuals at a high risk of developing CHD. Hypertension accelerates
the atherosclerotic process, especially if hyperlipidemia is also present and
contributes importantly to CHD. In the past, emphasis was placed on the
importance of diastolic blood pressure. Many investigators feel that
systolic blood pressure is a better predictor of CHD than is the diastolic.
However, both components are significant risk factors. The risk role of
"mild" hypertension is generally accepted (14).
3. Serum cholesterol
It is nearly three decades since it became clear that elevation of serum
cholesterol was one of the factors which carried an increased risk for the
development of myocardial infarction. Today, there is a vast body of
evidence showing a triangular relationship between habitual diet, blood
cholesterol-lipoprotein levels and CHD and that these relationships are
judged to be causal (1). There is no population, in which CHD is common,
that does not also have a relatively high mean level of cholesterol (i.e.
greater than 200 mg/dl in adults). This is illustrated in Fig. 2 (1) which
shows the cultural differences in serum cholesterol levels between two
countries, Japan and Finland - Japan having the lowest incidence and
Finland the highest incidence of CHD.
Fig. 3 shows that the risk of CHD rises steadily with the serum
cholesterol concentration (26). The 10-years' experience of the Seven
Countries Study (27) showed that serum cholesterol concentration is an
important risk factor for the incidence of CHD at levels perhaps 220 mg/dl
or more. This supports the notion of a "threshold level" of cholesterol, that
is, a certain level beyond which there is an association.
The strength of the dietary-fat hypothesis is that observations in the Seven Countries Study (among others) fitted it well - that is, the Japanese had low fat
diets, low serum cholesterol and low incidence of CHD while the East Fins were at the other extreme (Fig. 2). The weakness of the hypothesis is that studies
of individuals have not shown such a relationship. This has been attributed to genetic and dietary intake differences between individuals (1).
When we look at the various types of lipoproteins, it is the level of low-density lipoprotein (LDL) cholesterol that is most directly associated with CHD
(28). While very low-density lipoprotein (VLDL) has also been shown to be associated with premature atherosclerosis, it is more strongly associated with
peripheral vascular disease (e.g., intermittent claudication) than with CHD. High-density lipoprotein (HDL) cholesterol is protective against the development
of CHD - the higher its mean level in a group of individuals, the lower the incidence of infarction in that group (28). HDL should be more than 30 mg/dl.
To further refine CHD risk prediction based on serum lipid levels, a total "cholesterol/HDL ratio" has been developed. A ratio of less than 3.5 has been
recommended as a clinical goal for CHD prevention (29).
With newer techniques, high-density and low-density . lipoproteins have been further subdivided into sub-fractions. i Recent evidence indicates that
levels of plasma apolipoprotein -A-I (the major HDL protein) and apolipoprotein-B (the major LDL protein) are better predictors of CHD than HDL
cholesterol "or LDL cholesterol respectively. Therefore, measurement of apolipoproteins may replace lipoprotein^ cholesterol determinations in assessing the
risk of CHD (30).)
/ 4. Other risk factors
(i) Diabetes : The risk of CHD is 2-3 times higher in diabetics than in non-diabetics. CHD is responsible for 30 to 50 per cent of deaths in diabetics over
the age of 40 years in industrialized countries (31).
(ii) Genetic factors : A family history of CHD is known to increase the risk of premature death. Genetic factors are probably the most important
determinants of a given individual's TC and LDL levels. However, the importance of genetic factors in the majority of cases is largely unknown.
(Hi) Physical activity : Sedentary life-style is associated with a greater risk of the development of early CHD. There is
evidence that regular physical exercise increases th< concentration of HDL (32) ahd decreases both body weigh and blood pressure which are
beneficial to cardiovascula health.
(iv) Hormones : The pronounced difference in the mortalit; rates for CHD between male and female subjects (Table 1 suggests that the
underlying factor may have a hormonal basis It has been hypothesized that hyperoestrogenemia may be th< common underlying factor that
leads both to atherosclerosi: and its complications such as CHD, stroke and periphera vascular disease (33).
(v) Type A personality : Type A behaviour is associated with competitive drive, restlessness, hostility and a sense of urgency or
impatience. Type-A individuals are more coronary prone tc CHD than the calmer, more philosophical Type B individuals (34).
(vi) Alcohol: High alcohol intake, defined as 75 g or more per day is an independent risk factor for CHD, hypertension and all cardiovascular diseases (14). The evidence that moderate alcohol intake leads to a reduction in the risk of CHD is unsubstantiated (35).
(vii) Oral contraceptives : Women using oral contraceptives have higher systolic and diastolic blood pressure. The risk of myocardial
infarction in women seems to be increased by oral contraceptives, and the risk is compounded by cigarette smoking (36).
(viii) Miscellaneous : The possible role of dietary fibre, sucrose and soft water have been debated (5). Dyspnoea on exertion and low vital
capacity haye also been cited as possible risk factors.
PREVENTION OF CHD
In the 1960s the issue was whether CHD could be prevented or not. Studies were launched, reported and debated. The accumulated
evidence led to a broad consensus of expert opinion that CHD is preventable (14). This is best expressed in a report of the WHO Expert
Committee on the Prevention of CHD (1) which recommended the following strategies :
a. Population strategy
(i) prevention in whole populations
(ii) primordial prevention in whole populations
b. High risk strategy
c. Secondary prevention
a. Population strategy
CHD is primarily a mass disease. The strategy should therefore
be based on mass approach focusing mainly on the control of
underlying causes (risk factors) in whole populations, not merely
in individuals. This approach is based on the principle that small
changes in risk factor levels in total populations can achieve the
biggest reduction in mortality (16). That is, the aim should be to
shift the whole risk-factor distribution in the direction of
"biological normality" (1). This cannot obviously be done by
medical means alone; it requires the mobilization and involvement
of the whole community to alter its life-style practices that are
associated with CHD.
Specific interventions:
The population strategy centres round the following key areas:
1. Dietary changes : Dietary modification is the principal
preventive strategy in the prevention of CHD. The WHO
Expert Committee (1) considered the following dietary changes
to be appropriate for high incidence populations :
reduction of fat intake to 20-30 per cent of total
energy intake
consumption of saturated fats must be limited to less
than 10 per cent of total energy intake; some of the
reduction in saturated fat may be made up by
mono- and poly-unsaturated fats
a reduction of dietary cholesterol to below 100 mg
per 1000 kcal per day
an increase in complex carbohydrate consumption
(i.e., vegetables, fruits, whole grains and legumes)
avoidance of alcohol consumption; reduction of salt
intake to 5 g daily or less
2. Smoking : As far as CHD is concerned, present evidence
does not support promotion of the so-called "safer cigarette"
(14). The goal should be to achieve a smoke-free society, and
several countries are progressing towards this goal.
To achieve the goal of a smoke-free society, a comprehensive
health programme would be required which includes effective
information and education activities, legislative restrictions, fiscal
measures and smoking cessation programmes.
1.Blood pressure : It has been estimated that even a small
reduction in the average blood pressure of the whole population
by a mere 2 or 3 mm Hg would produce a large reduction in the
incidence of cardiovascular complications (37, 38). The goal of
the population approach to high blood pressure would thus be to
reduce mean population blood pressure levels. This involves a
multifactorial approach based on a "prudent diet" (reduced salt
intake and avoidance of a high alcohol intake), regular physical
activity and weight control. The potential benefits and the safety
and low cost of this advice would justify its implementation.
2.Physical activity : Regular physical activity should be a part
of normal daily life. It is particularly important to encourage
children to take up physical activities that they can continue
throughout their lives (1).
PRIMORDIAL PREVENTION .
A novel approach to primary prevention of CHD is primordial
prevention (1). It involves preventing the emergence and spread of
CHD risk factors and life styles that have not yet appeared or
become endemic. This applies to developing countries in particular.
These countries should seek to preserve their traditional eating
patterns and life-styles associated with low levels of CHD risk
factors. \ \Lf ~i "fef>^
Since the aetiology of CHD is multifactorial the approach to
Since 1951, (one of the best known large prospective v studies, the
Framingham Study, has played a major role in establishing the nature
of CHD risk factors and their relative importance (49, 50). The major
risk factors of CHD are elevated serum cholesterol, smoking,
hypertension and sedentary habits7]Accordingly, the four main
possibilities of intervention in CHD prevention are: reduction of serum
cholesterol, the cessation of smoking, control of hypertension
andjDromotion of physical activity.
Risk factor trials can be "single factor" trials or "multi/ factor" trialsABoth the approaches are complementary and
both are needed. Early trials of CHD prevention concentrated
. 'on one factor (e.g., dietary cholesterol). Later emphasis swung
''away from unifactorial to multifactorial approach.
JThe widely reported intervention trials are : (a) The
>"5 Stanford Heart Disease Prevention Programme in California
(b) The North Kerelia Project in Finland, (c) The Oslo Study,
Association.
2.WHO (1980). Sixth Report of World Health Situation.
3.Stamler, J. (1985). N. Eng. J. Med., 312 : 1053.
4.WHO (1983). Bull WHO, 61: 45
5.WHO (1985) Primary Prevention of CHD EURO Rep and Studies 98.
Copenhagen.
6.Rose, G. (1982) European Heart J. 3, Suppl B. 18
7.Bradely, N. (1984). In : Medical Annual, D.J.P. Gray (ed). John Wright
and Sons.
8.WHO (1984). World Health Statis. Annual
9.Sarvothan, S.G. and Berry, J.N. (1968). Circulation, 37 : 339
10.Dewan, B.D. et al (1974). Indian Heart J., 26 : 68
11.Sinha, B.C. (1970). Jr. Ind. Med. Assoc, 55 : 171
12.Slone, D. et al (1978). N. Eng. J. Med. 298 : 1273
13.Shaper A.G. etal (1981). Brit. Med. J. 283 : 179
14.WHO (1979). Tech. Rep. Ser., No. 636
23 a. WHO (1996), Tech. Rep. Ser. No. 862, Hypertension control
1.Bain, C. etal (1978). Lancet, 1 : 1087
2.Wald, N.J. (1976). Lancet, 1 : 136
3.Kannel, W.B. (1976). Am. J. Cardiol, 37 : 269
4.Keys, A. (1980). Seven Countries : a multivariate analysis of death and
CHD, Harvard University Press, Cambridge, M.A.
5.Gordon, T. et al (1977). Am. J. Med., 62 : 707
6.Superko, H.R. et al (1985). Am. J. Med., 78 : 826
7.Schaefer, E.J. (1985). N. Eng. J. Med., 312 : 1300
8.WHO (1985). Techn. Rep. Ser., 727
9.Miller, N.E. et al (1979) Lancet, 1:111
10.Phillips, G.B. (1985). Am. J. Med., 78 (3) 363
11.Jenkins, CD. et al (1974). N. Eng. J. Med., 290 : 1271
12.WHO (1986) Techn. Rep. Ser, No. 732
13.Mann, J.I. et al (1976). Brit. Med. J., 2 : 445
14.WHO (1986). Techn. Rep. Ser., No. 732
15.Rose, G. (1981). Brit. Med. J., 282 : 1847
16.Puska, P. et al (1979). Brit. Med. J., 2 : 1173
17.Multiple risk factor Intervention Trial Research Group (1982). JAMA,
248 : 1465
18.Farquhar, J. et al (1977). Lancet, 1 : 1192
19.Salonen, J.T. et al (1983). Brit. Med. J., 286 : 1857
20.Lancet (1985). 1 : 320
21.Hjermann. I. et al (1981). Lancet, 2 : 1303
22.Lipid Research Clinics Programme (1984). JAMA, 251 : 351
23.Glasunov, I. et al (1973). Int. J. Epl, 2 (2) 137
24.Rose, G. (1975). Brit. J. PSM, 29 : 147
25.G. Lamm (1979) In : Measurement of Levels of Health, WHO Reg.
Publ. EURO Ser. No. 7
26.Dawber, T.R. (1980). The Framingham Study, Cambridege, M.A.,
Harvard University Press.
27.Kannel, W.B. et al (1976). Am. J. Cardiol., 38 : 46
28.Lawrence M. Tierney, Jr. Stephen J. Mcphee Maxine A. Papadakis,
Current Medical Diagnosis and Treatment, 41st Ed., 2002, Large
Publication
References
HYPERTENSION
Hypertension is a chronic condition of concern due to its role in the
causation of coronary heart disease, stroke and other vascular
complications. It is the commonest cardiovascular disorder, posing a
major public health challenge to population in socioeconomic and
epidemiological transition. It is one of the major risk factors for
cardiovascular mortality, which accounts for 20-50 per cent of all deaths.
Definition of hypertension is difficult and, by necessity arbitrary. Sir
George Peckering first fomulated a concept that blood pressure in a
population is distributed continuously as a bell-shaped curve with no real
separation between normotension and hypertension (1). There is also a
direct relation between cardiovascular risk and blood pressure : the higher
the blood pressure, the higher the risk of both stroke
_____1______________________i_ II 1
A_ -_____________________"____AL J:..:J:___________I:______
Category
Normal
<85
High normal
130-139
85-90
Hypertension
Stage 1 (mild)
140-159
90-99
160-179
> 180
100-109
> 110
Stage 2 (Moderate)
Stage 3 (Severe)
Diastolic blood
pressure
(mm of Hg)
< 130
Source : (1)
When systolic and diastolic blood pressure fall into different
categories, the higher category should be selected to classify the
individual's blood pressure. "Isolated systolic hypertension" is defined as a
systolic blood pressure of 140 mm of Hg or more and a diastolic blood
pressure of less than 90 mm of Hg.
Organ damage
Although the extent of organ damage often correlates with the level of
blood pressure, it is not always the case. In addition
TABLE 2
Classification of hypertension by extent of organ damage
Stage I
Stage II
HYPERTENSION 295
become muffled (phase IV) and then disappear (phase V). Most of
the studies have used phase V to measure diastolic blood pressure.
The systolic and diastolic pressures should be measured at least
three times over a period of at least 3 minutes and the lowest
reading recorded. For reasons of comparability, the data should be
recorded everywhere in a uniform way.
For details of measurement procedure, such standard references
as those published by WHO (3, 4, 5) and the American Heart
Association (6) should be consulted.
Classification
Hypertension is divided into primary (essential) and secondary.
Hypertension is classified as "essential" when the causes are
generally unknown. Essential hypertension is the most prevalent
form of hypertension accounting for 90 per cent of all cases of
hypertension. Hypertension is classified as "secondary" when some
other disease process or abnormality is involved in its causation.
Prominent among these are diseases of kidney (chronic glomerulonephritis and chronic pyelonephritis), tumours of the adrenal
glands, congenital narrowing of the aorta and toxemias of
pregnancy. Altogether, these are estimated to account for about 10
per cent or less of the cases of hypertension.
Magnitude of the problem
Although blood pressure is easily measured, it had taken several
decades to realise that arterial hypertension is a frequent, worldwide health disorder (7).
"Rule of halves"
Hypertension is an "iceberg" disease. It became evident in the
early 1970s that only about half of the hypertensive subjects in the
general population of most developed countries were aware of the
condition, only about half of those aware of the problem were
being treated and only about half of those treated were considered
adequately treated (8). Fig. 1 illustrates this situation (9). If this
was the situation in countries with highly developed medical
services, in the developing countries, the nroDortion treated would
be far too less.
The areas of the circles shown in Fig. 1 correspond to the actual
proportions observed in several population based studies and
1.Undiagnosed hypertension
2.Diagnosed hypertension
3.Diagnosed but untreated
4.Diagnosed and treated
5.Inadequately treated
6.Adequately treated
INCIDENCE : The concept of incidence has limited value in
hypertension because of the variability of consecutive readings in
individuals, ambiguity of what is "normal" blood pressure and the
insidious nature of the condition (10).
PREVALENCE : In some industrialized countries, up to 25 per
cent of adults have diastolic pressures above 90 mm Hg (11).
Prevalence in the developing countries seems to be similar to that
in European or other technically developed societies ranging from
10 per cent to as much as 20 per cent among adults (7). Only a few
populations, either living at high altitudes or belonging to primitive
cultures (e.g., a small number of ethnic groups living in the Pacific
islands, Asia, Africa and South America) seem to have
exceptionally low levels of blood pressure (12).
PREVALENCE IN INDIA : The data are derived from two
well-planned studies which screened all persons aged 20-60 years
and followed WHO suggested criteria for diagnosis (13). The one
in Rohtak is taken to represent the urban population (14), and the
other in a village in Haryana to represent rural population in India
(15). The prevalence of hypertension was 59.9 and 69.9 per 1000
in males and females respectively in the urban population, and
35.5 and 35.9 per 1000 in males and females respectively in the
rural population.
MORTALITY : High blood pressure is a major risk factor for
stroke, CHD, heart or kidney failure. The higher the pressure, the
greater the risk and lower the expectation of life. Mortality rates
from hypertension are also misleading, as hypertension is a grossly
underreported factor in cardiovascular mortality. The bulk of
mortality associated with hypertension is due to cardiovascular
disease. In western countries, it is mainly coronary heart disease; in
Japan and Taiwan and possibly in India death from stroke is more
common.
Uniform trends
Interestingly, hypertension is one of the chronic diseases which
has shown the largest decline in mortality in some countries during
the last four decades (Table 3). Although the number of deaths in
women exceed those in men, the rate of fall is similar in both
sexes. This fall is attributed to the use of more effective drugs
introduced during the past 15-20 years to control hypertension. It is
interesting to note that the rate of fall in mortality continues (16).
TABLE 3
Hypertensive disease in England & Wales
(death rate per 100,000)
Source : (16)
"Tracking" of blood pressure
If blood pressure levels of individuals were followed up over
Time
______________________________________HYPERTENSION 297
itself implies a disorder initiated by tension or stress. Since stress is
nowhere defined, the hypothesis is untestable (2). However, it is an
accepted fact that psychosocial factors operate through mental
processes, consciously or unconsciously, to produce hypertension.
Virtually all studies on blood pressure and catecholamine levels in
young people revealed significantly higher noradrenalin levels in
hypertensives than in normotensives. This supports the contention
that overactivity of the sympathetic nervous system has an
important part to play in the pathogenesis of hypertension (17).
(i) SOCIO-ECONOMIC STATUS : In countries that are in posttransitional stage of economic and epidemiological change,
consistently higher levels of blood pressure have been noted in
lower socio-economic groups. This inverse relation has been noted
with levels of education, income and occupation. However, in
societies that are transitional or pre-transitional, a higher
prevalence of hypertension have been noted in upper socioeconomic groups. This probably represents the initial stage of the
epidemic of CVD (1).
(j) OTHER FACTORS : The commonest present cause of
secondary hypertension is oral contraception, because of the
oestrogen component in combined preparations. Other factors such
as noise, vibration, temperature and humidity require further
investigation (7).
PREVENTION OF HYPERTENSION
The low prevalence of hypertension in some communities
indicates that hypertension is potentially preventable (11). The
WHO has recommended the following approaches in the
prevention of hypertension :
1. Primary prevention
(a)Population strategy
(b)High-risk strategy
2. Secondary prevention
1. PRIMARY PREVENTION
Although control of hypertension can be successfully achieved
by medication (secondary prevention) the ultimate goal in general
is primary prevention. Primary prevention has been defined as "all
measures to reduce the incidence of disease in a population by
reducing the risk of onset" (23). The earlier the prevention starts
the more likely it is to be effective.
In connection with primary prevention, terms such as
"population strategy" and "high-risk strategy" have become
established (7, 24). The WHO has recommended these approaches
in the prevention of hypertension. Both the approaches are
complementary.
a. POPULATION STRATEGY:
The population approach is directed at the whole population,
irrespective of individual risk levels. The concept of population
approach is based on the fact that even a small reduction in the
average blood pressure of a population would produce a large
reduction in the incidence of cardiovascular complications such as
stroke and CHD (11). The goal of the population approach is to
shift the community distribution of blood pressure towards lower
levels or "biological normality" (17). This involves a multifactorial
approach, based on the following nonpharmacotherapeutic
interventions :
(a) NUTRITION : Dietary changes are of paramount
importance. These comprise : (i) reduction of salt intake to an
average of not more than 5 g per day (ii) moderate fat intake (iii)
the avoidance of a high alcohol intake, and (iv) restriction of
energy intake appropriate to body needs, (b) WEIGHT
REDUCTION : The prevention and correction of obesity (Body
Mass Index greater than 25) is a prudent way of reducing the
Practitioner Series,
Churchill Livingstone
3.WHO (1983). Bu//WHO, 61 (1)53
4.WHO (1978). Techn. Rep. Ser., No. 628
5.WHO (1962). Techn. Rep. Ser., No. 231
6.American Heart Association (1981). Circulation, 64 : 510 A
7.WHO (1983). Techn. Rep. Ser., No. 686
8.Strasser, T. (1972). WHO Chronicle, 26 : 451
9.WHO (1974). WHO Chronicle, 28 (3) 11
10.Pedoe, H.T. (1982). In : Epidemiology of Diseases, D.L. Miller and R.T.D.
Farmer (eds), Blackwell, Oxford
STROKE
The term "stroke" (syn : apoplexy) is applied to acute severe
manifestations of cerebrovascular disease. It causes both physical
and mental crippling. WHO defined stroke as "rapidly developed
clinical signs of focal (or global) disturbance of cerebral function;
lasting more than 24 hours or leading to death, with no apparent
cause other than vascular origin" (1). The 24 hours threshold in the
definition excludes transcient ischaemic attacks (TIA).
The disturbance of cerebral function is caused by three
morphological abnormalities, i.e., stenosis, occlusion or rupture of
the arteries. Dysfunction of the brain ("neurological deficit")
manifests itself by various neurological signs and symptoms that
are related to extent and site of the area involved and to the
underlying causes. These include coma,
Subarachnoid haemorrhage
Cerebral haemorrhage
Cerebral thrombosis or embolism
Occlusion of pre-cerebral arteries
Transcient cerebral ischaemia (of more than 24 hours)
Ill-defined cardiovascular disease (i.e., the underlying
pathology in the brain is not determined).
Problem
Stroke is a world-wide health problem. It makes an important
contribution to morbidity, mortality and disability in developed as
well as developing countries. Although there are substantial
differences in frequency from place to place, cerebral thrombosis is
usually the most frequent form of stroke encountered in clinical
studies, followed by haemorrhage. Subarachnoid haemorrhage and
cerebral embolism come next as regards both mortality and
morbidity (2). However, stroke from cerebral haemorrhage is more
common in Japan than elsewhere (1).
a. MORBIDITY:
A WHO Collaborative Study in 12 countries (1) showed, in the
populations studied, stroke incidence rates ranged from 0.2 to 2.5
per 1000 population per year, the variation being mainly due to
differences in the age structure of the populations involved. Agestandardized rates for men were 2 per 1000 in Colombo (Sri
Lanka), 4 to 8 in most European countries, but 15 in Akita (Japan).
Female rates were on average 30 per cent lower. The highest
morbidity figures come from Japan.
There is no reliable information on stroke in India. Analysis of
data from major urban University Hospitals suggest that nearly 2
per cent of all hospital cases, 4.5 per cent of medical and 20 per
cent of neurological admissions are from stroke (3).
A random survey on 258,576 residents in urban areas of Vellore
revealed only 147 hemiplegic subjects, presumed to be of vascular
origin. Thus the prevalence rate for hemiplegia in South India was
reported to be 56.9 per 100,000 as compared to 150 to 186 per
100,000 for USA and Europe (3).
b. MORTALITY:
Stroke is one of the leading causes of death and disability
throughout the world. In developed countries, coronary heart
disease and cerebrovascular diseases (particularly stroke) are
responsible for between 40 and 50 per cent of all deaths (4). Of
these 10 to 12 per cent are due to stroke. There is evidence that
mortality from stroke has been declining in many countries for
several years. Some of the decline occurred before modern
treatment methods became available, indicating that the fall in
stroke was associated with social and economic changes.
The WHO Collaborative Study (1) showed that both in
developed and developing countries, nearly one-third of stroke
patients died within 3 weeks and 48 per cent died within one year.
The unfavourable prognostic factors were old age, hypertension and
impairment of consciousness.
Natural history
Our knowledge of the natural history of stroke is far from
complete (Fig. 1).
STROKE 299
Stroke control programme
The aim of a stroke control programme is to apply at
community level effective measures for the prevention of stroke.
The first priority goes to control of arterial hypertension which is
a major cause of stroke. As transcient ischaemic attacks (TIA)
may be one of the earliest manifestations of stroke, their early
detection and treatment is important for the prevention of stroke
(2). Control of diabetes, elimination of smoking, and prevention
and management of other risk factors at the population level are
new approaches. Treatment for acute stroke is largely the control
of complications. Facilities for the long-term follow-up of
patients are essential. The education and training of health
personnel and of the public form an integral part of the
programme. For any such programme, reliable knowledge of the
extent of the problem in the community concerned is essential
(2).
In summary, control of stroke that was once considered an
inevitable accompaniment to aging is now being approached
through primary prevention. It has generated the hope that stroke
can be tackled by community health action.
References
^T J
*
I
possible
intervention
/F
>K
streptococcus that has been incriminated as the causative agent. It has been
suggested that not all strains of group A streptococci lead to RF; it is
believed that there might be some strains with "rheumatogenic potential".
The serotype that has attracted special emphasis is M type 5 which is
frequently associated with RF (10). All group A streptococci are sensitive
to penicillin. Unfortunately, the group consists of a great number of
immunologically different types with little cross immunity, defying all
attempts to produce an effective vaccine. Recently the virus (coxsackie B4) has been suggested as a causative factor and streptococcus acting as a
conditioning agent. There are many gaps in our knowledge about the
causative agent and underlying pathogenic mechanisms, (b) CARRIERS :
Carriers of group A streptococcus are frequent, e.g., convalescent,
transcient and chronic carriers. In view of the high carrier rate, their
eradication is not even theoretically possible (11).
2. HOST AND ENVIRONMENTAL FACTORS :
(a) AGE : RF is typically a disease of childhood and adolescence (5-15
years). Mention has already been made about the high incidence of
"juvenile mitral stenosis" in India (11, 12). The initial attack of RF occurs
at a young age, progresses to valvular lesions faster and is associated with
pulmonary arterial hypertension. The cause of the "juvenile" disease in
India is not known, (b) SEX : The disease affects both sexes equally (c)
IMMUNITY : An immunological basis for RF and RHD has been
proposed. The most prevalent concept is the toxic-immunological
hypothesis. According to this theory, group A streptococcal products have
certain toxic products, and components of the streptococcus and of host
tissues have an antigenic cross-relationship, leading to immunological
processes that result in an attack of RF (2). (d) SOCIO-ECONOMIC
STATUS : RF is a social disease linked to poverty, overcrowding, poor
housing conditions, inadequate health services, inadequate expertise of
health - care providers and a low level of awareness of the disease in the
community. It declines sharply when the standard of living is improved,
but even in the most affluent countries, there are areas where the disease
still exists (e) HIGH-RISK GROUPS : The school-age children between 5
and 15 years; slum dwellers; and those living in a closed community (e.g.,
barracks).
Table 1 summarizes the effects of environmental factors on RF and
RHD.
TABLE 1
Direct and indirect results of enviromental and health-system determinants on rheumatic
fever and rheumatic heart disease
Determinants
Socioeconomic and
environmental factors :
(poverty, undernutrition,
overcrowding, poor housing).
Health-system related factors :
-inadequate expertise
of health-care providers;
Effects
Rapid spread of group A
streptococcal strains.
Difficulties in accessing health
care.
Source : (3)
Clinical features
(a) FEVER : Fever is present at the onset of acute illness and may be
accompanied by profuse sweating. It may last for about 12 weeks or
longer and has a tendency to recur, (b) POLYARTHRITIS: This occurs in
90 per cent of cases. Large joints like ankles, knees, elbows and wrists are
involved; uncommonly smaller joints of hands and feet may be involved.
The pain and swelling come on quickly and also subside spontaneously
within 5-7 days. There is no residual damage to the joint, (c) CARDITIS :
Occurs in 60-70 per cent of cases. It starts early in the course of RF
Moreover RHD may not be preceded by a clinically apparent attack of RF.
All layers of the heart- pericardium, myocardium and the heart valves - are
involved. The involvement of heart is manifested by tachycardia, cardiac
murmurs, cardiac enlargement, pericarditis and heart failure. The most
common ECG finding is the first degree AV block, (d) NODULES :
Nodules below the skin tend to appear 4 weeks after the onset of RF. They
are small, painless and non-tender. They last for a variable period of time
and then disappear leaving no residual damage. (e) BRAIN
INVOLVEMENT: This manifests as abnormal jerky purposeless
movements of the arms, legs and the body. It gradually disappears leaving
no residual damage, (f) SKIN : Various types of skin rash are known to
occur. It is thus obvious that except carditis all other manifestations of RF
do not cause permanent damage.
Diagnosis
The 2002-2003 WHO criteria for the diagnosis of RF and RHD are
based on revised Jones criteria (Table 2) and facilitate the diagnosis of:
a.
b.
c.
d.
e.
f.
a primary episode of RF
recurrent attacks of RF in patients without RHD
recurrent attacks of RF in patients with RHD
rheumatic chorea
insidious onset rheumatic carditis
chronic RHD.
Criteria
a
Recurrent attack of RF in a
patient without established
rheumatic heart disease.15
Recurrent attack of RF in a
patient with established
rheumatic heart disease.
Rheumatic chorea.
Insidious onset rheumatic
carditis.b
Chronic valve lesions of RHD
(patients presenting for the
first time with pure mitral
stenosis or mixed mitral valve
disease and/or aortic valve
disease).d
*
Major manifestations
- carditis
-polyarthritis
-chorea
-erythema marginatum
-subcutaneous nodules
** Minor manifestations
- clinical; fever, polyarthralgia
- laboratory; elevated acute phase
reactants (erythrocyte
sedimentation rate or leukocyte
count)
*** Supporting evidence of
- electrocardiogram; prolonged
a preceding streptococcal
P-R interval
infection within the
- elevated or rising
last 45 days
antistreptolysin-O or other
streptococcal antibody, or
-a positive throat culture, or
-rapid antigen test for group A
streptococci, or
-recent scarlet fever.
a Patients may present with polyarthritis (or with only polyarthralgia or
monoarthritis) and with several (3 or more) other minor
manifestaions, together with evidence of recent group A
streptococcal infection. Some of these cases may later turnout to be
rheumatic fever. It is prudent to consider them as cases of "probable
rheumatic fever" (once other diagnoses are excluded) and advise
regular secondary prophylaxis. Such patients require close follow-up
and regular examination of the heart. This cautious approach is
particularly suitable for patients in vulnerable age groups in high
incidence settings.
b Infective endocarditis should be excluded.
c Some patients with recurrent attacks may not fulfil these criteria.
d Congenital heart disease should be excluded.
Source : (3)
CANCER
Cancer may be regarded as a group of diseases characterised by
an (i) abnormal growth of cells (ii) ability to invade adjacent
tissues and even distant organs, and (iii) the eventual death of the
affected patient if the tumour has progressed beyond that stage
when it can be successfully removed. Cancer can occur at any site
or tissue of the body and may involve any type of cells.
The major categories of cancer are : (a) Caremomas, which
arise from epithelial cells lining the internal surfaces of the various
organs (e.g. mouth, oesophagus, intestines, uterus) and from the
skin epithelium; (b) Sarcomas, which arise from mesodermal cells
constituting the various connective tissues (e.g. fibrous tissue, fat
and bone); and (c) Lymphomas, myeloma and leukaemias arising
from the cells of bone marrow and immune systems.
The term "primary tumour" is used to denote cancer in the
organ of origin, while "secondary tumour" denotes cancer that has
spread to regional lymph nodes and distant organs. When cancer
cells multiply and reach a critical size, the cancer is clinically
evident as a lump or ulcer localized to the organ of origin in early
stages. As the disease advances, symptoms and signs of invasion
and distant metastases becomes clinically evident (1).
Problem statement
WORLD
Cancer afflicts all communities worldwide, approximately 10
million people are diagnosed with cancer and more than 6 million
die of the disease every year. About 22.4 million persons were
living with cancer in the year 2000 (2). This represents an increase
of around 19 per cent in incidence and 18 per cent in mortality
since 1990. The incidence and mortality world wide are shown in
Table 1.
TABLE 1
Global burden of cancer incidence and mortality, 2000
(in thousands)
Site
Lung
Breast
Colorectum
Stomach
Liver
Prostate
Cervix uteri
Oesophagus
Bladder
Non-Hodgkin
lymphoma
Oral cavity
Leukaemia
Pancreas
Ovary
Kidney
Incidence
Male
Female
901
498
558
398
542
278
259
166
337
1050
445
317
165
470
133
76
120
169
144
115
97
112
100
192
70
118
Mortality
Male
810
254
405
383
204
226
99
93
80
109
111
56
Female
292
372
237
241
164
233
110
33
67
47
85
101
114
34
Source : (3)
CANCER 303
with poor prognosis. On the other hand, appropriate intervention is
often effective in avoiding fatal outcome following diagnosis of
breast cancer. Hence this particular cancer, which rank second in
terms of incidence (Table 1), is not among the top three causes of
death from cancer, which are respectively cancers of the lung (17.8
per cent of all deaths), stomach (10.4 per cent) and liver (8.8 per
cent).
The most conspicuous feature of the distribution of cancers
between the sexes is the male predominance of lung cancer.
Stomach, oesophageal and bladder cancer are also much more
common in males (Table 1). For the most part, differences in
distribution between the sexes are attributable to differences in
exposure to causative agents rather than to variation in the
susceptibility. For other tumour types, including cancers of
pancreas and colorectum, there is little difference in the sex
distribution. Generally speaking, the relationship of incidence to
mortality is not affected by sex. Thus for example, the prognosis
following diagnosis of liver or pancreatic cancer is dismal for both
males and females. Many other tumour types are more responsive
to therapy, so that cancers of breast, prostate and uterine cervix are
the cause of death in only a minority of patients diagnosed (3).
The burden of cancer is distributed unequally between
developed and developing countries, with particular cancer types
exhibiting different patterns of distribution.
The total cancer burden is highest in effluent societies, mainly
due to a high incidence of tumour associated with smoking and
western lifestyle, i.e., cancer of the lung, colorectum, breast and
prostate. In developing countries, up to 25 per cent of tumours are
associated with chronic infections, e.g. hepatitis B (liver cancer),
human papillomaviruses (cervical cancer) and Helicobacter pylori
(stomach cancer). In some western countries, cancer mortality rates
have recently started to decline, due to reduction in smoking
prevalence, improved early detection and advances in cancer
therapy (3).
TABLE 2
Leading cancers in the 6 Population Based Cancer Registries 1997 - Males
Rank
1.
2.
3.
4.
5.
Bangalore
Barshi
Bhopal
Chennai
Delhi
Mumbai
Stomach
(8.2)
Esophagus
(6.5)
Trachea, Bronchus
and Lung (6.2)
Hypo pharynx
(5.3)
Prostate
(4.0)
Hypo pharynx
(4.4)
Trachea, Bronchus
and Lung (13.7)
Stomach
(12.5)
Trachea, Bronchus
and Lung (13.5)
Trachea, Bronchus
and Lung (10.6)
Esophagus
(4.2)
Liver
(3.6)
Myeloid Leukemia
(2.6)
Penis
(2.4)
Esophagus
(8.8)
Tongue
(8.5)
Other and unspec.
parts of mouth (7.5)
Hypopharynx
(6.5)
Trachea, Bronchus
and Lung (10.8)
Esophagus
(8.8)
Prostate
(6.0)
Tongue
(5.7)
Larynx
(9.6)
Prostate
(7.9)
Uri. Bladder
(6.1)
Tongue
(5.5)
Esophagus
(7.2)
Prostate
(6.8)
Larynx
(6.1)
Tongue
(5.4)
Figures in the parentheses are the Age Adjusted incidence Rates per 100,000
RPC
Rank
Bangalore
Barshi
Bhopal
Chennai
1.
Ut. Cervix
(21.6)
Ut. Cervix
(22.0)
Ut. Cervix
(20.7)
Ut. Cervix
(29.8)
Breast
(20.5)
Esophagus
(6.6)
Stomach
(4.9)
Other and unspec.
parts of mouth (4.5)
Breast
(8.9)
Esophagus
(2.6)
Ovary
(2.3)
Gum
(1.5)
Breast
(19.3)
Esophagus
(5.3)
Ovary
(4.9)
Other and unspec.
parts of mouth (4.5)
Breast
(26.0)
Stomach
(5.8)
Esophagus
(5.4)
Ovary
(4.8)
2.
3.
4.
5.
Figures in the parentheses are the age adjusted incidence rates per 100,000.
Source : (6)
1997 - FP
Delhi
Breast
(29.8)
Mumbai
Breast
(28.0)
Ut. Cervix
(24.1)
Ovary
(10.0)
Gall bladder
(9.8)
Lymphoma NOS
(3.5)
Ut. Cervix
(17.0)
Ovary
(8.2)
Esophagus
(6.3)
Trachea, Bronchus
and Lung (4.6)
TABLE 3
Age-standardized cancer incidence : selected sites, selected registries, per 100,000, by sex
Registry
China (Shanghai)
Colombia (Cali)
England & Wales
India (Mumbai)
Japan (Miyagi)
Senegal (Dakar)
Slovakia
USA, SEER (whites)
Oral M
F
2.2
4.9
2.7
16.4
2.1
2.4
6.8
7.8
Stomach M
1.8
F
58.3
3.1
1.0
8.8
0.9
1.6
1.0
4.1
48.4
18.5
8.9
79.6
3.7
31.7
10.0
Lung
M
Liver M
Cervix F
24.6
F
34.4
11.6
54.7
18.5
8.5
25.5
7.8
6.0
36.0
2.0
14.5
4.3
2.8
1.6
4.9
11.2
25.6
5.1
2.3
1.4
0.8
2.5
4.0
9.0
2.8
1.0
25.1
72.0
15.7
29.6
1.1
70.0
72.6
9.7
19.0
3.5
8.7
0.1
6.8
27.2
48.0
11.7
20.6
10.0
17.2
15.0
8.9
CANCER 305
causally related to hepatocellular carcinoma. The relative risk of
Kaposi's sarcoma occurring in patients with HIV infection is so high
that it was the first manifestation of the AIDS epidemic to be
recognized. Non-Hodgkin's lymphoma, a cancer of the lymph nodes
and spleen is a late complication of AIDS. The Epstein-Barr virus
(EBV) is associated with 2 human malignancies, viz. Burkitt's
lymphoma and nasopharyngeal carcinoma. Cytomegalovirus (CMV) is
a suspected oncogenic agent and classical Kaposi's sarcoma is
associated with a higher prevalence of antibodies to CMV. Human
papilloma virus (HPV) is a chief suspect in cancer cervix. Hodgkin's
disease is also believed to be of viral origin. The human T-cell
leukaemia virus is associated with adult T-cell leukaemia/ lymphoma in
the United States and southern parts of Japan (12). (f) PARASITES :
Parasitic infections may also increase the risk of cancer, as for example,
schistosomiasis in Middle jJoEast producing carcinoma of the bladder./
(g) CUSTOMS, pZUABITS AND LIFE-STYLES : To the above" causes
must be a'rtadded customs, habits and lifestyles of people which may
be ^associated with an increased risk for certain cancers. The familiar
examples are the demonstrated association between smokino and lung
cancer, tobacco and betel chewing and oral cancer Jetc (13). (h)
OTHERS : There are numerous other environmental factors such as
sunlight, radiation, air and water pollution, medications (e.g.,
oestrogen) and pesticides which are related to cancer.
2. GENETIC FACTORS :
Genetic influences have long been suspected. For example,
retinoblastoma occurs in children of the same parent. Mongols are
more likely to develop cancer (leukaemia) than normal children.
However, genetic factors are less conspicuous and more difficult to
identify. There is probably a complex interrelationship between
hereditary susceptibility and environmental carcinogenic stimuli in
the causation of a number of cancers.
Cancer control
Cancer control consists of a series of measures based on present
medical knowledge in the fields of prevention, detection,
diagnosis, treatment, after care and rehabilitation, aimed at
reducing significantly the number of new cases, increasing the
number of cures and reducing the invalidism due to cancer (14).
The basic approach to the control of cancer is through primary
and secondary prevention. It is estimated that at least one-third of
all cancers are preventable (15).
1. PRIMARY PREVENTION :
Cancer prevention until recently was mainly concerned with the
early diagnosis of the disease (secondary*prevention), preferably
at a precancerous stage. Advancing knowledge has increased our
understanding of causative factors of some cancers and it is now
possible to control these factors in the general population as well
as in particular occupational groups. They include the following :
(a) CONTROL OF TOBACCO AND ALCOHOL CONSUMPTION :
Primary prevention offers the greatest hope for reducing the number of
tobacco-induced and alcohol related cancer deaths. It has been estimated
that control of tobacco smoking alone would reduce the total burden of
cancer by over a million cancers each year (16). Some countries (e.g.,
Norway) have developed ambitious programmes to eradicate tobacco
smoking by the year 2000. (b) PERSONAL HYGIENE: Improvements in
personal hygiene may lead to declines in the incidence of certain types
of cancer, e.g., cancer cervix. (c) RADIATION: Special efforts should be
made to reduce the 20
amount of radiation (including medical
radiation) received by
CANCER 307
exposed to radiation. Unfortunately, it is not a sensitive tool.
Mammography is most sensitive and specific in detecting small
tumours that are sometimes missed on palpation. The use of
mammography has three potential drawbacks: (i) exposure to
radiation. This may amount to a dose of 500 milliroentgen
compared to a 30-40 milliroentgen dose received in chest X-ray.
Therefore there has been concern about exposure to radiation from
repeated mammographies and the risk of breast cancer developing
as a result (ii) mammography requires technical equipment of a
high standard and radiologists with very considerable experience these two factors limit its more widespread use for mass screening
purposes, and (iii) biopsy from a suspicious lesion may end up in
a false-positive in as many as 5-10 cases for each case of cancer
detected (22).
Although recent evidence points to the superiority of
mammography over clinical examination in terms of sensitivity
and specificity (27), medical opinion is against routine
mammography on the very young. Women under 35 years of age
should not have X-rays unless they are symptomatic or a family
history of early onset of breast cancer (28).
3. Screening for lung cancer
At present there are only two techniques for screening for lung
cancer, viz. chest radiograph and sputum cytology. Mass
radiography has been suggested for early diagnosis at six monthly
intervals, but the evidence in support of this is not convincing. So
it is not recommended. It is doubtful whether the disease satisfies
the criteria of suitability for screening (see chapter 4).
EPIDEMIOLOGY OF SELECTED CANCERS
1. Oral cancer
Oral cancer is one of the ten most common cancers in the
world (29). Its high frequency in Central and South East Asian
countries (e.g., India, Bangladesh, Sri Lanka, Thailand, Indonesia,
Pakistan) has been well documented. Each year, about 5,75,000
new cases and 3,20,000 deaths occur worldwide (1). Table 3
shows the incidence of oral cancer in selected countries.
PROBLEM IN INDIA :
( C>ral cancer is a major problem inlndia and accounts for 50
to 70 per cent of all cancers diagnosedJ30, 31) as compared to
2 to 3 per cent in UK and USA (32).
d^O
EPIDEMIOLOGICAL FEATURES :
(a)Tobacco : Approximately 90 per cent of oral cancers in
South East Asia are linked to tobacco chewing and tobacco
smoking. During 1966-1977, a large epidemiological survey
was carried out in different parts of the country. In this 10-year
follow-up study of 30,000 individuals in the three districts of
Ernakulam (Kerala), Srikakulam (Andhra) and Bhavnagar
(Gujarat), the results indicated that (i) oral cancer and
precancerous lesions occurred almost solely among those who
smoked or chewed tobacco, and (ii) oral cancer was almost
always preceded by some type of precancerous lesion (33, 34).
The case about tobacco is further strengthened by the findings
that the cancer almost always occurred on the side of the mouth
where the tobacco quid was kept (29) and the risk was 36 times
higher than for non-chewers if the quid was kept in the mouth
during sleep (35J.
(b)Alcohol : Data indicate that oral cancer can also be caused
by high concentrations of alcohol, and that alcohol appears to
have a synergistic effect in tobacco users (29).
(c)Pre -cancerous stage : The natural history of oral cancer
shows that often a precancerous stage precedes the
development of cancer. The precancerous lesions (leukoplakia,
erythroplakia) can be detected for up to 15 years prior to their
<->
cancer >
in situ
Invasive
cancer
CANCER 309
oestrogen as well as progesterone are important factors in
increasing breast cancer risk (43). In short, hormones appear to
hold the key to the understanding of breast cancer.
(f) PRIOR BREAST BIOPSY : Prior breast biopsy for benign
breast disease is associated with an increased risk of breast
cancer.
(g) DIET : Current aetiological hypotheses suggest that
cancer of the breast is linked with a high fat diet and obesity. It
is not known how dietary fat influences breast cancer risk at a
cellular level (43).
(h) SOCIO-ECONOMIC STATUS : Breast cancer is common
in higher socio-economic groups. This is explained by the risk
factor of higher age at first birth.
(i) OTHERS : (i) Radiation : An increased incidence of breast
cancer has been observed in women exposed to radiation. (M)
Oral contraceptives : Oral contraceptive appears to have little
overall effect on breast cancer, although prolonged use of oral pills
before the first pregnancy or before the age of 25 may increase the
risk in younger women (50).
PREVENTION
a. PRIMARY PREVENTION:
Current knowledge of the aetiology of breast cancer (44) offers
little prospect of primary prevention. However, the aim should be
towards elimination of risk factors discussed above and promotion
of cancer education. The average age at menarche can be increased
through a reduction in childhood obesity, and an increase in
strenuous physical activity; and the frequency of ovulation (after
menarche) decreased by an increase in strenuous physical activity
(51). There is also good reason for reducing fat intake in the diet.
b. SECONDARY PREVENTION:
Breast screening leads to early diagnosis of breast cancer,
which in turn influences treatment and, hopefully, mortality. An
important component of secondary prevention is follow-up, i.e., to
detect recurrence as early as possible; to detect cancer in the
opposite breast at an early stage; and to generate research data that
might be useful (47).
No major improvement in survival rates has yet been shown by
current treatment modalities. Some cases progress rapidly even if
diagnosed at an apparently early stage, others surviving for 20
years even after metastatic spread. However, in general, the
removal of the tumour early is more likely to be curative than
removal at a later stage (25).
4. Lung cancer
MAGNITUDE OF THE PROBLEM :
Lung cancer has been known in industrial workers from the late
19th century. It came into prominence as a public health problem
in the Western world in 1930s - at first in men, and later (in 1960s)
among women (52) and has followed the increasing adoption of
cigarette smoking first by men and later by women. According to
WHO reports, between 1960 and 1980, the death rate due to lung
cancer increased by 76 per cent in men and by 135 per cent in
women (53, 36). At present lung cancer (including cancer of the
trachea and bronchus) is the most common cancer in the world,
with 51% of cases occurring in developed countries, and 75%
occurring in men. Globally, 85% of cases in men and 46% in
women are due to smoking. In developed countries the proportions
are 91% for men and 62% for women, and in developing countries
76% for men and 24% for women (1). If present trends continue
lung cancer is likely to be the most common fatal cancer in
Western women in 10 years or so outstripping even breast cancer
(52).
In countries where cigarette smoking has only recently begun to
be widely adopted, lung cancer deaths still remain
low, but it may be expected that they will rise soon. In others, such
as Poland, where the use of cigarettes began earlier, the rise is
already occurring. The total burden of lung cancer in any country
is directly related to the amount and duration of cigarette smoking
(54).
It is not easy to assess the problem of lung cancer in developing
countries because of lack of accurate statistics. In India, a third of
all the men are addicted to tobacco smoking before reaching the
age of 20 years (8). Lung cancer accounts for 6.8 per cent of all
malignancies in India. If the "smoking epidemic" is not controlled,
an epidemic of lung cancer can be predicted in many developing
countries.
EPIDEMIOLOGICAL FEATURES:
a. AGE AND SEX :
About a third of all lung cancer deaths occur below the age of
65. In many industrialized countries, the incidence of lung cancer
is at present increasing more in females than in males (55).
b. RISK FACTORS:
(i) Smoking : Tobacco smoking was first suggested as a cause
of lung cancer in the 1920s. Subsequent studies proved the causal
relationship between cigarette smoking and lung cancer. Two
studies in India showed that the lung cancer risk for cigarette
smokers is 8.6 times the risk for non-smokers (56,57). The risk is
strongly related to the number of cigarettes smoked, the age of
starting to smoke and smoking habits, such as inhalation and the
number of puffs and the nicotine, the tar content and the length of
cigarettes. Those who are highly exposed to "passive smoking"
(somebody else's smoke) are at an increased risk of develoDing
lung cancer. It has been calculated that in countries where smoking
has been a widespread habit, it is responsible for 90 per cent of
lung cancer deaths (58). The strongest evidence that cigarette
smoking is responsible for lung cancer is the incidence reduction
that occurs after cessation of smoking. This has been convincingly
demonstrated in a 20-year prospective study on male British
doctors (59).
The most noxious components of tobacco smoke are tar, carbon
monoxide and nicotine. The carcinogenic role of tar is well
established. Nicotine and carbon monoxide, particularly, contribute
to increased risk of cardiovascular diseases through enhancement
of blood coagulation in the vessels, interference with myocardial
oxygen deHvery, and reduction of the threshold for ventricular
fibril! ?>ion (8).
A study in India has shown that there is no difference between
the tar and nicotine delivery of the filter and non -filter cigarettes
smoked in India, so that a filter gives no protection to Indian
smokers. The "king-size" filter cigarettes deliver more tar and
nicotine than ordinary cigarettes. Bidi smoking appears to carry a
higher lung cancer risk than cigarette smoking owing to the higher
concentration of carcinogenic hydrocarbons in the smoke (8).
(ii) Other factors : Besides cigarette smoking, there are other
factors which are implicated in the aetiology of lung cancer. These
include air pollution, radioactivity, and occupational exposure to
asbestos, arsenic and its compounds, chromates, particles
containing polycyclic aromatic hydrocarbons and certain nickelbearing dusts. A number of studies have shown an interaction
between smoking and asbestos exposure.
PREVENTION
1. Primary prevention :
In lung cancer control, primary prevention is of greatest
importance. The most promising approach is to control the
"smoking epidemic", because 80 to 90 per cent of all cases of
requires
at local,
smoking
2. SECONDARY PREVENTION:
This rests on early detection of cases and their treatment. At
present, there are only two procedures capable of detecting
presymptomatic, early-stage lung cancer. These are the chest X-ray
and sputum cytology. But screening for early-stage lung cancer is
less attractive, more expensive and appears to have less potential
for reducing mortality than primary prevention. Therefore, mass
screening for lung cancer is not recommended as a routine public
health policy (55).
Efforts to find effective treatment for lung cancer have met with
only limited success. For untreated patients, the median survival is
2 to 3 months, compared to 10 -14 months for patients receiving
combined chemotherapy. In view of these limitations,
Blackwell, Oxford
24.Pettersson, F. et al (1985). Int.J.Epi., 14 (4) 521
25.WHO (1984). Bull WHO, 62 (6) 861-869
26.Cole, F and H. Austin (1981). Am.J.Pub.Health, 71 : 572-574
27.Editorial (1985). Lancet, 1 : 851
28.Tucker, A.K. (1985). Practitioner, 229-217
29.WHO (1984). Bull WHO, 62 (6) 817-830
30.Jayant, K. et al (1977). Br.J.of Cancer, 35: 232
31.Jayant, K. (1977). Ind.J.of Cancer, 14 : 293
32.Warnakulasuriya, K.A.A.S. et al (1984). Bull WHO, 62 (2) 243-250
33.Mehta, F.S. et al (1982), Bull WHO, 60 (3) 441 - 446.
34.Gupta, P.C. et al (1980), Community Dentistry and Oral
Epidemiology, 8 : 287 - 333
35.Wahi, P.N. (1968), Bull WHO, 38 : 495
36.WHO (1985). Wkly Epi,Rec, 60 (17). 125-129
37.Reddy, C.R.R.M. et al (1976). Ind.J.Cancer, 13 : 161
38.Zaninetti, R et al (1986). Int.J.Epi. 15 (4) 477
39.Brinton, L.A. et al (1986). Int.J.Cancer, 38 : 339
40.The WHO Collaborative Study of Neoplasis and Steroid
Contraceptives (1985). Brit.Med.J., 290 : 961-965
41.Parkin, D.M. et al (1984). Bull WHO, 62 (2) 163-182
42.Logan, W.P.D. (1975). W.H. Statis.Rep., : 232-251
43.Pike, M.C. and R.K. Ross (1984). Br.Med.Bull, 40 (4) 351 -354
44.Miller, A.B. and Bulbrook, R.D. (1980). N.Eng.J.Med., 303 : 1246-1248
45.Clemmesen, J. (1979). In: Measurement of Levels of Health, WHO
Reg.Publ.EURO Ser.No.7, p. 199
46.Hughes L.E. and Courtney, S.R (1985). Brit.Med.J. 290 : 1229 (editorial)
47.Hislop, T.G. et al (1986). Int.J.Epi., 15 (4) 469
48.MacMahon, B. et al (1970). Bull WHO, 43 : 209-217
49.Marks, M. (1985). Practitioner, 229 : 225
50.Pike, M.C. et al (1983). Lancet, 2 : 926-929
51.Frisch, R.E. et al (1981). JAMA, 246 : 1559-1563
52.Muir, C.S. (1981). World Health, Sept-Oct, pp 8-11
53.WHO (1985). WHO Chronicle, 39 (3) 109-111
54.WHO (1975). Techn.Rep.Ser., No. 568
55.WHO (1982). Bull WHO, 60 (6) 809-819
56.Notani, P.N. et al (1977). Int.J.Cancer, 14 : 115
57.Jussawalla, D.J. and Jain, D.K. (1979). Brit. J .Cancer 40 : 437
58.WHO (1979). Techn.Rep.Ser., No. 636
59.Doll, R. and Peto, R. (1976). Brit.Med.J., 2 : 1525
DIABETES MELLITUS
action of insulin, a hormone that controls glucose, fat and amino acid
metabolism. Characteristically, diabetes is a long-term disease with
variable clinical manifestations and progression. Chronic hyperglycemia,
from whatever cause, leads to a number of complications - cardiovascular,
renal, neurological, ocular and others such as intercurrent infections.
Classification
The classification adopted by WHO (2) is given in Table 1. TABLE 1
Clinical classification of diabetes mellitus
1. Diabetes mellitus (DM)
i) Insulin-dependent diabetes mellitus (IDDM, Type 1) ii) Noninsulin dependent diabetes mellitus (NIDDM, Type 2) iii)
Malnutrition-related diabetes mellitus (MRDM) iv) Other types
(secondary to pancreatic, hormonal, drug-induced, genetic and other
abnormalities)
1.Impaired glucose tolerance (IGT)
2.Gestational diabetes mellitus (GDM)
Source (2)
IDDM (Insulin-dependent diabetes mellitus) is the most severe form of
the disease. Its onset is typically abrupt and is usually seen in individuals
less than 30 years of age. It is lethal unless promptly diagnosed and
treated. This form of diabetes is immune-mediated in over 90 per cent of
cases and idiopathic in less than 10 per cent cases. The rate of destruction
of pancreatic (3 cell is quite variable. Rapid in some individuals and slow
in others. Type 1 diabetes is usually associated with ketosis in its untreated
state. It occurs mostly in children, the incidence is highest among 10-14
year old group, but occasionally occur in adults. It is catabolic disorder in
which circulating insuline is virtually absent, plasma glucagon is elevated,
and the pancreatic (3 cells fail to respond to all insulinogenic stimuli.
Exogenous insuline is therefore required to reverse the catabolic state,
prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose
(3).
NIDDM is much more common than IDDM. It is often discovered by
chance. It is typically gradual in onset and occurs mainly in the middleaged and elderly, frequently mild, slow to ketosis and is compatible with
long survival if given adequate treatment. Its clinical picture is usually
complicated by the presence of other disease processes.
Impaired glucose tolerance (IGT) describes a state intermediate- "at
risk" group - between diabetes mellitus and normality. It can only be
defined by the oral glucose tolerance test (see Table 2).
Insuline resistance syndrome (Syndrome X)
TABLE 2
Diagnostic values for the oral glucose tolerance test
Glucose (mg/dt)
Whole blood
Diabetes mellitus
(a) Fasting value
(b) 2 hrs after glucose load
Impaired glucose tolerance
(a) Fasting value
(b) 2 hrs after glucose load
Source (2)
Plasma
Venous
Capillary
>120
>180
>120
>200
< 120
120-180
< 120
140-200
Venous
Capillary
>140
>200
>140
>200
< 140
140-200
< 140
160-220
TABLE 3
Estimated prevalence of diabetes mellitus, urban/rural and
male/female ratio in adult (age 20 + ) population of SEAR
countries in 1995
Country
Prevalence
%
Number
(000)
Bangladesh
Bhutan
DPR Korea
India
Indonesia
Maldives
Myanmar
Nepal
Sri Lanka
Thailand
2.2
2.1
2.9
3.8
4.1
2.5
2.4
2.2
2.5
2.4
1285
17
443
19397
4546
2.7
588
225
275
863
Ratio
Urban/
Rural
Male/
Female
0.50
0.11
3.30
1.38
0.84
0.93
0.72
0.31
0.61
0.68
1.42
1.21
1.19
1.35
1.05
1.45
1.17
1.25
1.15
1.19
Source : (5, 6)
A bulk of evidence from studies on migrants indicates that the
ethnic, presumably genetic, vulnerability of Asians manifests into
diabetes when subjected to unfavourable lifestyles. Populationbased surveys completed recently in Bangladesh, India and
Indonesia have shown considerable increase in the prevalence rate
of the disease in both urban and rural dwellers when compared to
results obtained earlier.
Natural history
1. AGENT:
The underlying cause of diabetes is insulin deficiency which is
absolute in IDDM and partial in NIDDM. This may be due to a
wide variety of mechanisms: (a) pancreatic disorders
-inflammatory, neoplastic and other disorders such as cystic
fibrosis, (b) defects in the formation of insulin, e.g., synthesis of an
abnormal, biologically less active insulin molecule; (c) destruction
of beta cells, e.g., viral infections and chemical agents, (d)
decreased insulin sensitivity, due to decreased numbers of
adipocyte and monocyte insulin receptors. (e) genetic defects, e.g.,
mutation of insulin gene; and (f) autoimmunity. Evidence is
accumulating that the insulin response to glucose is genetically
controlled. The overall effect of these mechanisms is reduced
utilization of glucose which leads to hyperglycemia accompanied
by glycosuria.
2. HOST FACTORS :
(a) AGE : Although diabetes may occur at any age, surveys
indicate that prevalence rises steeply with age. NIDDM usually
comes to light in the middle years of life and thereafter begins to
rise in frequency. Malnutrition related diabetes affects large
number of young people. The prognosis is worse in younger
diabetics who tend to develop complications earlier than older
diabetics, (b) SEX : In some countries (e.g., UK) the overall malefemale ratio is about equal (8). In south-east Asia, an excess of
male diabetics has been observed (1), but this is open to question,
(c) GENETIC FACTORS: The genetic nature of diabetes is
undisputed. Twin studies showed that in identical twins who
developed NIDDM, concordance was approximately 90 per cent
(2), thus demonstrating a strong genetic component. In IDDM
(type 1 diabetes), the concordance was only about 50 per cent
indicating that IDDM is not totally a genetic entity, (d) GENETIC
MARKERS : IDDM is associated with HLA-B8 and B15, and more
powerfully with HLA-DR3 and DR4. The highest risk of IDDM is
carried by individuals with both DR3 and DR4. On the other hand
NIDDM is not HLA-associated (2). (e) IMMUNE MECHANISMS
: There is some evidence of both cell-mediated and of humoral
activity against islet cells. Some people appear to have defective
immunological mechanisms, and under the influence of some
environmental "trigger", attack their own insulin producing cells,
(f) OBESITY : Obesity particularly central adiposity has long been
accepted as a risk factor for NIDDM and the risk is related to both
the duration and degree of obesity. The association has been
repeatedly demonstrated in longitudinal studies in different
populations, with a striking gradient of risk apparent with
increasing level of BMI, adult weight gain, waist circumference or
waist to hip ratio. Indeed waist circumference or waist to hip ratio
(reflecting abdominal or visceral adiposity) are more powerful
determinant of subsequent risk of type 2 diabetes than BMI (4).
Central obesity is also an important determinant of insuline
resistance, the underlying abnormality in most cases of type 2
diabetes. In some instances obesity reduces the number of insuline
receptors on target cells. Voluntary weight loss improves insuline
sensitivity and in several randomized controlled trials has been
shown to reduce the risk of progression from impaired glucose
tolerence to type 2 diabetes (9, 10). However, many obese subjects
are not diabetic. Thus obesity by itself is inadequate to account for
all, or even most, cases of NIDDM; physical inactivity and/or
deficiencies of specific nutrients may also be involved (2). Obesity
appears to play no role in IDDM pathogenesis (11). (g)
MATERNAL DIABETES : Offsprings of diabetic pregnancies
including gastational diabetes are often large and heavy at birth,
tend to develop obesity in childhood and are at high risk of
developing type 2 diabetes at an early age. Those born to
TABLE 4
Summary of strength of evidence on lifestyle factors and risk of
developing type 2 diabetes
Evidence
Decreased
risk
Insufficient
NSP1
r|-3 fatty acids
Low glycaemic
index foods Exclusive
breastfeeding1.
Vitamin E
Chromium
Magnesium
Moderate alcohol
Increased
risk
Overweight and
obesity
Abdominal
obesity
Physical inactivity
Maternal diabetes0
Saturated fats
Intrauterine growth
retardation
Total fat intake
Trans fatty acids
Excess alcohol
*7\
Weight (kg)
_J
Height2(m)
(2) Ponderal index
Height (cm)
Cube root of body weight (kg)
(3) Broca index
= Height (cm) minus 100
For example, if a person's height is 160 cm,
his ideal weight is (160-100) = 60 kg
(4) Lorentz's formula
Ht (cm) - 150
= Ht (cm) - 100------------------------------------2 (women) or 4 (men)
_________________________________________________OBESITY 319
mortality is brought about mainly by the increased incidence of
hypertension and coronary heart disease. There is also an excess number of
deaths from renal diseases. Obesity lowers life expectancy. More
information is needed about the relationship between different degrees of
obesity and morbidity and mortality.
TABLE 3
Moderately
increased
Slightly increased
NIDDM
CHD
Gallbladder
disease
Dyslipidaemia
Hypertension
Insulin resistance
Osteoarthritis
(knees)
Hyperuricaemia
gout
Breathlessness
Sleep apnoea
References
Livingstone
BLINDNESS
A compilation published by WHO in 1966 (1) lists 65 definitions of
blindness. As might be expected the definitions differed widely. Terms
such as total blindness, economic blindness and social blindness were in
vogue, The 25th World Health Assembly in 1972 noted the complexity of
the problem and considered the need for a generally accepted definition of
blindness and visual impairment for national and international
comparability. Taking into consideration existing definitions, the WHO
proposed a uniform criterion and defined blindness as "visual acuity of
less than 3/60 (Snellen) or its equivalent" (2). The WHO International
Classification of Diseases (1975 revision) described the levels of visual
impairment (see Table 1). In order to facilitate the screening of visual
acuity by non-specialized personnel, in the absence of appropriate vision
charts, the WHO has now added the "inability to count fingers in daylight
at a distance of 3 meters" to indicate less than 3/60 or its equivalent (3).
Categories
of visual
impairment
Low vision
Blindness
TABLE 1
Categories of visual impairment
Visual acuity
Maximum
Minimum
less than
equal to or
better than
1
6/18
6/60
2
6/60
3/60
3/60 (finger
counting at
3 meters)
1/60 (finger
counting at
1 meter)
No light
perception
1/60 (finger
counting at
1 metre)
light perception
4
5
Source : (4)
Table 1 shows differentiation between "low vision"
(categories 1 and 2) and "blindness" (categories 3, 4 and 5). If
TABLE 2
Status of eye health in the SEA Region, by country (2000)
Country
Prevalence of
blindness (%)
No. of
blind
persons
Bangladesh
1.0
1,300,000
Bhutan
0.8
5,600
India
0.7
6,800,000
Indonesia
1.5
2,948,761
Maldives
0.8
1,959
Myanmar
0.9
427,617
Nepal
0.8
325,918
Sri Lanka
Thailand
0.5
0.3
92,920
242,341
Prevalence
of cataract
(%)
CSR*
IOL
rate
(%)**
60
500
30
74
1,019
100
77
3,400
34
53
350
20
64
700
35
64
500
50
72
900
85
70
74
1,337
1,667
100
90
*
Cataract surgical rate : Number of cataract surgery per one million population per year.
**
Intraocular lenses
Source : (6)
\^J
62.6 per cent
19.7 per cent
5.8 per cent
4.7 per cent
0.9 per cent
6.2 per cent
Source : (7)
Epidemiological factors
(a) AGE : About 30 per cent of the blind in India are said to
lose their eyesight before they reach the age of 20 years, and many
under the age of 5 years. Refractive error, trachoma, conjunctivitis
and malnutrition (vitamin A deficiency) are
21
_________________________________________
BLINDNESS 321
important causes of blindness among children and the younger
age groups; cataract, refractive error, glaucoma and diabetes
are causes of blindness in middle age; accidents and injuries
can occur in all age groups, but more importantly in the age
group 20 to 40 years, (b) SEX : A higher prevalence of
blindness is reported in females than in males in India. This
has been attributed to a higher prevalence of trachoma,
conjunctivitis and cataract among females than in males (13).
(c) MALNUTRITION : Malnutrition as a cause of blindness
was hardly recognized a few years ago. It is closely related not
only with low vitamin A intake, but also with infectious
diseases of childhood especially measles and diarrhoea (which
precipitate malnutrition). In many cases protein energy
malnutrition (PEM) is also associated with blindness. Severe
blinding corneal destruction due to vitamin A deficiency (e.g.,
keratomalacia) is largely limited to the first 4-6 years of life
and is especially frequent among those 6 months to 3 years of
life, (d) OCCUPATION : It has long been recognized that
people working in factories, workshops and cottage industries
are prone to eye injuries because of exposure to dust, airborne
particles, flying objects, gases, fumes, radiation (usually
welding flash), electrical flash, etc. Many workers including
doctors are known to have developed premature cataracts
while exposed to x-rays, ultraviolet rays or heat waves, (e)
SOCIAL CLASS : There is a close relationship between the
incidence of blindness and socioeconomic status. Surveys
indicate that blindness is twice more prevalent in the poorer
classes than in the well-to-do (13). (f) SOCIAL FACTORS:
Many people lose their eyesight because of meddlesome
ophthalmology by quacks. The basic social factors are
ignorance, poverty, low standard of personal and community
hygiene and inadequate health care services.
Changing concepts in eye health care
Recent years have witnessed a change from acute
intervention (cure) typical of clinical ophthalmology to
comprehensive eye-health care which includes the following
concepts :
1. Primary; eye care :
One of the most significant developments in the field of
eye health care over the last few years has been the concept of
primary eye care, that is, the inclusion of an eye-care
component in primary health care system. The idea of primary
eye care, as one of the main ingredients of a primary health
care approach to blindness, has rapidly gained acceptance the
world over. It is today recognized as a model for eye care at
the community level. The promotion and protection of eye
health, together with on-the-spot treatment for the commonest
eye diseases, are its cornerstones. The final objective of
primary eye care is to increase the coverage and quality of eye
health care through primary health care approach and thereby
improve the utilization of existing resources.
2. Epidemiological approach :
The epidemiological approach which involves studies at
the population level has been recognized. It focuses, among
other things, on the measurement of the incidence, prevalence
of diseases and their risk factors. The local epidemiological
situation will determine the action needed.
3. Team concept:
In many developing countries, there is only one eye
specialist for more than a million people. Increasingly,
therefore, health care leans on the use of auxiliary health
personnel to fill many gaps. In India this gap is filled by
village health guides, ophthalmic assistants, multi-purpose
workers and voluntary agencies.
of blindness
\L_x
\*y
The concept of avoidable blindness (i.e., preventable or
curable blindness) has gained increasing recognition during recent
years. A great many of the causes of blindness lend themselves to
prevention and/or control - whether by improving nutrition, by
treating cases of infectious diseases, or by controlling the
organisms which cause infection, or by improving safety
conditions - particularly on the roads, at work or in the home (16).
The components for action in national programmes for the
prevention of blindness comprise the following :
1. INITIAL ASSESSMENT
The first step is to assess the magnitude, geographic distribution
and causes of blindness within the country or region by prevalence
surveys. This knowledge is essential for setting priorities and
development of appropriate intervention programmes.
2. METHODS OF INTERVENTION (11)
(a) Primary eye care :
A wide range of eye conditions (e.g., acute conjunctivitis,
ophthalmia neonatorum, trachoma, superficial foreign bodies,
xerophthalmia) can be treated/prevented at the grass-root level by
locally trained primary health workers (e.g., village health guides,
multi-purpose workers) who are the first to make contact with the
community. For this purpose, they are provided with essential
drugs such as topical tetracycline, vitamin A capsules, eye
bandages, shields, etc. They are also trained to refer difficult cases
(e.g., corneal ulcer, penetrating foreign bodies, painful eye
conditions and infections which do not respond to treatment) to the
nearest PHC or district hospital. Their activities also involve
promotion of personal hygiene, sanitation, good dietary habits and
safety in general. Currently, there is one village health guide for
1000 population and 2 multipurpose workers for 5000 population
in India.
In short, primary eye care is based firmly in primary health
care which is ".........essential health care........... made universally
accessible to individuals and families in the community through
their full participation and at a cost that the community and
country can afford ...." (Article VI of the Declaration of Alma Ata,
1978).
(b) Secondary care :
Secondary care involves definitive management of common
blinding conditions such as cataract, trichiasis, entropion, ocular
trauma, glaucoma, etc. This care is provided in PHCs and district
hospitals where eye departments or eye clinics are established. The
secondary care may involve the use of mobile eye clinics. For
instance, cataract accounts for over 80 per cent of blindness in
India. The eye camp approach to make cataract surgery available
has been highly successful, and has received
______________________________________________BLINDNESS 323
intake of foods rich in vitamin A, lack of personal hygiene, etc. Health
education is an important long-term measure in order to create community
awareness of the problem; to motivate the community, to accept total eye
health care programmes, and to secure community participation.
4. EVALUATION
Evaluation should be an integral part of intervention programmes to
measure the extent to which ocular diseases and blindness have been
alleviated, assess the manner and degree to which programme activities
have been carried out, and determine the nature of other changes that may
have been produced (19).
Cause
deaths
Female
causes
Total No.
% of all
% of all causes of of
deaths due to injury (000)
of deaths
Male
TABLE 2
Prioritization of injury problem in the member countries
of the WHO South-East Asia Region
Country
" _ . _ _
-2S<3
g | R
!S-a Injury
"S |
Road traffic
1 1
113
1111 Burns
_'
_
3
4
3
3
5
5
Workrelated
2
43
2
2
2
2
4
4
Poisoning
5
2
5
5
2
Drowning
3 3 2
6
3
1
6
7
2
2
Disaster
5 - 1
_______
Violence, suicide 45
4
445
4
43
3 Falls
2
_ _ _
- 6
(1 = highest priority, 7 = lowest priority) Source : (11)
NDIA
Accidents are definitely on an increase in India. Increasing mechanization
in agriculture and industry, induction of semiskilled and unskilled
workers in various operations and rapid ncrease in vehicular traffic have
resulted in an increase in morbidity and mortality due to accidents.
Overcrowding, lack of awareness and poor implementation of essential
Unintentional
3551
6.2
44.64
24.0 Road
traffic
1192
2.1
16.81
6.25 accidents
Poisoning'
350
0.6
4.35
2.41 Falls
392
0.7
4.56
3.01 Fires
312
0.5
2.32
3.71 Drowning
382
0.7
5.06
2.32 Other injuries
923
1.6
11.51
6.34
Intentional
1604
2.8
22.38
8.92 Self
inflicted .
873
1.5
10.56
6.32 Violence
559
1.0
8.61
2.78 War
172
0.3
2.99
0.32
Total
5155
9.0
67.02
32.99
Source : (8)
Accidents are not the prerogative of developed nations. In developing
countries accidents are shown to be as numerous as in developed countries.
It is increasing rapidly as a cause of death in absolute numbers and in terms
of proportion (9).
Of the 5.1 million deaths from injuries globally, more than one-fourth
are estimated to occur in the South-East Asia Region. Road traffic injuries
alone are ranked as the primary cause of disease among children in the age
group of 5-14 years, and the third leading cause among people between the
age of 15-29 years in 2000. It is an irony that thousands of children saved
from nutritional and infectious diseases were killed or miamed by injuries
(10).
Injuries due to road traffic, occupational accidents, burns, poisoning,
suicides and violence are observed to be major causes of mortality and
morbidity in the Region. Table 2 shows the causes of injuries by
importance in the SEAR countries. Road traffic injuries are the most
common injuries in all the countries of the Region, except in DPR Korea
and Maldives. With 16-18 per cent annual increase in motorization in the
Region, the rate of road traffic injuries is higher than in other parts of the
world. Persons injured in road traffic accidents occupy nearly 10-30 per
cent of beds in hospitals (10).
Cause
1998
A Natural disasters
Un-natural causes
1.
Road accidents
b.
Rail-Road accidents
c.
22762
235647
Traffic accidents
a.
2.
Drowning
3.
Fire
4.
Poisoning
5. Collapse of structure
(house, building etc.)
6.
Falls
1999
27506
244412
17366 B
238517
93996
99541
98038
76732
81036
80118
2799
2836
1282
14465
15669
23041
21457
25898
28400
16638
21996
25467
24262
25734
23395
2412
2386
2233
6201
6613
2917
2303
7.
Firearms
8.
Factory accidents
642
9.
Killed by animals
730
Source : (12)
2000
667
692
7087
2634
625
669
TYPES OF ACCIDENTS
1. Road traffic accidents
In many countries, motor vehicle accidents rank first among all
fatal accidents. During 2002 there were almost 1.19 million deaths
from road accidents in the world. In addition, for every death there
are as many as 50-100 minor injuries and 10-20 serious injuries
requiring long periods of expensive care, nursing and treatment
(10).
In 2002 the global rate of deaths from road traffic injuries was
about 19.0 per 100,000 people. The rate was 27.6 per 100000 for
males and 10.4 per 100000 for females. Adults aged 15-44 years
account for more than 50 per cent of deaths and more than 1.8 lac
children under 15 years of age die in road accidents (13). In
developing countries, a large proportion of vehicles involved in
accidents are two-wheelers. Compared to cars, they are unstable
and provide little protection for their riders in accidents. In these
countries, pedestrians are more frequently involved in road
accidents than others, whereas in developed countries four
wheelers are more frequently involved in the accidents. Fig. 1
shows the difference.
Developing countries are very different from the industrialized
countries with regard to the environment and the mix of vehicles
in the traffic stream. The following are the more important
differences (14):
1.Large numbers of pedestrians and animals share the
roadway with fast-moving and slow-moving (e.g., bullock
carts) vehicles. There is almost no segregation of pedestrians
from wheeled traffic
2.Large numbers of old, poorly maintained vehicles
3.Large numbers of motor cycles, scooters, and mopeds
4.Low driving standards
5.Large numbers of buses, often overloaded
6.Widespread disregard of traffic rules
7.Defective roads, poor street lighting, defective layout of
cross roads and speed breakers
8.Unusual behaviour of men and animals
In South-East Asia Region countries, semi-urban and rural
areas contribute 60-80 per cent of road accident injuries, although
all media attention is focussed on urban road accidents. Recent
estimates shows that road accidents amount
to atleast 1-2 per cent GDP loss to the nations around the world
(11J.
2. Domestic accidents
By "domestic accident" is meant an accident which takes place
in the home or in its immediate surroundings, and, more generally,
all accidents not connected with traffic, vehicles or sport (15). The
most frequent causes of domestic accidents are :
1.drowning
2.burns (by a flame, hot liquid, electricity, crackers or fire
works, chemicals)
3.poisoning (e.g., drugs, insecticides, rat poisons,
kerosene)
4.falls
5.injuries from sharp or pointed instruments
6.bites and other injuries from animals
DROWNING : It is estimated that during the year 2002, about
98 thousand lives were lost due to drowning in SEAR countries
and it was responsible for about 2.74 million DALYs lost (8).
Bangladesh and Maldives have identified drowning as the most
common cause of accidental deaths. India recorded 21996 deaths
due to drowning in the year 2000. A hospital based study from
Thailand reports that 35 per cent of the injury-related deaths among
children were due to drowning (11). Most of the drowning related
deaths take place in ponds, rivers, or the ocean, or during floods
and cyclones. Very few of them are swimming pool related. In
Bangladesh, since water transport is used more frequently because
of the need to cross-waterways in the delta region, there are
frequent reports of boats capsizing with passengers and vehicles on
board.
Victims of drowning have a very slim chance of survival after
immersion. The victim loses consciousness after approximately 2
minutes of immersion, and irreversible brain damage can take
place after 4-6 minutes. Therefore, prevention strategies are more
important.
BURNS : An estimated 184000 persons died of burn injuries in
the countries of SEAR in 2002, with 6.55 million DALYs lost due
to burns (8). India recorded 25467 deaths due to burns during the
year 2000 (12). The fire related mortality in the SEAR accounts for
more than half of the global burden of fire-related burns. About
two-thirds of the global burden of fire-
Rapid industrialization has also resulted in mortality and morbidity of many workers in hazardous industries.
The unique features common to the workplace in this region are that the manual labour content is high and the man-machine interaction is
unsafe. In addition, there is greater emphasis on attempts to change the worker's behaviour, but designs that provide automatic protection are
ignored. Children and people who are challenged physically as well as mentally are at a greater risk of encountering occupational injuries
(11).
4/Railway accidents K ~ ^ b(^
v/ith the increase in number of trains and passengers, the increase in the number of accidents and casualties resulting therefrom is not
unexpected (16). During 2000, about 16638 people died of railway accidents in India (12). The main factor involved in railway accidents is
human failure""!
5. Violence
An estimated 1618000 persons died in 2002 due to violence or intentional injuries (homicide, suicide and war) world-wide, of which
386000 were in SEAR countries (8). The accurate statistics are not available, as not all those injured go to the hospital or state that the injury
is because of violence. Violence behind closed doors are grossly unreported.
Violence is reported to be increasing rapidly. It also follow the same epidemiological pattern as any other disease (host, agent and
environment), i.e. a motivated person who injures; a suitable target; and a suitable environment or the absence of a guardian, all coinciding in
time and space. Often, it may only be possible to initiate steps for prevention after an episode of violence has already taken place.
Some of the risk factors for violent behaviour are (11) :
-Exposure to violence and societal acceptability of violence as a means to solve problems. The image of violence as an acceptable and
effective tool for solving problems, whether across international borders, on the street, or around the home, may spill over into real
behaviour.
-Availability of lethal weapons like fire-arms significantly increases the possibility of both fatal and non-fatal injuries;
Consumption of alcohol and other drugs is linked to almost 2/3 of cases of violence according to several studies.
Violence due to war and political unrest is fairly common in several countries. Organized and unorganized, ethnic and communal violence
are well known in some places.
Suicides have been increasing at an alarming rate in SEAR countries. Incidence rates of 11 per lac population in Bangladesh, 36 per lac
population in India, 8 per lac in Sri Lanka and 22 per lac in Thailand per year have been reported. Nearly 70 per cent of suicides in all
countries have been reported in the age group of 15-34 years with male-female ratio of 1:1.2 to 1:3 from different countries. Poisoning,
hanging, self-immolation and drowning are the most commonly reported methods of suicide (10).
Multiple causation
Accidents are a complex phenomena of multiple causation (Fig. 2). The aetiological factors may be classified into two broad categories human and environmental. Up to 90 per cent of the factors responsible for accidents are attributed to human failure. Many of the
psychological circumstances in which accidents occur are still poorly known (5).
PREVENTION
Accidents don't just happen; they are caused. The causes in a given situation must be identified by epidemiological methods. Since accidents
are multifactorial, they call for an intersectoral approach to both prevention and care of the injured. The various measures comprise the
following :
1. Data collection
There should be a basic reporting system of all accidents. The national data should be supplemented by special surveys and in-depth studies.
These studies will bring out the risk factors, the circumstances and chain of events leading up to the accident. These details are rarely provided
by the basic reporting system. Detailed environmental data relating to the road, vehicle, weather, etc must also be collected. The police
have a statutory duty in many countries to investigate accidents, for legal as well as preventive purposes; the data collecting systems should
recognise this and take police records as their starting point (3). Without adequate data collection, analysis and interpretation there could be no
effective counter-measures, evaluations and strategies for prevention.
2. Safety education
There is a widespread belief that accidents are inevitable; this fatalistic attitude must be curbed. Safety education must begin with school
children. The drivers need to be trained in proper maintenance of vehicles and safe driving. Young people need to be educated regarding risk
factors, traffic rules and safety precautions. They should also be trained in first aid. It has been aptly said that "if accident is a disease, education
is its vaccine".
7. Enforcement of laws
Legislation embodies codified set of rules. These are enforced
by the State to prevent accidents. These include driving tests,
medical fitness to drive, enforcement of speed limits, compulsory
wearing of seat belts and crash helmets, checking of blood alcohol
concentration, road-side breath testing for alcohol, regular
inspection of vehicles, periodic reexamination of drivers over the
age of 55, etc. In addition, there are factory and industrial laws to
ensure safety of the people at work.
8. Rehabilitation services
Rehabilitation consists of a number of elements which each
injured person should benefit from. These are medical
rehabilitation, social rehabilitation, occupational rehabilitation, etc.
The aim of rehabilitation is to prevent, reduce or compensate
disability and thereby handicap.
9. Accident research
The future of accident prevention is in research. Such research
will be concerned with gathering precise information about the
extent, type and other characteristics of accidents, correlating
accident experience with personal attributes and the environments
in which accidents occur, investigating new and better methods of
altering human behaviour; seeking ways to make environments
safer; and evaluating more precisely the efficiency of control
measures. This area is now termed accidentology.
References
1.Hogarth, J. (1978). Glossary of Health Care Terminology, WHO, Copenhagen
2.WHO (1957). Techn. Rep. Ser., No.118
3.WHO (1984). Techn. Rep. Ser., 703
4.WHO (1976). The epidemiology of road traffic injuries, European Sr. No.2,
WHO Copenhagen
5.WHO (1982). The epidemiology of accident traumas and resulting disabilities,
EURO Reports and Studies, 57, WHO, Copenhagen
6.WHO (1980). International classification of impairments, disabilities, and
handicaps, WHO, Geneva
7.WHO (1995). The World Health Report 1995, Report of the Director-General
WHO
8.WHO (2004), The World Health Report 2004, Changing history
9.Amor, A.J. (1979). World Health, June 1979
10.WHO (2002), Health Situation in the South-East Asia Region 1998-2000,
Regional Office for SEAR, New Delhi
11.WHO (2002), Injuries in South-East Asia Region, Priorities for Policy
and'Action, SEA / Injuries / Al
12.Govt, of India, Health Information of India 2000-2001, DGHS, New Delhi.
13.Health Action, Road Safety, A Collective Responsibility, April 2004
14.WHO (1981). Seat belts and other devices to reduce injuries from traffic
accidents, EURO Reports and Studies 40, WHO, Copenhagen
1
7
"Those who would benefit most from a service are least likely to obtain it"
Since India became free, several measures have been
undertaken by the National Government to improve the health of
the people. Prominent among these measures are the NATIONAL
HEALTH PROGRAMMES, which have been launched by the
Central Government for the control/ eradication of communicable
diseases, improvement of environmental sanitation, raising the
standard of nutrition, control of population and improving rural
health. Various international agencies like WHO, UNICEF,
UNFPA, World Bank, as also a number of foreign agencies like
SIDA, DANIDA, NORAD and USAID have been providing
technical and material assistance in the implementation of these
programmes. A brief account of these programmes which are
currently in operation is given below :
VECTOR BORNE DISEASE CONTROL PROGRAMME
Directorate of National Anti Malaria Programme (NAMP) is
the national nodal agency for prevention and control of major
vector borne diseases of public health importance namely malaria,
filaria, Japanese encephalitis, Kala-azar and dengue / dengue
haemorrhagic fever. Till 2002-2003, the centrally sponsored
schemes viz. national anti-malaria programme, national filaria
control programme and kala-azar control programme, had been
operative in the country on cost sharing basis between centre and
states. There was no specific centrally sponsored programme for
JE and dengue/DHF, and the states were managing these diseases
out of their own resources and with limited need based support and
technical guidance from the directorate of NAMP. However, in
pursuance of the concept of convergence, the Government of India
has approved a National Vector Borne Disease Control Programme
(NVBDCD) from the year 2003-2004 by inclusion of JE and
dengue/DHF with other three ongoing programmes (1).
Q\
divided
into
preparatory,
attack,
consolidation
and
maintenance phases.
In the beginning, malaria eradication programme was highly
successful. But very soon setbacks appeared in the form of focal
outbreaks. The resurgence had grown to epidemic proportions.
The annual incidence of malaria cases in India escalated from
50,000 in 1961 to a peak of 6.4 million cases in 1976.
Revised Strategy
Considering the resurgence of malaria as well as the situation
in the neighbouring countries, the Govt, of India in the Ministry of
Health appointed several task forces and Expert Committees on
malaria to review the situation (2). Based on their
recommendations, a/Modified Plan of Operation (MPO) to control
malaria was evolved, and put into operation from April 1977 (3j)
^.. D^|
MODIFIED PLAN OF OPERATION
1. Objectives :
The Modified Plan of Operation under the NMEP came into
force from 1st April 1977 with the following objectives.
-to prevent deaths due to malaria
-to reduce malaria morbidity
-to maintain agricultural and industrial production by
undertaking intensive antimalarial measures in such areas
-to consolidate the gains so far achieved.
Flexibility in the policies according to the epidemiological
situation and local conditions is an essential feature in this
programme.
2. Reclassification of endemic areas
The report of the consultative committee of experts indicated
that in order to stabilise the malaria situation in the country, areas
with Annual Parasite Incidence 2 and above should be taken up
for spray operations. This led to the abolition of the earlier
phasing of the antimalaria units as attack, consolidation and
maintenance phase areas, and reclassification of areas according
to Annual Parasite Incidence.
3. Areas with API more than 2
(a) SPRAYING ^AlUreas with API 2 and above are brought
under regular insecticidal spray with 2 rounds of DDT, unless\i the
vector is refractory. Where the vector is refractory to DDT, J-3
rounds of malathion are recommendedTj\reas refractory both \\ to
DDT and malathion are to be treated with 2 rounds of synthetic
pyrethroids spray at intervals of 6 weeks. DDT, malathion and
pyrethroids dosage applied are 1.0, 2.0 and
_____________
The surveillance worker will visit each house in his area once a
fortnight and enquire :{a) whether there is a fever case in the
house, including guests or visitors in the house, and (b) whether
there was a fever case in the house between his previous visit and
the present visit. If the answer to either of these two questions is
"yes'\ the surveillance worker/MPW collects a blood film (thick and
thin on the same slide) and administers a single dose (600 mg for
an adult and proportionate doses for others) of chloroquine
according to the prescribed NMEP schedule. This is known as
"presumptive treatment". The surveillance worker/MPW makes
necessary entries in the stencil or house card about his visit and
despatches the blood slides at least twice a week to the unit
laboratory (primary health centre) for microscopic examination. He
is required to collect the blood slides from the subcentres and fever
treatment depots and send these to the laboratory. If the blood film
is reported positive for malaria parasite, the surveillance
worker/MPW returns to the patient and administers a course of
radical treatment for malaria, as prescribed.
Passive surveillance
The search for malaria cases by the local health agencies such
as the primary health centres, sub-centres, hospitals, dispensaries
and local medical practitioners is known as "passive surveillance".
Their contribution to case detection is by no means small, because
cases of fever which escape the net of active surveillance workers
are screened by the passive surveillance agencies. The passive
agencies collect blood smears from all fever cases and also from
those with history of recent fever. After the collection of blood
smear, a single dose treatment for malaria is administered as is
done under the active surveillance programme. The blood slides
are collected by the local surveillance worker/MPW and sent to the
unit laboratory for microscopic examination. The results of the
blood examination are communicated to the local surveillance
worker/MPW for institution of radical treatment.
Parameters of malaria surveillance
By definition surveillance also implies the continuing scrutiny
of all aspects of occurrence and spread of a disease, that are
pertinent to effective control. Included in these are the systematic
collection and evaluation of field investigations, etc. The following
parameters are widely used in the epidemiological surveillance of
malaria : a. Annual parasite incidence (API); b. Annual blood
examination rate (ABER); c. Annual falciparum incidence (AFI);
d. slide positivity rate (SPR); e. Slide falciparum rate (SFR).
Malaria control through primary health care
A new approach to malaria control was approved by WHO in
1978, i.e. implementation of malaria control in the context of the
primary health care strategy. This is because several anti-malarial
activities, including drug distribution, can be carried out by the
most peripheral level of primary health care system with
community participation, where such system has been developed.
Malaria control within the framework of PHC demands national
commitment, community participation and intersectoral
cooperation. Strategies and approaches are being adjusted to
control malaria through primary health care.
In 1999, the Government of India decided to drop the term
"National Malaria Eradication Programme" and renamed it
"National Anti-Malaria Programme".
The anti-malarial activities have been intensified with additional
inputs in 100 selected districts of the states of Andhra Pradesh,
Bihar, Gujarat, Maharashtra, Madhya Pradesh, Rajasthan and
Orissa. In 19 cities/towns in these states and in the states of
Karnataka, Tamil Nadu and West
No.
778
907
5744
290
75
40
350
Source : (10)
Mobile Leprosy Treatment Units provide services to the leprosy
patients in the non-endemic districts. Each MLTU consists of one
medical officer, one non-medical officer, one non-medical
supervisor, two para medical workers and a driver.
Under the NLER the State Leprosy Officer is the chief
coordinator and technical advisor to the concerned State
Government. At the Central level, the leprosy division of the
Directorate General of Health Services, New Delhi is responsible
for planning, supervision and monitoring the programme. The
division is under the control of a Deputy Director General who
advises the Government on all anti-leprosy activities.
MODIFIED LEPROSY ELIMINATION CAMPAIGN (MLEC) :
A mid - term appraisal of the programme in April 1997 indicated
that while the progress of the programme is satisfactory at national
level, it is uneven in some states. It was decided to launch a
leprosy elimination campaign by giving short term orientation
training in leprosy to health staff including medical officer, health
workers and volunteers; increase public awareness about leprosy;
and house to house search has been conducted to detect new
leprosy cases throughout the country for a period of six days. This
first round of campaign led to detection of 4.63 lakh cases. Second
campaign was carried out from January to March 2000 with
detection of 2.13 lakh cases. Third campaign was carried out from
October 2001 to February 2002 with detection of 1.65 lakh cases,
and Fourth campaign was carried out from August 2002 to March
2003 leading to detection of 1.04 lakh cases. The fourth campaign
was different from first three campaigns. In this, the states were
divided into three categories (13).
Category I - It included 8 endemic states namely Bihar, Uttar
Pradesh, Chhattisgarh, Madhya Pradesh, West Bengal, Uttaranchal
and Orissa. The activities included IEC and reorientation training,
voluntary reporting of cases and active search for new cases. The
voluntary reporting centres were organized in all urban areas and
in those rural blocks where prevalence rate was less than 5 per
10,000 population. In all rural areas with prevalence rate more than
5 per 10,00 population, active search through house to house visit
by a team of health workers and trained volunteers were carried
out.
Category II - These included 14 moderate to low endemic states
namely Andhra Pradesh, Arunachal Pradesh, Goa, Gujarat,
Karnataka, Maharashtra, Tamil Nadu, Chandigarh, Daman & Diu,
Dadra and Nagar Haveli, Pondicherry, Andaman & Nicobar
Islands, Delhi and Lakshadweep. The activities were extensive IEC
with training to engaged staff and passive case detection through
voluntary reporting centres.
Category III - These included 13 very low endemic states
namely Haryana, Punjab, Himachal Pradesh, Nagaland, Sikkim,
Tripura, Meghalaya, Mizoram, Jammu and Kashmir, Assam,
Manipur, Rajasthan and Kerala. Here extensive IEC and passive
detection in all the health centres were carried out.
The fifth MLEC was carried out during December 2003 to
(i) one case infects less than one new person annually; (ii)
the prevalence of infection in age group below 14
years is brought down to less than 1 percent, against
about 30 percent as at present.
(b) Operational or short term objectives
(i) to detect maximum number of TB cases among the
outpatients attending any health institution with
symptoms suggestive of tuberculosis and treat them
effectively (ii) to vaccinate newborns and infants with
BCG (iii) to undertake the above objectives in an integrated
manner through all the existing health institutions in
the country.
District Tuberculosis Programme (DTP)
NTP operates through the District Tuberculosis Programme (DTP)
which is the backbone of the NTP Over 600 TB clinics have been set
up in the country, of which 390 have been upgraded todate as District
TB Centres (DTC) to undertake district-wise TB control in
association with general health and medical institutions. It was
evolved by the National Tuberculosis Institute, Bangalore, and was
accepted by the Govt, of India for implementation in 1962. District
Tuberculosis Centre (DTC) is the nucleus of the DTP The function of
DTC is to plan, organize and implement the DTR in the entire
district, in association with general health services. The health
institutions available for inclusion in DTP are - government general
hospitals and community health centres, primary health centres,
tuberculosis clinics other than DTC and out patient departments of
tuberculosis sanatoria and hospitals (TBC), other health
institutions like dispensaries, health units, hospitals including those
managed by the government health schemes (e.g., CGHS, Railways,
etc.), Employees State Insurance Scheme, local bodies, religious
missions, voluntary organizations and private charitable societies.
It is important that only such PHIs (peripheral health
institutions) are selected for implementation of the programme, which
are under the charge of qualified Medical Officers, these are called
implementable PHIs. When DTP activities are introduced in an
organised manner in a PHI, it is considered to be implemented PHI.
A team of trained medical and paramedical personnel are available
at these centres. Besides the DTC, 330 TB clinics are functioning in
the country with 47,600 beds available for tuberculosis patients (15).
17 TB training and demonstration centres have been established
in major States of the country. Two premier TB institutes, namely
National Tuberculosis Institute, Bangalore established in 1959, and
Tuberculosis Chemotherapy Centre, Chetput, Chennai established
in 1956 conduct training and research activities.
The activities of DTC include case finding and treatment. The
treatment is free and is offered on domiciliary basis from all the
health institutions. It is organized in such a manner that patients are
expected to collect drugs once a month on fixed dates from the
nearest treatment centre. When the patient fails to collect his drugs
on the "due date", a letter is written to him (first action) and in the
event of no response for 7 days a home visit is paid (second action)
by the health staff.
ORGANIZATION:
A District Tuberculosis Programme consists of one District
Tuberculosis Centre (DTC) and on an average 50 peripheral health
institutions comprising of PHCs, general hospitals, rural
dispensaries, etc.
To implement the programme, a specially trained team of key
programme personnel (trained at the National Tuberculosis
Institute, Bangalore for a period of 13 weeks) is posted at each
DTC. The team consists of :
1 District Tuberculosis Officer (DTO)
ft4 (All patients are provided short-course chemotherapy free of charge. During the intensive phase of chemotherapy all the
rJ drugs are administered under direct supervision called Direct Observed Therapy Short-term (DOTS). DOTS is a community-based
tuberculosis treatment and care strategy which combines the benefits of supervised treatment, and the benefits of community-based care
and support. It ensures high cure rates through its three components: appropriate medical treatment, supervision and motivation by a
health or non-health worker, and monitoring of disease status by the health services. DOTS is given by peripheral health staff such as
MPWs, or through voluntary workers such as teachers, anganwadi workers, dais, ex-patients, social workers etc. They are known as
DOT 'Agent' and paid incentive/honorarium of Rs 150 per patient completing the treatment)
The success of DOTS depends on five components :
- Political commitment
Good quality sputum microscopy
-Directly observed treatment
-Uninterrupted supply of good quality drugs
-Accountability
The drugs are supplied in patient-wise boxes containing the full course of treatment, and packaged in blister packs. For the intensive
phase, each blister pack contains one day's medication. For the continuation phase, each blister pack contains one weeks supply of
medication. The combipack drugs for extension of intensive phase are supplied separately.
The country situation of tuberculosis is discussed in detail on page 147. As far as the RNTCP is concerned, by March 2004, nearly 76
per cent of the population in 26 states/ UTs (about 851 million) are covered under RNTCP. India has become the second largest country
in the world in terms of population coverage under DOTS. Since the inception of the programme in 1993, nearly 2.8 million patients
have been placed on the treatment (0.9 million in the year 2003 alone), thus saving 0.5 million additional lives (1).
Diagnostic facilities for RNTCP are available in 7800 laboratories in the country. The proportion of the confirmed sputum positive
cases has doubled than the previous programme and is at par with the international standards. The success rate is about 86 per cent,
compared to 25 per cent of previous programme. The death rates under the RNTCP have been cut 7-fold, from 29 per cent to less than 5
per cent (1). More than 3 lakh health' staff has been trained till the end of 2003. About 700 NGOs and more than 3000 private
practitioners are involved with the programmes. More than 31,000 community volunteers are providing DOTS under RNTCP (1).
The trends of RNTCP in India is as follows :
Trends
1999
2000
2001
2002
45
105
52
101
37
38
61
49
23
60
50
31
52
60
85
86
In India, out of estimated 4.58 million HIV-positive cases, around 1.6 million are estimated to be co-infected with HIV and tuberculosis.
Action plan for TB / HIV coordination is being implemented jointly by RNTCP and NACO.
Surveillance for multi-drug resistance is being carried out at various sites of the country. Among the sputum smear +ve patients put on
treatment, about 1.7 per cent cases are paediatric cases, the children below 14 years of age. Guidelines are being developed for diagnosis and
treatment for such cases.
Goals for the Tenth Five Year Plan
The goals for the Tenth Five Year Plan are indicated in Table 2.
TABLE 2
Goals for tuberculosis control for Tenth Five Year Plan
Indicator
Coverage under
350 650 800 900
RNTCP (population in million)
Number of patients
2.08 2.50 3.04 3.42
Total number of
0.52 0.61 0.75 0.85
patients put on DOTS treatment (million)
New sputum smear
0.21 0.24 0.29 0.33
Cure rate of new
83
84
>85 >85
sputum smear positive patients in RNTCP (%)
2006 2007
1000 1070
3.80 4.07 examined (million)
0.94 1.00
0.37
>85
Source : (8)
The National Tuberculosis Control Programme has been accorded high priority by the government. With the inclusion of NTP in the 20
point programme, there is expansion of essential activities under the programme. There has been considerable increase in budget allotment.
The international agencies like WHO, USAID, DANIDA, World Bank etc. are providing the assistance to RNTCP and NTP.
NATIONAL AIDS CONTROL PROGRAMME
With the spread of AIDS from one country to another it became necessary to initiate a national control programme. The Govt, of India in
1985 constituted a task force to look into this matter. It began by pilot screening programme of high-risk population. National AIDS Control
Programme was launched in 1987. In the year 1992, the Ministry of Health and Family Welfare set up a National AIDS Control Organization
as a separate wing to implement and closely monitor the various components of the programme. The Government of India launched a 5 year
HIV/AIDS Control Project from September 1992 to September 1997 as 100 per cent centrally sponsored project for all states/UTs. The project
was later on extended upto March 1999 (10).
The Phase II (1999-2004) of the National AIDS Control Programme has become effective from 9th November, 1999. It is also a 100%
centrally sponsored scheme implemented in 32 States/UTs and 3 Municipal Corporations namely Ahmedabad, Chennai and Mumbai through
AIDS Control Societies. The three new states of Chhattisgarh, Uttaranchal and Jharkhand are in the process of establishing their State AIDS
Control Societies.
"Learning for life" has been prepared and distributed to all the
states. State AIDS Control Societies are responsible to cover the
students of secondary and higher secondary schools. Colleges and
universities are being covered under the "University Talk AIDS
Project". It is being implemented in collaboration with the
Department of Sports and Youth Affairs (13).
INFORMATION, EDUCATION, COMMUNICATION AND
SOCIAL MOBILIZATION : The objective of the IEC strategy in
the national AIDS control programme are : to raise awareness,
improve knowledge and understanding among the general public
about AIDS infection and STD, routes of transmission and
method of prevention; to promote desirable practice such as
avoiding multiple sex partner, use of condom, sterilization of
needles/syringes and voluntary blood donation, to mobilize all
sectors of society to integrate messages and programme on AIDS
into their existing activities; to create a supportive environment
for the care and rehabilitation of persons with HIV/AIDS (21).
In the present day, awareness campaign through multimedia
has made easy the efforts to reach a larger segment of people. The
print media, electronic media, press campaign, interpersonal
publicity and field publicity hold the key to success. A massive
media campaign was launched by NACO in 1996 through well
designed generic materials. Posters, pamphlets, booklets,
newspaper, advertisements, film clippings, TV spots, radio spots,
wall paintings and cinema slides were prepared in Hindi and all
regional languages. IEC programming cannot exist in isolation.
FAMILY HEALTH AWARENESS CAMPAIGN (FHAC) (13,
22) : The importance of reproductive tract infections (RTI)
including sexually transmitted diseases (STD) has increased with
the introduction of HIV/AIDS epidemic in the country. Early
diagnosis and effective treatment of RTI / STD can significantly
reduce transmission of HIV/AIDS. The Family Health Awareness
Campaign is an effort to address the key issues related to
reproductive health in the country, especially in rural and
marginalized population. The period of the campaign is of 15 days
and dates are decided by the states as per their convenience. There
is a paradigm shift in FHAC strategy since 2003. The objectives
of the campaign are :
(i) To raise the awareness levels regarding HIV/AIDS in rural and
slum areas and other vulnerable groups of the population ;
(ii) To make people aware about the services available under the
public sector for management of RTI/STD ;
(iii)To facilitate early detection and prompt treatment of RTI /
STD cases by utilizing the infrastructure available under
primary health care system, including provision of drugs;
(iv)To strengthen the capacity of medical and paramedical
professionals working under health care system to respond to
HIV/AIDS epidemic adquately.
(v) To use safe blood from licensed blood banks and blood
storage centres
(vi) To be aware that HIV can be transmitted from the infected
mother to her baby during pregnancy, delivery and breastfeeding.
PREVENTION OF HIV TRANSMISSION FROM MOTHER TO
CHILD : The project using Nevirapine, single dose, to the mother
and child has been started from 1st October, 2001 at 11 centres
viz. Maharashtra (5), Chennai (3), Bangalore (1), Hyderabad (1)
and Imphal (1). The results of the study are encouraging. The
intervention will be carried out in phased manner giving priority
to 6 states with high prevalence of HIV
TABLE 3
Development of infrastructure for eye care
Current
Achievement
'tem
Strengthening of PHCs
Central Mobile Units
Strengthening of Distt. Hospitals
Upgrading of Depts. of
Ophthalmology in Medical Colleges
Establishment of Regional Institutes
Ophthalmic Assistant Training Centres
District Mobile Units
State Ophthalmic Cells
Establishment of DBCSs
Eye Banks (Govt.)
Paramedical Ophthalmic Assistants posted
5633
80
445
82
11
39
341
21
512
166
4881
Source : (10)
The organizational structure for the national programme for
control of blindenss is as shown in Fig. 2
Administration
Central t Ophthalmology Section, Directorate I
General of Health Services, Ministry I
of Health & FW, New Delhi
State
District
f
I
^
\
Secondary
Level
Primary
Level
TABLE 4
'
Percentage decline in vaccine preventable
diseases from year 1987 to 2001
Disease
1987
2001
Poliomyelitis
28257
268
99.05
12952
163786
11849
247519
4954
28900
1354
45301
61.75
82.36
95.75
81.70
Diphtheria
Pertussis
NNT
Measles
% Decline
Source : (13)
Pulse Polio Immunization Programme was launched in the
country in the year 1995. Under this programme children under
five years of age are given additional oral polio drops in December
and January every year on fixed days. Since then there is a
significant decline in the incidence of poliomyelitis. Following the
success of the polio eradication programme, the next likely
diseases for elimination are measles and neonatal tetanus.
INTRODUCTION OF HEPATITIS-B VACCINE
A pilot project for the introduction of Hepatitis-B vaccine in the
National Immunization Programme was initiated in June 2002.
Under this project Hepatitis-B vaccine is being administered to
infants along with the primary doses of DPT vaccine on 6th, 10th
and 14th week. The project is being implemented in 33 districts
and 15 metropolitan cities. In the project areas auto-disable
syringes are being introduced. It will be implemented for a period
of two years (1).
URBAN MEASLES CAMPAIGN
A special campaign, with assistance of UNICEF was taken up
for covering the slum localities in urban areas during 1998. In
1998-99, 13 cities were covered under this programme. In 19992000, 50 more cities were covered. The emphasis is on covering
all unprotected children up to the age of 3 years with single dose
of measles vaccine. Based on the experience from these cities,
more will be targeted in the coming years.
NEONATAL TETANUS ELIMINATION
Neo-natal tetanus still continues to be a problem in many
districts particularly in the larger states. In order to achieve early
elimination of neo-natal tetanus, ICMR has advised that efforts
should be made to cover all women in reproductive age group with
three doses of tetanus toxoid vaccine through a campaign
approach. Based on the these recommendations, Rajasthan and
Madhya Pradesh have implemented campaigns during the year
1998-99 and 1999-2000. In Rajasthan campaign only married
women up to the age of 30 years were targeted with 3 doses of
tetanus toxoid.
Intensification of immunization programme has contributed to a
significant decline in Infant Mortality Rate in the last few years.
The decline is particularly pronounced after 1990 as compared to
earlier years. During that year IMR declined by 11 points to 80 per
thousand live births (28).
REPRODUCTIVE AND CHILD HEALTH PROGRAMME
Reproductive and child health approach has been defined as
"people have the ability to reproduce and regulate their fertility,
women are able to go through pregnancy and child birth safely, the
outcome of pregnancies is successful in terms of maternal and
infant survival and well being, and couples are able to have sexual
relations free of fear of pregnancy and of contracting disease" (33).
Reproductive and child health approach has been defined as
"people have the ability to reproduce and regulate their fertility,
women are able to go through pregnancy and child birth safely, the
outcome of pregnancies is successful in terms of maternal and
infant survival and well being, and couples are
Client approach to
health care
Child Survival
and Safe Motherhood
component
Prevention/Management
of RTI/STD
AIDS
FIG. 4 RCH
Package
The main highlights of the RCH programme are :
1.The programme integrates all interventions of fertility
regulation, maternal and child health with reproductive health
for both men and women.
2.The services to be provided will be client oriented, demand
driven, high quality and based on needs of community through
decentralised participatory planning and target free approach.
3.The programme envisages upgradation of the level of
facilities for providing various interventions and quality of care.
The First Referral Units (FRUs) being set-up at sab-district
level will provide comprehensive emergency obstetric and new
born care. Similarly RCH facilities at PHCs will be
substantially upgraded.
4.It is proposed to improve facilities of obstetric care, MTP and
IUD insertion in the PHCs. Also for IUD insertion at subcentres.
5.Specialist facilities for STD and RTI will be available in all
district hospitals and in a fair number of sub-district level
hospitals.
6.The programme aims at improving the out-reach of services
primarily for the vulnerable group of population who have been,
till now, effectively left out of planning process, e.g. special
programme will be taken up for urban slums, tribal population
and adolescents; NGOs and voluntary organizations will be
involved in a much larger way to improve out-reach and make it
people's programme; practitioners of Indian System of Medicine
will be trained and research and development in Indian System
of Medicine will be supported to improve range of RCH
services; the Panchayat Raj functionaries will have a central role
in determining the need of the local population for RCH
services generally and for contraceptives particularly under the
target free approach. The Panchayat will also be the agency for
implementing the programme and for extending financial
support to women for taking them to specialist at sub-divisional
hospitals for delivery.
The RCH programme is based on a differential approach.
Inputs in all the districts have not been kept uniform. While the
care components are the same for all districts, the weaker
TABLE 5
Key indicators of reproductive health in India
(Survey report September to December 1999)
Indicator
CMW age 15-44 years
*With any ANC
*With full ANC
Institutional delivery
Safe delivery
Women having
*Pregnancy complications
*Delivery complications
*Post delivery complications
CMW age 15-44 years
*With symptoms of RTI/STD
*Aware of AIDS
Males age 20 - 54 years
*With symptoms RTI/STD
*Aware of AIDS
Percentage
67.2
14.8
35.0
41.9
34.8
36.4
42.0
28.8
41.1
12.7
57.4
Source : (10)
CMW refers to currently married women who had the last live/
still birth since January 1995
Safe delivery refers to institutional delivery and home delivery
attended by doctor/nurse/ANM
Full ANC refers to 3 ANC check up + at least one TT injection +
100 tablets of IFA.
Pregnancy complications : Percent women who reported any of
the following complications : swelling of hands and feet, visual
disturbance, bleeding, convulsions, weak or no movement of
foetus and abnormal presentation
Delivery complications : percent of women who reported any of
the following complications : premature labour, obstructed
labour, prolonged labour
Post delivery complications : percent women who reported any
of the following complications : high fever, lower abdominal
pain, foul smelling vaginal discharge, excessive bleeding and
dizziness or severe headache.
NATIONAL GUINEA - WORM
ERADICATION PROGRAMME
India launched its National Guinea-worm Eradication
Programme in 1984 with technical assistance from WHO. From
the very beginning the programme was integrated into the national
health system at village level. With well defined strategies, an
efficient information and evaluation system, intersectoral
coordination at all levels and close collaboration with WHO and
UNICEF, India was able to significantly reduce the disease in
affected areas. The country has reported zero cases since August
1996. In February 2000, the International Commission for the
Certification of Dracunculiasis Eradication recommended that
India be certified free of dracunculiasis transmission (35).
NATIONAL CANCER CONTROL PROGRAMME
In India, it is estimated that there are about 2 million cancer
cases at any given point of time with about 0.7 million new cases
coming every year. The Government of India started the National
Cancer Control Programme in a limited form during the year 197576 when central assistance of Rs. 2.5 Lakh was provided to
institutions for purchase of Cobalt Therapy units for treatment of
cancer patients. This scheme continued during the Sixth and
Seventh Plan period. At the same time ten major institutions were
recognised as Regional Cancer Centres which receive financial
assistance from the Government. During the Eighth five year plan
emphasis was on prevention, early detection of cancer and
augmentation of treatment facilities in the country. The following
new schemes have been initiated starting from the year 1990-1991.
(a) Scheme for District Projects : The scheme envisages
177
113
243
9
37
42
37
76
Paper No.
10, SEARO, New Delhi.
18.Govt, of India, Annual Report 1993-94, Ministry of Health and Family Welfare.
19.Govt, of India, Annual Report 1992-93, DGHS, New Delhi
20.Allan, D. (1987). WorldHealth, Jan-Feb, 1987, p. 9.
21.Grant, J.R (1987). World Health, Jan-Feb, 1987, p. 10.
22.Govt, of India (1987). Centre Calling, Nov. 1987.
23.UNICEF (1987). The State of the World's Children, Oxford University Press,
Oxford.
24.Govt, of India, Reproductive and Child Health Programme, Schemes for
Implementation October 1997, Department of Family Welfare, Ministry of Health
and Family Welfare, New Delhi
25.Govt, of India (1997) Manual of the Training of Trainers of Health and Family
Welfare, Rural Health Division, Directorate of Family Welfare, Ministry of Health
and Family Welfare, New Delhi.
29.WHO (1985). Health Care in SEAsia, Reg. Publ. SEARO, Sr. No. 14.
30.Bookhive's, 8th Five Year Plan (1992-97) by E. Chandran, issues of
interest, Series No. 4
current
"Delay the first, postpone the second and prevent the third"
Demography, as understood today, is the scientific study of
human population. It focuses its attention on three readily
observable human phenomena : (a) changes in population size
(growth or decline) (b) the composition of the population and (c)
the distribution of population in space. It deals with five
"demographic processes", namely fertility, mortality, marriage,
migration and social mobility. These five processes are
continuously at work within a population determining size,
composition and distribution.
Community medicine is vitally concerned with population,
because health in the group depends upon the dynamic relationship
between the numbers of people, the space which they occupy and
the skill that they have acquired in providing for their needs. The
main sources of demographic statistics in India are population
censuses, National Sample Surveys, registration of vital events,
and adhoc demographic studies.
Demographic Cycle
The history of world population since 1650 suggests that there
is a demographic cycle of 5 stages through which a nation passes:
(1) FIRST STAGE (High stationary)
This stage is characterised by a high birth rate and a high death
rate which cancel each other and the population remains
stationary. India was in this stage till 1920.
(2) SECOND STAGE (Early expanding)
The death rate begins to decline, while the birth rate remains
unchanged. Many countries in South Asia and Africa are in this
phase. Birth rates have increased in some of these countries
possibly as a result of improved health conditions, and shortening
periods of breast feeding (1).
,i^UHIRD STAGE((Late expanding (__The death rate declines still
further, and the birth rate tends to fall. The population continues to
grow because births exceed deaths. India has entered this phasejf
In a number of developing countries (e.g., China, Singapore) birth
rates have declined rapidly.
(4) FOURTH STAGE (Low stationary)
This stage is characterised by a low birth and low deathjate. with
the result that the population becomes stationarylZero^ population
growth has already been recorded in Austria during' 1980-85.
Growth rates as little as 0.1 were recojekd in UK, Denmark,
Sweden and Belgium during 1980-85Jn short, most industrialized
countries have undergone a demographic transition shifting from a
high birth and high death rates to low
Kirtn ^r-vH Ic-viii ^02 + h va+/->c
Populatio
n
(million)
791
978
1262
1650
2526
3037
3696
4066
4432
5000
5385
5884
6054
6225
0.4
0.5
0.6
1.1
1.79
1.92
1.89
1.72
1.63
1.7
1.6
1.4
1.1
TABLE 3
Crude birth and death rates in selected developed and
developing countries in 2002
Country
India
Bangladesh
Pakistan
Sri Lanka
Thailand
Myanmar
Nepal
China
Japan
Singapore
UK
USA
24
29
36
17
18
24
33
15
9
10
10
15
9
8
10
7
7
11
10
7
8
5
10
8
Source : (9)
The world's birth rate fell below 30 for the first time around
1975 and had declined to about 22 during 2002 (9). In most of the
world the decline reflected falling birth rates and a global trend
towards smaller families. The outstanding examples are Singapore
and Thailand. In Singapore, in 32 years, the birth rate fell from 23
per thousand in 1970 to 10 in 2002; and, in Thailand from 37 to 18
during the same period (Table 4).
FIG. 1 Ten most
populous countries of the world
1.Population figure for India is as per Census 2001 (Provisional)
2.Population figures fdr U.S.A. and Japan are as per census 2000
3.Other figures are based on World Population prospects, 1998
Revisions (vol. II), United Nations.
Source : (7)
Three countries of SEAR, i.e. India (16.87 per cent), Indonesia
(3.49 per cent) and Bangladesh (2.13 per cent) are among the most
populous ten countries of the world. At present India's population
is second to that of China. According to UN projections India's
population will reach 1.53 billion by the year 2050, and will be the
highest population in the world. The trend of population increase in
South East Asia Region countries is as shown in Table 2.
TABLE 2
Trends in increase of population of SEAR countries (in
thousands)
Country
India
Bangladesh
Bhutan
DPR Korea
Indonesia
Maldives
Myanmar
Nepal
Sri Lanka
Thailand
Total
1985
767940
99310
1451
18942
167332
184
37544
16503
16060
51128
1176394
2002
1049549
143809
2190
22541
217131
309
48852
24609
189110
62193
1589293
2005
(Projected)
1082184
139911
2313
25416
226938
355
53479
27439
19858
62612
1640505
Source : (9)
Birth and death rates
The glaring contrasts in birth and death rates in selected
countries are as shown in Table 3.
TABLE 4
Reduction in the crude birth and death rates in
selected countries, 1970-2002
Country
Bangladesh
Nepal
India
Sri Lanka
Thailand
Singapore
China
Pakistan
2002
29
33
24
17
18
10
15
36
Crude
1970
21
22
17
8
9
5
8
18
death rate
2002
8
10
9
7
7
5
7
10
Source : (9)
In all these countries, key factors in fertility decline included
changes in Government attitudes towards growth, the spread of
education, increased availability of contraception and the extension
of services offered through family planning programmes, as well
as the marked change in marriage patterns.
Death rates have also declined worldwide over the last decades.
The global death rate declined from 11.0 (between 1975-1980) to 9
per thousand population during 2002, a reduction of 18 per cent.
The decline in the crude death rate of the South East Asia Region
has been more marked, from 14.1 to 8.2 per 1000 population (10).
In countries with a relative young population, crude death rates
are mainly affected by infant and child mortality. With
improvement in maternal and child health services, successful
implementation of the expanded programme on immunization,
diarrhoeal disease and acute respiratory infection control
programmes, as well as with the control of other infectious
diseases, there has been marked reduction in infant and child
mortality rates, which are reflected in the declining crude death
rates.
Growth rates
When the crude death rate is substracted from the crude birth
rate, the net residual is the current annual growth rate, exclusive of
migration. The relation between the growth rate and population
increase is as shown in Table 5.
State
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Uttar Pradesh
Maharashtra
Bihar
Andhra Pradesh
Tamil Nadu
Rajasthan
Karnataka
Gujarat
Population
1.3.2001
(million)
166.05 '
96.75
82.87
80.22
75.72
62.11
60.38
56.47
52.73
50.59
16.17
9.42
8.07
7.81
7.37
6.05
5.88
5.50
5.14
4.93
Source : (7).
Age and Sex Composition
The age-sex composition of India's population according to the
National Family Health Survey-2 done in 1998-99 is as shown in
Table 8.
Male
0-4
11.2
11.1
12.8
12.1
10.4
8.5
7.8
6.7
6.6
5.1
4.5
3.4
2.6
2.9
2.0
3.3
100.0
12.4
11.8
10.3
9.3
8.7
7.1
6.4
4.7
4.2
3.1
3.3
3.0
2.0
2.8
100.0
5-9
10-14
15-19
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70+
Total
Female
Sex ratio
{Sex ratio is defined as "the number of females per 1000
maIes"T]One of the basic demographic characteristics of the
population is the sex composition. In any study of population,
analysis of the sex composition plays a vital role. The sex
composition of the population is affected by the differentials in
mortality conditions of males and females, sex selective migration
and sex ratio at birth.
The trends in the sex ratio in the country from 1901 onwards
are as shown in Table 9.
The sex ratio in India has been generally adverse to women,
i.e., the number of women per 1,000 men has generally been less
than 1,000. Apart from being adverse to women, the sex ratio has
also declined over the decades. Kerala has a sex ratio of 1,058
females per 1,000 males in 2001. It is the only state with a sex
ratio favourable to females.
^0
Females per
1000 males
Year
Source : (14)
Age pyramids
The age structure of a population is best represented as shown
in Fig.2.
Such a representation is called an "Age Pyramid". A vivid
contrast may be seen in the age distribution of men and women in
India and in Switzerland. The age pyramid of India is typical of
under-developed countries, with a broad base and a tapering top. In
the developed countries, as in Switzerland, the pyramid generally
shows a bulge in the middle, and has a narrower base.
1901
972
1911
1921
1931
1941
1951
1961
1971
1981
1991
2001
964
955
950
945
946
941
930
934
927
933 *>*}
Source : (7)
Dependency Ratio
The proportion of persons above 65 years of age and children
below 15 years of age are considered to be dependent
INDIA (2001)
SWITZERLAND (2001)
DEMOGRAPHIC TRENDS IN
INDIA 35;
on the economically productive age group (15-64 years). The
ratio of the combined age groups 0-14 years plus 65 years and
above to the 15 - 65 year age group is referred to as the total dependency ratio.
) Year
Total
dependency
Child
dependency
Old-age
dependency
1990
69
61
2000
2010
(projected)
62
54
54
45
8
9
Source : (10)
Density of population
One of the important indices of population concentration is
the density of population. In the Indian census, density is
defined as the number of persons, living per square kilometre.
The trends of the density in the country from 1901 onwards are
as shown in Table 11.
V"
23
Source : (7)
Year
per sq.km
1901
1911
1921
1931
1941
1951
1961
1971
1981
1991
2001
77
82
81
90
103
117
142
177
216
267
324
decision regarding the "desired family size" and the effective limitation of
fertility once that size has been reached.
TABLE 10
Trends in dependency ratio in India (per 100)
TABLE 11
Density of population in India 1901-2001
India
Bangladesh
Nepal
Sri Lanka
Myanmar
China
Pakistan
UK
USA
Japan
Switzerland
1990
2002
3.9
4.6
5.2
2.6
4.0
2.2
6.0
1.8
2.0
1.6
1.5
3.1
3.5
4.3
2.0
2.9
1.8
5.1
1.6
2.1
1.3
1.4
Source : (9)
Urbanization
Growing urbanization is a recent phenomenon in the
developing countries. The proportion of the urban population in
India has increased from 10.84 per cent in 1901 to 25.72 per
cent in 1991, and was 27.8 in the year 2001. In absolute terms,
the urban population in India was projected to be 285 million in
2001 as compared to 217.17 million in 1991. Fig. 3 indicates the
level of urbanization in the country.
220200
uO
Z
2
1805
*
160 _
140
Family size
^
While in common parlance, family size refers to the total
j=2
120
number of persons in a family /in demography, family size
< i nn
means the total number of children a woman has borne at
^
a point in time (13). The completed family size indicates the
cu
80
total number of children borne by a woman during her childobearing age, which is generally assumed to be between 15 and
z
60
45 years. The total fertility rate gives the approximate
^
__________________
magnitude of completed family sizeN
CC
20
60-
52.21
UJ50H
43.57
40-
34.45
O
UJ30O
28.30
20- 18.33
UJ
U
DC
UJ
CM
10-
n-
Male
literacy rate
Female
literacy rate
Total literacy
rate
71
44
58
62
76
77
35
44
51
49
61
64
79
72
80
76
86
76
78
76
71
82
94
76
56
56
59
51
68
64
60
56
51
65
88
54
69
64
70
64
77
70
69
67
61
73
91
65.38
Source : (7)
Table 13 shows that Kerala continues to occupy the top rank in
the country with about 91 per cent literates. Mizoram (88.49
percent and Lakshadweep (87.52 per cent) closely follow Kerala.
On the other end is Bihar and Jharkhand with literacy rate of only
49 per cent. The states which have literacy rates
FERTILITY 355
below the national average are Arunachal Pradesh, Andhra
Pradesh, Bihar, Jammu & Kashmir, Uttar Pradesh, Rajasthan, MR
and Orissa etc.
Government of India has made education compulsory up to
age 14 years in the country. Though considerable progress has
been made in expanding primary education, a major concern is
high drop out rates in the first few years of schooling (8).
Lite expectancy
expectancy - or expectation of life - at a given age is
I^Uhe average number of years which a person of that age may expect
to live, according to the mortality pattern prevalent in that country.
Demographers consider it as one of the best indicators of a country's
level of development and of the overall health status of its
population.}
Life expectancy at birth has continued to increase globally
over the years. For 1950 - 1955, the combined life expectancy at
birth for both sexes was 46.5 years. Five decades later by 2002, it
was 63 years-an increase of 16.5 years. The increase has been
more marked in less developed regions of the world than in the
developed regions (9). One of the goals of HFA/ 2000 was the
attainment of a life expectation of 64 years at birth for both males
and females (15).
Most countries in the world exhibit a sex differential in
mortality favouring women - females live longer than males as
shown in Table 14. Contrary to this biological expectation, the
life expectancy of women in Nepal and Maldives is lower than
that of men, while in Bangladesh and India it is almost equal.
Trends in life expectancy show that people are living longer,
and they have a right to a long life in good health, rather than one
of pain and disability. Health policy makers thus need to
recognize this changing demographic pattern and plan for
prevention and control of diseases associated with old age.
Tables 14 and 15 present life expectancy at birth in India and
those in selected countries. Japan leads in life expectancy for both
males and females,77.7 and 84.7 years respectively for the year
2001.
f^C (ife
FERTILITY
By fertility is meant the actual bearing of children. Some
demographers prefer to use the word natality in place of fertility. A
woman's reproductive period is roughly from 15 to 45 years - a
period of 30 years. A woman married at 15 and living till 45 with
her husband is exposed to the risk of pregnancy for 30 years, and
may give birth to 15 children, but this maximum is rarely
achieved. Information on fertility in India indicates that an average
woman gives birth to an average of six or seven children if her
married life is uninterrupted.
Fertility depends upon several factors. The higher fertility in
India is attributed to universality of marriage, lower age at
marriage, low level of literacy, poor level of living, limited use of
contraceptives and traditional ways of life. National Family Health
Survey 2 conducted in India during 1998-1999 provides some
detailed information of fertility trends, as shown in Table 16.
TABLE 16
Total fertility rate by selected background characteristics
racteristics
2.27
3.07
3.47
Males
Females
1901
1911
1921
1931
1941
1951
1961
1971
1981
1991
2001
23.63
22.59
19.42
26.91
32.09
32.45
41.89
46.40
50.90
58.10
62.80
23.96
23.31
20.91
26.56
31.37
31.66
40.55
44.70
50.00
59.10
64.00
2.64
DOI
2.26
1.99
complete
1 complete and above
2.78
TABLE 14
Expectation of life at birth - India
Year
eo-Buddhist
3.15
tribe
ward class
3.06
2.83
2.66
g index
2.37
2.85
2.10
2.85
TABLE 15
Expectation of life at birth in selected countries 2001
Nepal
Bangladesh
Myanmar
India
Sri Lanka
Thailand
2001 Male
Female
59.4
58.9
59.4
59.5
54.4
59.8
62.8
64.0
69.6
75.5
64.9
73.2
Source : (20)
Developed
countries
UK
USA
Sweden
Switzerland
Russian Federation
Japan
3.59
2.44
2.26
1.90
2.13
2.33
3.91
caste
Developing
countries
2001 Male
Female
75.4
80.4
74.0
79.7
77.4
82.4
75.8
82.2
60.6
72.9
77.7
84.7
(1996-1998)
Residence
Urban
Rural
Education
Illiterate
Literate, <
Middle schc
High schoo
Religion
Hindu
Muslim
Christian
Sikh
Jain
Buddhist/N
Other
No religion
Caste/tribe
Scheduled
Scheduled
Other back
Other Standard of
livin
Low
Medium
High
Total
Source : (14)
Some of the factors which have engaged attention of demographers
since long are discussed below.
1. Age at marriage
The age at which a female marries and enters the reproductive
period of life has a great impact on her fertility. The Registrar General
of India collected data on fertility on a national scale and found that
females who marry before the age of 18 gave birth to a larger number
of children than those
FERTILITY-RELATED STATISTICS
----------- -,
>
tQs
J *\\'
_______________________________________________
FERTILITY 357
a woman would have if she were to pass through her reproductive years
bearing children at the same rates as the women now in each age group
(24). It is computed by summing the age-specific fertility rates for all
ages; if 5-year age groups are used, the sum of the rates is multiplied by
5. This measure gives the approximate magnitude of "completed
familys
!3^^@
marriage rate :
General
Number of marriages within one year
Marriage = -------------------------------------------------- X 1000
pafe
Number of unmarried persons age
15-49 years
This rate is more accurate when computed for women than for
men because more men than women marry at the older ages (11).
Fertility trends
Researches indicate that the level of fertility in India is
beginning to decline. The crude birth rate which was about 49 per
thousand population during 1901-11 has declined to about 31.3 per
thousand population in 1991, and 25 per thousand population in
2002.
There are considerable inter-state variations in fertility trends. It
is significant that atleast ten states/UT have achieved net
replacement levels. The examples are Kerala, Tamil Nadu, Goa,
Delhi, Chandigarh, Mizoram etc. 14 states / UT have a total fertility
rate of more than 2.1 but less than 3.0, e.g., Orissa, Karnataka,
Andhra Pradesh, Maharashtra, Gujarat, Punjab, West Bengal,
Himachal Pradesh etc. However, there are 9 states / UT that have a
total fertility rate of over 3.0. They are Bihar, Uttar Pradesh,
Madhya Pradesh, Haryana, Assam, Rajasthan etc. Fig. 6 shows
crude birth rate and total fertility rate for major states in India.
lABLfc. 1/
Rural
Urban Combined
112.8
77.6
103.2
147.8
112.3
138.9
3.5
2.3
3.2
4.9
4.2
4.7
1.7
1.1
1.5
Source : (29)
TABLE 18
Age-specific fertility rates - all India (1999)
(per 1000 women)
Age group
Urban
15-19
20-24
25-29
30-34
35-39
40-44
45-49
30
166
154
74
32
11
3
Rural
60
232
193
115
64
29
10
Birth rate
39.9
41.7
41.2
37.2
33.9
29.5
28.3
27.5
27.2
26.4
26.1
25.0
Death rate
27.4
22.8
19.0
14.8
12.5
9.8
9.0
9.0
8.9
9.0
8.7
8.1
target couple has lost its original meaning. The term eligible
couple is now more widely used and has come to stay.
Couple protection rate (CPR)
Couple protection rate (CPR) is an indicator of the
prevalence of contraceptive practice in the community. It is
defined as the per cent of eligible couples effectively protected
against childbirth by one or the other approved methods of
family planning, viz. sterilization, IUD, condom or oral pills.
Sterilization accounts for over 60 per cent of effectively
protected couples (38) \Demographers are of the view that the
demographic goal of NR"R7= 1 can be achieved only if the CPR
exceeds 60 per cent (25*)J ^ 0v<\ ^) , V"^ (B) V ]
Couple protection rate is based on the observation-tnat 50 '
to 60 per cent of births in a year are of birth order 3 or more.
Thus attaining a 60 per cent CPR will be equivalent to cutting
off almost all third or higher order births, leaving 2 or less y
surviving children per couple (40).(Therefore, the previous
Small-family norm
\/,'
----- .... , ---_ u Dy lyyfj ^enu uLoeveniii rive rear nan;, diiu ou pei ceiu uy
Small differences in the family size will make big differences!^^ year 200OJn short CPR is a dominant factor in the in the birth rate.
The difference of only one child per family^-reduction of net reproduction rate.
Small differences in the family size will make big differences;>/
in the birth rate. The difference of only one child per family ^ over
a decade will have a tremendous impact on the population
growth.
The objective of the Family Welfare Programme in India is that
people should adopt the "small family norm" to stabilise the
country's population at the level of some 1533 million by the year
2050 AD. Symbolised by the inverted red triangle, the programme
initially adopted the model of the 3-child family. In the 1970s, the
slogan was the famous Do Ya Teen Bas. In view of the seriousness
of the situation, the 1980s campaign has advocated the 2-child
norm. The current emphasis is on three themes : "Sons or
Daughters - two will do"; "Second child after 3 years", and
"Universal Immunization".
A significant achievement of the Family Welfare Programme in
India has been the decline in the fertility rate from 6.4 in the 1950s
to 3.1 in 2002. The national target is to achieve a Net Reproduction
Rate of 1 by the year 2006, which is equivalent to attaining
approximately the 2-child norm. All efforts are being made
through mass communication that the concept of small family
norm is accepted, adopted and woven into lifestyle of the people.
Eligible couples
An "eligible couple" refers to a currently married couple
wherein the wife is in the reproductive age, which is generally
assumed to lie between the ages of 15 and 45. There will be at least
150 to 180 such couples per 1000 population in India. These
couples are in need of family planning services. About 20 per cent
of eligible couples are found in the age group 15-24 years (38). As
of 31st March 1999, there were about 168 million eligible couples
in the country. (39). On an average 2.5 million couples are joining
the reproductive group every year. The "Eligible Couple Register"
is a basic document for organizing family planning work. It is
regularly updated by each functionary of the family planning
programme for the area falling within his jurisdiction.
Target couples
In order to pin-point the couples who are a priority group within
the broad definition of "eligible couples", the term "target couple"
was coined. Hitherto, the term target couple was applied to couples
who have had 2-3 living children, and family planning was largely
directed to such couples. The definition of a target couple has been
gradually enlarged to include families with one child or even
newly married couples (36j with a view to develop acceptance of
the idea of family planning from the earliest possible stage. In
effect, the term
By all methods
By sterilization
52.8
15.2
21.2
52.8
49.4
56.3
39.6
45.9
49.3
65.5
36.1
30.4
38.0
32.2
37.6
46.2
45.5
12.5
16.7
35.4
32.3
44.8
34.5
28.0
40.0
35.2
22.9
39.3
17.3
27.2
26.5
29.0
1.Intra-Uterine Devices
2.Hormonal Methods
3.Post-Conceptional Methods
4.Miscellaneous
Female condom
The female condom is a pouch made of polyurethane, which
lines the vagina. An internal ring in the close end of the pouch
covers the cervix and an external ring remains outside the vagina. It
is prelubricated with silicon, and a spermicide need not be used. It
BARRIER METHODS
is an effective barrier to STD infection. ,However, high cost and
A variety of barrier or "occlusive" methods, suitable for both men acceptability are major problems. The 'failure rates during the first
and women are available. The aim of these methods is tot" prevent
year use vary from 5 per 100 women-years pregnancy rate to about
live sperm from meeting the ovum/Barrier method&C have
21 in typical users (46).
increased in popularity quite recently because of certain-"'
contraceptive and non -contraceptive advantages. The main
2. Diaphragm
contraceptive advantage is the absence of side effects
The diaphragm is a vaginal barrier. It was invented by a
associated with the "pill" and IUD. The non-contraceptive
German physician in 1882. Also known as "Dutch cap", the
advantages include some protection from sexually transmitted
diaphragm is a shallow cup made of synthetic rubber or plastic
diseases, a reduction in the incidence of pelvic inflammatory disease material. It ranges in diameter from 5-10 cm (2-4 inches). It has a
and possibly some protection from the risk of cervical cancer (42).
flexible rim made of spring or metal. It is important that a woman
Barrier methods require a high degree of motivation on the
be fitted with a diaphragm of the proper size. It is held in position
part of the user. In general they are less effective than either the pill
partly by the spring tension and partly by the vaginal muscle tone.
or the loop. They are only effective if they are used consistently and
This means, for successful use, the vaginal tone must be
carefully/)
reasonable. Otherwise, in the case of a severe degree of cystocele,
the rim may slip down.
a. PHYSICAL METHODS
ftV)
The diaphragm is inserted before sexual intercourse and must
1. Condom (43, 44)
remain in place for not less than 6 hours after sexual intercourse. A
Condom is the most widely known and used barrier device by
spermicidal jelly is always used along with the diaphragm. The
the males around the world. In India, it is better known by its trade
diaphragm holds the spermicide over the cervix. Side effects are
name NIRODH, a Sanskrit word, meaning prevention. Condom is
practically nil. Failure rate for the diaphragm with spermicide wiry
receiving new attention today as an effective, simple "spacing"
between 6 to 12 per 100 women-years (45). Y.^W&
method of contraception, without side effects. In addition to
ADVANTAGES (ihe primary advantage of the diaphragm is
preventing pregnancy, condom protects both men and women from
the almost J:otal absence of risks and medical
sexually transmitted diseases.
contraindications/DISADVANTAGES : Initially a physician or
other trained person will be needed to demonstrate the technique of
The condom is fitted on the erect penis before intercourse. The
inserting the diaphragm into the vagina and to ensure a proper fit.
air must be expelled from the teat end to make room for the
After delivery, it can be used only after involution of the uterus is
ejaculate. The condom must be held carefully when withdrawing it
completed. Practice at insertion, privacy for this to be carried out
from the vagina to avoid spilling seminal fluid into the vagina after
and facilities for washing and storing the diaphragm precludes its
intercourse. A new condom should be used for each sexual act.
use in most Indian families, particularly in the rural areas.
Condom prevents the semen from being deposited in vagina.
Therefore, the extent of its use has never been great.
The effectiveness of a condom may be increased by using it in
conjunction with a spermicidal jelly inserted into the vagina before
If the diaphragm is left in the vagina for an extended period,
intercourse. The spermicide serves as additional protection in the
there is a remote possibility of a toxic shock syndrome, which is a
unlikely event that the condom should slip off or tear.
state of peripheral shock requiring resuscitation (48).
Condoms can be a highly effective method of contraception, if
Variations of the diaphragm include the cervical cap, vault cap
they are used correctly at every coitus. Failure rates for the condom
and the vimule cap. These devices are not recommended in the
vary enormously. Surveys have reported pregnancy rates varying
National Family Welfare Programme.
from 2-3 per 100 women-years to more than 14 in typical users
3. Vaginal sponge
(45). Most failures are due to incorrect use.
Another barrier device employed for hundreds of years is the
The ADVANTAGES of condom are : (a) they are easily
sponge soaked in vinegar or olive oil, but it is only recently one
available (b) safe and inexpensive (c) easy to use; do not require
has been commercially marketed in USA under the trade name
medical supervision (d) no side effects (e) light, compact and
TODAY for the sole purpose of preventing conception. It is a
disposable, and (f) provides protection not only against pregnancy
small polyurethane foam sponge measuring 5 cm x 2.5 cm,
but also against STD. The DISADVANTAGES are : (a) it may slip
saturated with the spermicide, nonoxynol-9. The sponge is far less
off or tear during coitus due to incorrect use, and (b) interferes
effective than the diaphragm, but it is better than nothing (45). The
with sex sensation locally about which some complain while others
failure rate in parous women is between 20 to 40 per 100 womenget used to it. The main limitation of condoms is that many men do
years and in nulliparous women about 9 to 20 per 100 womennot use them regularly or carefully, even when the risk of
years (46).
unwanted pregnancy or sexually transmitted disease is high.
II Terminal methods
1Male sterilization
2Female sterilization
b. CHEMICAL METHODS
In the 1960s, before the advent of IUDs and oral
contraceptives, spermicides (vaginal chemical contraceptives)
were used widely. They comprise four categories (49):
________________________________________________IUDs 365
described the ideal IUD candidate as a woman :
-who has borne at least one child has no
history of pelvic disease
-has normal menstrual periods is
willing to check the IUD tail
-has access to follow-up and treatment of potential problems,
and
is in a monogamous relationship
The federation does not, however, rule out women who do not
conform to this profile (57).
An important finding that has recently emerged is that the IUD
is not a method of first choice for nulliparous women. They have
more problems with IUD such as expulsions, low abdominal pain
and pelvic infection, than other women. IUDs such as copper-T,
which are smaller and more pliable are better suited to the small
uterus of the nulliparous women, if they cannot use or accept
alternative methods of contraception.
In 1985, the American College of Obstetricians and
Gynaecologists stated that IUDs are "not recommended for women
who have not had children or who have multiple partners, because
of the risk of PID and possible infertility" (57).
Timing of insertion
Although the loop can be inserted at almost anytime during a
woman's reproductive years (except during pregnancy), the most
propitious time for loop insertion is during menstruation or within
10 days of the beginning of a menstrual period (55). During this
period, insertion is technically easy because the diameter of the
cervical canal is greater at this time than during the secretory
phase. The uterus is relaxed and myometrial contractions which
might tend to cause expulsion are at a minimum (50). In addition,
the risk that a woman is pregnant is remote at this time.
IUD insertion can also be taken up during the first week
after delivery before the woman leaves the hospital
^("immediate postpartum insertion"). Special care is required with
insertions during the first week after delivery because of
j the greater risk of perforation during this time. Furthermore,
immediate post-partum insertion is associated with a high
expulsion rateT}^ convenient time for loop insertion is 6-8 weeks
after delivery ("post-puerperal insertion"). Post-puerperal insertion
of an IUD has several advantages. It can be combined with the
follow-up examination of the women and her child. IUD insertion
can also be taken up immediately after a legally induced first
trimester abortion. But IUD insertion immediately after a second
trimester abortion is not recommended (51). Since there is a risk of
infection, most physicians still do not approve of an IUD insertion
after an illegal abortion (51).
Follow-up
An important aspect of IUD insertion is follow-up which is
sadly neglected. The objectives of the follow-up examination are :
(a) to provide motivation and emotional support for the woman (b)
to confirm the presence of the IUD, and (c) diagnose and treat any
side-effect or complication (55). The IUD wearer should be
examined after her first menstrual period, for the chances of loop
expulsion are high during this period; and again after the third
menstrual period to evaluate the problems of pain and bleeding;
and thereafter at six-month or one-year intervals depending upon
the facilities and the convenience of the patient.
The IUD wearer should be given the following instructions : (a)
she should regularly check the threads or "tail" to be sure
that the IUD is in the uterus; if she fails to locate the threads, she
must consult the doctor (b) she should visit the clinic whenever she
experiences any side-effects such as fever, pelvic pain and
bleeding (c) if she misses a period, she must consult the doctor.
SIDE-EFFECTS AND COMPLICATIONS
1. Bleeding
The commonest complaint of women fitted with an IUD (inert
or medicated) is increased vaginal bleeding. It accounts for 10-20
per cent of all IUD removals (57). The bleeding may take one or
more of the following forms : greater volume of blood loss during
menstruation, longer menstrual periods or mid-cycle bleeding (54).
From the woman's point of view, irregular bleeding constitutes a
source of personal inconvenience; from a medical point of view,
the concern is iron-deficiency anaemia. Usually bleeding or
spotting between periods settles within 1-2 months (55). The
patient who is experiencing the bleeding episodes should receive
iron tablets (ferrous sulfate 200 mg, three times daily).
Studies have shown that the greatest blood loss is caused by the
larger non-medicated devices. Copper devices seem to cause less
average blood loss. Menstrual blood loss is consistently lower
when hormone-releasing devices are used (51).
If the bleeding is heavy or persistent or if the patient develops
anaemia despite the iron supplement, the IUD should be removed.
Since there is often a direct relationship between the bleeding and
the size and configuration of the IUD (56), a change of IUD from
the Lippes Loop to one of copper devices is advised. In most
women, removal of the device is rapidly followed by a return to
the normal menstrual pattern. If an abnormal pattern persists, a full
gynaecological examination is required to ensure that there is no
pelvic pathology (51).
2. Pain
Pain is the second major side-effect leading to IUD removal.
WHO estimates that 15-40 per cent of IUD removals appear to be
for pain only (51). Pain may be experienced during IUD insertion
and for a few days thereafter, as well as during menstruation (57L
It may manifest itself in low back ache, cramps in the lower
abdomen and occasionally pain down the thighs. These symptoms
usually disappear by the third month (55).
If during insertion, the pain is particularly severe, it is possible
that the device may have been incorrectly placed in the uterus or
there is a disparity in size between the device and the uterine
cavity. Severe pain can also indicate a uterine perforation (51).
Pain could also be due to infection. Pain is more commonly
observed in nullipara and those who have not had a child for a
number of years (58, 59).
Slight pain during insertion can be controlled by analgesics
such as aspirin and codein. If pain is intolerable, the IUD should be
removed. In place of a Lippes Loop, a copper device can be tried.
If the woman decides not to have an IUD, another method of
contraception should be prescribed.
3. Pelvic injection
Pelvic inflammatory disease (PID) is a collective term that
includes acute, subacute and chronic conditions of the ovaries,
tubes, uterus, connective tissue and pelvic peritoneum and is
usually the result of infection (56). Studies suggest that IUD users
are about 2 to 8 times more likely to develop PID than noncontraceptors (60). Risk associated with IUD use is greater among
women who have a number of sexual partners (61) possibly
because of greater potential for exposure to STDs. The greater risk
of PID with IUD use may be due to introduction of bacteria
s"Vfl I-------------------------------------------------------------------------who cannot tolerate the adverse effects of oral pills may find the
IUD.an acceptable alternative. It does not interfere with lactations
However, because of expulsion and possible side effects Wye.
menstrual irregularities, IUDs should preferably be used in settings
where follow-up facilities are available. Evidence to date shows
that for a fully informed woman, the IUD can provide a
satisfactory, highly effective, relatively low-risk method of
contraception.
HORMONAL CONTRACEPTIVES
Hormonal contraceptives when properly used are the most
effective spacing methods of contraception. Oral contraceptives of
the combined type are almost 100 per cent effective in preventing
pregnancy. They provide the best means of ensuring spacing
between one childbirth and another. More than 65 million in the
world are estimated to be taking the "pill" of which about 10
million are estimated to be in India.
Gonadal steroids
To physicians in general medicine, the term "steroid" refers to
adrenocortical hormones, while to those in gynaecology, it implies
gonadal steroidsyi.e., oestrogens and progestogens.
a. Synthetic oestrogens : Two synthetic oestrogens are used
in oral contraceptives. These are ethinyl oestradiol and
mestranol. Both are effective. In fact, mestranol is inactive until
converted into ethinyl oestradiol in the liver (65).
b. Synthetic progestogens : These are classified into three
groups - pregnanes, oestranes and gonanes. (i) Pregnanes :
These include megestrol, chlormadinone and medroxy
progesterone acetate. The pregnane progestogens are now not
recommended in oral contraceptives because of doubts raised by
the occurrence of breast tumours in beagle dogs,
(ii) Oestranes : These are also known as 19-nortestosterones,
e.g., norethisterone, norethisterone acetate, lynestrenol,
ethynodiol diacetate and norethynodrel. These are all
metabolised to norethisterone before becoming active. For some
women, oestranes are more acceptable than gonanes.
(iii) Gonanes : The most favoured gonane is levonorgestrel (65).
Classification
Hormonal contraceptives currently in use and/or under study
may be classified as follows :
A. Oral pills
1.Combined pill
2.Progestogen only pill (POP)
3.Post-coital pill
4.Once-a-month (long-acting) pill
5.Male pill
B. Depot (slow release) formulations
1.Injectables
2.Subcutaneous implants
3.Vaginal rings
A. ORAL PILLS
1. Combined pill
The combined pill is one of the major spacing methods of
contraception. The "original pill" which entered into the market in
the early 1960s contained 100-200 meg of a synthetic oestrogen
and 10 mg of a progestogen. Since then, a number of
improvements have been made to reduce the undesirable sideeffects of the pill by reducing the dose of both the oestrogen and
progestogen. At the present time, most formulations of the
combined pill contain no more than 30-35 meg of a synthetic
oestrogen, and 0.5 to 1.0 mg of a progestogen. The debate
continues about the minimum effective dose of the progestogen in
the pill which will produce
Mortality
Ever users
Rate
Controls
15-24 Years
Non-smokers Smokers
0.0
10.5
0.0
0.0
25 -34 Years
Non-smokers Smokers
4.4
14.2
2.7
4.23
35-44 years
Non-smokers Smokers
21.5
63.4
6.4
15.2
45 + years
Non-smokers Smokers
52.4
206.7
11.4
27.9
Source : (80)
The above findings led to the progressive reduction of the
oestrogen content to the minimum levels necessary to maintain
contraceptive effect. In spite of this reduction, it became clear by
1980 that some of the untoward vascular effects (e.g.,
hypertension) persisted, in addition to metabolic effects which are
attributed to the progestogen content of the pill. It became clear
that progestogen levels must also be minimal to avoid the
complications of pill use.
2. Carcinogenesis
A review prepared by WHO (81) concluded that there was no
clear evidence of a relationship, either positive or negative
between the use of combined pill and the risk of any form of
cancer. However,/he WHO Multicentre case-control study on the
possible association between the use of hormonal contraceptives
and neoplasia indicated a trend towards
___________________________HORMONAL CONTRACEPTIVES
369
Wa
3. Metabolic effects
^-*
A great deal of attention has been focused recently on the
metabolic effects induced by oral contraceptives. These have
included the elevation of blood pressure, the alteration in serum
lipids with a particular effect on decreasing high-density
lipoproteins, blood clotting and the ability to modify carbohydrate
metabolism with the resultant elevations of blood glucose and
plasma insulin {83). These effects are positively related to the dose
of the progestogen component (84). Family planning specialists
have voiced a growing concern that the adverse effects associated
with oral contraceptives could be a potential long-range problem
for the users in that they may accelerate atherogenesis and result in
clinical problems such as myocardial infarction and stroke.
4. Other adverse effects
(i) Liver disorders : The use of the pill may lead to
hepatocellular adenoma and gall bladder disease. Cholestatic
jaundice can occur in some pill users, (ii) Lactation : Preparations
containing a relatively high amount of oestrogen adversely affect
the quantity and constituents of breast milk (82) and less frequently
cause premature cessation of lactation. In a WHO study (82) users
of the combined pill experienced a 42 per cent decline in milk
volume after 18 weeks, compared with a decline of 12 per cent for
users of progestogen-only minipills and 0.16 per cent for controls
using non-hormonal preparations. Women taking oral
contraceptives, no matter what type, excrete small quantities of
hormones in their breast milk, but little is known about the longterm impact, if any, on the child (79). (iii) Subsequent fertility: In
general, oral contraceptive use seems to be followed by a slight
delay in conception (85). The proportion of women becoming
pregnant within 2 months of discontinuing the pill may range from
15-35 per cent (86). It is not known whether the prolonged use of
the pill beyond 5-10 years affects subsequent fertility, (iv) Ectopic
pregnancies : These are more likely to occur in women taking
progestogen-only pills, but not in those taking combined pills, (v)
Foetal development : Several reports have suggested that oral pills
taken inadvertently during (or even just before) pregnancy might
increase the incidence of birth defects of the foetus, but this is not
yet substantiated (87).
5. Common unwanted effects
(i) Breast tenderness : Breast tenderness, fullness and
discomfort have been observed in women taking oral pills. Breast
engorgement and fullness are said to be dependent on progestogen;
pain and tenderness are attributed to oestrogen. (ii) Weight gain :
About 25 per cent of users complain of weight gain. It is usually
less than 2 kg, and occurs during the first 6 months of use. This is
attributed to water retention, in which case restriction of salt intake
is usually effective, (iii) Headache and migraine : Migraine may
be aggravated or triggered by the pill. Women, whose migraine
requires treatment with vasoconstrictors such as ergotamine,
should not take oral pills, (iv) Bleeding disturbances : A small
minority of women using oral contraceptives may complain of
break-through bleeding or spotting in the early cycles. A few
women may not have a withdrawal bleeding at the end of a cycle.
Women should be forewarned of these possibilities.
b. Beneficial effects
The single most significant benefit of the pill is its almost 100
per cent effectiveness in preventing pregnancy and thereby
removing anxiety about the risk of unplanned pregnancy. Apart
from this, the pill has a number of non-contraceptive health
24
a. DMPA
Depot-medroxyprogesterone acetate (DMPA or Depo-provera)
has been in use since 1960s. The standard dose is an intramuscular
injection of 150 mg every 3 months. It gives protection from
pregnancy in 99 per cent of women for at least 3 months (90). It
exerts its contraceptive effect primarily by suppression of
ovulation. However, it also has an indirect effect on the
endometrium and direct action on the fallopian tubes and on the
production of cervical mucus, all of which may play a role in
reducing fertility (90). DMPA has been found to be a safe, effective
and acceptable contraceptive which requires a minimum of
motivation or none at all. Another advantage is that it does not
affect lactation. Therefore in the experience of several countries,
DMPA has proved acceptable during the postpartum period as a
means of spacing pregnancies. However, the side-effects of DMPA
(viz. weight increase, irregular menstrual bleeding and prolonged
infertility after its use) are disadvantages limiting the age groups
for which the drug could regularly be used. As now practised in a
number of countries, this contraceptive should find good use
among multiparae of age over 35 years who have already
completed their families. Some countries do not allow the use of
DMPA in view of its effect on subsequent fertility. Available
information suggests that there are no cardiovascular risks
associated with depot injections. It also appears that there is no
excess risk of breast cancer (92).
b. NET-EN
Norethisterone enantate (NET-EN) has been in use as a
contraceptive since 1966. However, it has been less extensively
used than DMPA. It is given intramuscularly in a dose of 200 mg
every 60 days. Contraceptive action appears to include inhibition
of ovulation, and progestogenic effects on cervical mucus. A
slightly higher (0.4) pregnancy rate (failure rate) has been reported
as compared to DMPA.
Administration
The initial injection of both DMPA and NET-EN should be
given during the first 5 days of the menstrual period. This timing is
very important to rule out the possibility of pregnancy. Both are
given by deep intramuscular injection into the gluteus maximus.
The injection site should never be massaged following injections.
(90). Although compliance with regular injection intervals should
be encouraged , both DMPA and Net-EN may be given two weeks
early or two weeks late (91).
Side-effects
Both DMPA and NET-EN have similar side effects, the mo;
common being disruption of the normal menstrual cycle
manifested by episodes of unpredictable bleeding, at time
prolonged and at other times excessive. In addition, man; women
using DMPA or NET-EN may become amenorrhoeic The
unpredictable bleeding may be very inconvenient to th< user; and
amenorrhoea can be alarming, causing anxiety Studies showed
that women discontinuing DMPA becam< pregnant some 5.5
months (average) after the treatmen period. At 2 years, more than
90 per cent of previous user: became pregnant (90). A study is in
progress in India tc examine the return of fertility among women
who discontinuec NET-EN (90). The potential long-term effects of
DMPA anc NET-EN are not yet known.
Contraindications
These include cancer of the breast; all genital cancers;
undiagnosed abnormal uterine bleeding; and a suspected
malignancy (90).
The particular advantage of DMPA and NET-EN is that they
are highly effective, long-lasting and reversible contraceptives.
Checklists have been developed for auxiliaries primarily for the
screening of women who can be given injectable contraceptives
without being examined by the physician; they can also be utilized
in follow-up visits (90).
B. COMBINED INJECTABLE CONTRACEPTIVES (91)
These injectables contain a progestagen and an oestrogen. They
are given at monthly intervals, plus or minus three days. Combined
injectable contraceptives act mainly by suppression of ovulation.
The cervical mucus is affected, mainly by progestagen, and
becomes an obstacle to sperm penetration. Changes are also
produced in endometrium which makes it unfavourable for
implantation if fertilization occurs, which is extremely unlikely.
In clinical trials, Cyclofem / Cyclo-provera and Mesigyna have
both been found to be highly effective with 12 month failure rates
of 0.2 per cent or less for Cyclofem / Cycloprovera and 0.4 per
cent for Mesigyna. The side-effects are similar to progestagen only
injectables, but are much less. Data on return to ovulation and
fertility are limited.
The contraindications are confirmed or suspected pregnancy;
past or present evidence of thromboembolic disorders;
cerebrovascular or coronary artery disease; focal migraine;
malignancy of the breast; and diabetes with vascular
complications. Combined injectables are not suitable for women
who are fully breast feeding until 6 months post -partum. It is less
suitable for women with risk factors for oestrogen.
2. Subdermal implants
The Population Council, New York has developed a subdermal
implant known as Norplant for long-term contraception. It
consists of 6 silastic (silicone rubber) capsules containing 35 mg
(each) of levonorgestrel (93). More recent devices comprise
fabrication of levonorgestrel into 2 small rods, Norplant (R)-2,
which are comparatively easier to insert and remove. The silastic
capsules or rods are implanted beneath the skin of the forearm or
upper arm. Effective contraception is provided for over 5 years.
The contraceptive effect of Norplant is reversible on removal of
capsules. A large multicentre trial conducted by International
Committee for Contraception Research (ICCR) reported a 3-year
pregnancy rate of 0.7. The main disadvantages, however, appear to
be irregularities of menstrual bleeding and surgical procedures
necessary to insert and remove implants.
ABORTION
Abortion is theoretically defined as termination of pregnancy
before the foetus becomes viable (capable of living independently).
This has been fixed administratively at 28 weeks, when the foetus
weighs approximately 1000 g.. Abortion is sought by women for a
variety of reasons including \ birth control. In fact, in some countries
(e.g., Hungary) ther legal abortions exceed live births.
Abortions are usually categorised as spontaneous and induced.
Spontaneous abortions occur once in every 15 pregnancies (97).
They may be considered "Nature's method of birth control".
Induced abortions, on the other hand, are deliberately induced they may be legal or illegal. Illegal abortions are hazardous; they
are usually the last resort of women determined to end their
pregnancies at the risk of their own lives.
The actual incidence of abortion world-wide is not known.
Estimates range from 30-55 million a year or about 40-70 per 1000
women of reproductive age, with an abortion ratio of 260-450 per
1000 live births (98). In India it has been computed that about 6
million abortions take place every year, of which 4 million are
induced and 2 million spontaneous.
Abortion hazards
Abortions, whether spontaneous or induced, whether in hands
of skilled or unskilled persons are almost always fraught
The shortest cycle minus 18 days gives the first day of the
fertile period. The longest cycle minus 10 days gives the last day
of the fertile period. For example, if a woman's menstrual cycle
varies from 26 to 31 days, the fertile period during which she
should not have intercourse would be from the 8th day to the 21st
day of the menstrual cycle, counting day one as the first day of the
menstrual period. Fig. 8 shows the fertile period and the safe
period in a 28-day cycle.
However, where such calculations are not possible, the couple
can be advised to avoid intercourse from the 8th to the 22nd day of
the menstrual cycle, counting from the first day of the menstrual
period (106).
The drawbacks of the calendar method are : (a) a woman's
menstrual cycles are not always regular. If the cycles are irregular,
it is difficult to predict the safe period (b) it is only possible for this
method to be used by educated and responsible couples with a high
degree of motivation and cooperation (c) compulsory abstinence of
sexual intercourse for nearly one half of every month - what may
be called "programmed sex" (d) this method is not applicable
during the postnatal period and (e) a high failure rate of 9 per 100
woman-years (45). The failures are due to wrong calculations,
inability to follow calculations, irregular use and "taking chances".
Two medical complications have been reported to result from
the use of safe period; ectopic pregnancies and embryonic
abnormalities. Ectopic pregnancies may follow conception late in
the menstrual cycle and displacement of the ovum; embryonic
abnormalities may result from conception involving either an overaged sperm or over-aged ovum. If this is correct, the safe period
may not be an absolutely safe period (107).
4. Natural family planning methods
The term "natural family planning" is applied to three methods:
(a) basal body temperature (BBT) method (b) cervical mucus
method, and (c) symptothermic method. The principle is the same
as in the calendar method, but here the woman employs selfrecognition of certain physiological signs and symptoms associated
with ovulation as an aid to ascertain when the fertile period begins.
For avoiding pregnancy, couples abstain from sexual intercourse
during the fertile phase of the menstrual cycle; they totally desist
from using drugs and contraceptive devices. This is the essence of
natural family planning.
(a) Basal body temperature method (BBT)
The BBT method depends upon the identification of a specific
physiological event - the rise of BBT at the time of ovulation, as a
result of an increase in the production of progesterone. The rise of
temperature is very small, 0.3 to 0.5 degree C. When no ovulation
occurs (e.g., as after menarche, during lactation) the body
temperature does not rise. The temperature is measured preferably
before getting out of bed in the morning. The BBT method is
reliable if intercourse is restricted to the post-ovulatory infertile
period, commencing 3 days after the ovulatory temperature rise
and continuing up to the beginning of menstruation. The major
drawback of this method is that abstinence is necessary for the
entire preovulatory period. Therefore, few couples now use the
temperature method alone (108).
(b) Cervical mucus method
This is also known as "Billings method" or "ovulation method".
This method is based on the observation of changes in the
characteristics of cervical mucus. At the time of
____________________.
AGE
15-19
20-24
25-29
30-34
35-39
40-44
45-49
RESIDENCE
Urban
Rural
EDUCATION
Illiterate
Literate, < middle school
complete
Middle school complete
High school complete
and above
RELIGION
Hindu
Muslim
Christian
STANDARD OF LIVING INDEX
Low
Medium
High
25.6
18.4
8.1
3.1
1.1
0.2
0.1
1.6
5.9
10.5
11.1
9.1
5.5
3.0
27.1
24.4
18.6
14.1
10.2
5.7
3.1
6.7
8.9
6.7
7.8
13.4
16.7
7.8
8.4
8.5
6.1
16.2
14.5
11.1
8.8
6.1
6.3
17.1
15.1
8.0
11.0
8.7
7.1
11.0
6.1
15.1
22.0
14.8
9.0
8.5
6.7
8.8
7.2
6.1
17.9
15.6
12.8
of India. In Rajasthan, Madhya Pradesh and Orissa it is aboui 1618 per cent.
The National Family Health Survey-2 results show thai
although current use of contraception has increased and the extent
of unmet need has declined in most of the states in India, there is a
need for considerable improvement in the coverage and quality of
family planning services, especially in the four large states of Uttar
Pradesh, Bihar, Madhya Pradesh and Rajasthan.
Contraception and adolescence (122)
Adolescence is the period between puberty and the end of
physiological maturation, which occurs between ages 15-19 years.
Pregnancy in adolescence constitute between 10 and 20 per cent of
all pregnancies in most developing countries and in some
developed countries such as the USA. Their number is constantly
rising. These are often "at risk" pregnancies. Many are undesired,
and occur in unmarried adolescents who then resort to legal or
illegal abortion, performed under unsatisfactory medical
conditions. This has serious health and even life-threatening
consequences for these young women -the ensuing mortality and
morbidity (especially secondary sterility) are quite considerable.
Prevention of undesired pregnancies and of sexually transmitted
diseases in young people through educational programmes dealing
with responsible sexual behaviour is a major public health
challenge. Adolescents are ambivalent about family planning : to
request contraception is to "reveal" one's sexuality. For this reason
adolescent girls sometimes choose the risk of an undesired
pregnancy and of an abortion.
Barrier methods : Condoms make barrier method worthwhile,
because they protect those adolescents, with occasional different
sexual partners, against STD and AIDS. However, condoms must
be properly used, and it depends on the man's behaviour. Young
men seem to be increasingly aware of the importance of
safeguarding their own health and that of their partners. Cervical
caps and diaphragms, on the other hand, are inappropriate for
adolescents since they require foreseeing of intercourse and
complicated manipulations, to which young people are loath.
Hormonal contraception : Hormonal methods are perfectly
suitable for adolescents, who generally do not suffer from such
problems as cardiovascular contraindications. In fact, these are
probably the most adequate methods, since they are completely
reversible, and in no way modify the future fertility of these young
women. In developed countries pills are usually preferred, but
trimestrial or monthly injections are also appropriate. Implants,
with their five year term, cover too long a period for certain
adolescents.
IUD : IUD are theoretically contraindicated, because of the risk
of pelvic infection and of secondary sterility. However, an
adolescent is better protected by an IUD than by illegal repeated
abortions. This method has the advantage of being discrete and
avoiding demanding routines.
Other methods; Periodic abstinence is not easy when cycles are
irregular and intercourse is unforeseen, and with new partners. In
certain countries, however, they are practically the only method
taught, for religious reasons, and poor protection is preferable to no
protection at all. Similarly, withdrawal is not very suitable method,
since young men are usually not very skilful.
Spermicides are not contraindicated, but have two
disadvantages - they are costly, and are not effective against STD
and AIDS.
In the year 2000, 42 per cent of the world population was under
25 year age group. An extremely large number of young people
will therefore be entering their reproductive years at that time. The
demographic future of the world will depend on
Source : (30)
__________________________________________________REFERENCES 381
assessed in
Delhi
of India 1991,
Provisional Population Totals, Paper 1 & 2 of 1991
6.Govt, of India (2000). Annual Report 1999-2000, Ministry of Health and Family
Welfare, New Delhi
7.National Family Health Survey NFHS 2 India 1998 - 99, International Institute
for Population Sciences, Mumbai, India MEASURE DHS + ORC & MACRO
8.Govt.ofIndia(1986).Hea/th/n/ormationo//ndial9S6, DGHSNew Delhi
9.World Bank (1987). World Development Report, 1987, Oxford University Press,
New Delhi
10.WHO (1996). Regional Health Report 1996, South-East Asia Region, New
Delhi
11.Govt, of India (1993). Health Information of India, 1992, DGHS, Nirman
Bhavan, New Delhi
12.UNDP (2002). Human Development Report 2002, Deepening democracy in a
fragmented world, Oxford University Press
13.UNDP (2003), Human Development Report 2003, Oxford University Press
14.Agarwala, S.N. (1977). India's Population Problems, 2nd Ed., Tata Mc Graw
Hill
15.Sadashiviah, K. et al (1981). J. Family Welfare, 27 (3) 39
16.Last, J.M. (1983). A Dictionary of Epidemiology, Oxford Medical Publications.
17.The John Hopkins University (1985). Population Reports, M.8, Sept-Oct. 85,
Baltimore, Maryland
18.Govt, of India (1986). Swasth Hind, Aug. 1986 Central Bureau of Health
Education, New Delhi.
19.Hogarth, J. (1978). Glossary of Health Care Terminology, WHO, Copenhagen
20.International Family Planning Perspectives (1983). 9 (3) 84, New York, USA
21.Govt, of India (2004). Annual Report 2003-2004, Ministry of Health and Family
Welfare, New Delhi
22.Govt, of India (2003), YearBook, Family Programme in India 1996-97,
Ministry of Health and Family Welfare, New Delhi
23.Govt, of India (2003), Health Information of India 2000 & 2001, DGHS, New
Delhi
194
11.P&P
In any community,
care which it gives to
mothers and children
constitute a priority group. In sheer numbers, they comprise
approximately 70 per cent of the population of the developing
countries. In India, women of the child-bearing age (15 to 44
years) constitute 19 per cent, and children under 15 years of age
about 40 per cent of the total population. Together they constitute
nearly 59 per cent of the total population. By virtue of their
numbers, mothers and children are the major consumers of health
services, of whatever form.
Mothers and children not only constitute a large group, but they
are also a "vulnerable" or special-risk group. The risk is connected
with child-bearing in the case of women; and growth, development
and survival in the case of infants and children. Whereas 50 per
cent of all deaths in the developed world are occurring among
people over 70, the same proportion of deaths are occurring among
children during the first five years of life in the developing world.
Global observations show that in developed regions maternal
mortality ratio averages at 30 per 100,000 live births; in developing
regions the figure is 480 for the same number of live births (1).
From commonly accepted indices, it is evident that infant, child
and maternal mortality rates are high in many developing
countries. Further, much of the sickness and deaths among mothers
and children is largely preventable. By improving the health of
mothers and children, we contribute to the health of the general
population. These considerations have led to the formulation of
special health services for mothers and children all over the world.
The problems affecting the health of mother and child are
multifactorial. Despite current efforts, the health of mother and
child still constitutes one of the most serious health problems
affecting the community, particularly in the developing countries.
The present strategy is to provide mother and child health services
as an integrated package of "essential health care", also known as
primary health care which is based on the principles of equity,
intersectoral coordination and community participation. The
primary health care approach combines all elements in the local
community necessary to make a positive impact on the health
status of the population, including the health of mothers and
children.
Mother and Child - One Unit
Mother and child must be considered as one unit. It is because:
(1) during the antenatal period, the foetus is part of the mother. The
period of development of foetus in mother is about 280 days.
During this period, the foetus obtains all the building materials and
oxygen from the mother's blood; (2) child health is closely related
to maternal health. A healthy mother brings forth a healthy baby;
there is less chance for a premature birth, stillbirth or abortion; (3)
certain diseases and
from 28 to 37 weeks
average 280 days
MCH problems
MCH problems cover a broad spectrum. At one extreme, the
most advanced countries are concerned with problems such as
perinatal problems, congenital malformations, genetic and certain
behavioural problems. At the other extreme, in developing
countries, the primary concern is reduction of maternal and child
mortality and morbidity, spacing of pregnancies, limitation of
family size, prevention of communicable diseases, improvement of
nutrition and promoting acceptance of health practices. Currently,
the main
health problems affecting the health of the mother and the child in
India, as in other developing countries, revolve round the triad of
malnutrition, infection and the consequences of unregulated
fertility (4). Associated with these problems is the scarcity of
health and other social services in vast areas of the country
together with poor socio-economic conditions.
1. MALNUTRITION
Malnutrition is like an iceberg; most people in the developing
countries live under the burden of malnutrition. Pregnant women,
nursing mothers and children are particularly vulnerable to the
effects of malnutrition. The adverse effects of maternal
malnutrition have been well documented-maternal depletion, low
birth weight, anaemia, toxemias of pregnancy, post-partum
haemorrhage, all leading to high mortality and morbidity. The
effects of malnutrition are also frequently more serious during the
formative years of life. Previously it was thought that malnutrition
was largely concentrated in school age children, and in toddlers.
Now it is realised that the intrauterine period of life is a very
important period from the nutritional standpoint. Infants born with
adequate birth weight have relatively low mortality even under
poor environmental conditions. The next critical period of
childhood is the period of weaning. Severe malnutrition coincides
with the age at which babies are usually weaned. Susceptibility to
infection and severity of illness are significantly less in well
nourished, than in malnourished children. Nutrition protection and
promotion is, therefore, an essential activity of MCH care.
Measures to improve the nutritional status of mothers and
children may be broadly divided into direct and indirect nutrition
interventions (4). Direct interventions cover a wide range of
activities, viz. supplementary feeding programmes, distribution of
iron and folic acid tablets, fortification and enrichment of foods,
nutrition education, etc. Indirect nutrition interventions have still
wider ramifications because they are not specifically related to
nutrition. These include measures such as control of communicable
diseases through immunization, improvement of environmental
sanitation, provision of clean drinking water, family planning, food
hygiene, education and primary health care. Nutritional
surveillance is becoming increasingly important for identifying
subclinical malnutrition, as it tends to be overlooked in both the
mother and the child. The primary health worker (community
worker) can play a vital role in improving the nutritional status of
mothers and children.
2. INFECTION
Maternal infections may cause a variety of adverse effects such
as foetal growth retardation, low birth weight, embryopathy,
abortion and puerperal sepsis. In industrial societies, the risk of the
mother acquiring infections during pregnancy is relatively low, but
in underdeveloped areas, the mother is exposed to significantly
higher risks. Many women are infected with cytomegalo viruses,
herpes simplex virus or toxoplasma during pregnancy.
Furthermore, as many as 25 per cent of the women in rural areas
suffer at least one bout of urinary infection (5).
As far as the baby is concerned, infection may begin with labour
and delivery and increase as the child grows older. Children may be
ill with debilitating diarrhoeal, respiratory and skin infections for as
much as a third of their first year of life. In some regions, the situation
is further aggravated by such chronic infections as malaria and
tuberculosis. The occurrence of multiple and frequent infections may
precipitate in the children a severe protein-energy malnutrition and
anaemia. When the child becomes ill, traditions, beliefs and taboos
enter into play; the indirect effect of infections may be more 5
important than the direct one in traditional societies (5, 6).
IMR per
1000 live
births
India
24
67
93
Pakistan
36
83
107
Bangladesh
29
51
77
Thailand
18
24
28
Sri Lanka
17
17
19
China
15
31
39
Country
Switzerland
Under-five
mortality rate
per 1000 live
births
UK
11
USA
15
Singapore
10
Japan
Source : (7)
MAINTENANCE OF RECORDS
The "Antenatal Card" is prepared at the first examination. It is
generally made of thick paper to facilitate filing. It contains a
Registration number, identifying data, previous health history, and
main health events. The Record is kept at the MCH/FP Centre. A
link is maintained between the Antenatal Card, Postnatal Card and
Under-fives' Card. Maintenance of records is essential for
evaluation and further improvement of MCH/FP services.
HOME VISITS
Home visiting is the backbone of all MCH services. Even if the
expectant mother is attending the antenatal clinic regularly, it is
suggested that she must be paid at least one home visit by the
Health Worker Female or Public Health Nurse. More visits are
required if the delivery is planned at home. The mother is
generally relaxed at home. The home visit will win her
confidence. The home visit will provide an opportunity to observe
the environmental and social conditions at home and also an
opportunity to give prenatal advice.
(2) Prenatal advice
A major component of antenatal care is antenatal or prenatal
advice. The mother is more receptive to advice concerning herself
and her baby at this time than at other times. The "talking points"
should cover not only the specific problems of pregnancy and
child-birth but overflow into family and child health care.
(i) DIET : Reproduction costs energy. A pregnancy in total
duration consumes about 60,000 kcal, over and above normal
metabolic requirements. Lactation demands about 550 kcal a day.
Further, child survival is correlated with birth weight. And birth
weight is correlated to the weight gain of the mother during
pregnancy. On an average, a normal healthy woman gains about
12 kg of weight during pregnancy. Several studies have indicated
that weight gain of poor Indian women averaged 6.5 kg during
pregnancy (11). Thus pregnancy imposes the need for considerable
extra calorie and nutrient requirements. If maternal stores of iron
are poor (as may happen after repeated pregnancies) and if enough
iron is not available to the mother during pregnancy, it is possible
that foetus may lay down insufficient iron stores. Such a baby may
show a normal haemoglobin at birth, but will lack the stores of
iron necessary for rapid growth and increase in blood volume and
muscle mass in the first year of life. Stresses in the form of malaria
and other childhood infections will make the deficiency more
acute, and many infants become severely anaemic during early
months of life. A balanced and adequate diet is therefore, of
utmost importance during pregnancy and lactation to meet the
increased needs of the mother, and to prevent "nutritional stress".
(ii) PERSONAL HYGIENE : Of equal importance is advice
regarding personal hygiene, (a) Personal cleanliness : The need to
bathe every day and to wear clean clothes should be explained.
The hair should also be kept clean and tidy, (b) Rest and sleep : 8
hours sleep, and at least 2 hours rest after midday meals should be
advised, (c) Bowels: Constipation should be avoided by regular
intake of green leafy vegetables, fruits and extra fluids. Purgatives
like caster oil should be avoided to relieve constipation, (d)
Exercise: Light household work is advised, but manual physical
labour during late pregnancy may adversely affect the foetus, (e)
Smoking: Smoking should be cut down to a minimum. Expectant
mothers who smoke heavily produce babies much smaller than the
average - it is because nicotine has a vasoconstrictor influence in
the uterus and induces a degree of placental insufficiency. The
adverse effects of smoking range from low birth-weight to an
increased risk of perinatal death of the infant (12). Women who
smoke
it rJ
TABLE 2
^
,p
Output of breast milk at different stages of lactation
Months of
lactation
Number
examined
0-2
20
530
3-4
5-6
7-8
9-10
18
14
14
17
640
730
660
600
11-12
13-15
16-18
19-24
25-36
37-38
30
11
29
14
12
4
525
515
440
400
425
345
Source : (27)
Family Planning
It has already been stressed that family planning is related to
every phase of maternity cycle. Every attempt should be made to
motivate mothers when they attend postnatal clinics or during
postnatal contacts to adopt a suitable method for spacing the next
birth or for limiting the family size as the case may be. Postpartum
sterilization is generally recommended on the 2nd day after
delivery. Although lactation confers some protection against
conception, it cannot be depended upon; contraceptives have to be
supplied immediately postpartum. To ask the mothei to come at the
time of her first menstruation may be too late. A contraceptive
must therefore be used that will not affect lactation in the
early postpartum period. In this
TABLE 3
Apgar Score
Sign
Score 1
Heart rate
Absent
Slow (below
100)
Over 100
Respiratory effort
Absent
Slow
Irregular
Good
crying
Muscle tone
Flaccid
Some flexion of
extremities
Active
movements
Reflex response
No response
Grimace
Cry
Colour
Blue, pale
Body pink
Extremities
blue
Completely
pink
Total score = 10
. Severe
depression
0-3
Mild
depression
4-7
No
depression
7-10
There are two main groups of low birth weight babies -those
born prematurely (short gestation) and those with foetal growth
retardation. In countries where the population of low birth weight
infants is less, short gestation period is the major cause. In
countries where the proportion is high (e.g. India), the majority of
cases can be attributed to foetal growth jretardation.
( A target birth weight of atleast 2.5 kg for 90 per cent of
)newBorn infants, and an adequate growth of children as
measured by weight-for-age, together constitute global
indicator number "8" for monitorifuj and evaluation of the
global strategy for Health for A11/200O] Y"^n%
^*IBy international agreement low birth weight has been denrlect
as a birth weight of less than 2.5 kg (up to and including 2499g),
the measurement being taken preferably within the first hour of
life, before significant postnatal weight loss has occurred (39).
Apart from birth weight, babies can also be classified into 3 groups
according to gestational age, using the word "pre-term", "term"
and "post-term", as follows (38) :
rj9( a. Pre-term : Babies born before the end of 37 weeks
India
26
Sri Lanka
Thailand
China
Bangladesh
Pakistan
USA
Singapore
Sweden
UK
Switzerland
17
7
6
30
21
8
8
4
8
6
Source : (42)
FEEDING OF INFANTS
A detailed discussion of the feeding of infants is outside th
scope of this book. However, a brief mention may be made c
some of the important aspects of the problem.
(1) Breast feeding
Under any circumstances, breast milk is the ideal food fo the
infant. No other food is required by the baby until 4-i months after
birth. Under normal conditions, Indian mother secrete 450 to 600
ml of milk daily with 1.1 gm protein per 10( ml. The energy value
of human milk is 70 kcals per 100 ml.
A child who is breast-fed has greater chances of surviva than a
child artificially fed. Prolonged breast feeding doe: protect the
infant from early malnutrition and some infections The data
suggest that infant mortality rates in developing countries are 5-10
times higher among children who have nol been breast-fed or who
have been breast-fed for less than 6 months. Despite the marked
advantages of breast-feeding, its popularity has declined
significantly in many parts of the world.
Among the advantages of breast milk are the following : (a) it is
safe, clean, hygienic, cheap and available to the infant at correct
temperature (b) it fully meets the nutritional requirements of the
infant in the first few months of life (c) it contains antimicrobial
factors such as macrophages, lymphocytes, secretory IgA, antistreptococcal factor, lysozyme and lactoferrin which provide
considerable protection not only against diarrhoeal diseases and
necrotising enterocolitis, but also against respiratory infections in
the first months of life (d) it is easily digested and utilized by both
the normal and premature babies (e) it promotes "bonding"
between the mother and infant (f) sucking is good for the baby - it
helps in the development of jaws and teeth (g) it protects babies
from the tendency to obesity (h) it prevents malnutrition and
reduces infant mortality (i) it provides several biochemical
advantages such as prevention of neonatal hypocalcemia and
hypomagnesaemia (48) and (j) it helps parents to space their
children by prolonging the period of infertility.
It is neither necessary nor desirable +o train a baby to "feed by
the clock". It should be explained to the mother, however, that
intervals between feeds are necessary for herself and for the baby,
though they may vary between 1 to 4 hours, according to the
baby's needs, size, strength of sucking and the mother's milk
supply.
(2) Artificial feeding
The main indications for artificial feeding are failure of breast
milk, prolonged illness or death of the mother. It is crucial for the
baby to be fed "breast-milk substitutes" - e.g., dried whole milk
powder, fresh milk from a cow or other animal or commercial
formulae.
PRINCIPLES OF ARTIFICIAL FEEDING
In planning an artificial feed, the nutritional needs of infants
should be kept in view. These include :
1.Infants require an average of 100 kcal of energy per kg of
body weight per day, i.e., about 150 ml of milk per kg of
body weight each day
2.The estimated protein requirement is about 2 g/kg of body
weight during the first 6 months; it declines to about 1.5 g/kg
by the end of one year. This works out to 13-14 g protein
daily during the first year of life. In terms of Calories, 8 to 10
per cent of Calories are given as protein
3.The carbohydrate requirement is about 10 g/kg of body
weight daily
70
20
5
kcal
64
Protein (g) 2.1
- Place milk, water, and sugar in pan
- bring to boil, then
cool
- pour into feeding utensil
100
150
180
20
10
103
3.0
0
10
135
4.5
0
10
153
5.4
Source : (50).
Artificial feeding is a hazardous procedure in poor homes
because of the dangers of contamination and over-dilution of the
feed.
The composition of cow's milk and human milk is given in
Table 6.
Table 6 shows that cow's milk and human milk are dissimilar in
many respects. The differences may be seen as great as the
difference between "brain" and "brawn", (a) Protein : One of the
striking difference is the low protein content of human milk; this is
about 3 times less than in cow's milk and lower than in most
mammals. The proteins in human breast milk and in cow's milk are
completely different. Human milk contains more cystine, essential
for the prematures, and less methionine than cow's milk. It is rich
in taurine, indispensable for infants, but which they, unlike adults,
are unable to synthesize. Breast milk is almost completely digested
and utilized for growth, whereas much of cow's milk protein is
excreted by the infant undigested producing whitish curdy stool.
Breast milk contains other proteins whose functions are not
nutritive, but anti-infective, e.g., IgG, lysogyme, living cells, etc.
Human milk is virtually a "living" fluid, (b) Fats : Mother's milk is
especially rich in fats, which represent between 35-50 per cent of
total energy value.
Cow's milk
Grammes per litre
Constituent
Breast milk
Grammes per litre
( PROTEINS :
11
33/
4
7
3.5
0
lto2
lto2
0.5
0.32
28
5
1.5 to 1.8
3.7
0.2 to 0.5
0.5
Traces
0.32
c
v
_(
/
1
!
\
i
TABLE 5
Quantities per feeding - assuming five feedings per day
3
Casein
Soluble proteins
Lactalbumin
Beta -lactoglobulin
Lactotransferrin
Immunoglobulin
Lysozyme
NON-PROTEIN:
NITROGENOUS
SUBSTANCES
LIPIDS :
"- Linoleic acid
^CARBOHYDRATES :
- Lactose
- Nitrogenous
oligosaccharides
MINERALS:
- Ca
P
Fe
VITAMINS :
- C
- D
ENERGY:
\
35
3.5
70
62
8
2
0.33
0.15 0.4 to 1.5
mg
60 mg
50 IU
640-720 kcal
2670-3000 kJ
35j
1
50)
50
0
1
~)
8
/
1 /
/ 0.3 to 0:5 mg
20 mg
/
25 IU /
650 kcal /
2717 kJ \
Source : (49)
There are two main ways in which the fats of human milk differ
from those of other milks - first, levels of essential polyunsaturated
fatty acids, especially linoleic acid and alpha -linoleic acid are
higher in human milk than in cow's milk; secondly, the fats of
human milk are easier for the baby to digest and absorb than are
those of cow's milk. With cow's milk, unabsorbed fatty acids tend
to bind with calcium and prevent it from being absorbed. Although
there is less calcium in human milk than in cow's milk, it is much
better absorbed, (c) Carbohydrate : Human milk contains more
lactose than most other milks. It may be specially useful for the
growing brain. In the intestine, lactose helps the "right" kind of
bacteria (i.e., Lactobacillus bifidus) to grow. Lactobacillus and
lactose help to keep the intestinal contents acidic, which inhibits
the growth of harmful bacteria. Lactose plays an important role in
maintaining low electrolyte concentration, (d) Vitamins and
minerals : If the mother takes adequate amount of vitamins, there is
no reason why the child should have a vitamin supplement. The
earlier teaching that human milk was deficient in vitamin D is no
longer accepted. Recent work has shown that vitamin D is present
in human milk in water-soluble form which was unknown to
nutritionists. Human milk contains more vitamin A and vitamin C
than cow's milk. Another factor which was supposed to be
deficient in human milk was iron, but again recent work has shown
that iron contained in human milk has a high level of
bioavailability, thanks to complex phenomena (the action of
lactoferrin, acidity of the digestive track, presence of appropriate
proportions of zinc and copper). The coefficient of uptake of the
iron in breast milk may be as high as 70 per cent, whereas it is only
30 per cent for cow's milk and infant formulas (49), and no iron
supplement is necessary for the baby reared on human milk.
Human milk is richer in copper, selenium and cobalt than cow's
milk. It contains less sodium than cow's milk
CONCEPT OF NORMALITY
When speaking of human growth and development mention
must be made of the difficulty of defining normality, fi normal
child may be defined as one whose characteristics fal within the
range of measurements accepted as normal for the majority of
children in the same (or reference) age group Conventionally,
these limits - the limits of normal variation -are assumed to include
two standard deviations above and below the mean (i.e., between
the 3rd and the 97th centiles). This presupposes the availability of
accurate measurement techniques of growth, and a sau^fectory set
of reference values or standards for comparison.
As far as physical development is concerned, we have
measurement techniques. For example, we measure growth in
terms of kilograms and centimetres. But very great difficulties are
encountered in connection with psychomotor, emotional and social
development; most measurement techniques are based on
observations such as "milestones of development."
1. Definition
A phenomenon peculiar to the paediatric age group is growth
and development. The term growth refers to increase in the
physical size of the body, and development to increase in skills and
functions. Growth and development are considered together
because the child grows and develops as a whole. Growth and
development include not only physical aspect, but also intellectual,
emotional and social aspects. Normal growth and development take
place only if there is optimal nutrition, if there is freedom from
recurrent episodes of infections, and if there is freedom from
adverse genetic and environmental influences. MCH care is
concerned with the process of growth and development, which is
the foundation of human life. It is the nature of this protess of
physical and psychological growth and development of the child
which is crucial for health or ill-health, for life or death.
Determinants of Growth and Development
It is beyond the scope of this book to delve into the subject of
growth and development which indeed is a vast one, except to
make a passing reference to some of the more important factors
influencing it. Briefly these are : (1) Genetic inheritance : Genetic
factors influence growth and development, especially height and
weight, mental and social development and personality (2)
Nutrition : Nutrition influences growth and development before as
well as after birth. In fact, retardation of growth rate is an
indication of malnutrition. When the diet is improved the child
begins to grow in height and weight. (3) Age: Growth rate is
maximum during foetal life, during the first year of life and then
again at puberty. At other periods, growth is slower. (4) Sex : At
about the age of 10 to 11 years, female children show a sudden
increase in height and weight. This growth spurt corresponds to
puberty. In male children, the growth spurt occurs a little later, i.e.,
between 12 and 13 years. (5) Physical surroundings: Sun-shine,
good housing, lighting and ventilation have their effects on growth
and development
2. Normal growth
"normal." However, the 6 per cent of the children outside this range may not necessarily be "abnormal", particularly if their growth is
parallel with their centile lines. A measurement outside 3 standard deviation (above 99th and below 1st centile) is more likely to indicate a
significant degree of abnormality, (iii) Thirdly, it is also possible to assess the growth of a child by such indices as weight for height, and
weight/ height. These are age-independent indices.
The assessment of growth may be longitudinal or cross-sectional. Longitudinal assessment of growth entails measuring the same child
at regular intervals. This provides valuable data about a child's progress. Cross-sectional studies are also essential to compare a child's
growth with that of his peers. Cross-sectional comparisons involve large number of children of the same age. These children are measured
and the range of their measurements (e.g., weight, height) is plotted, usually on percentile charts.
Reference values
For national and international comparisons and for monitoring, reference or "standard" values of growth are essential. The well known
reference standards are : (i) Harvard (or Boston) standards (53) : These are based on observations made on children in Boston from 1930
to 1956. They have been carefully compiled longitudinally on a large series of children, mostly from North European origin. They became
widely used throughout the world, (ii) WHO reference values (54, 55) : The Harvard values are being replaced by WHO reference values
for weight and height. These new values are based on extensive cross sectional data assembled by the United States National Centre for
Health Statistics (NCHS) which were considered the best available for international use. The WHO reference values may be used for
children upto 5 years of age since the influence of ethnic or genetic factors on young children at this age period is considered insignificant,
given the similar socio-economic environment. (Hi) Indian
standards (56) : The Indian Council of Medical Research (ICMR) undertook a nation-wide cross-sectional study during the year 1956 and
1965 to establish the much needed reference standards of growth and development of Indian children, for the country as a whole, as well as
for each of the states in the country. As the Indian data are based on measurements of children belonging to the lower socioeconomic
groups which form the majority of Indian communities, the values cannot be considered as representing standard values (57).
The use of local standards of reference is not recommended unless these are based on well-nourished and healthy samples of local
population. Further, local standards do not permit international comparisons (58). It was the opinion of WHO thai countries or regions
might eventually develop their own reference standards; in the interim, the WHO reference value should provide an effective substitute
(54).
Reference versus standard values
A distinction must be made between reference values anc standard values. If the values are derived from a populatior racially different
from the population under study, such value: should be considered as reference values only and not a; standard values (59). That is,
reference values cannot be usee as standard values applicable to a population racially different For example, it would be absurd to apply
the Harvarc standards of growth to Pigmies and Eskimos who are racialh different (58).
Surveillance of growth and development
Surveillance of growth and development is a specifii function of the mother and child health services. It is ar important component of
the routine anticipatory care o children. The main purpose of growth surveillance is to identif; those children who are not growing
normally. Surveillance alsc reflects the effectiveness of other components of child can
Increments
200 g 150 g
100 g 50 75 g
2.5 kg
2.0 kg
1st year
2nd year
3rd year
4th year
5th year
Source : (59)
Weight-for-age is often used to classify malnutrition and
determine its prevalence. Jelliffe suggested that 80 per cent of the
median weight-for-age of the reference be the cut-off point below
which children could be considered malnourished.
2. Height (length)-for-age
Height should be taken in a standing position without foot wear.
If the height machine is not available, the measuring scale fixed to
the wall can be employed. This arrangement is suitable for children
2 years and above. The measuring scale should be capable of
measuring to an accuracy of 0.1 cm (55). A very great effort should
be made to measure children accurately. Errors in the measurement
of a young child may lead to significant errors in the classification
of the nutritional status.
The length of a baby at birth is about 50 cm. It increases by
about 25 cm during first year, and by another 12 cm during the
second year. During growth spurt, boys add something like 20 cm
in their height, and girls gain about 16 cm. The spurt is followed
by a rapid slowing of growth. Indian girls reach 98 per cent of their
final height on an average by the age of 16.5
TABLE 7
Reference Standards of Weight of Boys and Girls up to the age of 10 years
Age (years)
-2SD
0
0.25
0.5
0.75
1.0
1.5
2.0
3
4
5
6
7
8
9
10
2.4
4.1
5.9
7.2
8.1
9.1
9.9
11.4
12.9
14.4
16.0
17.6
19.1
20.5
22.1
Boys
Median
3.3
6.0
7.8
9.2
10.2
11.5
12.69
14.6
16.7
18.7
20.7
22.9
25.3
28.1
31.4
+ 2SD
-2SD
Girls
Median
+2SD
4.3
7.7
9.8
11.3
12.4
13.9
15.2
18.3
20.8
23.5
26.6
30.2
34.6
39.9
46.0
2.2
3.9
5.5
6.6
7.4
8.5
9.4
11.2
12.6
13.8
15.0
16.3
17.9
19.7
21.9
3.2
5.4
7.2
8.6
9.5
10.8
11.9
14.1
16.0
17.7
19.5
21.8
24.8
28.5
32.5
4.0
7.0
9.0
10.5
11.6
13.1
14.5
18.0
20.7
23.2
26.2
30.2
35.6
42.1
49.2
Figures taken from United States Public Health Service, Health Resources Administration NCHS growth charts, Rockville, MD, 1976 (HRA 761120,25,3).
Full details on weight for age, height for age, and weight for height are given in the original publication as reproducted by WHO (Measuring
change in nutritional status, Geneva, World Health Organization, 1983).
years, and boys reach the same stage by the age of 17.75 years.
With the exception of a few ethnic groups, there is evidence
showing that all children have a similar growth potential.
Height is a stable measurement of growth as opposed to body
weight. Whereas weight reflects only the present health status of
the child, height indicates the events in the past also. The use of
growth (height) centile chart is particularly valuable in studying
the trend of height curve.
Low height for age : This is also known as nutritional stunting
or dwarfing. It reflects past or chronic malnutrition. The cut-off
point commonly taken for the diagnosis of stunting is 90 per cent
of the United States NCHS height-for-age values (61). Waterlow
recorded the use of 2SD below the median reference as the cut-off
point.
3. Weight-for-height
Height and weight are interrelated. Weight in relation to height
is now considered more important than weight alone. It helps to
determine whether a child is within range of "normal" weight for
his height. For example, a child on the 75th centile of both his
height and weight is neither over-weight nor under-weight, but a
child on the 75th centile of his weight chart and the 25th centile of
his height chart is clearly overweight.
Low weight for height : This is also known as nutritional
wasting or emaciation (acute malnutrition). It is associated with an
increased risk of mortality and morbidity (61). A child who is less
than 70 per cent of the expected weight-for-height is classed as
severely wasted.
The WHO has compiled reference value for children giving
weight according to height.
Weight Records :
Weight records are generally kept by all infant clinics; the aim
is the prevention of underfeeding, and in the developing world, the
weight chart is an important tool in the prevention of malnutrition.
<4. Head and chest circumference
-v lALbirth the head circumference is about 34 cm. It is about 2 m
more than the chest circumference. By 6 to 9 months, the *fwo
measurements become equal, after which the chest circumference
overtakes the head circumference. In severely malnourished children,
this overtaking may be delayed by 3 to 4 years due to poor
development of the thoracic cag^ In a ICMR study (56), the
crossing over of chest afta head?
circumference did not take place until the age of two years and six
months. This has been attributed to growth retardation in poor
Indian children.
Besides increase in height and weight, the term "growth" also
includes various physiological events which occur at predictable
periods such as, dentition, ossification of bones and secondary
sexual characteristics.
BEHAVIOURAL DEVELOPMENT
A closely related development is behavioural development. It is
assessed in four fields :
1.Motor development
2.Personal - social development
3.Adaptive development
4.Language development
The developmental landmarks or milestones of development
provide an estimate of the time when the child can be expected to
attain certain skills or points in development. Since the milestones
are averages, each child is bound to differ from the other. For
instance, some children sit up and speak earlier than others. Table
9 shows some of the normal developmental milestones and ages at
which these are reached in the Indian context. When a child takes
longer time to cross these milestones, the possibility of his being
mentally handicapped should not be overlooked.
The behavioural development of the child is a complex affair.
The work of ethnologists and sociologists show how quickly the
child's behaviour conform to the models adult society offers them.
For proper behaviour development, the child must be assured
emotional and moral stability, that is, a home where he will find
bonds of affection, regular discipline and parents who accept him
and provide him with models of balanced conduct. Many children
will not find themselves in ideal conditions. They consequently
have trouble with behaviour, speech, sleep and appetite and these
problems will have to be anticipated, diagnosed and treated.
THE GROWTH CHART
The growth or "road-to-health" chart (first designed by David
Morley and later modified by WHO) is a visible display of the
child's physical growth and development. It is designed primarily
for the longitudinal follow-up (growth monitoring) of a child, so
that changes over time can be interpreted.
It is important to note that in the weight-for-age chart, the
height of the child is not taken into consideration. This is
\ because weight is the most sensitive measure of growth, and
Milestones of Development
The 'milestones' given here are approximations and to assess any individual child, all types of growth development
and behaviour must be taken into account.
...............................
Age
Motor
development
6-8 weeks
3 months
4-5 months
6-8 months
crawling
stands with support
11
months
12-14
months
18-21 months
24 months
Language
development
Adaptive
development
Socio-personal
development
Looks at mother and smiles
listening
experimenting
with noises
increasing range of
sounds first words
joining words
beginning to run
short sentences
begins to reach
out for objects
transfers objects
hand to hand
releases objects
recognises mother
enjoys hide
and seek
suspicious of strangers
builds
beginning to explore
dry by day
Reference curves :
For purposes of comparison, growth charts are provided
with reference curves. These curves show the limits of normal
/-f growth./The WHO reference curves are based on extensive
-?-~ cross-sectional data of well-nourished healthy children, (f$
[\ffy assembled by the United States National Centre for Health '2. Growth chart used in India/
h~ There are 49 different types of growth charts in use in Indi.
(65). The growth chart recommended by the Government c
FIG. 4
A Growth Chart showing the direction of the growth curve
WEIGHT CURVE FROM BIRTH TO 5 YEARS OF AGE
India is shown in Fig. Sl^lt has four reference curves. The topmost curve corresponds to 80 per cent of the median (50th percentile) of the
WHO reference standard. The lower lines represent 70 per cent, 60 per cent and 50 per cent of that standard. 80 per cent median weight is
approximately equivalent to 2 SD below the median (or mean) which is the conventional lower limit of "normal range/ The purpose of these
lines is to indicate the degree of malnutrition, as recommended by the Indian Academy of Paediatrics.
The growth chart recommended by the Govt, of India shows three degrees of malnutrition: first-degree (Grade I), second-degree (Grade II)
and third-degree (Grade III) malnutrition. /According to this classification, if a child's weight is between Hhe 80 per cent and 70 per cent lines,
it indicates first-degree or mild malnutrition. If the weight is between 70 per cent and 60 per cent, it indicates second-degree or moderate
malnutrition. If the weight is below the 60 per cent line, it is third-degree or severe malnutrition. In addition, Grade IV, below 50 per cent has
also been added. vAny weight between the top two lines is considered satisfactory/
The growth charts being used in ICDS in India contain 3 reference lines in addition to the standard, representing 80 per cent, 60 per cent
and 50 per cent of the reference standard (64).
Uses of growth chart
A growth chart has many potential uses :
1. for growth monitoring which is of great value in child health care
1.diagnostic tool: for identifying "high risk" childn For example, malnutrition can be detected long bef< signs and symptoms of it
become apparent
2.planning and policy making: by gradi malnutrition, it provides an objective basis planning and policy making in
relation to child hea care at the local and central levels
3.educational tool: because of its visual character, 1 mother can be educated in the care of her own ch and encourage her to participate
more actively growth monitoring
4.tool for action: it helps the health worker on t type of intervention that is needed; it will help make referrals easier
5.evaluation: it provides a good method to evaluc the effectiveness of corrective measures and t impact of a programme or of special
interventions i improving child growth and development
6.tool for teaching: it can also be used for teachir for example, the importance of adequate feeding; t deleterious effects of diarrhoea.
The growth chart has been described as a passport to ch health care (65). It has won international recognition and now a standard method of
monitoring children's health ai nutritional status.
Alternative methods of growth monitoring
Growth charting is only one method of growth monitorin There are other indicators such as height-for-age, weight-fo
AGE IN MONTHS
Weights of average well-fed healthy children should be above the uppermost line I.
Children whose weight falls between lines I and III are under-nourished and require supplementary feeding at home.
Children whose weight falls below line III are severely malnourished. Consult the doctor and follow his advice.
Children whose weight falls below line IV will have to be hospitalized for treatment.
FIG. 5
Growth chart in use in India, showing use of several reference curves to
indicate the nutritional status of the child
height, and arm circumference. The last two are independent of
age and are particularly useful when age is not known.
GARE OF THE PRE-SCHOOL CHILD
Children between 1-4 years of age are generally called preschool age children or toddlers. In the history of health services of
many developing countries, their social and health needs were
realised rather late. Today, more than ever before, the pre -school
age child has become a focus for organized medical-social
welfare activities, and their death rate is considered a significant
indicator of the social situation in a country.
The pre-school age is distinguished by the following
characteristics :
1. Large numbers :
Pre-school age children (1-4 yrs) represent about 12 per cent of
the general population in India. A large majority of these children
live in rural and tribal areas and in urban slums. By virtue of their
numbers, they are entitled to a large share of health and social
services. Further, children are the human resources of the future.
Their development is in the interest of the total national
development; therefore, they need special attention.
Unfortunately, pre-school age children are comparatively less
attended to.
2. Mortality :
The pre-school age (1-4 years) mortality in India is as high as
11.2 per cent of all deaths. This high mortality which is largely
due to infection and malnutrition is characteristic of this
^
UNDER-FIVES' CLINIC
(j
1. Integration of care :
Conventional MCH services tended to be fragmented into
antenatal care, postnatal care, infant care, family planning etc. The
various components were dealt with separately by different staff or
departments. This approach has changed over the years. The trend
now is towards an "integrated" approach.
A. Family Planning
indicators
Crude birth
rate
Total fertility
rate
Couple
protection rate
B. Mortality indicators
per 1000
Infant
mortality
Neonatal
mortality
Maternal
mortality
Under 5
mortality
C. Services (% coverage)
Infants
(fully immunized)
- Measles
- DPT
- Polio
- BCG
Pregnant
women TT
Antenatal care
Institutional
deliveries
Deliveries
by trained
personnel
D Prevalence of low birth Weight babies
25.0
(2002)
3.1
(2002)
52
(2002)
23
21
2.6
2.1
64
(2002)
45
(1999)
4.07
(1998)
93
(2002)
56-50
56
(2002)
67
70
70
81
82.9
65
100
60
(1995-2002)
34
(1998-99)
42.3
(2000)
95
100
35
80
45
100
26
(1995-2000)
60
Meet all
needs
< 30
35
10
Source : (7, 77, 78, 79) and Annual Report (Govt, of India) 2003-2004
Organization of MCH/FP services
The mother and child health, and family planning services were
integrated in the fourth Five Year Plan, for better effectiveness.
They both are now an integral part of primary health care, which
places emphasis on community participation and intersectoral
coordination. The National Health Policy has provided the
necessary directives for reorienting and restructuring the health
services, based on primary health care approach, with short and
long-term goals.
The organizational pattern of MCH and Family planning
services cannot be considered apart. They are discussed in the
, ,.
J..
Source : (7)
Causes
v^
About 80 per cent of maternal deaths are due to directv causes
i.e. obstetric complications of pregnancy, labour and puerperium to
interventions or incorrect treatment. As shown in Fig. 8 the single
most common cause-accounting for a quarter of all maternal deaths is obstetric haemorrhage, generally occurring post-partum which can
lead to death very rapidly in the absence of prompt life-saving care.
Severe bleeding
Medical Causes
Obstetric causes:
Toxaemias of pregnancy
Haemorrhage
Infection
Obstructed labour
Unsafe abortion
Social Factors
MORTALITY IN INFANCY AND CHILDHOOD
Age at child birth
Parity
Too close pregnancies
Family size
Malnutrition
Poverty
Illiteracy
Ignorance and prejudices Lack
of maternity services
Shortage of health manpower
Delivery by untrained dais
Poor environmental sanitation
Poor communications and
transport facilities
Social customs, etc.
Newer approaches such as "risk approach" and primary health care are
steps in the right direction to reduce maternal mortality and morbidity.
Despite best antenatal care, some
Mortality rates are good indicators to measure the level health and
health care in different countries. They also help assessing the overall
socio-economic development of country and correlate well with certain
economic variab such as GNP. Medical and social progress have
substantic reduced mortality in childhood.
It has become customary to consider mortality in a around infancy
in a number of time periods convenient fr< both the analytical and
programmatic point of view as under
a.
perinatal period
b.
c.
d.
neonatal period
e.
Although perinatal period occupies less than 0.5 per cent (less than 168
hours) of the average life span, there are more deaths within this period
than during the next 30-40 years of life in many developing countries (90).
The value of perinatal mortality rate is that it gives a good indication of the
extent of pregnancy wastage as well as the quality and quantity of health
care available to the mother and the newborn. It reflects the results of
maternity care more clearly than the neonatal death rate.
(5)Malnutrition
Incidence
Perinatal mortality is a problem of serious dimensions in all countries.
It now accounts for about 90 per cent of all foetal and infant mortality in
the developed countries. In India, stillbirths are seldom registered.
Consequently, most studies on perinatal mortality in this country are
hospital-based. The perinatal mortality rate in India is reported to be 47.0
per 1000 live births in rural areas, 30.0 per 1000 live births in urban areas
and 44.0 per 1000 live births combined in rural and urban areas in 1999
(88). The national goal was to achieve a perinatal mortality rate between
30 and 35 by the year 2000.
In developed countries, perinatal mortality rates have gradually
declined during the past decades due to improved obstetric and perinatal
technologies to levels of 15-20 per 1000 total births and are still
decreasing. Their target is now to achieve a rate of 7-8 per 1000 total births
(51).
Social and biological variables
A number of social and biological factors are known to be associated
with perinatal mortality. The degree to which these factors influence
perinatal mortality varies from country to country. Many of these factors
also endanger the life of the mother, causing high maternal mortality. An
appreciation of these factors (at-risk factors) will certainly make the
greatest impact on reducing perinatal mortality. The overall risk is
increased in the following categories : (1) Low socio-economic status; (2)
High maternal age (35 years or more); (3) Low maternal age (under 16
years); (4) High parity (fifth and subsequent pregnancies, especially with
short intervals between pregnancies); (5) Heavy smoking (10 or more
cigarettes daily); (6) Maternal height - short stature (as compared with
average for locality); (7) Poor past obstetric history (one or more previous
stillbirths and neonatal deaths, one or more premature live-born infants);
(8) Malnutrition and severe anaemia; and (9) Multiple pregnancy.
For further details see page 419 under factors affecting infant mortality.
Causes of Perinatal Mortality
About two-thirds of all perinatal deaths occur among infants with less
than 2500 g birth weight. The causes involve one or more complications in
the mother during pregnancy or labour, in the placenta or in the foetus or
neonate.
Main causes : The main causes of death are intrauterine and birth
asphyxia, low birth weight, birth trauma, and intrauterine or neonatal
infections. The various causes of perinatal mortality may be grouped as
below :
(a) Antenatal Causes :
(1)
imbalance
and
inadequate
uterine preparation
(4)Blood incompatibilities
(6)Toxemias of pregnancy
(7)Antepartum haemorrhages
(8)Congenital defects
(9)Advanced maternal age
(b) Intranatal Causes:
(1)Birth injuries
(2)Asphyxia
(3)Prolonged effort time
(4)Obstetric complications
(c) Postnatal Causes :
(1)Prematurity
(2)Respiratory distress syndrome
(3)Respiratory and alimentary infections
(4)Congenital anomalies
(d) Unknown Causes :
In some cases; the causes are not clinically ascertainable.
Interventions for the reduction of perinatal mortality
Measures to reduce perinatal mortality rates are essential tc accelerate
the declining trend in neonatal and infant mortality rates. They are (9) : (a)
Advice to women with medica problems to avoid pregnancy till health
improves; (b) Birth spacing; (c) Tetanus toxoid immunization and IFA
tablets foi anaemia control; (d) Early treatment of materna complications;
(e) Institutional delivery for women at high risk (f) Immediate referral and
appropriate care of emergency obstetric complications; (g) Safe and clean
delivery practices (h) Essential newborn care; and (i) Resuscitation of
newborn; without spontaneous cry at birth.
International certificate of perinatal death
For international comparability, the 9th (1975) Revision o
International Classification of Diseases (ICD-9) recommendec a special
certificate of c^use of perinatal death. The ICD has also a list of 100
causes (the "P" list) for tabulation of perinata morbidity and mortality
(38).
Prevention of perinatal mortality
See page 420 under Preventive & Social Measures.
NEONATAL MORTALITY RATE
Neonatal deaths are deaths occurring during the neonata period,
commencing at birth and ending 28 completed days after birth. Neonatal
mortality rate is the number of neonata deaths in a given year per 1000
live births in that year.
The neonatal mortality rate is tabulated as :
Number of deaths of children under
28 days of age in a year
-----------------------------------------------=
Total live births in the same year
x 1000
1960
2002
India
146
67
Sri Lanka
Bangladesh
83
149
17
51
Pakistan
Thailand
Sweden
139
103
16
83
24
3
Switzerland
12
France
New Zealand
USA
UK
Japan
29
22
26
23
31
4
6
7
7
3
Source : (7)
There are wide variations between countries or regions the
levels of infant mortality. The world average of IMR 1 2002 has
been estimated at about 56 per 1000 live births ( However, IMR
varies from 5 per 1000 live births in t developed countries to
106 per 1000 live births in the lei developed countries. The
average in the developing countr was 62 per 1000 live births.
Although infant mortality declin significantly during 1960-2002,
the drop was greatest for t developed countries (80%) and
lowest for least develop countries (40%). The developed world
had a much grea reduction in infant mortality compared to child
mortality, wh in the developing world the situation was reverse
(7).
The IMRs in industrialized countries were around 200 even
more some 150 years ago. Even at the beginning of t 20th
century. USA, UK, Japan, France, etc, had rates abo 140 per
1000 live births. Within 50 years (1950) a spectacu fall in the
rate was observed in all developed countries. ] 1980s, most
developed countries achieved rates below 10 p 1000 live births.
Demographers opine that in most develop countries, further
decline in IMRs would be difficult to achie without some
revolutionary advances in perinatology. A further reduction in
infant mortality in developed countries w depend upon
preventing one of its principal causes, name congenital
abnormalities.
During 2002, the worst rates were in Sierra Leone (161
TABLE 15
Infant mortality in major states of India (2000)
State
Andhra Pradesh
Assam
Bihar
Gujarat
Haryana
Karnataka
Kerala
Madhya Pradesh
Maharashtra
Orissa
Punjab
Rajasthan
Tamil Nadu
Uttar Pradesh
West Bengal
All India
Rural
Urban
Combined
74
78
63
69
69
68
14
94
57
99
56
83
57
87
54
74
36
35
53
45
57
24
14
54
33
68
38
58
38
65
37
43
65
75
62
62
67
57
14
88
48
96
52
79
51
83
51
68
Source : (88)
There is plenty of evidence to show that better control of infant
mortality is related to a wider spread of literacy (particularly female
literacy) and primary health care. Also, the states with the highest infant
mortality are also the states with the highest fertility. Table 16 illustrates
the impact of the above variables on infant mortality.
TABLE 16
IMR, female literacy rate and birth rate in major Indian States
ctat:e
Andhra Pradesh
Assam
Bihar
Gujarat
Karnataka
Kerala
Madhya Pradesh
Maharashtra
Orissa
Haryana
Punjab
Rajasthan
Tamil Nadu
Uttar Pradesh
West Bengal
IMR
per 1000
live births
(2000)(2001)
. 65
75
62
62
57
14
88
48
96
67
52
79
51
83
51
Female
literacy
Rate
(2000)
51.17
56.03
33.57
58.60
57.45
87.86
50.28
67.51
50.97
56.31
63.55
44.34
64.55
42.98
60.22
Birth Rate
per 1000
population
21.3
26.9
31.9
25.2
22.0
17.9
31.2
20.9
24.3
26.9
21.5
31.2
19.2
32.8
20.6
Source : (88)
Table 16 shows that Kerala has managed to surpass all the Indian states
in certain important measures of social development. It has the lowest
infant mortality rate, the lowest birth rate and the highest literacy rate.
Mortality pattern
(a) Age : Deaths in the age-group 0-1 year account for 24.1 per cent of
the total deaths in the country (93). About 50 per cent of infant deaths
occur within the first month (neonatal period) of life. Of these, more than
half may die during the first week of birth. The risk of death is the greatest
during the first
after the third birth. The fate of the 5th and later children always worse
than the fate of the 3rd child. Infant mortali from nutritional deficiencies
are 3-4 times higher for infan born with fifth or higher birth order
compared to the first thre These deaths occur mostly in post-neonatal
period.
TABLE 17
. flV^
Neonatal mortality
(0-4weeks)
Post-neonatal mortality
(1-12 months)
1. Diarrhoeal diseases
2.Birth injury and difficult labour 2. Acute respiratory infections
3.Congenital anomalies
3. Other communicable diseases
4.Haemolytic diseases of newborn 4. Malnutrition
5.Conditions of placenta and cord 5. Congenital anomalies
6.Diarrhoeal diseases
6. Accidents
7.Acute respiratory infections
8.Tetanus
The principal causes of infant mortality in India are low birth weight,
respiratory infections, diarrhoeal diseases, congenital malformations and
cord infection. Neonatal deaths make a major contribution (70%) to infant
mortality. Whereas in developing countries, the high infant mortality is
mainly due to low birth weight, and the combined effects of infection
(e.g., diarrhoea, respiratory infections) and malnutrition, in developed
countries, it is mainly due to congenital anomalies, anoxia and hypoxia.
Factors affecting Infant Mortality
Infant mortality is due to the interaction of several factors in
combination. They may be classified as biological, economic and social
factors.
1. BIOLOGICAL FACTORS
(a) Birth weight:
Birth weight is a major determinant of infant and perinatal mortality
and morbidity. Babies of low birth weight (under 2.5 kg) and high birth
weight (over 4 kg) are at special risk. Virtually, all infants weighing less
than 1000 g at birth succumb. One major cause of low birth weight is poor
maternal nutrition - not only during pregnancy, but even before that. It has
been observed that the mother who was adequately nourished during her
own growing-up years has an excellent chance of delivering a normal size
baby even if she has taken an inadequate diet during her pregnancy. An
increase in birth weight would lower the perinatal and neonatal mortality.
(b) Age of the mother :
There is a definite relationship between the age of the mother and the
fate of the child. Infant mortality rates are greater when the mother is
either very young (below the age of 19 years) or relatively older (over 30
years). Very young mothers also tend to be poorer and less educated (95).
(c) Birth order :
The live births are classified according to their order of rank. The
highest mortality is found among first born, and the lowest among those
born second. The risk of infant mortality escalates
TABLE 18
Neonatal, postneonatal, infant, child, and under-five mortality rates for the 10 year period preceding the
survey by selected background characteristics, India, 1998-99
(Per thousand live births)
Background characteristic
Neonatal
mortality
(NN)
Postneonatal
mortality '
Infant
(PNN)
mortality
Residence
Rural
Urban
Mother's education
Illiterate
Literate, < middle complete
Middle school complete
High school complete and above
Religion
Hindu
Muslim
Christian
Standard of living index
Low
Medium
High
Sex of child
Male
Female
Mother's age at birth
<20
20-29
30-39
40-49
Birth order
1
2
3
4
5
6+
Previous birth interval
< 24 months
24-47 months
48+ months
Medical care 2
No care
One or two types of care
All three types of care
Birth size 3
Large
Average
Small
Very small
Total
Note : The period preceding the survey does
Child
mortality
Under-five j
mortality 1
5.7
35.5
28.0
15.8
79.7
49.2
34.6
17.0
111.5
65.4
55.3
40.5
33.7
24.3
31.2
18.0
14.4
8.5
86.5
58.5
48.1
32.8
39.7
18.4
10.5
44
122.8
75.8
58.1
37.1
50.4
38.0
29.8
26.7
20.8
19.4
77.1
58.8
49.2
32.4
25.4
19.7
107.0
82.7
68.0
55.8
47.0
30.9
33.1
23.4
11.8
88.8
70.3
42.7
45.2
26.1
9.1
130.0
94.6
51.5
50.7
44.6
24.2
26.6
74.8
71.1
24.9
36.7
97.8
105.9
63.1
40.7
48.7
61.9
29.7
22.6
27.9
44.3
92.7
63.3
76.7
106.2
31.0
28.7
37.4
57.2
120.8
90.2
111.2
157.4
52.4
43.8
38.5
44.7
48.7
62.5
22.4
22.0
23.2
28.4
27.5
38.6
74.9
65.7
61.7
73.1
76.2
101.1
18.9
25.7
33.9
36.8
42.0
49.8
92.3
89.8
93.5
107.3
115.0
145.9
71.7
35.5
24.1
37.8
22.6
14.4
109.5
58.1
38.5
49.2
31.4
13.6
153.3
87.7
51.5
53.6
35.8
22.2
35.5
19.0
11.8
89.1
54.8
34.0
.
-
32.8
30.0
47.5
110.0
47.7
18.1
19.9
28.3
37.0
25.3
50.9
49.9
75.9
147.2
73.0
30.6
101.4
Source : (78)
death is greatly enhanced if the last child was born less than 2
years ago, and if the mother already has four or more children.
Smaller sibship and longer spacing between pregnancies are
associated in all societies with improved infant and child survival.
6. Sanitation :
For infants and young children, the risk of dying is very closely
related to the environment in which they live. Exposure to
infections through contaminated food and polluted water, lack of
elementary hygiene, flies and poor housing pose hazards which the
young cannot escape. This is why infant mortality rate is
universally recognized not only as a most
In India for the year 1991, 1-4 year age mortality was estimated to be
11.2 per cent of total deaths. Like infant mortality, 1-4 year age mortality
also shows wide state-wise variations. The states reporting rates higher
than the national average are Madhya Pradesh 15.9, Rajasthan 14.9, Uttar
Pradesh 14.7, Bihar 14.5, Assam 12.7 and Haryana with 12 per cent of
total deaths in India (93). Kerala recorded the lowest with 2.2 per cent
followed by Tamil Nadu with 4.5 per cent.
Leading causes of death :
The leading causes of death in the 1 -4 year age group are shown in
Table 19.
TABLE 19
Leading causes of death in 1 -4 year age group
Developing countries
Diarrhoeal diseases
Respiratory infections
Malnutrition
Infectious diseases (e.g.,
measles, whooping cough)
Other febrile diseases
Accidents and injuries
Developed countries
Accidents
Congenital anomalies
Malignant neoplasms
Influenza
Pneumonia
Source : (4)
The leading causes of death in 1-4 year age group in developing
countries are diarrhoeal diseases and respiratory infections, closely
followed by other communicable diseases such as whooping cough and
measles. When combined with malnutrition these diseases have high case
fatality rates. In the developed countries deaths from infectious diseases
are quite rare, while accidents are the leading cause of death from the age
of one year. Four groups of home accidents have been identified - (a) falls
from unprotected stairs and balconies (b) suffocation (c) burns and scalds
(d) poisoning. Almost all accidents are preventable. The factors such as
congenital anomalies and neoplasms are not easy to prevent or to cure.
These conditions also affect children in developing countries, but their
relative importance is overshadowed by infections.
UNDER - 5 MORTALITY RATE (Child
Mortality Rate)
UNICEF defines this as the "annual number of deaths of children age
under 5 years, expressed as a rate per 1000 live births." More specifically,
it measures the probability of dying between birth and exactly 5 years of
age (1). UNICEF considers this as the best single indicator of social
development and well-being rather than GNP per capita, as the former
reflects income, nutrition, health care and basic education etc (104). The
rate is calculated by the formula :
Number of deaths of children less
than 5 years of age in a given
year
Child mortality rate = ---------------------------------X 1000
Number of live births in the same
year
The global average for under 5 mortality in 2002 was 82 per 1000 live
births. In the developed countries, the rate was 7 per 1000 live births, in
the developing world it was 90 per 1000 live births, and in the least
developed countries it was 158 per 1000 live births - 25 times higher than
the rate of an industrialized nation (7). Bad as that last rate is, it is not so
bad as it was 40 years ago, when in the developing countries about 287
children in every 1000 died before their fifth birthday. Child mortality has
declined significantly during the past years, although the pace of decline
has not been uniform among the
1960
2002
India
242
93
Sri Lanka
133
19
Thailand
148
28
China
225
39
Bangladesh
248
77
Pakistan
227
107
UK
27
7
USA
30
8
Japan
40
5
Singapore
40
4
Source : (7j
However, most of the reduction in under 5 mortality is due to decline
in infant mortality. This reduction was largely due to a 35 per cent drop in
vaccine preventable deaths as well as 13 per cent fewer deaths from acute
respiratory infection and 10 per cent fewer deaths from diarrhoea (43).
The estimated mortality among children under 5 by cause of death in the
developing countries during 1985, 1990, and 1993 is as shown in Table
21.
TABLE 21
Estimated mortality among children under 5 years by cause of death in
the developing countries
Cause of death
1985
1990
(in thousands)
1993
4730
4200
4110
3640
2955
790
295
495
740
590
3750
2870
275
295
275
955
375
250
75
195
3715
2740
290
280
290
940
360
190
100
170
195
Source : (43)
Child mortality rate in India
In India, the deaths among young children are monitored by the
Registrar General's Office. The SRS estimates of child mortality rate is
calculated as "the annual number of deaths in children < 5 years of age per
1000 < 5 years children (the international agencies calculate this rate as
per 1000 live births). That is why, while reviewing reports and analysing
data, these differences should be kept in mind (59).
The child mortality trend has shown a decline from 41.2 per 1000
children < 5 years in 1984 to 26.3 in 1990, i.e., a decline by 14.9 points.
This rate declined by 7 points during 1989 and 1990 alone. According to
the provisional reports for the year 1999 child mortality rate was 20.4 per
1000 < 5 children (105).
Deaths in children account for more than 34 per cent of the total
deaths. An estimated 7.1 lakh deaths occur annually due to diarrhoea and
9.6 lakh due to pneumonia. The younger the child, the higher is the
mortality rate. Low birth weight babies and under-nourished children also
have a high risk of dying.
1960
2000
India
75.8
90.7
Sri Lanka
Bangladesh
Pakistan
China
UK
USA
Japan
Singapore
86.7
75.2
77.3
77.5
97.3
97
96
96
98.1
92.3
89.3
96.1
99.3
99.2
99.5
99.6
Estimated incidence
per 1000 live births
6-8
0.5-2
0.5 - 4
0.5 - 4
10 - 12
17-30
Source : (103)
INDIA :
Population and hospital-based studies from different parts of India
show that 2.5 per cent of newborns have a birth defect, and this figure rises
to 4 per cent if the children are followed up to 5 years of age (107).
Congenital malformations already rank as the third most frequent cause of
perinatal mortality in India (108).
Birth defects in India :
The pattern of genetic disorders in India is given in Table 24.
In the whole of North India, neural tube defects or spina bifida are the
most common birth defects. The highest frequency of neural tube defects
is observed in Punjab (1 in 116 births), followed by Rajasthan (1 in 145
births) and Delhi (1 in 212 births). In Tamil Nadu it is 1 in 330 births, and
in Mumbai 1 in 450. The frequency is lowest in Kolkata. These figures
have been derived from hospital data (107).
TABLE 24
Genetic disorders in India
_.
Dlsorder
,
Prevalence
Total no.
________________________________(%)____________(millions)
Affected at birth
0.832
3
Congenital anomalies
2.5
0.569
Single gene
0.6
0.136
0.56
1.5
0.127
10.650
Chromosomal
In general population
behaviour and central
nervous system disorders'3
Late onset multifactorial
disorders0
10.1
27.390
can afford it may bring their lunch packets from home and during
lunch hours take their meals in school. Otherwise,
HANDICAPPED CHILDREN
Definitions
"Handicap" may be defined as "reduction in a person's capacity
to fulfil a social role as a consequence of an impairment,
inadequate training for the role, or other circumstances. Applied to
children, the term usually refers to the presence of an impairment
or other circumstances that are likely to interfere with normal
growth and development or with the capacity to learn" (120).
International Classification of Impairments, Disabilities and
Handicaps (ICIDH) : First published by WHO in 1980, this is an
attempt to produce a systematic taxonomy of the consequences of
injury and disease.
An impairment is defined as "any loss or abnormality of
psychological, physiological, or anatomical structure or function".
Impairments are disturbances at the level of the organ and include
defects, loss of limb, organ or other body structure and defects or
loss of mental function.
A disability is defined as "any restriction or lack (resulting from
an impairment) of ability to perform an activity in a manner or
within the range considered normal for a human being". The term
disability reflects the consequences of impairment in terms of
functional performance and activity by the individual; disability
thus represents disturbances at the level of the person.
A handicap is defined as a disadvantage for a given individual,
resulting from an impairment or a disability, that limits or prevents
the fulfilment of a role that is normal (depending on age, sex, and
social and cultural practice) for that individual. The term handicap
thus reflects interaction with and adaptation to the individual's
surroundings.
Handicap may be intrinsic or extrinsic. For example, blindness
is an intrinsic handicap, and loss of parents is an extrinsic
handicap. One handicap can give rise to further handicaps and the
terms "primary" and "secondary" are used to denote this
relationship. Blindness is a primary handicap; it can lead to
poverty, which will be secondary handicap.
Extent of the problem
Nearly 83 million of the world's population are estimated to be
mentally retarded, with 41 million having long-term or permanent
disability. It ranks fourth in the list of leading causes of disability.
Hearing loss (41 decibels and above) over the age of 3 is estimated
to affect 42 million people, ranking 3rd in the list. Disability
resulting from poliomyelitis has affected about 10 million people
(43). It is difficult to state how many people are mentally retarded
in India as the census estimates do not cover mental handicap.
About 16.15 million persons (1.9 per cent of the population) suffer
from some or the other physical disability in the country. About 3
per cent child population in 1-14 age group is affected by
developmental delay- (121).
Classification :
It is usual to classify handicapped children into the following
groups :
1.Physically handicapped
2.Mentally handicapped
3.Socially handicapped
1. Physically handicapped children
This category includes children who are blind, deaf and mute;
those with hare-lip, cleft palate, telipes; and the "crippled" - e.g.,
resulting from polio, cerebral palsy, congenital heart disease, road
accidents, burns, injuries, etc.
These conditions fall into three broad causative groups : (a) birth
defects (b) infections, and (c) accidents. These are all preventable
to a large extent through adequate prenatal, natal, postnatal
services, and genetic counselling.
2. Mentally handicapped children
Mental handicap is the present term used for mental retardation.
It is a condition of subaverage intellectual function combined with
deficits in adaptive behaviour. Terms which were previously used
such as idiot, moron and imbecile are now discarded. At least 2 per
cent of India's population are said to be suffering from some kind
of mental disability (122).
Causes
Mental handicap has many causes. These may be genetic, or
environmental and include prenatal as well as postnatal causes.
The possible and earliest time to recognise the problem of mental
retardation is to look for any delayed milestones and development.
The known causative factors include the following : (a) Genetic
conditions : Down's syndrome, Klinefelter syndrome, PKU, TaySach
disease,
galactosaemia,
microcephaly,
congenital
hypothyroidism involving both single and multiple gene action and
chromosomal abnormalities (b) Antenatal factors : These comprise
neural tube defects, Rh incompatibility, certain infections (e.g.,
rubella, cytomegalovirus, toxoplasmosis, syphilis), drugs and
irradiation (c) Perinatal factors : These include birth injuries,
hypoxia and cerebral palsy (d) Postnatal factors : Head injuries,
accidents, encephalitis, physical and chemical agents such as lead
and mercury poisoning may result in mental retardation (e)
Miscellaneous
:
Maternal
malnutrition,
protein-energy
malnutrition, iodine deficiency (endemic goitre), consanguinous
marriages, pregnancy after the age of 40 (late marriages) are all
known to be associated with mental retardation.
Categories of Mental Retardation
Psychologists have used the concept of IQ to classify the
degree of mental retardation. The IQ scores rest on the assumption
that intelligence distribution in the general public follow the
normal or Gaussian curve, with a mean of 100. The half of the
general population achieve scores above 100, and one half below.
The lower 3 per cent or so of the population achieve scores of 70
or less. They are usually considered to be mentally retarded. The
WHO gave the following classification of mental retardation :
Mild mental retardation
IQ
50-70
Moderate mental retardation
IQ
35-49
Severe mental retardation
IQ
20-34
Profound mental retardation
IQ
under 20
Children scoring above 70 are no longer described as mentally
handicapped. The number of mild cases far exceed the severe and
profound cases. English statistics which have been widely quoted
suggest that, among 100 mentally handicapped persons, the
following proportion will be found : 70 mild, 20 moderate and 5
severe cases. In other words, a very great majority of cases of
mental handicap are of the mild type and potentially capable of
being taught to make a fairly adequate social adaptation in
appropriate circumstances (123).
Severe mental retardation is uncommon. The great majority of
severely handicapped children remain more or less dependent
throughout life. Mental retardation often involves psychiatric
disturbances. It has been stressed that the IQ range suggested must
not be applied too rigidly. IQ level is not necessarily constant
during the individual's life span.
Services
Pregnant women
Nursing mothers
Health check-up
Supplementary nutrition
Nutrition and health education
Supplementary nutrition
Immunization
Health check-up
Referral services
Supplementary nutrition
Immunization, Health check-up
Referral services Non-formal
education
Source : (135)
The strategy adopted in ICDS is one of simultaneous delivery
of early childhood services. While the health component forms a
major component, ICDS is much more than a mere health
programme for delivery of social services input for development.
The blue print for the scheme was prepared by the Department
of Social Welfare in 1975. Considering the magnitude of the task,
it was decided to take up on an experimental basis 33 projects in
the year 1975-76 in 4 urban, 19 rural and 10 tribal areas spread
over 22 states and the Union Territory of Delhi. The projects were
sanctioned in October 1975. The Government of India decided to
expand the project to cover 100 areas by 1978-79.
Delivery of Services
1. Supplementary nutrition :
Supplementary nutrition is given to children below 6 years, and
nursing and expectant mothers from low income group. The type
of food depends upon local availability, type of beneficiary,
location of the project etc. The aim is to supplement nutritional
intake by about 200 Cal and 8-10 grams of protein for children
below 1 year; about 300 Cal and 15 grams of protein for children
between 1-6 years; and about 500 Cal and 25 grams of protein for
pregnant women and nursing mothers. Supplementary nutrition is
given in 300 days a year (136). Adequate funds for supplementary
nutrition is provided in the State Plan under Minimum Need
Programme. Children are weighed every month. Nutrition
education and health education is given to mothers of children
suffering from 1st degree of malnutrition. Supplementary nutrition
(therapeutic food) is given to children suffering from 2nd and 3rd
degree malnutrition. Children suffering from 4th degree
malnutrition are recommended hospitalization.
2. Nutrition and health education
Nutrition education and health education is given to all women
in the age group 15-45 years, giving priority to nursing and
expectant mothers. It is imparted by specially organized courses in
village during home visits by anganwadi workers.
3. Immunization
Immunization of children against 6 vaccine preventable
diseases is beina done, while for exDectant mothers.
and dislike of change are some of the mental changes in the aged.
Reduced income leads to a fall in the living standards of the
elderly; it does have mental and social consequences. (2) Sexual
adjustment: Between 40 and 50, there is cessation of reproduction
by women and diminution of sexual activity on the part of men.
During this phase, physical and' emotional disturbances may occur.
Irritability, jealousy and despondency are very frequent. (3)
Emotional disorders : Emotional disorders result from social
maladjustment. The degree of adaptation to the fact of ageing is
crucial to a man's happiness in this phase of life. Failure to adapt
can result in bitterness, inner withdrawal, depression, weariness of
life, and even suicide.
Health status of the aged in India
A few hospital based studies have been made in India on the
health status of the aged persons, but such studies provide only a
partial view of the spectrum of illness in the aged. The overall data
on aged are scarce. The main causes of illness are arthritis,
cataract, bronchitis, avitaminosis, ear diseases, hypertension,
diabetes, rheumatism, helminthic infestations, accidents, etc. The
findings of an ICMR survey conducted in 1984-85 of elderly
persons over 60 year of age attending geriatric clinics in rural areas
is as shown in Table 25.
TABLE 25
Percentage of elderly reporting various ailments
Ailment
Reported percentage
Visual impairment/complaint
88.0
40.0
18.7
17.4
16.1
13.3
9.0
8.5
8.2
3.5
Source : (140)
Secondary
Tertiary
Health habits
smoking
alcohol abuse
obesity
nutrition
sleep
Coronary heart
disease risk factors
Screening for
hypertension, diabetes
peridental disease
dental caries
sensory impairment
medication side effects
colo-rectal cancer
breast cancer,
cervical cancer
Rehabilitation
physical deficits
cognitive deficits
functional deficits
Immunization
influenza
pneumovax
tetanus
Injury prevention
Iatrogenesis
prevention
Oesteoporosis
prevention
Caretaker support
Introduction of
support necessary
to prevent loss of
autonomy
prostatic cancer
nutritionally-induced
anaemias
depression, stress
urinary incontinence
podiatric problems
fail risk
tuberculosis
syphilis
Stroke prevention
Myocardial infarction
Source : (141)
References
1.WHO (1996), The World Health Report 1996, Report of the Director General
2.Menon, M.K.K. (1975). J. Obs&Gynae. of India, XXXV, 113
3.WHO (1969). Report of Training Courses on Organization of MCH Field
__________________________________________________REFERENCES 437
and
Health", Geneva
Health in India,
chapter 14, Health Problem of Specialized Groups.
37.German, PS., Fried, L.P., Annual Review of Public Health, Vol.10, 1989, P.325
I II
"What people eat is not calories but food, and consideration of fads, flavours and
variations of appetite can make nonsense of the dietician's theories"
Nutrition may be defined as the science of food and its
relationship to health. It is concerned primarily with the part played
by nutrients in body growth, development and maintenance (1).
The word Nutrient or "food factor" is used for specific dietary
constituents such as proteins, vitamins and minerals. Dietetics is
the practical application of the principles of nutrition; it includes
the planning of meals for the well and the sick. Good nutrition
means "maintaining a nutritional status that enables us to grow
well and enjoy good health" (2). The subject of nutrition is very
extensive. Since our concern is with community aspects of
nutrition, the subject will be dealt with in five sections : dietary
constituents, nutritional requirements, assessment of nutritional
status, nutritional problems in public health and nutritional
programmes in India.
Changing concepts
Through centuries, food has been recognized as important for
human beings, in health and disease. The history of man to a large
extent has been a struggle to obtain food. Until the turn of the
century the science of nutrition had a limited range. Protein,
carbohydrate and fat had been recognized early in the 19th century
as energy-yielding foods and much attention was paid to their
metabolism and contribution to energy requirements (3). The
discovery of vitamins at the turn of the present century has
"rediscovered" the science of nutrition. Between the two World
Wars, research on protein gained momentum. By about 1950, all
the presently known vitamins and essential amino acids had been
discovered. Nutrition gained recognition as a scientific discipline,
with roots in physiology and biochemistry. In fact nutrition was
regarded as a branch of physiology and taught as such to medical
students.
Great advances have been made during the past 50 years in
knowledge of nutrition and in the practical application of that
knowledge. Specific nutritional diseases were identified and
technologies developed to control them, as for example, protein
energy malnutrition, endemic goitre, nutritional anaemia,
nutritional blindness and diarrhoeal diseases.
While attention was concentrated on nutrition deficiency
diseases during the first decades of the century, the science of
nutrition was extending its influence into other fields -agriculture,
animal husbandry, economics and sociology. This led to "green
revolution" and "white revolution" in India and increased food
production. However, studies of the diets and state of nutrition of
people in India showed that poorer sections of the population
continued to suffer from malnutrition despite increased food
production. One result was that for the first time the problem of
nutrition began to attract international attention (3) as a cause of
social problems. International activities in the field of nutrition
initiated by the League of Nations, later continued by FAO, WHO
and UNICEF form a striking part of the story.
___________________________________________PROTEINS 439
2. Classification by chemical composition :
1) Proteins
2) Fats
3) Carbohydrates
4) Vitamins 5)
Minerals
3. Classification by predominant function
1)Body-building foods, e.g., milk, meat, poultry, fish, eggs,
pulses, groundnuts, etc.
2)Energy-giving foods, e.g., cereals, sugars, roots and tubers,
fats and oils.
3)Protective foods, e.g., vegetables, fruits, milk
4. Classification by nutritive value :
1)Cereals and millets
2)Pulses (legumes)
3)Vegetables
4)Nuts and oilseeds
5)Fruits
6)Animal foods
7)Fats and oils
8)Sugar and jaggery
9)Condiments and spices
10)Miscellaneous foods
NUTRIENTS
Nutrients are organic and inorganic complexes contained in
food. There are about 50 different nutrients which are normally
supplied through the foods we eat. Each nutrient has specific
functions in the body. Most natural foods contain more than one
nutrient. These may be divided into :
{i) Macronutrients : These are proteins, fats and carbohydrates
which are often called "proximate principles" because they form
the main bulk of food. In the Indian dietary, they contribute to the
total energy intake in the following proportions.
Proteins
7 to 15 per cent
Fats
10 to 30 per cent
Carbohydrates
65 to 80 per cent
(ii) Micronutrients : These are vitamins and minerals. They are
called micronutrients because they are required in small amounts
which may vary from a fraction of a milligram to several grams. A
short review of basic facts about these nutrients is given below.
PROTEINS
The word protein by derivation means that which is of first
importance. Indeed they are of the greatest importance in human
nutrition. Proteins are complex organic nitrogenous compounds.
They are composed of carbon, hydrogen, oxygen, nitrogen and
sulphur in varying amounts. Some proteins also contain
phosphorus and iron and occasionally other elements. Proteins
differ from carbohydrates and fats in that they contain nitrogen,
this usually amounting to about 16 per cent. Proteins constitute
about 20 per cent of the body weight in an adult.
Essential amino acids
Proteins are made up of smaller units, called amino acids. Some
24 amino acids are stated to be needed by the human body, of
which 9 are called "essential" because the body cannot synthesize
them in amounts corresponding to its needs, and therefore, they
must be obtained from dietary proteins. They are : leucine,
isoleucine, lysine, methionine, phenylalanine, threonine, valine,
tryptophan and histidine. Evidence is now accumulating that
histidine is essential even for adults (6). Non-essential amino acids
include arginine,
are divided into saturated fatty acids such as lauric, palmitic and
stearic acids, and unsaturated fatty acids which are further
divided into monounsaturated (MUFA) (e.g., oleic acid) and
polyunsaturated fatty acids (PUFA) (e.g., linoleic acid and alinolenic acid). Table 1 shows the fatty acid content of different
fats.
The polyunsaturated fatty acids are mostly found in vegetable
oils, and the saturated fatty acids mainly in animal fats. However,
there are exceptions, as for example, coconut and palm oils,
although vegetable oils, have an extremely high percentage of
saturated fatty acids. On the other hand,- fish oils, although they
are not vegetable oils, contain poly and mono-unsaturated fatty
acids.
TABLE 1 ^^TjJ)
Fats
Coconut oil
Palm oil
Cotton seed oil
Groundnut oil
Safflower oil
Sunflower seed oil
Corn oil
Soya bean oil
Butter
Monounsaturated
fatty acids
(MUFA)
Polyunsatu- !
rated fatty j
acids (PUFA)
6
44
25
50
15
27
27
24
37
25
2
10
50
317565
65
623
50
92
46
25
19
10
8
8
14
60
25
Margarine
Source : (11)
TABLE 2
"\ v Afeiw */
Dietary source
Linoleic acid
Safflower oil
73
Corn oil
Sunflower oil
Soyabean oil
Sesame oil
Groundnut oil
Mustard oil
Palm oil
Coconut oil
Meat, eggs
milk (fat)
Soyabean oil
Leafy greens
Fish oil
57
56
51
40
39
15
9
2
0.5-0.3
0.4-0.6
7
Varied
10
Arachidonic acid
Linolenic acid
Eichosapentaenoic acid
Source : (12)
Sources
The dietary sources of fats may be classified as :
Per cent
content
_______________________________________________FATS 441
(a)ANIMAL FATS : The major sources of animal fats are ghee,
butter, milk, cheese, eggs, and fat of meat and fish. Animal fats
with few exceptions like cod liver oil and sardine oil are mostly
saturated fats.
(b)VEGETABLE FATS : Some plants store fat in their seeds,
e.g., groundnut, mustard, sesame, coconut, etc. They are sources
of vegetable oils.
(c)OTHER SOURCES : Small quantities of fat (invisible fat) are
found in most other foods such as cereals, pulses, nuts and
vegetables. For example, rice carries 3 per cent of fat, wheat 3 per
cent, jowar 4 per cent and bajra 6.5 per cent. Large cereal
consumption, as in India, provides considerable amounts of
"invisible fat". Moreover, the body can convert carbohydrate into
fat.
Functions
Fats have always been equated with calories. They are high energy
foods, providing as much as 9 kcal for every gram. By supplying
energy, fats spare proteins from being used for energy. Besides
providing energy, fats serve as vehicles for fat-soluble vitamins. Fats
in the body support viscera such as heart, kidney and intestine; and
fat beneath the skin provides insulation against cold. Without fat,
food is limited in palatability. ..
It is only recently that the "non-calorie" roles of fats have been
discovered. For example vegetable fats are rich sources of essential
fatty acids which are needed by the body for growth, for structural
integrity of the cell membrane and decreased p'atelet adhesiveness.
Diets rich in EFA have been reported to reduce serum cholesterol
and low-density lipoproteins (13). Polyunsaturated fatty acids are
precursors of prostaglandins - a group of compounds, now
recognised as "local hormones"; they play a major role in controlling
many of the physiological functions of the body such as vascular
homeostasis, kidney function, acid secretion in stomach, gastrointestinal motility, lung physiology and reproduction. Cholesterol is
essential as a component of membranes and nervous tissue and is a
precursor for the synthesis of steroid hormones and bile acids. Thus
fats and oils are useful to the body in several ways.
Calorie
intake
Kerala
Tamil Nadu
Andhra Pradesh
Gujarat
Orissa
U.P.
2140
1871
2340
2375
2468
2115
3
10
17
19
6
4
V/
Per cent
as energy
53.52
35.96
41.22
51.29
26.73
25.03
Source : (12)
Hydrogenation
When vegetable oils are hydrogenated under conditions of
optimum temperature and pressure in the presence of a
22.3
14.7
15.5
19.8
9.8
10.7
catalyst, the liquid oils are converted into semi-solid and solid fat.
The resulting hydrogenated fat is known as "vanaspati" or vegetable
ghee, which is a popular cooking medium in India.
During the process of hydrogenation, unsaturated fatty acids are
converted into saturated acids and the EFA content is drastically
reduced. The main advantage of vanaspati is its ghee-like consistency
and its keeping quality even in hot humid climates. Since vanaspati is
lacking in fat-soluble vitamins, it is fortified with vitamins A and D
by government regulation to the extent of 2500 IU of vitamin A and
175 IU of vitamin D per 100 grams.
Refined oils
Refining is usually done by treatment with steam, alkali, etc.
Refining and deodorization of raw oils is done mainly to remove the
free fatty acids and rancid materials which may be present in them.
Refining does not bring about any change in the unsaturated fatty
acid content of the oil. It only improves the quality and taste of oils.
Refined oils are costly.
I- A. J JFats and disease
(a) OBESITY: A diet, rich in fat, can pose a threat to human
health by encouraging obesity. In fat people, adipose tissue may
increase up to 30 per cent, (b) PHRENODERMA : Deficiency of
essential fatty acids in the diet is associated with rough and dry skin, a
condition known as phrenoderma or "toad skin". This condition is
reported in Kerala, Karnataka and Gujarat (15). It is characterised by
horny papular eruptions on the posterior and lateral aspects of limbs
and on the back and buttocks. Phrenoderma can be .cured rapidly by
the administration of linseed or safflower oil which are rich in EFA,
along with vitamins of the B-complex group, (c) CORONARY
HEART DISEASE : High fat intake (i.e., dietary fat representing 40
per cent or over of the energy supply and containing a high
proportion of saturated fats) has been identified as a major risk factor
for CHD (16). Epidemiological studies indicate that LDL and VLDL
fractions are atherogenic and HDL exerts a protective effect against
the development of atherosclerosis. There is evidence indicating an
inverse relationship between EFA intake and CHD mortality. (d)
CANCER : In recent years, there has been some evidence that diets
high in fat increase the risk of colon cancer and breast cancer (17). (e)
OTHERS : The skin lesions of kwashiorkor and those induced by
EFA deficiency are similar. The possible association between the skin
lesions of kwashiorkor and EFA deficiency has attracted attention
(18).
Fat requirements
[In developed countries, dietary fats provide 30 to 40 per
cent of total energy intake. The WHO Expert committee on
Prevention of Coronary Heart Disease (16) has recommended
only 20 to 30 per cent of total dietary energy to be provided by
fats. At least 50 per cent of fat intake should consist of
vegetable oils rich in essential fatty acids. The Indian Council
of Medical Research (1989) has recommended a daily intake of
not more than 20 per cent of total energy intake through fafsj
For further details see Table 31.
J
CARBOHYDRATE
The third major component of food is carbohydrate, which is the
main source of energy, providing 4 kcals per gram. Carbohydrate is
also essential for the oxidation of fats and for the synthesis of certain
non-essential amino acids. There are three main sources of
carbohydrate, viz., starches, sugar and cellulose. Starch is basic to the
human diet. It is found in abundance in cereals, roots and tubers.
Sugars comprise monosaccharides (glucose, fructose and galactose)
and disaccharides (sucrose, lactose and maltose). These free sugars
are highly water soluble and easily assimilated. Free sugars
State
Kerala, Meghalaya, Sikkim
Andhra Pradesh, Karnataka, Manipur, Orissa,
Punjab, Chandigarh, Lakshadweep, Mizoram
Haryana, Himachal Pradesh, J & K,
Maharashtra, Nagaland, Tamil Nadu, Arunachal
Pradesh, Delhi, Goa, Pondicherry
Assam, Bihar, Gujarat, Madhya Pradesh,
Rajasthan, Tripura, Uttar Pradesh, West Bengal,
Andaman and Nicobar Islands
Source : (189)
There are indications of declining trends of vitamin i deficiency. In a
nation-wide survey of the prevalence and caus of blindness during 197174, VAD accounted for 0.3% of th total cause of blindness in the
country. The proportion ha declined to 0.04% in a similar survey during
1986-89. Numbe of keratomalacia has declined significantly. Repeat
survey (1975-79 and 1988-90) by the National Nutrition Monitorin
Bureau in Andhra Pradesh, Gujarat, Karnataka, Kerala, Madhy Pradesh,
Maharashtra, Orissa and Tamil Nadu, documented decline of overall
prevalence rate of Bitot's spots from 1.8% t 0.7%. Vitamin A
administration to children 9 months to 3 yeai of age has been included in
the CSSM programme.
Functions
The functions of vitamin D are as summarised in Table 8.
TABLE 8
Functions of vitamin D and its metabolites
Intestine :
Bone :
Kidney :
Recommended allowances
The recommended daily intake of vitamin A is
micrograms for adults. The detailed recommendations
given in Table 7. A^,
Q^Sy*
60
ar
or
B-carotene
(meg)
Adults
Man
Woman
Pregnancy
Lactation
Infants 0 to 12 months
600
600
600
950
350
2400
' 2400
2400
3800
1200
400
600
1600
2400
600
2400
Children
1 to 6 years
7 to 12 years
Adolescents
13 to 19 years
Other ;
Source : (37)
Sources
Group
source : (i>)
Toxicity
An excess intake of retinol causes nausea, vomiting, anorexia and sleep
disorders followed by skin desquamation and then an enlarged liver and
papillar oedema. High intakes of carotene may colour plasma and skin, but
do not appear to be dangerous (25, 34). The teratogenic effects of massive
doses of vitamin A is the most recent focus of interest (35).
Butter Eggs
Milk, whole
Fish fat
ug/per lOOg
0.5-1.5
1.25-1.5
0.1 5-30
30-100
200-750
500-10,000
VITAMIN D
The nutritionally important forms of Vitamin D in man are Calceferol
(Vitamin D2) and Cholecalciferol (Vitamin D3). Calciferol may be derived
by irradiation of the plant sterol, ergosterol. Cholecalciferol is the
naturally occurring (preformed) vitamin D which is found in animal fats
and fish liver oils. It is also derived from exposure to UV rays of the
sunlight which convert the cholesterol in the skin to vitamin D.
Deficiency
(1) Rickets : Vitamin D deficiency leads to rickets, which is usually
observed in young children between the age of six months and two years.
There is reduced calcification of growing bones. The disease is
characterised by growth failure,
___________________________________________VITAMINS 445
bone deformity, muscular hypotonia, tetany and convulsions due
to hypo-calcemia. There is an elevated concentration of alkaline
phosphate in the serum. The bony deformities include curved legs,
deformed pelvis, pigeon chest, Harrison's sulcus, rickety rosary,
kyphoscoliosis, etc. The milestones of development such as
walking and teething are delayed. (2) Osteomalacia : In adults,
vitamin D deficiency may result in osteomalacia which occurs
mainly in women, especially during pregnancy and lactation when
requirements of vitamin D are increased.
Both rickets and osteomalacia are frequently reported in India,
although they do not appear to be a problem of public health
importance. In the world as a whole, their prevalence has declined
as a result of changes in social customs (e.g., purdah system), and
the expansion of mother and child health services leading to better
care and feeding of infants and children (3). In the developing
countries today, rickets as a menace to child health is
overshadowed by the prevalence of protein energy malnutrition.
Prevention
Prevention measures include (a) educating parents to expose
their children regularly to sunshine; (b) periodic dosing
(prophylaxis) of young children with vitamin D; and (c) vitamin D
fortification of foods, especially milk. Some industrialised
countries still carry out the last measure. Periodic dosing and
education appear to be the most practical approaches in developing
countries.
Fraser (39) urges caution concerning oral supplementation,
because orally administered vitamin D appears to bypass the
protective mechanism that prevent excessive 25 (OH) D3
formation. The margin of safety with oral vitamin D between the
nutrient requirement and toxic intake is narrow.
Vitamin D is stored in the body in fatty tissues and in the liver.
An excessive intake is harmful and may result in anorexia, nausea,
vomiting, thirst, and drowsiness. The patient may lapse into coma,
while cardiac arrhythmias and renal failure may occur. The effects
are due to hypercalcemia induced by increased intestinal
absorption and mobilization of calcium from bone. Recent
literature contains warning against the administration of amounts
of vitamin D that greatly exceed accepted requirement levels. This
warning applies to pregnant women also since manifestations of
hypercalcemia may develop in utero (4).
Daily requirements
The daily requirements of vitamin D are (9) :
Adults
2.5 meg (100 IU)
Infants and children
5.0 meg (200 IU)
Pregnancy and lactation
10.0 meg (400 IU)
(One international unit (IU) of vitamin D = 0.025(xg of
calciferol - that is, to convert IU to micrograms, divide by 40)
VITAMIN E
(Tocopherol)
Vitamin E is the generic name for a group of closely related and
naturally occurring fat soluble compounds, the tocopherols. Of
these alpha-tocopherol is biologically the most potent. Vitamin E
is widely distributed in foods. By far the richest sources are
vegetable oils, cotton-seed, sunflower seed, egg yolk and butter.
Foods rich in polyunsaturated fatty acids are also rich in vitamin E.
The usual plasma level of vitamin E in adults is between 0.8 and
1.4 mg per 100 ml (37). While there is no doubt that man requires
tocopherol in his diet, there is no clear indication of dietary
deficiency. The role of vitamin E at the molecular level is little
understood. The current
mg/100 g
0.45
0.21
0.06
0.48
0.24
1.01
0.90
Foods of animal
origin
Milk, cow's
Egg. hen's
Mutton Liver,
sheep
mg/100 g
0.05
0.10
0.18
0.36
mg/100 g
Foods of vegetable
origin
mg/100 g
Liver, sheep
1.70
Whole cereals
0.10-0.16
Milk, cow's
Egg, hen
0.19
0.40
Milled cereals
Pulses
0.03-0.08
0.21-0.32
Meat
0.14
Leafy veg.
0.15-0.30
Source : (157J
Deficiency
Deficiency of riboflavin, or ariboflavinosis is widespread in
India particularly in population where rice is the staple. The most
common lesion associated with riboflavin deficiency is angular
stomatitis, which occurs frequently in malnourished children and
its prevalence is used as an index of the state of nutrition of groups
of children (3). Other clinical signs suggestive (but not specific)
include cheilosis, glossitis, nasolabial dyssebacia, etc. Studies
conducted at National Institute of Nutrition in India showed that
subclinical riboflavin deficiency (as judged by the erythrocyte
glutathione reductase activation test) was present in over 80 per
cent of low income group children and adults (45). Hyporiboflavinosis, even when severe, seldom incapacitates the
individual, but it may have subtle functional effects such as
impaired neuromotor function, wound healing and perhaps
increased susceptibility to cataract (45). Riboflavin deficiency
almost always occurs in association with deficiencies of other Bcomplex vitamins such as pyridoxine; it is usually a part of a
multiple deficiency syndrome.
Requirement
There are no real body stores of riboflavin. Daily requirement is
0.6 mg per 1000 kcal of energy intake (9). For further details see
Table 31.
NIACIN
Niacin or nicotinic acid is essential for the metabolism of
carbohydrate, fat and protein. It is also essential for the normal
functioning of the skin, intestinal and nervous systems. This
vitamin differs from the other vitamins of the B -complex group in
that an essential amino acid, tryptophan serves as its precursor.
Another characteristic of niacin is that it is not excreted in urine as
such, but is metabolised to at least 2 major methylated derivatives :
N-methyl-nicotinamide and N-methyl pyridones.
Sources
Foods rich in niacin and//or tryptophan are liver, kidney meat,
poultry, fish, legumes and groundnut. Milk is a poor source of
niacin but its proteins are rich in tryptophan which is converted in
the body into niacin (about 60 mg of tryptophan is required to
result in 1 mg of niacin). In many cereals, especially maize, niacin
occurs in "bound" form unavailable to the consumer.
Deficiency
Niacin deficiency results in pellagra. The disease is
characterised by three D's - diarrhoea, dermatitis and
_______________________________________________VITAMINS 447
Deficiency
Folate deficiency may occur simply from a poor diet. It is
commonly found in pregnancy and lactation (48) where requirements
are increased. It results in megaloblastic anaemia, glossitis, cheilosis
and gastrointestinal disturbances such as diarrhoea, distension and
flatulence. Severe folate deficiency \ may cause infertility or even
sterility. There is also evidence / that the administration of folic acid
antagonists (e.g., alcohol, pyrimethamine, and cotrimoxazole) in
I^tfprevention
VS^) early pregnancy may produce abortions or congenital malformations.
O^ Pellagra is a preventable disease. A good mixed diet" containing
The laboratory diagnosis of folate deficiency is based on
milk and/or meat is universally regarded as an essential part of measurement of serum and red cell folate concentrations, usually
prevention and treatment. Avoidance of total dependence on maize by microbiological assay (49).
or sorghum is an important preventive measure. Pellagra is a disease
of poverty. Given modern knowledge and opportunities for Requirement
economic, agricultural and social development, there is every reason
Body stores of folate are not large, about 5-10 mg, and
to hope that this disease could be eliminated (3).
therefore, folate deficiency can develop quickly. Folic acid
requirements are greatest in conditions where there is rapid cell
Requirement
multiplication, such as during growth in young children and during
The recommended daily allowance is 6.6 mg/1000 kcal of
pregnancy (49). Folic acid supplementation during pregnancy has
energy intake (9). For further details see Table 31.
been found to increase the birth weight of infants and decrease the
incidence of low birth weight babies. Intake values recommended
VITAMIN B6
by ICMR (1989) are given below:
Per day
Pyridoxine (vitamin B5) exists in three forms : pyridoxine,
pyridoxal and pyridoxamine. It plays an important role in the
a)Healthy adults
100 meg
metabolism of amino acids, fats and carbohydrate. It is widely
b)Pregnancy
400 meg
distributed in foods, e.g., milk, liver, meat, egg yolk, fish, whole
c)Lactation
150 meg
grain cereals, legumes and vegetables. Pyridoxine deficiency is
d)Children
100 meg
associated with peripheral neuritis. Riboflavin deficiency impairs
the optimal utilization of pyridoxine. INH, an antituberculosis drug
VITAMIN B12
is a recognized antagonist, and patients receiving INH are often
provided with a supplement of pyridoxine (10 mg/day).
Vitamin B12 is complex organo-metallic compound with a
cobalt
atom. The preparation which is therapeutically used is
The requirements of adults vary directly with protein intake.
cyanocobalamine, which is relatively cheap. Vitamin B12
Adults may need 2 mg/day; during pregnancy and lactation, 2.5
cooperates with folate in the synthesis of DNA, so deficiency of
mg/day. Balanced diets usually contain pyridoxine, therefore
either leads to megaloblastosis. Vitamin B12 has a separate
deficiency is rare.
biochemical role, unrelated to folate, in synthesis of fatty acids in
myelin (25). The physiological mechanism for its absorption
PANTOTHENIC ACID
requires intrinsic factor from the stomach, and the complex is
There is a long standing evidence for a relation between
absorbed only at a special site in the terminal ileum.
pantothenic acid and adrenal cortical function. Recent work
Sources
indicates a more specific role for pantothenic acid in the
biosynthesis of corticosteroids (7). Human blood normally contains
Good sources are liver, kidney, meat, fish, eggs, milk and
18 to 35 mg of pantothenic acid per 100 ml, mostly present in the
cheese. Vitamin B12 is not found in foods of vegetable origin. It is
cells as coenzyme A. The daily requirement is set at 10 mg (37). All
also synthesized by bacteria in colon. Unlike folic acid, vitamin B12
foods contribute to dietary intake. About 3 mg are excreted daily in
is relatively heat stable. Liver is the main storage site of vitamin
urine.
B12. About 2 mg are stored in liver, and another 2 mg elsewhere in
the body. These stores are sufficient to tide over any deficiency for
FOLATE
one to three years. Because of these reserves, deficiency of vitamin
B12 appears to be rare. Unlike folic acid, vitamin B12 is relatively
The recommended name is folate, alternative name is folacin and
heat stable.
the usual pharmaceutical preparation is folic acid (25).
Folic acid occurs in food in two forms : free folates and bound
folates. The total folates represent both the groups. In man, free
folate is rapidly absorbed, primarily from the
Deficiency
Vitamin B12 deficiency is associated with megaloblastic
Vegetables :
Amla
Guava
Lime
Orange
Tomato
Germinated Pulses
Bengal gram
600
212
63
30
27
Source : (157)
g Decency ^ g,
16
Amaranth
Cabbage
Spinach
Brinjal
Cauliflower
Potatoes
Radish
99
124
28
12
56
17
15
Requirement
The estimated requirement for vitamin C has recently been
raised from 40 to 60 mg with much larger doses advocated by
some. The normal body when fully saturated contains about 5 g of
vitamin C. Daily intakes recommended by the ICMR (9) are given
in Table 31.
MINERALS
More than 50 chemical elements are found in the human body,
which are required for growth, repair and regulation of vital body
functions. These can be divided into three major groups : (a)
MAJOR MINERALS : These include calcium, phosphorus,
sodium, potassium and magnesium (b) TRACE ELEMENTS :
These are elements required by the body in quantities of less than a
few milligrams per day, e.g. iron, iodine, fluorine, zinc, copper
cobalt, chromium, manganese, molybdenum, selenium, nickel, tin,
silicon and vanadium (51). Many more have been added to the list
in the last few years, (c) TRACE CONTAMINANTS WITH NO
KNOWN FUNCTION : These include lead, mercury, barium,
boron, and aluminium.
Only a few mineral elements (e.g., calcium, phosphorus,
sodium, iron, fluorine, iodine) are associated with clearly
recognizable clinical situations in man. For none of the other
elements do we know with any certainty for their metabolic roles,
and much less the clinical effects of dietary insufficiency (52). The
bioavailability of minerals such as iron and zinc may be low in a
total vegetarian diet because of the presence of substances such as
phytic acid. Besides, large amounts of dietary fibre may interfere
with proper absorption. Man is not likely to suffer from trace
element deficiencies as long as he is omnivorous. Surveys have
shown that mineral deficiencies are no greater among vegetarians
than among non-vegetarians. In fact, man's need for trace elements
has not yet been precisely determined. Trace elements should not
be used as dietary supplements, since excessive amounts can have
injurious effects.
CALCIUM
Calcium is a major mineral element of the body. It constitutes
1.5-2 per cent of the body weight of an adult human. An average
adult body contains about 1200 g of calcium of which over 98 per
cent is found in the bones. The amount of calcium in the blood is
usually about 10 mg/dl. The developing foetus requires about 30 g
of calcium. There is a dynamic equilibrium between the calcium in
the blood and that in the skeleton; this equilibrium is maintained by
the interaction of vitamin D, parathyroid hormone, and probably
calcitonin.
Functions
Ionized calcium in the plasma has many vital functions
including formation of bones and teeth, coagulation of blood,
contraction of muscles, cardiac action, milk production, relay of
electrical and chemical messages that arrive at a cell's surface
membrane to the biochemical machinery within the cell, keeping
the membranes of cells intact and in the metabolism of enzymes
and hormones. It also plays a crucial role in the transformation of
light to electrical impulses in the retina. In short, the calcium ion
controls many life processes ranging from muscle contraction to
cell division.
Sources
Calcium is readily available from many sources. By far the best
natural sources are milk and milk products, (e.g., cheese, curd,
skimmed milk and butter milk), eggs and fish. A litre of cow's milk
provides about 1200 mg of calcium, and human milk about 300
mg. Calcium occurs in milk as calcium
_______________________________________________MINERALS 449
V * ^r\S J
r^7
VIABLE mf
MCHC
(per cent)
Adult males
13
34
12
34
11
34
11
34
Children, 6 to 14 years
12
34
At all ages the normal MCHC should be 34; values below that
indicate that red cells are hypochromic, which occurs in iron
deficiency anaemia. A haemoglobin level of 10 to 11 g/dl has been
defined as early anaemia; a level below 10 g/dl as marked anaemia
(61).
Age Group
Infants (5-12 months)
Children (1-12 years)
Adolescents (13-16 years)
0.7
1.0
1.8 (males)
2.4 (females)
0.9
Adults, males
Adults, females :
Menstruation
2.8
Pregnancy (first half)
0.8
(second half)
3.5
Lactation
2.4
Post-menopause
0.7
Source : (61)
The recommended dietary intakes of iron are given in Table 31.
IODINE
Iodine is a essential micronutrient. It is required for the synthesis
of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3)
containing respectively 4 and 3 atoms of iodine. Iodine is essential in
minute amounts for the normal growth and development and well
being of all humans. The adult human body contains about 50 mg of
iodine, and the blood level is about 8-12 micrograms/dl (37).
Sources
The best sources of iodine are sea foods (e.g., sea fish, sea salt)
and cod liver oil. Smaller amounts occur in other foods, e.g., milk,
meat, vegetables, cereals, etc. The iodine content of fresh water is
small and very variable, about 1-50 micrograms/L (37).
___________________________________________MINERALS 451
About 90 per cent of iodine comes from foods eaten; the
remainder from drinking water. The iodine content of the soil
determines its presence in both water and locally grown foods.
The deficiency is geochemical in nature.
Goitrogens
"Goitrogens", are chemical substances leading to the
development of goitre. They interfere with iodine utilization by
the thyroid gland. They may occur in food and water. The brassic
group of vegetables (e.g., cabbage, cauliflower) may contain
goitrogens. Most important among the dietary goitrogens are
probably cyanoglycosides and the thiocyanates.
Deficiency
The most obvious consequence of iodine deficiency is goitre
but recent studies have indicated that there is a much wider
spectrum of disorders, some of them so severe as to be disabling.
They include : (a) hypothyroidism (b) retarded physical
development and impaired mental function
(c) increased rate of spontaneous abortion and stillbirth
(d) neurological cretinism, including deaf-mutism; and
(e) myxedematous cretinism, including dwarfism and severe
mental retardation. To express this state of affairs more
accurately, the term "endemic goitre", is now replaced by the
term Iodine Deficiency Disorders (IDD) to refer to all the
effects of iodine deficiency on human growth and development
which can be prevented by correction of iodine deficiency
(64, 65, 66). The spectrum of IDD is as shown in Table 15.
TABLE 15
The spectrum of iodine-deficiency disorders in
approximate order of increasing severity
Disorders
Levels of severity
Goitre
- Grade I
-Grade II
. Sources
-Grade III
LJhe principal sources of fluorine available to man are :
- Multinodular
V*',
,\(a) Drinking water : The major source of fluorine to man is
- Varying combinations of
\
drinking water. In most parts of India, the fluoride content of
clinical signs (depending
drinking water is about 0.5 mg/L, but in fluorosis-endemic
on age of onset, duration
^areas, it may be as high as 3 to 12 mg/L (68). (b) Foods :
and severity)
<. Fluorides occur in traces in many foods, but some foods such
| as sea fish,, cheese and tea are reported to be rich in
fluorides (46).
Variable severity
Deficiency/Excess
Fluorine is often called a two-edged sword. Prolonged ingestion
of fluorides through drinking water in excess of the daily
- Unilateral
requirement is associated with dental and skeletal fluorosis; and
- Bilateral
inadequate intake with dental caries. The use of fluoride is
recognized as the most effective means available for the prevention
of dental caries.
- Muscle weakness in legs,
arms, trunk
Requirement
) f-3
-Spastic diplegia
Y,
| The recommended level of fluorides in drinking water in this
-Spastic quadriplegia
fp
\ country is accepted as 0.5 to 0.8 mg per litre (69, 70). In
/ temperate countries where the water intake is low, the optimum
- Hypothyroid cretinism
5 level of fluorides in drinking water is accepted as 1 to 2 mg per
- Neurological cretinism
X-l~
\
OTHER TRACE ELEMENTS
Hypothyroidism
aDelayed
Subnormal intelligence
motor milestones I
Mental deficiency
Hearing defects
Speech defects
Strabismus (squint)
Nystagmus
Spasticity (extrapyramida)
Neuromuscular weakness
Endemic cretinism
Intrauterine death
(spontaneous abortion,
miscarriage)
>
I
J
Zinc yA^(g)
NUTRITIONAL PROFILES OF
PRINCIPAL FOODS
When planning balanced diets, it is important to know what
foods are available according to origin, approximate chemical
composition, predominant function and how to combine them to
increase nutritive value. Since each food has a different
'Nutritional profile, an intake of different types of foods is
xfesired to achieve optimum health.
\l. Cereals and millets
CEREALS
Cereals (e.g., rice, wheat) constitute the bulk of the daily diet.
Rice is the staple food of more than half the human race. Next to
rice, wheat is the most important cereal. Maize ranks next to rice
and wheat in world consumption. Maize is also used as food for
cattle and poultry because it is rich in fat, besides being cheaper
than rice or wheat.
Cereals are the main sources of energy (carbohydrates). They
also contribute significant quantities of proteins (6 to 12 per cent),
minerals and B-group vitamins. The yellow variety of maize
contains significant amounts of carotene. In terms of energy,
cereals provide about 350 kcal per 100 grams. Considering the
large amounts in which they are consumed, cereals contribute 70 to
80 per cent of the total energy intake, and more than 50 per cent of
protein intake in typical Indian diets.
Cereal proteins are poor in nutritive quality, being deficient in
the essential amino acid, lysine. The proteins of maize are still
poorer, being deficient in lysine and tryptophan (a precursor of
niacin). However, if cereals are eaten with pulses, as is common in
the traditional Indian diets, cereal and pulse proteins complement
each other and provide a more balanced and "complete" protein
intake. Some strains of maize contain an excess of leucine which
interferes with the conversion of tryptophan into niacin; this
aggravates the pellagragenic action of maize.
Table 16 gives the nutritive value of some common cereals.
TABLE 16
Nutritive value of cereals (Values per 100 g.)
Protein
(g)
Fat
Carbohydrate
Thiamine
Niacin
Riboflavin
Minerals
Energy
(g)
(g)
(mg)
(mg)
(mg)
(g)
(kcal)
Raw Rice
Milled
Wheat
Whole
6.8
11.81
0.5
78.2
0.06
1.9
0.06
0.6
345
1.5
71.2
0.45
5.0
0.17
1.5
346
Maize
dry
11.1
3.6
66.2
0.42
1.8
0.1
1.5
342
Source : (157)
Rice
Rice is the staple food of more than half the human race. The
rice grain consists of 3 parts - the germ (embryo), the inner
endosperm, and the outer pericarp and aleurone grain layer. The
endosperm is composed mostly of starch; the outer pericarp
aleurone layer and germ contain most of the essential nutrients.
The protein content of rice varies from 6-9 per cent. Rice proteins
are richer in lysine than the other cereal proteins, and for this
reason, rice protein is considered to be of better quality. Rice is a
good source of B group vitamins, especially
have been developed by which the finished product does not give
any bad odour.
TABLE 17
Effect of Milling on Rice
Wheat
Next to rice, wheat is the most important cereal. The nutritive
composition of wheat is given in Table 16/The protein , content of
wheat varies from 9 to 16 per cent,(_the limiting amino acids are
lysine and threonineT^The wheat grain is much less subjected to
loss of essential TTutrients during processing than rice. In India, the
bulk of wheat is consumed as whole grain wheat flour or atta.
Maida or white flour which represents 70 per cent extraction of
wheat is poorer from the nutrition standpoint. The whiter the flour
the greater the loss of vitamins and minerals. Thus whole grain
wheat flour is richer source of vitamin B than refined white flour.
3
c
JZ
5
~
2
o
a.
J3
CO
>
V
L
Maize
Maize (Corn, bhutta) ranks next to rice and wheat in world
consumption, and in certain areas it is the principal source of
proteins and energy both. It is also used as a food for cattle and
poultry. The yellow variety of maize contains significant amount of
carotenoid pigments. Maize is fairly rich in fat (Table 16). The
proteins of maize are deficient in tryptophan and lysine; and some
strains contain an excess of leucine. Studies indicate that excess of
leucine interferes in the conversion of tryptophan into niacin, and
thus aggravates the pellagragenic action of maize. Maize is also
used in the manufacture of breakfast foods such as cornflakes.
Maize flour or corn flour is widely used in the preparation of
custards and table desserts. The incorporation of opaque-2 gene
into maize has greatly improved the quality of its protein.
MILLETS
The term "millet" is used for smaller grains which are
ground and eaten without having the outer layer removed;
ythey are jowar (sorghum), bajra (pearl millet), ragi, kodo and a
Mew others known as "minor millets" or pseudocereals (73).
^Jhe nutritive value of millets is as shown in Table 18.
TABLE 18
Nutritive value of millets (values per 100 g)
,
Protein
Fat
Carbohydrate
Minerals
Calcium
Iron
Thiamine
Riboflavin
Niacin
Energy
(g)
(g)
(g>
(g)
(mg)
(mg)
(mg)
(mg)
(mg)
(kcal)
Jowar
Bajra
Ragi
10.4
1.9
72.6
1.6
25.0
4.1
0.3
1.3
3.1
349
11.6
5.0
67.5
2.3
42.0
8
0.3
0.25
2.3
361
7.3
1.3
72.0
2.7
344.0
3.9
0.2
0.18
2.3
328
Source : (157)
Jowar (sorghum)
Jowar is also known as kaffir corn or Milo. It is a major crop
grown in India next only to wheat and rice. For several population
groups, it is a staple diet. The protein content of jowar varies from
9 to 14 per cent, and the proteins are limiting in lysine and
threonine. Certain varieties of jowar have a high leucine content
and consumption of these varieties is associated with pellagra. This
disorder is often seen in the Telengana and Marathwada regions
where jowar is predominantly consumed.
360
347
335
432
17.1
24.0
22.3
43.2
ThiaFat ( Cal
cium Iron mine
3
mg
mg
mg
5.3 202 4.6 0.30
1.4 154 3.8 0.42
1.7 73 2.7 0.45
19.5 240 10.4 0.73
2.9
2.0
2.9
3.2
30
00
Source : (157)
Anti-nutritional factors : In the raw state, pulses have some antinutritional factors such as phytates and tannins which adversely
affect the availability of some nutrients to the body. However,
most of the antinutritional factors are destroyed by heat. Presence
of high amounts of certain sugars known as oligosaccharides is
known to be associated with flatulence (74).
Soyabean
Soyabean is the richest among pulses. It contains about 40 per
cent of protein, 20 per cent of fat and 4 per cent of minerals. The
proteins of soyabean are of relatively high nutritive value. The
limiting amino acid is methionine. Soyabean can be cooked and
eaten as dhal. It can be tried in other forms like mixing its powder
with atta for chappatis, soyabean milk and curd and in baby
____________________________________________________MILK 45
After oil extraction in the case of some, the residue (oilseed cake)
can be formulated into acceptable foods rich in protein. For
example, groundnut flour is used in the manufacture of Indian
Multipurpose Food, balahar and balanced malt food. Due partly to
their high fat content and partly to their high cellulose content,
nuts are not easily digestible. However nuts eaten in a mixed diet
are an extremely valuable source of protein. Peanuts for human
consumption should be thoroughly dried and properly stored to
avoid the growth of Aspergillus flavus which produces "aflatoxin".
5. Fruits
Fruits are protective foods. They are invaluable in human
nutrition because they are good sources of vitamins and minerals.
One special feature which distinguishes fruits fromV other foods is
that they can be eaten raw and fresh. This makes the vitamins and
minerals present in fruit easily available.
Nutritive Value
(1) Vitamins : Fruits are prized for their vitamins. Most fruits
contain significant amounts of ascorbic acid. The orange, guava
and the Indian gooseberry (amla) are particularly rich in ascorbic
acid. One medium sized orange can provide enough juice to meet
the daily requirement of ascorbic acid of an adult. Apart from
ascorbic acid, several fruits contain good amounts of carotene. The
papaya and mango are excellent sources of carotene. (2) Minerals
: Fruits are good sources of minerals especially sodium and
potassium. Some fruits like sitaphal (custard apple) are rich in
calcium. Dried fruits like raisins, dates and apricots are good
sources of calcium and iron. Fruits also contain a great variety of
organic acids which are responsible for the sources of unripe fruits.
The intake of fruits leads to an alkaline urine. (3) Carbohydrate :
Fruits in general have a low energy value but some fruits like
banana and mango contain good amounts of carbohydrate and can
act as good source of energy. Pectin, a kind of sugar, present in
fruits like guavas is helpful in the preparation of fruit jellies. The
fruit sugars are easily digestible and completely absorbed. The
more ripe a fruit is, the higher its sugar content. (4) Cellulose :
Fruits contain cellulose which assists in normal bowel movements.
Nutrition experts recommend a daily intake of 85 grams or
more of fresh fruit for maintenance of good health. Fruits are
costly and it may not be within the reach of all to afford them
daily. If green leafy vegetables are included in the daily diet, the
need for fruit as an essential item in the diet is much reduced. The
aim in nutrition education should be to promote the intake of
seasonal fruits which are cheaper and easily available. The costly
fruits are not necessarily the best in respect of nutrients. The food
values of some common fruits are as given in Table 20.
TABLE 20
Nutritive value of some common fruits
(per 100 g of edible portion)
Name
Fresh Fruits:
Banana
Grapes
Guava
Mango
Orange
Papaya
Sitaphal
Amla
Dry fruits:
Dates
Raisins
Source : (157)
Calories
Calcium
(mg)
Iron
(mg)
Carotene
104
71
51
74
48
32
104
58
10
20
10
14
26
17
17
50
0.5
1.5
0.27
1.3
0.32
0.5
4.31
1.2
124
0
0
2210
2240
2740
0
9
317
308
120
87
7.3
7.7
44
2.4
tea)
Vit. C
(mg)
7
1
212
16
68
57
37
600
3
1
6. Animal foods
Foods of animal origin include meat, poultry, fish, eggs, mill
and dairy products. They provide high quality proteii (containing
all the essential amino acids) and good amounts o fat, besides
some vitamins and minerals. Vitamin B 12 is one o the rare
nutrients found only in animal foods. Since they an expensive,
animal foods are consumed in small amounts ii most developing
countries. Even small amounts of anime foods add considerably
to the nutritive value of the diel Among animal foods, cow's milk
and hen's egg are perhap nature's two most nearly perfect foods.
Milk
Milk is the best and most complete of all foodsjt is secretei by
IFTe animals to serve as the sole and wholesome food fo their
suckling young ones. It is a fine blend of all the nutrient necessary
for growth and development of the young ones Thus milk is a
good source of proteins, fats, sugars, vitamin and minerals.
Hi) Proteins : The chief protein of milk is casein; it occurs ii
combination with calcium as calcium caseinogenate. The othe
proteins are lactalbumin and lactglobulilri^Animal milks contaii
nearly three times as much protein as human milk. Mill proteins
contain all the essential amino acids. Human mill proteins contain
greater amounts of tryptophan and sulphur containing amiao acids
(especially cystein) than the anima milk proteins. ^n^Pai: The fat
content of milk varies from 3.' per cent in human milk to 8.8 per
cent in buffalo milk. Humai milk contains a higher percentage of
linoleic acid and oleic ack than anirjaalmilks. Milk fat is a good
source of retinol an< vitamin D.jfiii) Sugar : The carbohydrate in
all milks is lactosi or milk sugafjlt is found nowhere else in nature.
It is less swee than cane sugar and is readily fermented by lactic
acid bacilli Human milk contains more sugar than animal
milks
Minerals : Milk contains almost all known minerals needec the
body such as calcium, phosphorus, sodium, potassium
magnesium, cobalt, copper, iodine, etc. Milk is particularly rid in
calcium; it is however a poor source of irqrjltyj Vitamins Milk is a
good source of all vitamins except vitamin_CJ J^.^4|
Human and animal milks are as compared in Table 21 which
illustrates that milk is to a great extent species-specific.
TABLE 21
Nutritive value of milks compared
(Value per 100 grams)
Fat
(g)
Protein
Lactose
Calcium
(g)
(g)
(mg)
Iron
(mg)
Vitamin C
(mg)
Minerals
(g)
Water
(g)
Energy
(kcal)
Source : (157)
(
\
Buffalo
Q/Z
Cow
Goat
Human
6.5
4.1
4.5
3.4
4.3
5.1
210
3.2
4.4
120
3.3
4.6
170
1.1
7.4
28)
0.2
1
0.8
81.0
117
0.2
2
0.8
87
67
0.3
1
0.8
86.8
72
"
3
0.1
88
65
Milk products
Toned milk:
The term "toned" is an Indian coinage. It is a blend of natural
milk and "made-up" milk. It contains 1 part of water, 1 part of
natural milk and 1/8 part of skim milk powder. The mixture is
stirred, pasteurised and supplied in bottles. Toned milk has a
composition nearly equivalent to cow's milk. It is cheaper and yet
a wholesome product.
Vegetable milk
Milk prepared from certain vegetable foods (viz. groundnut,
soyabean) is termed "vegetable milk". It may be used as a
substitute for animal milk. The Central Food Technological
Research Institute, Mysore has perfected techniques for the
preparation of vegetable milk (75).
Ms
" legg contains all the nutrients except carbohydrate and vitamin C.
About 12 per cent of egg is made of shell, 58 per I cent of egg white,
and 30 per cent of egg yolk. An egg weighing 60 grams contains 6 g
of protein, 6 g of fat, 30 mg of calcium and 1.5 mg of iron, and
supplies about 70 kcal of energy. Egg proteins have all the nine
essential amino acids needed by the body in right proportions.
Nutritionists consider egg protein as the best among food proteins. In
fact, egg protein is the standard against vvhich the quality of other
proteins is compared. Except for vitamin C, egg contains all the fatsoluble and water-soluble vitamins in appreciable amounts. Important
minerals such as calcium, phosphorus, iron, zinc and other trace
elements are present in the eggTlBarring milji, no other food can
supply such a diverse range oTnutrientsfNet protein utilization (NPU)
which combines in a single value trie biological value and V
digestibility, is 100 for egg compared to 80 for meat and 75 for!
muOftaw egg white is not assimilated by the intestinal mucosa/
therefore it must be cooked before consumption. Boiling destroys
'avidin', a substance which prevents the body from obtaining biotin,
one of the B-complex vitamins. Boiled egg is therefore nutritionally
superior to raw egg. In recent years the cholesterol content of egg
(250 mg/egg) has generated a sense of fear because of the risk of
CHD. A reduction in intake of eggs is advised for those at risk of
CHD. This should not distract others from eating eggs. Eggs or no
eggs, cholesterol is formed in the body endogenously and is controlled
by what is known as feedback mechanism.
Fish
Fish is nutritious food rich in proteins (15 to 25 per cent) with a
good biological value and a satisfactory amino acid balance. The
fat of fish is rich in unsaturated fatty acids and A and D vitamins.
Fish liver oils are the richest source of vitamins A and D. Fish
bones when eaten are an excellent source of calcium, phosphorus
and fluorides. Fish are less rich in iron (0.7 to 3 mg per 100 g) than
meat. Fresh water fish do not contain iodine, but sea fish do. Of all
the sea foods, oysters and lobsters are the richest in iodine. There is
practically no carbohydrate in fish. The fish proteins are easily
digested. The nutritive value of diet is greatly enhanced by
inclusion of fish.
Meat
The term "meat" is applied to the flesh of cattle, sheep and
goats. Meats contain 15 to 20 per cent of protein, which is less than
that found in pulses, but meat proteins are a good source of
essential amino acids. Iron contained in meat (2 to 4 mg per 100 g)
is more easily absorbed than iron in plants and this is another
major quality of meat. In addition, meat contains varying amounts
of fat, which is composed of non-essential saturated fat. The
energy provided by meat depends upon its fat content. Besides
iron, meat provides minerals such as zinc and B-vitamins. It is
poor in calcium (10 to 25 mg per 100 g)
Fat
Minerals
Meat, Goat
21.4
3.6
1.1
Fish
Egg. hen*
19.5
13.3
2.4
13.3
1.5
1.0
Liver goat
20.0
3.0
1.3
AH
______________________________________________ENERGY 457
Tea
Cocoa
(g)
1.8
0.9
7.2
Fat
(g)
Carbohydrate (g)
Kcal
2.2
17.8
98.0
1.1
16.4
79.0
8.8
26.2
213.0
Protein
Soft drinks
Some are carbonated (e.g., soda water incorporating carbon
dioxide under high pressure) and others non-carbonated such as
fruit juices. The principal ingredients of soft drinks are carbon
dioxide, sugars, acids such as citric acid or tartaric acid, colouring
and flavouring agents. Fruit beverages comprise fruit juices,
squashes and cordials. Fruit squashes and cordials are diluted with
water before consumption.
Alcoholic beverages
These are beer, whisky, rum, gin, arrack, etc. The alcoholic
content of these beverages varies widely from 5 to 6 per cent in
beers to 40 to 45 per cent in whisky, rum, gin and brandy. Alcohol
supplies about 7 kcal per gram.
b. Vinegar
Natural vinegar is made from fermentation of fruits, malt and
molasses. It contains a minimum of 3.7 per cent acetic acid.
Synthetic vinegar should not be harmful if it is free from lead,
copper, arsenic or mineral acids. Synthetic vinegar should be
distinctly labelled "SYNTHETIC" according to Prevention of Food
Adulteration Act rules.
NUTRITIONAL REQUIREMENTS
Basic concepts
The science of human nutrition is mainly concerned with
defining the nutritional requirements for the promotion, protection
and maintenance of health in all groups of the population. Such
knowledge is necessary in order to assess the nutritional adequacy
of diets for growth of infants, children and adolescents, and for
maintenance of health in adults of both sexes and during pregnancy
and lactation in women (76). In this context, a variety of terms
have been used to define the amount of nutrients needed by the
body such as : optimum requirements, minimum requirements,
recommended intakes or allowances, and safe level of intake. Of
these, the term "recommended daily intake" or allowance (RDA)
has been widely accepted (1).
Recommended daily allowance (RDA)
The term "recommended daily intake "is defined as the amounts
of nutrient sufficient for the maintenance of health in
rather than weight where practical (79). The ICMR standards are
based on age, and not on body weight (except during the first year
of life).
Children above the age of 13 years need as much energy as
adults. This is because they show a good deal of physical activity,
almost equal to hard work by adults. This is also the age when
puberty sets in and there is a spurt in growth and an increase in
metabolic rate. This fact should be borne in mind when planning
dietaries for children.
(c) Adults : The energy requirements decrease with age because
of a fall in BMR and a decrease in physical activity in most
persons. In general, there is a 2 per cent decline of resting
metabolism for each decade for adults (37). The FAO/WHO
committee suggested that after the age of 40 years, requirements
should be reduced by 5 per cent per each decade until the age of
60, and by 10 per cent for each decade thereafter (78).
TABLE 24
Recommended daily intake for energy
Body
weight
Kg.
Group
118
108
Ikcal/kg/day
12.03
18.87
26.37
1240
1690
1950
5.1
7.0
8.1
35.4
31.5
47.8
46.7
57.1
49.9
2190
1970
2450
2060
2640
2060
9.1
8.2
10.2
8.6
11.0
8.6
Infancy
0-6 months 7-12
months
Children
1 -3 years
4-6 years 79 years
Adolescents
10-12 years
13-15 years
16-18 years
(males)
(females)
(males)
(females)
(males)
(females)
Adults
Ref Males
(light work)
(moderate work)
(heavy work)
60
2425
2875
3800
Ref Females
(light work)
(moderate work)
(heavy work)
50
1875
2225
2925
10.1
12.0
15.8
7.8
9.3
12.2
+ 300
+ 1.25
+ 550
+ 400
+2.3 +
1.68
Pregnancy
Lactation
(first 6 months)
(6-12 months)
Source : (9)
TABLE 25
Daily intake of energy
Age
Body weight
Kg
-1 year(average)
1 to 3 years
4 to 6 years
7 to 9 years
Reference man
Reference woman
kcal/kg/24 hrs.
(approximate)
112
12.0
18.8
26.3
60
50
100
90
80
45
40
PROTEIN 45!
Nutritional individuality
TABLE 26
Group
Recommended
protein intake
g/day
Recommended
energy intake
kcal/day
Protein
energy
ratio (%]
60
50
2900
2200
8.3
9.1
65
75
2500
2750
10.4
10.9
Reference adult
(Moderate activity)
Man
Woman
Pregnant woman
Lactating woman
(0-6m)
Assessment of protein
Preschool children :
1-3 years
21
1240
6.8
4 - 6 years
7 - 9 years
29
40
1690
1950
6.9
8.2
67
62
75
60
2450
2060
2640
2060
10.9
12.0
11.4
11.7
Adolescents ;
13 - 15 yrs. Boys
Girls
16-18 yrs. Boys
Girls
Nutrients per
100 g
kcal
Protein
(g)
Fish
PE%
(Kcal)
100
20.0
80
80
67
3.2
13
20
Dhal
350
21.0
84
24
Rice
350
7.0
28
Potato
100
1.6
Banana
100
1.0
Tapioca
160
0.7
Milk (cow)
If the PE is less than 4 per cent, the subject will be unable to eat
enough to satisfy protein requirements. It is recommended that
protein should account for approximately 15 to 20 per cent of the
total daily energy intake (81).
Dietary intakes
It is customary to express requirement in terms of grams per kg
of body weight. This principle applies to all age groups, although
absolute additions in units of grams of protein per day are made for
pregnancy and lactation.
The ICMR Expert Group (9) suggested an intake of one gram
of protein per kg of body weight for adult males and females,
assuming a NPU of 65 for the dietary protein. Table 28 gives the
protein intakes for individuals of different ages and physiological
states.
^^J^f*
Particulars
Man
sedentary work
(60 kg)
Woman
(50 kg)
Infants
Children
*
-.-.,-.
Adolescents
moderate work
heavy work
sedentary work
moderate work
heavy work
pregnancy
lactation (0 to 6 m)
0 to 3 months
3 to 6 months
6 to 9 months
9 to 12 months
1 to 3 years
4 to 6 years
7 to 9 years
Males
10 to 12 years
13 to 15 years
16 to 18 years
Females
10 to 12 years
13 to 15 years
16 to 18 years
fl^
Protein allowance
(g/kg/day)
(g/day)
r------' \
/
! '
60.0
1
*
50.0
i
1
1
+ 15.0
+ 25.0
2.37aTl
1.8(a)
1.65(b) \
1.5(b)
1.83
1.52
1.48
22.0
30.0
41
1.46
1.40
1.31
54
70
78
1.45
1.33
1.21
57
65
63
65 relative to egg
Source : (9)
Vulnerable groups
The protein requirements of women are increased during
pregnancy by about 14 g per day; and during lactation by about 25
g per day (during 0 to 6 months), over and above their normal
requirements.
Young children (0 to 6 years) require proportionately more
protein for each kilogram of body weight than adults. They are
more vulnerable to malnutrition.
The ICMR Expert Group (9) has not made any
recommendations for the elderly. It seems reasonable to assume
that the requirement of the aged are not less than that for young
adults, because it is an accepted fact that protein utilization is less
efficient in the elderly (6).
All estimates of protein requirement are valid only when the
energy requirements are fully met. If the total energy intake is
inadequate some dietary protein will be diverted to provide energy.
It is now accepted that there are no body protein stores which can
be filled up by a high protein intake.
At present there is no evidence that higher intakes of protein
confer greater benefit, although the possibility cannot be ruled out.
Most people, if they can, apparently choose to eat more protein
than the physiological requirement. The question remains whether
high protein intakes, far from being beneficial, may actually be
harmful (7).
Amino acid requirements
The protein intake must also satisfy the need for essential
amino acids. The 1985 WHO Expert Committee Report on Energy
and Protein Requirements (6) gives current estimates of amino
acid requirements (in mg/kg per day) at different ages. These are
reproduced in Table 29.
TABLE 29
Estimates of amino acid requirements at different ages
mg/kg per day
Infants Children
Amino acid
(3-4 (2 years)
months)
Histidine
Isoleucine
Leucine
Lysine
Methionine + cystine
Phenylalanine + tyrosine
Threonine
Tryptophan
Valine
Total essential
amino acids
Schoolboys
(10-12 years) Adults
A
B
28
8-12
70
161
103
58
125
87
17
93
742
31
73
64
27
69
37
12.5
38
352
30
45
60
27
27
35
4
33
261
28
44
44
22
22
28
3.3
25
216
10
14
12
13
14
7
3.5
10
84
Fat intake
g/day
Energy %
20*
9
30
45
22
25
12.5
17.5
9
15
4.5
5.7
3
3
* About half of this will come from invisible fat present in the foods.
Source : (9)
CARBOHYDRATE
The recommended intake of carbohydrate in balanced diets is
placed so as to contribute between 50 to 70 per cent of total energy
intake. Most Indian diets contain amounts more than this,
providing as much as 90 per cent of total energy intake in some
cases, which makes the diet imbalanced. This needs to be
corrected through nutrition education.
OTHER RECOMMENDED INTAKES
(a) Fat soluble vitamins
The daily requirement of vitamins A and D are given in
on which a
A%
.
_____________________________
BALANCED DIET 461
TABLE 31
J>" SiQjmary of
RDA for Indians
Group
Particulars
i Wt 1
Body
_______________(kg
Sedentary work
Man
Net
energy
Protein
Fat
Cal- I Iron
cium
Kcal/d
g/d
j
g/d
2425
Moderate work j 60
Heavy work
'
J mg/d Retinol
mg/d
2875
3800
60
20
400
28
600
1875
2225
2925
+300
50
20
400
30
600
+ 15
30
1000
38
600
1000
30
950
0-6 months
6-12 months
5.4
8.6
108/kg
98/kg
+25
+ 18
2.05/kg
1.65/kg
12.2
119.0
1240
1690
22
30
7-9 years
26.9
1950
41
54
57
nfants
+550
+400
Boys
Girls
10-12years
10-12 years
35.4
31.5
2190
1970
Boys
13-15 years
147.8
2450
Girls
13-15years
600
2400
10
0.2-1.0
J46.7
2060
3oys
16-18 years
157.1
2640
3irls
16-18 years
600
2400
10
100 0.2-1.0
49.9
2060
70
1.2
16
65
12
78
1.3
/
63
12
45
500
350
12
18
400
400
26
600
\ 34 '
19
600
400
25 j
600
22
41
1.5
22
14
600
2.0
28
40
loo
I 50
1.6 17
22
14
500j 30
2.0
40
1=^
80 per cent, are the "intermediate" ones, that is the mild and moderate
cases which frequently go unrecognized. The problem exists in all the
States and that nutritional marasmus is more frequent than kwashiorkor.
In the 1970s, it was widely held that PEM was due to protein
deficiency. Over the years, the concept of "protein gap" has given place to
the concept of "food gap". That is, PEM is primarily due to (a) an
inadequate intake of food (food gap) both in quantity and quality, and (b)
infections, notably diarrhoea, respiratory infections, measles and intestinal
worms which increase requirements for calories, protein and other
nutrients, while decreasing their absorption and utilization. It is a viscious
circle - infection contributing to malnutrition and malnutrition
contributing to infection, both acting synergistically (Fig. 1).
------------------------------.----------------------l
--:
^ ^^-
. _
Appetite loss
Nutrient loss
Malabsorption
Altered metabolism
-------
Weight loss
________._______ Growth faltering
Immunity lowered
Mucosal damage
i-'
FIG.l Malnutrition/Infection
cycle
Source : (186)
There are numerous other contributory factors in the web of causation,
viz. poor environmental conditions, large family size, poor maternal
health, failure of lactation, premature termination of breast feeding, and
adverse cultural practices relating to child rearing and weaning such as the
use of over-diluted cow's milk and discarding cooking water from cereals
and delayed supplementary feeding (187).
Malnutrition is self-perpetuating. A child's nutritional status at any
point of time depends on his or her past nutritional history, which may
particularly account for the present status. To some extent, this nutritional
history is linked to the mother's health and nutritional status. This in turn
has been influenced by her living conditions and nutritional history during
her own childhood (Fig. 2).
Nutritional status of
-------- woman of child-bearing ------------------------ ,
__________age_______
"
Nutritional status at
puberty
^
~~
Nutritional status of
pregnant woman
L---- .__^_---- ,.
Girl's nutritional
status
:
:
:
> m - 2 SD
< m - 2 SD
> m - 2 SD
Normal
Wasted
< m - 2 SD
Stunted
;--.
TABLE 32
Principal Features of Severe PEM
FEATURE
S
KWASHIORKOR
MARASMU
S
CLINICAL
Muscle wasting Fat
wasting Oedema
Weight for height
Mental changes
ALWAYS PRESENT
Obvious
Severe loss of subcutaneous fat
None
Very low
Sometimes quiet and apathetic
CLINICAL
Appetite Diarrhoea Skin
changes
Hair changes Hepatic
enlargement
SOMETIMES PRESENT
Usually good
Often (current and past)
Usually none
Seldom None
Poor
Often (current and past)
Diffuse pigmentation, sometimes 'flaky
paint dermatosis'
Sparse, silky, easily pulled out
Sometimes, due to accumulation of fat
BIOCHEMICAL
Serum albumin
Urinary urea per g creatinine
Hydroxyproline/creatinine ratio
Normal
Source : (185)
TABLE 34
Interpretation of indicators
Weight of the child
^ jog
Weight of a normal child at same height
Weight/Height =
(%)
Height/Age =
(%)
. '<
is'-.-
Nutritional
status
Stunting (% of
height/age)
Wasting (% of
weight/height)
Normal
Mildly impaired
>95
87.5 - 95
>90
80-90
Moderately impaired
Severely impaired
80 - 87.5
<80
70-80
<70
Source : (186)
Arm circumference : (186)
Arm circumference yields a relatively reliable estimation of the
body's muscle mass, the reduction of which is one of the most
striking mechanisms by which the body adjusts to inadequate
energy intakes. Arm circumference cannot be used before the age
of one year; between ages one and five years, it hardly varies.
An arm circumference exceeding 13.5 cm is a sign of a
satisfactory nutritional status, between 12.5 and 13.5 cm it
indicates mild-moderate malnutrition and below 12.5 cm, severe
malnutrition.
For the purpose of comparison, growth charts are provided with
reference curves. These curves show the limit of normal growth.
The WHO reference curves are based on extensive cross-sectional
data of well-nourished healthy children, assembled by the National
Centre for Health Statistics (NCHS). Malnutrition is defined by
WHO as a weight for age below the median minus two standard
deviations of the NCHS reference population (156).
Preventive Measures
There is no simple solution to the problem of PEM. Many types
of actions are necessary. The following is adapted from the 8th
FAO/WHO Expert Committee on Nutrition (1) for the prevention
of PEM in the community :
(a) Health Promotion
1.Measures directed to pregnant and lactating women
(education, distribution of supplements)
2.Promotion of breast feeding.
3.Development of low cost weaning foods : the child should be
made to eat more food at frequent intervals
4.Measures to improve family diet
5.Nutrition education - Promotion of correct feeding
practices.
6.Home economics
7.Family planning and spacing of births
8.Family environment
(b) Specific Protection
1.The child's diet must contain protein and energy-rich foods.
Milk, eggs, fresh fruits should be given if possible.
2.Immunization
3.Food fortification
^V i ()TABLE 35
VitarniTTA prophylaxis schedule
Individual
Timing
Children < 12
months of age
55mg(100 000IU)
Children > 12
months of age
Newborn
Women of Child
bearing age
Pregnant and
lactating women
110mg(200 000IU)
Sbtlrce : (30)
6 months, and 1 and 2 years of age (41). One tablet of iron and
folic acid containing 20 mg of elemental iron (60 mg of ferrous
sulphate) and 0.1 mg of folic acid should be given daily!*}
(2) Iron fortification
The WHO experts (49) did not recommend iron fortification
strategy for control of anaemia in regions where its prevalence is
high. However, recent studies in India at the National Institute of
Nutrition, Hyderabad showed that simple addition of ferric orthophosphate or ferrous sulphate with sodium bisulphate was enough
to fortify salt with iron (100). When consumed over a period of 1218 months, iron fortified salt was found to reduce prevalence of
anaemia significantly. Fortification of salt with iron has been
accepted by the Govt, of India as a public health approach to
reduce prevalence of anaemia. Commercial production of iron
fortified salt was started in 1985(100).
Iron fortification has many advantages over iron
supplementation. As salt is a universally consumed dietary item,
all segments of the population stand to benefit. No special delivery
systems are required (61).
(3) Other strategies
There are other strategies such as changing dietary habits,
control of parasites and nutrition education. These are longterm
measures applicable to situations where the prevalence and
severity of anaemia are lower. Cost and time involved to meet the
desired goals through these strategies are disproportionately high
(61).
5. Iodine deficiency disorders (IDD)
Iodine deficiency is yet another major nutrition problem in
India. Till recently, iodine deficiency was equated with goitre.
In recent years, it has become increasingly clear that iodine
deficiency leads to a much wider spectrum of disorders
commencing with the intrauterine life and extending through
childhood to adult life with serious health and social
implications. Table 15 presents the iodine deficiency disorders
in approximate order of increasing severity. The social impact
of iodine deficiency arises not so much from goitre as from the,
effect on the central nervous system (65).
V'Qf
The Problem
V-*"
Whereas goitre has ceased to be a major problem in many
developed countries (although not eradicated) it continues to be a
serious health problem in many Third World Countries. For
example iodine deficiency is a health problem of considerable
magnitude in India and the neighbouring countries of Bangladesh,
Bhutan, Myanmar, Indonesia, Nepal, Sri Lanka and Thailand.
More people are affected and levels of severity are higher in
South-East Asia than anywhere else in the world (101).
It has always been thought in India that goitre and cretinism
were only found to a significant extent in the "Himalaya goitre
Belt" which is the world's biggest goitre belt. It stretches from
Kashmir to the Naga Hills in the east, extending about 2400 km
and affecting the northern States of Jammu and Kashmir,
Himachal Pradesh, Punjab, Haryana, Delhi, Uttar Pradesh, Bihar,
West Bengal, Sikkim, Assam, Arunachal Pradesh, Nagaland,
Mizoram, Meghalaya, Tripura and Manipur. In recent years
renewed surveys outside the conventional goitre belt have
identified endemic foci of iodine deficiency and the associated
IDD in parts of Madhya Pradesh, Gujarat, Maharashtra, Andhra
Pradesh, Kerala and Tamil Nadu. More and more new areas are
being identified. Even areas near the sea coast like Bharuch district
in Gujarat and Ernakulam district in Kerala are found goitreaffected. In short, no State in India can be said to be entirely free
from goitre (Fig. 3).
in India
The magnitude of the problem in India is far greater than what
had been estimated in 1960s, when it was estimated that about 9
million persons were affected by goitre (102). Currently, no less
than 140 million people are estimated to be living in goitreendemic regions of the country. In the sub-Himalayan goitre belt of
India alone, nearly 55 million are estimated to be suffering from
endemic goitre, with an average goitre prevalence rate of about 36
per cent (66). In one particular district (Gonda) of Uttar Pradesh
known to be highly endemic, the prevalence of neonatal
hypothyroidism has been measured at the extremely high rate of 15
per cent (66).
Goitre control
There are four essential components of national goitre control
programme. These are iodized salt or oil, monitoring and
surveillance, manpower training and mass communication.
1. Iodized Salt
The iodization of salt is now the most widely used prophylactic
public health measure against endemic goitreiln India the level of
iodization is fixed under the Prevention of^ Food Adulteration
(PFA) Act and is not less than 30 ppm at the" production point, and
not less than 15 ppm of iodine at the consumer level
(100J?\lodized salt is most economical, convenient and effective
means of mass prophylaxis in endemic areas. Under the national
IDD control activities, the Govt, of India proposed to completely
replace common salt with iodized salt in a phased manner by 1992
(100).
Recently the National Institute of Nutrition at Hyderabad has
come out with a new product, common salt fortified with iron and
iodine. Community trials have been launched to examine the
efficacy of the "two-in-one" salt (100).
Iodized oil : Another method which has demonstrated its
efficacy for controlling goitre is intramuscular injection of iodized
oil (mostly poppy-seed oil). Scientists at the National Institute of
Nutrition, Hyderabad have now successfully developed a process
to produce iodized oil in safflower. or safola oil (103).
The advantage of the injection procedure is that an average dose
of 1 ml will provide protection for about 4 years. Although more
expensive than iodated salt, this method has the advantage that it
can be applied rapidly and in places where iodization of salt is not
feasible or iodated salt is in short supply. However, the difficulty
with this procedure is one of logistics, i.e., in reaching every victim
or potential victim of IDD for the injection, which means this
approach is less
Prepathogenic period
Period of pathogenesis
Reserves
exhausted
Non.
specific _____.
__________________.
Death
_> T
reserves
____.
*
signs and
symptoms
Physiological
and metabolic
alterations
IIlness
Permanent
dama e
2
0N
-c
Mortality data
10
Anthropometric studies
Dietary surveys
Biochemical studies
FIG.5 Methods of nutritional assessment and their relationship to the natural history of
disease
Method
Normal value
Vitamin A
Serum retinol
20 mcg/dl
Thiamine
Thiamine pyrophosphate
(TPP) stimulation of RBC
transketolase activity
RBC glutathione
reductase activity
stimulated by flavine
adenine dinucleotide
Urine N -methyl
nicotinamide
1.00-1.23 (ratio)
Riboflavin
Niacin
1.0-1.2 (ratio)
Folate
Serum folate
6.0 mcg/ml
Vitamin B12
160 mcg/ml
160 mg/L
Vitamin C
Vitamin K
Protein
Prothrombin time
Serum albumin (g/L)
11-16 seconds
35
Transferrin (g/L)
Thyroid-binding pre-albumin
(mg/L)
20
250
15 mcg/108 cells
Source : (132)
4. Functional indicators
Static indices of nutritional status (biochemical indicators) will
continue to play an important role as they are well-established and
familiar to practitioners and public health workers. Functional
indices of nutritional status are emerging as an important class of
diagnostic tools. Some of these are given in Table 37.
TABLE 37
Functional indices of nutritional status
System
1. Structural integrity
Erythrocyte fragility
Capillary fragility
Tensile strength
2. Host defence
Leucocyte chemotaxis
Leucocyte phagocytic capacity
Leucocyte bactericidal capacity
T cell blastogenesis
Delayed cutaneous hypersensitivity
3. Hemostasis
Prothrombin time
4. Reproduction
Sperm count
5. Nerve function
Nerve conduction
Dark adaptation
EEG
6. Work capacity
Heart rate
Vasopressor response
Nutrients
Vit.E.Se
Vif.C
Cu
P/E, Zn
P/E, Fe
P/E, Fe, Se
P/E, Zn
P/E, Zn
Vit.K
Energy, Zn
P/E, Vit Bl, B12
Vit A, Zn
P/E
P/E, Fe
Vit.C
Source : (133)
5. Assessment of dietary intake
The value of nutritional assessment is greatly enhanced when it
is supplemented by an assessment of food consumption. Direct
assessment of food consumption involves dietary surveys which
may be household inquiries or individual food consumption
surveys. Well organized survey methods for this purpose are
available (134,135).
A diet survey may be carried out by one of the following
methods : (i) WEIGHMENT OF RAW FOODS : This is the
method widely employed in India as it is practicable and if
properly carried out is considered fairly accurate. The survey team
visits the households, and weighs all food that is going to be
cooked and eaten as well as that which is wasted or discarded. The
duration of the survey may vary from 1 to 21 days, but commonly
7 days which is called "one dietary cycle". (ii) WEIGHMENT OF
COOKED FOODS : Foods should preferably be analysed in the
state in which they are normally consumed, but this method is not
easily acceptable among people (iii) ORAL QUESTIONNAIRE
METHOD : This is useful in carrying out a diet survey of a large
number of people in a short time. Inquiries are made
retrospectively about the nature and quantity of foods eaten during
the previous 24 or 48 hours. If properly carried out, oral
questionnaire method can give reliable results. A diet survey may
also include collection of data relating to dietary habits and
practices.
The data that is collected have to be translated into (a) mean
intake (grams) of food in terms of cereals, pulses, vegetables,
fruits, milk, meat, fish and eggs, and (b) the mean intake of
nutrients per adult man value or "consumption unit". This exercise
requires the use of suitable tables of food composition. An
excellent guide for carrying out this analysis is the Indian Council
of Medical Research (ICMR) publication : "Nutritive Value of
Indian Foods" (53).
A diet survey provides information about dietary intake
patterns, specific foods consumed and estimated nutrient intakes. It
indicates relative dietary inadequacies as judged by present
standards. Not only will such information be valuable for planning
health education activities, but it will also allow an assessment to
be made of the extent and nature of changes needed in the
agriculture and food production industries.
Growth
Monitoring
Nutritional
Assessment
Strategy
Preservation of
normal growth
Detection of
undernutrition
Approach
Educational-Motivational
Enrolment
All infants
Representative
sample
Age
Representative
ages at longer
intervals
Number
DiagnosticInterventional
Trained Worker
Weight card
Simple, emphasis
growth
Precise, nutritional
status
Nutritional
emphasis
Maintaining good
nutrition
Detect
malnutrition
Response
Early home
intervention based
on local knowledge
Nutritional
rehabilitation often
with supplements
Response time
Brief, resumption of
normal growth
Long, regain of
good nutrition in
community
Interventions
Source : (139)
Food supplements
of communitywide response,
such as
food subsidy
Malnutrition
rehabilitation,
often in special
centre
Indicator
Maternal Nutrition
Infant and preschool
child nutrition
birth weight
proportion being breast fed and
proportion on weaning foods, by age in
months, mortality rates in children aged
1,2,3 and 4 years, with emphasis on 2year-olds If age known :
height for age
weight for age If
age unknown :
the population (175). What makes the situation most serious is that
malnutrition's main victims are children under the age of 15. But
children under the age of 5 years are hit the hardest. On a global
scale the five principal nutritional deficiency diseases that are
being accorded the highest priority action are kwashiorkor,
marasmus, xerophthalmia, nutritional anaemias and endemic goitre
(175). These diseases represent the tip of the "iceberg" of
malnutrition; a much larger population are affected by "hidden"
malnutrition which is not easy to diagnose.
The effects of malnutrition on the community are both direct
and indirect. The direct effects are the occurrence of frank and
subclinical nutrition deficiency diseases such as kwashiorkor,
marasmus, vitamin and mineral deficiency diseases. The indirect
effects are a high morbidity and mortality among young children
(nearly 50 per cent of total deaths in the developing countries occur
among children under 5 year of age as compared to less than 5 per
cent in developed countries), retarded physical and mental growth
and development (which may be permanent), lowered vitality of
the people leading to lowered productivity and reduced life
expectancy. Malnutrition predisposes to infection and infection to
malnutrition; and the morbidity arising therefrom as a result of
complications from such infectious diseases as tuberculosis and
gastro-enteritis is not inconsiderable. The high rate of maternal
mortality, stillbirth and low birth-weight are all associated with
malnutrition.
In the more developed countries of the world nutritional
problems are somewhat different. Overnutrition is encountered
much more frequently than undernutrition. The health hazards
from overnutrition are a high incidence of obesity, diabetes,
hypertension, cardiovascular and renal diseases, disorders of liver
and gall bladder. From this brief review, it is obvious that the
consequences of malnutrition are ominous.
Ecology of Malnutrition
Malnutrition is a man-made disease. It is a disease of human
societies. It begins quite commonly in the womb and ends in the
grave. The great advantage of looking at malnutrition as a problem
in human ecology is that it allows for variety of approaches
towards prevention. Jelliffe (1966) (129) listed the ecological
factors related to malnutrition as follows : conditioning influences,
cultural influences, socio-economic factors, food production and
health and other services.
(1)CONDITIONING INFLUENCES : Infectious diseases are
an important conditioning factor responsible for malnutrition,
particularly in small children. Diarrhoea, intestinal parasites,
measles, whooping cough, malaria, tuberculosis all contribute
to malnutrition. In fact it is a vicious circle - infection
contributing to malnutrition, and malnutrition causing an
otherwise minor childhood ailments to become killers. It has
been shown that where environmental conditions are poor,
small children may suffer from some infection or the other for
almost half of their first three years of life. The interrelationship
between malnutrition and infection has been well documented.
(2)CULTURAL INFLUENCES : Lack of food is not the only
cause of malnutrition. Too often there is starvation in the midst
of plenty. People choose poor diets when good ones are
available because of cultural influences which vary widely from
country to country, and from region to region. These may be
stated as follows : (a) Food habits, customs, beliefs, traditions
and attitudes : Food habits are among the oldest and most
deeply entrenched aspects of any culture. They have deep
psychological roots and are associated with love, affection,
warmth, self image and social prestige. The family plays an
important role in shaping the food habits, and these habits are
passed from one generation to another. Rice is the staple cereal
in the eastern and southern States of India and wheat is the
______________________
staple cereal in the northern States. During the second World War,
when wheat was made available in place of rice in South India
people refused to buy wheat because it was not their staple cereal.
The story is told of a Philippine student who died of beriberi after
writing an essay explaining how the disease could be prevented.
The crux of the problem is that many customs and beliefs apply
most often to vulnerable groups, i.e. infants, toddlers, expectant
and lactating women. Papaya is avoided during pregnancy because
it is believed to cause abortion. In Gujarat, valuable foods such as
dhals, leaf greens, rice and fruits are avoided by the nursing
mother. There is a widespread belief that if a pregnant woman eats
more, her baby will be big and delivery difficult. Certain foods are
"forbidden" as being harmful for the child. Then there are certain
beliefs about hot and cold foods, light and heavy foods (b)
Religion : Religion has a powerful influence on the food habits of
the people. Hindus do not eat beef, and Muslims pork. Some
orthodox Hindus do not eat meat, fish, eggs and certain vegetables
like onion. These are known as food taboos which prevent people
from consuming nutritious foods even when these are easily
available, (c) Food fads : In the selection of foods, personal likes
and dislikes play an important part. These are called "food-fads".
The food fads may stand in the way of correcting nutritional
deficiencies, (d) Cooking practices : Draining away the rice water
at the end of cooking, prolonged boiling in open pans, peeling of
vegetables, all influence the nutritive value of foods, (e) Child
rearing practices : These vary widely from region to region and
influence the nutritional status of infants and children. Examples of
this situation are premature curtailment of breast feeding, the
adoption of bottle feeding and adoption of commercially produced
refined foods, (f) Miscellaneous : In some communities, men eat
first and women eat last and poorly. Consequently, the health of
women in these societies may be adversely affected. Chronic
alcoholism is another factor which may lead to serious
malnutrition.
(3) SOCIO-ECONOMIC FACTORS : Malnutrition is largely
the by-product of poverty, ignorance, insufficient education,
lack of knowledge regarding the nutritive value of foods,
inadequate sanitary environment, large family size, etc. These
factors bear most directly on the quality of life and are the true
determinants of malnutrition in society. The speed with which
populations are growing in many developing countries is
another important factor to reckon with. It has made the
solution of the malnutrition problem more difficult. In short,
the causes of malnutrition are built into the very nature of
society, in the socioeconomic and political structures, both
nationally and internationally (175).
(4) FOOD PRODUCTION : Increased food production
should lead to increased food consumption. The average
Indian has 0.6 hectare of land surface compared to 5.8 hectare
per head in the developed countries. The per capita arable
land for an average Indian is only 0.3 hectare (176). Yields per
hectare are only about one-fourth those achieved in the
industrial countries. Given the best technology known at
present, most developing countries could increase their food
production several fold. But increased food production will not
solve the basic problem of hunger and malnutrition in much of
the developing world. Scarcity of food, as a factor responsible
for malnutrition, may be true at the family level; but it is not
true on a global basis, nor is it true for most of the countries
where malnutrition is still a serious problem. It is a problem of
uneven distribution between the countries and within the
countries. It is said that there will be very little malnutrition in
India today if all the food available can be equitably distributed
in accordance with physiological needs (169).
(5) HEALTH AND OTHER SERVICES: The health sector can,
if properly organised and given adequate resources can combat
>^W)
Pasteurization of milk
^Ls
Pasteurization may be defined as the heating of milk to such
temperatures and for such periods of time as are required to destroy
any pathogens that may be present while causing minimal changes
in the composition, flavour and nutritive value (WHO, 1970)
(172). There are several methods of pasteurization. Three are
widely used : (1) Holder (Vat) Method : In this process, milk is
kept at 63-66 deg C for at least 30 minutes, and then quickly
cooled to 5 deg C. Vat method is recommended for small and rural
communities. In larger cities, it is going out of use. (2) HTST
Method : Also known as "High Temperature and Short Time
Method". Milk is rapidly heated to a temperature of nearly 72 deg
C, is held at that temperature for not less than 15 seconds, and is
then rapidly cooled to 4 deg C. This is now the most widely used
method. Very large quantities of milk per hour can be pasteurized
by this method. (3) UHT Method : Also known as "ultra-high
temperature method." Milk is rapidly heated usually in 2 stages
(the second stage usually being under pressure) to 125 deg C, for a
few seconds only. It is then rapidly cooled and bottled as quickly
as possible.
Pasteurization is a preventive measure of public health
importance and corresponds in all respects to the modern principles
of supplying safe milk. Pasteurization kills nearly 90 per cent of
the bacteria in milk including the more heat-resistant tubercle
bacillus and the Q fever organisms. But it will not kill thermoduric
bacteria nor the bacterial spores. Therefore, despite pasteurization,
with subsequent rise in temperature, the bacteria are bound to
multiply. In order to check the growth of microorganisms,
pasteurized milk is rapidly cooled to 4 deg C. It should be kept
cold until it reaches the consumer. Hygienically produced
pasteurized milk has a keeping quality of not more than 8 to 12
hours at 18 deg C.
Tests of pasteurized milk
(1) Phosphatase test : This test is widely used to check the
efficiency of pasteurization. The test is based on the fact that raw
milk contains an enzyme called phosphatase which is destroyed on
heating at a temperature which corresponds closely with the
standard time and temperature required for pasteurization. At 60
deg C for 30 minutes phosphatase is completely destroyed.
Consequently, the test is used to detect inadequate pasteurization or
the addition of raw milk. (2) Standard Plate Count : The
bacteriological quality of pasteurized milk is determined by the
standard plate count. Most countries in the West enforce a limit of
30,000 bacterial count per ml of pasteurized milk. (3) Coliform
Count: Coliform organisms are usually completely destroyed by
pasteurization, and therefore, their presence in pasteurized milk is
an indication either of improper pasteurization or postpasteurization contamination. The standard in most countries is
that coliforms be absent in 1 ml of milk.
MEAT HYGIENE
The term "meat" includes various tissues of animal origin. The
diseases which may be transmitted by eating unwholesome meat
are: (1) TAPE WORM INFESTATIONS :
Meat inspection
Animals intended for slaughter are subjected to proper
antemortem and postmortem inspection by qualified veterinary
staff. The principal causes of antemortem rejection of animals are
emaciation, exhaustion, pregnancy, sheep-pox, foot-rot,
actinomycosis, brucellosis, febrile conditions, diarrhoea and other
diseases of an infectious nature rendering meat unfit for human
consumption. The main causes of the postmortem rejection are
cysticercus bovis, liver fluke, abscesses, sarcocystis, hydatidosis,
septicaemia, parasitic and nodular infections of liver and lungs,
tuberculosis, cysticercus cellulosae, etc. (173). The characteristics
of good meat are that it should be neither pale pink nor a deep
purple tint, firm and elastic to touch, should not be slimy and have
an agreeable odour.
Slaughter houses
Slaughter houses are the places where animals, whose flesh is
intended for human consumption, are killed. The hygiene of the
slaughter house is of paramount importance to prevent the
contamination of meat during the process of dressing. The
following minimum standards for slaughter houses have been
suggested under the Model Public Health Act (1955) in India
(174). (1) Location : Preferably away from residential areas (2)
Structure : Floors and walls upto 3 feet should be impervious and
easy to clean (3) Disposal of wastes : Blood, offal, etc. should not
be discharged into public sewers but should be collected
separately. (4) Water supply : should be independent, adequate and
continuous (5) Examination of animals : Antemortem and
postmortem examination to be arranged. Animals or meat found
unfit for human consumption should be destroyed or denatured. (6)
Storage of meat : Meat should be stored in fly-proof and rat-proof
rooms; for overnight storage, the temperature of the room shall be
maintained below 5 deg C. (7) Transportation of meat : Meat shall
be transported in fly-proof covered vans. (8) Miscellaneous :
Animals other than those to be slaughtered should not be allowed
inside the shed.
FISH
Fish deteriorates or loses its freshness because of autolysis
which sets in after death and because of the bacteria with which
they become infected. Stale fish should be condemned. The signs
of fresh fish are : (1) it is in a state of stiffness or rigor mortis, (2)
the gills are bright red and (3) the eyes are clear and prominent.
Fish is the intermediate host of the tape worm,
Dibothriocephalus latus. This cestode is communicable to man,
but is very rarely encountered. Sewage, bacteria and viruses (e.g.,
the virus of hepatitis type A) may be concentrated in shellfish such
as oysters, and fish may carry Vibrio parahaemolyticus,
Salmonella spp., Clostridium botulinum type E, and other
organisms (144). Consumption of certain fish may sometimes give
rise to 'fish poisoning'.
TINNED FISH : When called upon to inspect tinned fish (or
meat or any food), the following points should be noted : the tin
must be new and clean without leakages or rusting; there should be
no evidence of having been tampered with such as sealed
openings; on opening the tin, the contents should not be blown out
which indicates decomposition.
EGG
Although the majority of freshly laid eggs are sterile inside,
(1)Viral diseases
(2)Parasites
1. Neurolathyrism
The cause of neurolathyrism is a toxin, Beta oxalyl amino
^x
>
**?
---------------------------3^
---------------------------
(d) the cost of fortification must not raise the price of the food
beyond the reach of the population in greatest need.
Finally, an adequate system of surveillance and control is
indispensable for the effectiveness of food fortification. Food
fortification is a long-term measure for mitigating specific
problems of malnutrition in the community.
Adulteration of foods
Adulteration of foods is an age-old problem. It consists of a
large number of practices, e.g., mixing, substitution, concealing
the quality, putting up decomposed foods for sale, misbranding or
giving false labels and addition of toxicants. Adulteration results
in two disadvantages for the consumer : first, he is paying more
money for a foodstuff of lower quality; secondly, some forms of
adulteration are injurious to health, even resulting in death, as for
example, adulteration of mustard oil with argemone oil causing
epidemic dropsy or adulteration of edible oils with trycresyn
phosphate (TCP) resulting in paralysis and death.
Food adulteration practices vary from one part of the country
to another, and from time to time. Our knowledge about the
current practices of food adulteration is by no means complete.
Table 40 shows the types of adulteration seen in India (152).
/TABLE 40
A_prulteration of foods
Food material
Cereals such as
wheat, rice
Dais
Haldi (Turmeric) powder
Dhania powder
TABLE 42
A Mid-day School Meal
Foodstuffs
g/day/child
75
30 8
30
30
ANNEXURE I Nutrition
Assessment Schedule
Serial No.
Name :
Address :
District:
Date :
Age :
Sex :
Village :
CLINICAL:
(1)General appearance:
(2)Hair :
(3)Face:
(4)Eyes :
(1)Lips:
(2)Tongue :
(3)Teeth:
(4)Gums:
(5)Glands:
(6)Skin :
(1)Nails:
(2)Oedema:
(3)Rachitic changes :
(4)Internal Systems :
ANTHROPOMETRIC :
Weight (kg) :
Head circumference (cm) :
Height (cm) :
Chest circumference (cm) :
Mid-upper-arm circumference (cm) :
Skinfold :
LABORATORY
(1)Haemoglobin : (specify method)
(2)Stool : negative/ascariasis/ancylostomiasis/giardiasis/amoebiasis/strongyloides/others (state) :
(3)Blood smear : negative/M.T/B.T./Filaria
Investigator
Adult Man
Adult Woman
Sedentary
Moderate
work
Children
Heavy
work
1-3
years
Boys
10-12
years
Girls
Sedentary
Moderate
work
Heavy
work
Cereals
Pulses
460
40
520
50
670
60
410
40
440
45
575
50
175
35
270
35
420
45
380
45
Leafy vegetables
Other vegetables
Roots and tubers
Milk
Oil and Fat
Sugar or Jaggery
40
60
50
150
40
30
40
70
60
200
45
35
40
80
80
250
65
55
100
40
50
100
20
20
100
40
50
150
25
20
50
100
60
200
40
40
40
20
10
300
15
30
50
30
20
250
25
40
50
50
30
250
40
45
50
50
30
250
35
45
4-6
years
10-12
years
Source : (9)
ANNEXURE 5 Exercise
and Physical Activity
ANNEXURE 3 Suggested
Substitution for Non-Vegetarians
Food item which can
50% of pulses
(20-30 g)
1.
2.
100% of pulses
(40-60 g)
1.
2.
10 g of fat or oil
Source : (9)
ANNEXURE 4 Additional Allowances
During Pregnancy and Lactation
Food
items
During
pregnancy
Cereals
Pulses
Milk
Fat
Sugar
35 g.
15 g.
100 g.
10 g.
Total
Calories
(kcal)
118
52 83
40
During
lactation
60 g.
30 g.
100 g.
10 g. 10
g.
293
Calories
(kcal)
203
105
83
90
40
521
Source : (9)
6 (Km/hr)
4 (Km/hr)
Kcal/hr
210
300
86
Activity
Kcal/hr
750
655
522
Shuttle
Table Tennis
Tennis
Volley Ball
Dancing
Fishing
Shopping
Typing
Sleeping
348
245
392
180
372
222
204
108
57
353
160
Standing
Sitting
132
86
360
* Approx. energy expenditure for 60 Kg reference man. Individuals with higher body weight will be spending more calories than those with
lower body weight. Reference woman (50 kg) will be spending 5% less calories.
ANNEXURES 485
ANNEXURE 6 Approximate Calorific Value
Preparation
one serving
Quantity for
Calories
(Kcal)
Rice
Phulka
Paratha
Puri
1 cup
INo.
INo.
1 No.
170
80
150
100
Bread
Poha
Upma
Idli
Dosa
Kichidi
2 slices
1 cup
1 cup
2Nos.
INo.
1 cup
170
270
270
150
125
200
1 cup
1 cup
1 cup
220
220
220
1/2 cup
1 cup
100
110
3. Vegetable
With gravy
Dry
4. Non-Vegetarian
Boiled egg
1 cup
1 cup
170
150
INo.
90
Omelette
INo.
160
Fried egg
INo.
160
Mutton curry
Chicken curry
Fish fried
3/4 cup
3/4 cup
2 big pieces
260
240
220
Fish cutlet
Prawn curry
Keema kofta curry
2Nos.
3/4 cup
3/4 cup
(6 small koftas)
190
220
240
Bajji or pakora
Besan ka pura
Chat (Dahi-pakori)
Cheese balls
Dahi vada
Vada
Masala vada
Masala dosa
8Nos.
INo.
5 pieces
2Nos.
2Nos.
2 Nos.
2Nos.
INo.
280
220
220
250
180
140
150
200
Pea-kachori
Potato bonda
Sago vada
Samosa
2 Nos.
2 Nos.
2 Nos.
INo.
380
200
210
200
2 Nos.
INo.
200
170
1 slice
200
2tbsp
120
5. Savoury snacks
6.
ts
2 pieces
Chikki
Fruit cake
1. Cereal
Wheat porridge
Semolina porridge
Cereal flakes with milk
(corn/wheat/rice)
2. Pulse
Plain dhal
Sambar
Quantity for
one serving
Preparation
8.
400
21 pieces
piece
Rice puttu
1/2 cup
Sandesh
2 Nos.
Double ka meetha
1/2 cup
Halwa (kesari)
1/2 cup
Jelly/Jam
ltsp
Custard (aramel)
1/2 cup
Srikhand
1/2 cup
Milk chocolate
25 g
Ice-cream
1/2 cup
Beverages
Tea
(2 tsp sugar +
1 cup
50 ml. toned
milk)
Coffee
(2 tsp sugar +
1 cup
10 ml toned
milk)
Cow's milk
(2 tsp sugar)
1 cup
Buffalo's milk
(2 tsp sugar)
1 cup
Lassi
(2 tsp sugar)
1 glass
(200 ml)
Squash
1 glass
Syrups (Sherbat)
Cold drinks
Fresh lime juice
Calories
(Kcal)
(200 ml)
1 glass
(200 ml)
1 bottle
(200 ml)
1 glass
290
270
280
140
280
320
20
160
380
140
200
75
110
180
320
110
75
200
150
60
(200 ml)
Nuts
Almonds
Cashewnuts
Coconut (fresh)
Coconut (dry)
Peanuts
Fresh fruits
Apple
Banana
Grapes
Guava
Jackfruit
Mango
Mosambi/orange
Papaya
Pineapple
Sapota
Custard apple
Watermelon/muskmelon
Serving
Calories
10 Nos.
10 Nos.
1/4
1/4 50
Nos.
85
95
130
140
90
1 medium
1 medium
30 Nos.
1 medium
4 pieces
1 medium
1 medium
1 piece
1 piece
1 medium
1 medium
1 slice
65
90
70
50
90
180
40 80
50
80
130
15
^AIAHQ
v^aictuo
Beetroot
Carrot
Cucumber
Onion
Radish
1 medium 1
medium
1 medium
1 medium
1 medium
30
20
15
25
10
Tomato
Tamarind (with jaggery)
1 tbsp
1 tbsp
10
60
Tomato
Source : (191)
1 medium
10
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habits, customs and beliefs reacting on his body and mind. It has
been aptly said that even a person with a broken leg may present
complex social and personal factors which may influence his
recovery. Thus there has been a shift from the earlier concept of
visualizing disease in terms of a specific germ to the involvement
of "multiple factors" in the causation of disease. Good doctors are
being identified as those who treat people, and bad ones as those
who treat cases. As a result of this new outlook, concepts of
sociology are increasingly being used in the study of disease in
human societies.
How much effect social changes might have on health of the
people is shown in Fig. 1.
It suggests that health is influenced by four sets of variablesindividual predispositions, ecological predispositions, current
circumstances, and opportunities. These variables are in turn
influenced by the major sources of social changes : economic,
political, educational and other systems. The health status of the
people can feed back into and influence factors relating to social
structure which may in turn influence the predisposing variables,
and therefore health (2).
HEALTH OUTCOME
Medicine and the social sciences are concerned, in their own special way, with human behaviour. Specialists in community health, clinical
medicine, epidemiology are all seeking the cooperation and help of social scientists in understanding problems such as the social component
of health and disease, "illness behaviour" of people, efficient use of medical care and the study of medical institutions. A brief sketch of the
current interest of these disciplines in social science is given below :
1. COMMUNITY HEALTH
Community health workers are often faced with the problem of why people who need a particular service are least likely to use it or fail to
secure the total benefit which is expected. A case in point is immunization against communicable diseases. Although, there is a wide range of
prophylactic vaccines, immunization has not gained universal acceptance. The family planning programme in India is a recent example of a
health service of which people are not making use to the extent desired. Similarly, health programmes relating to mother and child health care
services, improvement of water supplies, installation of sanitary latrines, improvement of dietary patterns and infant rearing practices have all
proved abortive or only partially successful. The resistance of the people is felt not only in the field of community health, but in fact even in
fields designed to improve their general standard of living. The central question in community health is : why do people behave as they do?
This is the basic problem which the social scientists are studying in India, and are often asked to explain this failure of health measures. In the
western countries, social scientists are working on problems of mental health, hospital organisation, social class difference in disease,
rehabilitation, and professional roles and relationships. In industries, the social scientists are invited to look into the relationships between
members of a team who are concerned with doing a job in order to improve the overall performance of the work team. In short, the social
scientists are stepping in increasing numbers into the field of community health. The theme common to community health and social sciences
is human behaviour. Many community health problems in essence are social problems, and vice versa.
2. CLINICAL MEDICINE
During the past half century, the scientific content of medicine has increased enormously. The acute communicable diseases have been
brought under control, and good medical care is available to more people than ever before. This has brought to a sharp focus, the so called
"modern diseases" such as cardiovascular disease, cancer, diabetes and mental illness. These diseases have defied "cure" and prevention, and
are currently the major causes of morbidity and mortality in developed societies. The clinicians also tend to believe that "psychophysiological
stress reactions" are involved in cases of rheumatoid arthritis, obesity, ulceration of intestine, skin diseases, constipation, diarrhoea and
epilepsy. It has become apparent that control of these diseases involves not merely medical care but basic changes in the behaviour and habits
of the patients, which is a field of specialization of social scientists. The social scientists are asked to investigate the life situations of the
patients with a view to discover linkages between specific life situations and specific types and cases of illness.
The clinicians have also shown interest in what is known as "illness behaviour" of patients, i.e., why different people react in different ways
to the same disease process or regimen of treatment. It is not known why some people (whether by reason of education, religion, social class
difference or occupational status) make light of symptoms and some respond in an exaggerated manner, to the slightest pain or
______________________________________PSYCHOLOGY 4i
COMMUNICATIONS
The term "communications" refers to a social process - the
flow of information, the circulation of knowledge and ideas, and
the propagation of thoughts. The role of communications in
community health is to help motivate people to accept ideas; the
ultimate aim of communications is to bring about changes in
behaviour. The mass media (e.g., song and drama, radio talks,
posters) are extensively used as vehicles of dissemination of
information.
SOCIAL DEFENCE
A new concept has come into vogue in recent times - the
concept of social defence. It covers the entire gamut of preventive,
therapeutic and rehabilitative services for the protection of society
from antisocial, criminal or deviant conduct of man. Included in
this are measures relating to the prevention and control of juvenile
delinquency, eradication of beggary, social and moral hygiene
programmes, welfare of prisoners, prison reforms, elimination of
prostitution, control of alcoholism, drug addiction, gambling and
suicides (12). Many States in India have enacted the Children Act
for the prevention and control of juvenile delinquency. Under the
Suppression of Immoral Traffic in Women and Girls Act, services
are being provided for the elimination of prostitution in society.
Social defence is a system developed to defend society against
criminality not merely by treating and defending the offended, but
also by creating such conditions in the community which are
conducive for a healthy and wholesome growth of human life. The
Government of India renamed the Central Bureau of Correctional
Services as National Institute of Social Defence in 1975. This
Institute is under the Department of Social Welfare.
.--.
PSYCHOLOGY
Psychology is defined as "the study of human behaviour - of
how people behave and why they behave in just the way they do".
A knowledge of psychology is essential to know others better; to
differentiate between the normal and abnormal; and to help
promote mental health in individuals and families.
Scope of Psychology
Psychology is vast in its scope, as indicated by the numerous
branches of psychology, e.g., normal psychology, abnormal
psychology, educational psychology, social psychology, child
psychology, applied psychology, psychoanalysis, etc. Medical
psychology deals with patients suffering from disorders of the
mind. Persons trained in medicine and psychology are called
psychiatrists. Thus psychology includes every aspect of human life
and every type of human relation.
BEHAVIOUR
The theme common to community medicine and psychology is
human behaviour. The main concern of psychology is to study
human behaviour. Human behaviour is the result of physical and
mental factors (body and mind) interacting in complicated ways.
The broad categories of factors that may influence individual
and community health behaviour include : knowledge, beliefs,
values, attitudes, skills, finance, materials, time, and the influence
of family members, friends, co-workers, opinion leaders, and even
health workers themselves. Serious consideration must also be
given to the community or social context in which a given type of
behaviour occurs. Pervasive issues such as norms, male/female
roles, ethnic discrimination, poverty, unemployment, and
educational opportunities may limit the ability of some of the
sections of the community to
Sympathy
Pity
Lust
Grief
_________________________________________EMOTIONS 495
which drives an individual to a certain action. It also determines
human behaviour. Motivation may be positive (the carrot) or
negative (the stick) : Without motivation, behavioural changes
cannot be expected to take place. Positive motivation is often
more successful than negative motivation. Motivation is not
manipulation. A motivated person acts willingly and knowingly.
The terms motives, needs, wants, desires and urges are all used
synonymously; these terms are interrelated and interdependent.
Kinds of needs and urges :
It is difficult to define human needs. There are many kinds of
needs and urges : (a) Biologic needs : These are survival needs. A
hungry man needs food, a thirsty man water, a sick man medicine.
There are other needs such as sleep, rest, recreation and fresh air.
The doctor should be aware of these needs in the day-to-day care
of the patients, (b) Social needs : The need for company, the need
for love and affection, the need for recognition, the need for
education are all social needs. Some of these needs are met by the
family, and some by the community, (c) Economic needs :
Economic security, that is security from want, is one which
everyone desires, (d) Ego -integrative needs : The desire for
prestige, power and self-respect come in this category.
Motivation is contagious; it spreads from one motivated person
to another. We make use of motives and incentives in community
health work. Motivation of eligible couples for a small family
norm is an important activity in the National Family Welfare
Programme. Motivation is required to enlist people's participation
in community health work.
INCENTIVES
Incentives are among the factors that stimulate motivation and
encourage specific behaviours. Incentives can be either intrinsic or
extrinsic, material or psychological, self determined or selected by
others. An intrinsic incentive is the benefit that comes from
solving one's own problems. Extrinsic incentives are rewards that
do not relate directly to the goal towards which the desired
behaviour is aimed, for example, financial compensation of
individuals undergoing sterilization operation for family planning.
Material incentives are tangible goods or services; psychological
incentives include the satisfaction, self-esteem, or enhanced
capabilities gained through a proposed course of action (13).
LEGISLATION
Legislation can serve as an important tool to support, promote
and sustain activities at the community level. Laws should satisfy
requirements and, at the same time be compatible with the
political, cultural, social, and economic situation of the country.
This is essential because laws may antagonize the population and
make the community uncooperative.
OBSERVATION
Treatment involves lot of correct observation of the patient's
condition. Observation involves two mental activities -perception
and attention. Hippocrates, the Father of Medicine, laid the
foundation of modern medicine by accurate observation of signs
and symptoms. By observing an apple fall, Newton formulated the
theory of gravitation. By observation penicillin was discovered.
Observation is a psychological skill. It consists of the noting of the
phenomena of life as they occur. It requires correct use of the
senses of seeing, hearing, touch, smell, movements etc. A doctor
should cultivate the habit of correct observation. Correct
observation leads to correct thinking, reasoning and learning.
Observation promotes attention. To observe more carefully
LEARNING
Learning is any relative permanent change in behaviour that
occurs as a result of practice or experience. It means acquiring
something new - new knowledge, new techniques, new skills, new
fears and new experiences.
Learning is necessary for man's survival and for human
progress. It includes not only acquiring knowledge but also skills
and formation of habits, and development of perception. Learning
depends largely upon intelligence. Learning also depends upon
motivation, and motivation depends on the need students feel to
learn. Learning is a continuous process. It is both conscious and
unconscious.
Conditions affecting learning
(1) Intelligence : Learning depends upon the intelligence or
mental faculty of an individual. It involves the activity of sensory
adjustment and motor mechanisms of the body. The mental faculty
is related to heredity, nutrition and IQ. Children with low IQ are
poor learners; they may not learn at all. (2) Age; The curve of
learning reaches its peak between 22 and 25 years of age. After the
age of 30, there is a sharp decline. It has been appropriately said :
You cannot teach an old dog a new trick . (3) Learning situation :
Physical facilities for learning, viz, institutions, teachers, textbooks,
audio-visual aids promote learning. (4) Motivation . In order to
learn effectively, there must be adequate motivation. The powerful
motives are encouragement, praise, rew?.. J and success. These
stimulate learning. (5) Physical health : rt Physically handicapped
person, e.g. deaf, dumb, chronically sick cannot learn. (6) Mental
health : Worries, anxieties, and fears interfere with learning.
Types of learning
There are 3 types of learning :
(1)Cognitive learning (knowledge)
(2)Affective learning (attitudes)
(3)Psychomotor learning (skills)
Psychologists have experimented a good deal with animals and
man to find out how learning takes place. They have proposed a
number of theories : (1) Learning fay conditioned reflex : It is well
known that when dogs see food, they begin to salivate; this is an
inborn reflex. Pavlov, the Russian physiologist discovered that if a
bell was rung when the dogs were fed, eventually, salivation could
be induced by the ringing of the bell alone. This is called
conditioned reflex. The psychologists proposed that learning takes
place partly by the mechanism. (2) Trial and error: The lower
animals such as apes and cats learn by trial and error method. We
also learn a good deal by this method. A child tries and tries again
using a number of approaches until accidentally the ideal
approaches, becomes obvious. This method of learning is very
slow, laborious and primitive, (3) Learning by observation and
imitation : We learn a good deal by observation and imitation. A
child copies or imitates gestures, facial expressions and movements
such as walking. He learns language by observation and imitation.
Observation is an important element in medical examination.
Observation promotes attention, discrimination and recognition. It
was by observation, Hippocrates, Father of Medicine, separated
medicine from magic. Part of the doctor's and nurse's education has
always been to observe the patient's condition, and to make
decisions based on these observations, (4) Learning by doing : In
this type of learning there is coordination of muscular responses
with sensory impulses. Nursing skills (e.g., bed making, applying
bandages, giving bath) are learnt by doing. Learning to type-write
or learning a new game or a musical
_______________________________________PERSONALITY 497
the pros and cons of the situation to be able to make a correct
decision. It is essential for a person's mental health that conflicts
should be resolved as quickly as possible, within a reasonable
period of time, before emotional disturbances occur.
DEFENCE MECHANISMS
When an individual is faced with problems, difficulties or
failures, he employs certain ways or devices to achieve health,
happiness or success. These are called defence mechanisms.
Psychologists have identified a number of such defence
mechanisms, which include the following :
1. Rationalization
Instead of accepting failure and correcting himself, the
individual tries to make excuses and justifies his behaviour. It is
like the proverbial fox declaring that the grapes were sour, when it
could not reach them. This is called rationalization. It is a facesaving device.
2. Projection
Sometimes the individual blames others for his mistakes or
failures. It is just like the student saying that he could not score
good marks in the examination because, his teacher did not like
him.
3. Compensation
Many people make use of compensation to enhance their selfesteem and prestige. The familiar example is that the student who
is not good in his studies may distinguish himself in sports or
dramatics, music or other activities.
4. Escape mechanism
Some individuals adopt what is known as an "escape
mechanism" to overcome failure or defeat. Some students pretend
illness and do not appear for examinations. This is an escape
phenomenon. Then there are others who take to alcohol or drugs
trying to solve their problems. This is also an escape phenomenon.
5. Displacement
An office clerk badly snubbed by his superior takes it out on his
wife and children on reaching home. This is like a rebound
phenomenon. It is trying to escape from one situation and fixing
blame on another situation.
6. Regression
Some people resort to childhood practices (e.g., weeping when
something goes wrong) as a mode of adjustment.
The above list of "defence mechanisms" serves to illustrate the
various modes of adjustments the individual adopts to escape from
realities. He is either too keen to hide his faults, or run away from
his troubles and problems. A mentally healthy person will not use
defence mechanisms for achieving success or happiness.
PERSONALITY
The term "personality" is a key word in psychology. It implies
certain physical and mental traits which are characteristic of a
given individual; these traits determine to some extent, the
individual's behaviour or adjustments to his surroundings. The
terms personality and human behaviour are inter-related.
Psychology, in its broader concept, implies study of human
personality. It is important to bear in mind that the personality of
the doctor affects very much the well-being of the patient.
Components of personality
There are at least 4 components of human personality :
(1) PHYSICAL : These are the physical traits or features of an
individual namely height, weight, colour, facial expression,
physical health, etc. To the layman, a good personality means an
impressive, symmetrical and healthy body. (2) EMOTIONAL : A
person's emotions also go into the makeup of his personality.
Emotions are the feelings we have -fear, anger, love, jealousy,
guilt, worries. These feelings affect an individual's personality. (3)
INTELLIGENCE : Personality also implies intellectual ability. An
intelligent person will have a forceful personality. A person with
sub-normal intelligence is described as a "dull" person. (4)
BEHAVIOUR : Behaviour is a reflection of one's personality. It is
partly dependent upon our feelings and partly on the expectations
of the society. Behaviour is described in such terms as gentle, kind,
affectionate, balanced, submissive and aggressive. When we assess
human personality, all these components must be taken into
consideration.
Personality traits
A trait is described as tendency to behave in a consistent
manner in variable situations. Human personality is a bundle of
traits. The basic personality traits are established by the age of 6
years. Some traits, we cultivate (e.g., good manners); some, we
may conceal (e.g., kindliness); and some, we modify depending
upon the society in which we are placed (e.g., sense of humour).
The following are some of the personality traits :
Cheerfulness
Loyalty
Good manners
Reliability
Sportsmanship
Sense of humour
Honesty
Tactfulness
Kindliness
Willing to help others.
The personality traits we look for in a doctor are kindliness,
honesty, patience, tolerance, perseverance, consciousness,
thoroughness and initiative. It is possible to cultivate these traits.
The Swiss Psychiatrist, Carl Jung (1875-1961) divided
personalities into 2 types - extrovert and introvert. The
extrovert is a person who is thought to be dashing, practical, active,
showing-off and easily mixes with people. An introvert is a person
who is reserved, shy and generally keeps to himself. Most people
exhibit characteristics of both.
Development of personality
Human life consists of definite stages of growth, and each stage
is marked by distinctive psychology. (1) INFANCY : The first one
year of life is called infancy. The infant is hardly a social creature.
There is rapid physical and mental growth. The infant is totally
dependent on the mother. By the end of first year, the infant is able
to stand up for a short while and tries to walk with a little support.
He enjoys simple tricks and games.
(2) PRE-SCHOOL CHILD: This stage is marked by
considerable growth of brain. The child feeds himself, speaks,
loves his home, fears dark, loves stories and wants to assume
responsibility. He begins to mix with other small children.
(1)SCHOOL-AGE : The school-age period ranges from 5 to 15
years. The school going child is active all the time. By the age of 8,
the mental powers are fully developed. The brain of the child at the
age of 8 years is almost of the same size as an adult. The child
begins to reason. There is a gradual detachment from the family,
and greater attachment to his playmates and friends. He begins to
form groups. The period of childhood terminates with the onset of
puberty, which is about 11 years in the case of girls and 13 in the
case of boys.
(2)ADOLESCENCE : Adolescence or "teenage" is a turbulent
Mental age
The first tests of intelligence were devised by Binet and Simon
(1896). They developed the concept of mental age. That is, a child
who could do the five-year tests but who could not go on to the
six-year level, was credited with mental age of five years. The
concept of mental age indicated the level of intelligence achieved,
but it gave no indication of the brightness or dullness of the
individual concerned. Terman revised these tests, defining
intelligence as the capacity to use abstract ideas for solving
problems. Gessel indicated four sectors of intellectual development
for consideration : (a) motor ability (b) adoptive behaviour (c)
language development and (d) personal-social behaviour.
Intelligence Quotient
This is an improvement over the concept of mental age. It is
obtained by dividing the mental age by chronological age, and
multiplying by 100.
THINKING
Man is called a thinking animal. Thinking includes perception,
memory, imagination and reasoning. It is an active mental process.
Imaginative thinking is a mental process, it involves thinking in the
absence of original sensory stimuli. Daydreaming and thinking
about our future plans are examples of imaginative thinking. The
highest form of thinking is said to be creative thinking , e.g., an
artist painting a picture. Creative thinking is said to be responsible
for new inventions, new views of life and new discoveries. The
anatomical basis of thinking is cerebral cortex. In fact, the purpose
of education is to teach people to think, and not merely to
memorise facts and figures.
Problem solving
An aspect of thinking is problem solving. It is regarded as the
highest stage in human learning. Some problems in life are
relatively simple; there are others which are more difficult and
complex calling for thinking and reasoning. REASONING requires
intelligence. There are several steps in the reasoning process collection of information on the subject, the arrangement of data
carefully, observation of the implications, drawing conclusions and
testing the conclusions. An intelligent person reasons well.
Reasoning is not always foolproof. Fallacies may also occur.
INTELLIGENCE
Intelligence is an important aspect of personality. It has not
been satisfactorily defined as yet. The widely accepted definition is
that it is the ability to see meaningful relationships between things.
It includes perceiving, knowing, reasoning and remembering.
Psychologists believe that intelligence results from an interplay
between hereditary and environmental factors. Some psychologists
emphasize genetic factors as having major significance while
others emphasize environmental factors.
There is considerable relationship between a person's degree of
intelligence and range of activities, the level of achievement and
the depth of understanding possible to him. As psychologists
observed the differences between animals and human beings, and
the differences between organisms of the same species, they were
impressed by the fact that there are variations in the case and
adequacy with which adjustments to new situations occur. It was
out of such observations that the concept of intelligence arose.
Mental age
IQ =--------------------------- X 100
Chronological age
_____________________________
been constructed mostly to meet practical necessities. Naturally, if
large numbers of subjects are to be tested, it would be more
convenient to test them in large group to save time and trouble.
But under particular situations, such as in a guidance clinic, each
individual could be tested separately and would need to be tested
separately. To suit these different requirements, we now have both
group tests and individual tests. In a group test, all the subjects
must start at one time and finish at the same time just as in an
examination. Here, the time factor is constant. One's intelligence is
measured in terms of the amount of work successfully completed
within the given time. Individual tests on the other hand need not
necessarily depend on a constant time factor. Time tests can also
be used for individuals. Strictly speaking, all tests of intelligence
are measures of performance. However, the term performance is
customarily applied to tests which call for a minimal
understanding and use of language. These tests provide a measure
of fundamental psychological process, such as reasoning and
seeing relationship, without at the same time depending upon
particular cultural or educational opportunities. They enable us to
measure the intelligence of individuals : - (1) who are too young to
have learned a language, (2) who are illiterate through lack of
educational opportunity or feeble-mindedness, and (3) who speak
only a foreign tongue.
As the child grows older, his intelligence undergoes a gradual
increase. There is an improvement with age in his versatility of
adjustment - in the readiness with which he gathers information
and acquires new skills which enable him to adjust to the changing
circumstances of his environment. When a normally healthy
school child, whose educational opportunities have been average,
is tested year after year, his I.Q. remains fairly constant. Changes
in educational opportunities lead to fluctuations in I.Q. There are
cases on record, too, where the I.Q. rose considerably after
glandular therapy.
The chief values of discovering a child's I.Q. are that :
(1)those of low I.Q. can be taken aside for special education in
line with their capacity to acquire intelligent behaviour;
(2)those of very high capacity can be selected for education in
keeping with their capacity; (3) intelligence tests as an aid in the
determination of the right time to enter school; (4) the use of
intelligence test in maintaining the adjustment of a pupil to his
work; (5) the selection of applicants for college and professional
school; (6) the use of intelligence test in educational guidance; and
(7) the use of intelligence test to the therapist (16).
Measurement of disability
There have been many attempts to measure or record in
standardized form the aspects of behaviour, psychological
functions and social performance. One of the most important is
Wing's comprehensive Handicaps, Behaviour and Skills Schedule
(HBS) which has been used in epidemiological studies to assess
the total child population in terms of detailed scales of specific
abilities and disabilities. Results from these surveys have raised
important questions about ethnic differences in disability profiles,
individual programme planning, defining new syndromes of
disability and the possibilities of new parameters for classification.
The HBS is essentially a research tool, but Wing has developed
from it a small practical schedule for use in service contexts using
what had emerged as the most important aspect of mobility,
communication and social interaction. The resulting Disability
Assessment Schedule (DAS) is being used in several communities
as a source of high quality routine data for total population (17).
SOCIAL PSYCHOLOGY 49
SOCIAL PSYCHOLOGY
Social psychology is an important branch of psychology, is
defined as the science of behaviour of the individual i society.
That is, it studies the behaviour of the individual i: group, crowd,
mob, audience and other social situations. 1 also studies the
attitudes of the individuals towards cultural am social values.
Group behaviour
Man is a social being. From birth till death, he is associatec
with people. He is born in particular culture which is made ur. of
customs, laws, ideals, art, literature, crafts, science technology and
institutions. All these act on the individual anc influence his social
behaviour. Group behaviour is also knowr as social behaviour.
Social interaction
(a)Inter-personal relationships : The individual learns many
things from his parents, teachers and friends. This is known as
person-to-person interaction.
(b)Inter -group relationships : The individual is a member of a
group, of a family and of a community. He has to follow the
traditions of the group. For example, in many communities in
India the person is not permitted to marry outside his caste.
This is the result of person-to-group interaction.
The individual, through social interaction and social learning
acquires patterns of behaviour prevalent in his society, and is
accepted as a member of that community. This process of
adaptation is. known as socialization. Social interaction converts
the biological organism into human, social and moral.
As a result of social interaction, the individual acquires attitudes
towards persons, things, situations and issues. Social attitudes are
shared by others in the community, e.g., attitude to prohibition,
family planning, child marriage, etc. In any democratic society,
people's attitudes are a matter of vital importance to the State.
Croup morale
Every group has leaders. They are responsible for the solidarity
of the group behaviour and the morale of the people in the group.
Groups work together. They have definite programmes and
objectives. Often their members think, feel and act together. Many
community problems can be solved by group effort. We can
approach the group through group discussions. The problem is one
of how to make these group activities happy and satisfying
experiences for those who participate in them.
SOCIOLOGY
Sociology is the science of society. It deals with the study of
relationship between human beings, it also deals directly with the
study of human behaviour. Whereas the unit of study of
psychology is the individual, the unit of study of sociology is the
group. Sociology studies man in the context of society and as a
part of it.
Medical sociology is a specialization within the field of
sociology. Its main interest is in the study of health, health
behaviour and medical institutions. Illness is viewed not only as a
medical problem but also as a psychological and social problem.
The problems presented by patients are not always purely medical
but also psycho-social. Diseases such as tuberculosis, leprosy,
sexually transmitted diseases have a big social component in their
aetiology. Medical scientists are increasingly turning their attention
to the study of social, behavioural and cultural factors of illness. A
social approach to disease treatment is also emphasized. The
doctor needs to
Events characterizing
Beginning of phase
End of phase
I.
II.
III.
IV.
V.
VI.
Marriage Birth of
1st child Birth of
last child 1st child
leaves home
L ast child has left
home of parents
1st spouse dies
Formation Extension
Complete extension
Contraction
Completed contraction
Dissolution
Source : (18)
Such a model, however, tends to apply only to areas of low
mortality and requires amendment in high mortality situations to
reflect the early death of children and even the death of the mother
before any of the children are old enough to leave home.
Moreover, "leaving home" is essentially an American and
European phenomenon that has little or no relevance in many
developing countries in Africa and Asia. A number of variations
and exceptions, then, to the typical life-cycle such as the early
death of children or one spouse, divorce, childlessness, etc., need
to be taken into account.
Family cycle and stress
Structure
Each family experiences its own dynamics of formation,
growth, maturation, and dissolution. Crises confronted may be
divided into those that are transitional in the family life cycle (e.g.,
birth of first child or loss of spouse) or nontransitional (e.g., acts of
war, uprooting, mental disorders, etc.). Family sociologists have
studied effects of sudden shifts in economic status, migration,
uprooting, disasters, physical change or
V*^2"
(l. NUCLEAR FAMILY
The nuclear or elementary family is universal in all human
v societies. It consists of the married couple and their children
*.:, while they are still regarded as dependents. They tend to
' -; occupy the same dwelling space} In the nuclear family, the
husband usually plays a dominant role in the household. The
absence of parents, grandparents, uncles, aunts and near
relatives places a greater burden on the nuclear family in terms
of responsibilities for child rearing. The husband-wife
relationship is likely to be more intimate in the nuclear family
than in the joint family. The term "new families" has come
recently into vogue; it is applied to those under 10 years
duration and consists of parents and children. The concept is
important in view of studies relating to family planning (20).
9.7
II
11.1
IIIN
11.8
HIM
13.0
IV
15.0
17.0
flow of the conversation will slow down and the interview may
take the form of questions and answers. Further, the interviewee
will be conscious that his statements are being recorded. The
researcher should jot down only important points.
9 CLOSING THE INTERVIEW
An interview should not be ended abruptly. The interviewee
should not feel, at the close of the interview, that he has divulged
many of his secrets to a stranger. The researcher should bring the
interview to a natural close, followed by the usual forms of
greetings.
10 REPORT
Soon after the interview, the report should be compiled when
the mind is still fresh about the narration.
OPERATIONAL RESEARCH
The term 'operational research' was coined during the World
War II in connection with the best use of a new invention, the
radar. Since the war, the term has spread rapidly in Britain and
America and it has come to mean today more than the study of the
use of new inventions - the study of the whole systems of services
rendered in industry, administration, education and health services
(38).
Operational research is defined as the application of scientific
methods of investigation to the study of complex human
organisations and services. A mathematician working on atomic
structure is pursuing pure research; an engineer designing a new
plant for an industry is pursuing applied research. In operational
research, one is concerned all the time with the activities of a group
of people with the purpose of inducing beneficial changes. Thus,
operational research is a sociological science, and has an immense
social content which distinguishes it from pure or applied research.
The main objective of operational research is "to develop new
knowledge about institutions, programmes, use of facilities, the
people working in these activities and the individuals and
communities served by them" in order to secure optimal utilisation
of resources in men, material and money in the service of the
community (38). A new area of operational research is emerging,
i.e., "health operational research" (39).
Phases in operational research
The procedure to be adopted in operational research differs
according to the nature of the study. The usual procedure adopted
generally consists of the following phases.
1.Formulation of the problem.
2.Collection of relevant data, if necessary, by a suitable
sample.
3.Analysis of data and formulation of hypothesis.
4.Deriving solutions from the hypothesis or "model."
5.Choosing the optimal solution and forecasting
results.
6.Testing of solution, e.g., pilot projects.
7.Implementing the solution in the whole system.
Operational research team
Operational research is a team work job and involves several
workers. The composition of the team varies with the type of
research. The minimum composition in social medicine
applications is probably a public health administrator, an
epidemiologist, a statistician, and a social scientist. This is in
addition to ancillary workers such as clerks, peons and field
workers. The team is headed by a director who is responsible for
the whole project.
Dowry system
Dowry started as an innocent custom, a symbol of love from
parents to their daughter on the eve of her marriage. But it has, in
recent years, grown into a social evil with many instances of brideburning and suicides. These are symptoms of societal corruption.
Under the Dowry Prohibition (Amendment) Act, 1986
the minimum punishment for taking or abetting the taking of
dowry has been raised to 5 years imprisonment and a fine of Rs.
15,000. What is required is a sustained effort to go into the root
causes of these evils. Well-entrenched social customs cannot be
easily erased by an Act of Parliament.
Drug addiction
Drug addiction is defined as a state of periodic or chronic
intoxication detrimental to the individual and society produced by
the repeated intake of habit-forming drugs.
Drug abuse has reached an alarming proportion in recent years.
"Drug culture" is fast making inroads into the lives of young
people from all walks of life.
To call a person a drug addict, the following criteria must be
satisfied :
(1)Psychological dependence : there is an overpowering
desire (compulsion) to take the drug and obtain it by any
means.
(2)Physical dependence : when the drug is withdrawn, the
patient shows "withdrawal symptoms" such as irrational and
violent behaviour, nausea, diarrhoea, watering of eyes and
nose, etc.
(3)Development of tolerance : there is a tendency to increase
the dose.
Simultaneously with medical treatment, changes in
environment (home, school, college, social circle) are important.
The patient must effect a complete break with his group, otherwise
the chances of relapse are 100 per cent. Psychotherapy has a
valuable place in the management of the addict.
Preventive measures include education of target groups and the
general public through TV, radio, leaflets, and posters to create
awareness of the problem. The Government have promulgated an
Act called the "Narcotic Drugs and Psychotropic Substances Act"
which came into force in 1985 to combat this problem.
Alcohol abuse
Alcoholism is world-wide social and medical problem. Over the
past 30 to 40 years, alcohol consumption has increased in quantity
and frequency. The age at which people start drinking has also
declined. The population groups at great risk are those undergoing
rapid socio-economic and cultural changes; they view alcohol as a
symbol of prestige and social status.
Drinking by adults serves as a role model for the young. The
identification of risk factors is essential for prevention. As drinking
patterns vary considerably, the prevention of alcoholism is not
easy. A widespread public education and discussion, and
investigation of public attitudes may result in measurable
improvement. This should be combined with social welfare and
health services.
Unmarried mothers
We do not have accurate statistics regarding unmarried mothers
in India. Because of social customs and traditions in India, the
problem of unmarried mothers in India must be insignificant. Such
mothers have a multiplicity of needs - not only for medical
termination of pregnancy but for
The blind
The deaf
The orthopaedically handicapped
The leprosy affected
The mentally retarded
The emotionally and socially handicapped
4.5 Million
2.0 Million
4.2 Million
3.2 Million
3 to 4 Million
6 to 8 Million
The above figures are not static, but ever growing. In all
civilized countries, the State looks after the handicapped. The
rehabilitation services available for the handicapped in India are as
follows : (1) medical care facilities (2) education for the blind, deaf
and the orthopaedically handicapped (3) vocational training (4) job
placement and sheltered workshops (5) pensions, scholarships and
allowances for the education and training of the handicapped.
SOCIAL AGENCIES
Social welfare services have always been an integral part of the
socio-cultural tradition of India. Soon after Independence, on the
basis of a survey made by the Planning Commission, it was
estimated that there were 10,000 voluntary organizations in the
field of social welfare. Today the number is likely to be much
greater. The activities are coordinated and assisted by the Ministry
of Social Welfare and Women's Affairs. An autonomous Central
Social Welfare Board is the main agency of the Ministry for
undertaking and implementing programmes for women through the
voluntary sector. Activities include welfare, training, health care,
provision of women's hostels, as well as legal aid and support to
women being exploited by families or employers. A few of the
principal agencies are listed below :
1.All India Women's Conference, 6 Bhagwandas Road, New
Delhi 110001
2.National Association of Rural Women, Room No. 9/ 104,
Jamnagar Hutments Block 11, Mansingh Road, New Delhi 11
3.National Council of Women, 12 Circular Road, Patna,
800001
4.India Social Institute, Department of Women's
Development, 24 Benson Road, Bangalore 560046
5.Centre of Science for Villages, Magan, Sangrahalaya,
Wardha - 442001 '
6.Eastern India Women's Association
E Ahmed Building, Lakhtokia, Guwahati
COMMUNITY SERVICES Administrative
pattern of the country
(1) CENTRE
India is a Union of 26 States and 6 Union territories. The
Constitution of India came into force on 26 January, 1950. The
Union Executive consists of the President, the Vice President, the
Prime Minister and the Council of Ministers. Rules of business
have been framed under the Constitution.
India is a sovereign Democratic Republic with a Parliamentary
form of government. Sovereignty ultimately rests with the people.
The Parliament consists of the President,
and the two Houses of Parliament - The Rajya Sabha and the Lok
Sabha. The Rajya Sabha consists of 250 indirectly elected
members, and the Lok Sabha 544 directly elected members. The
main functions of Parliament are to make laws for the country, and
to make finances available to the Government. The Parliament is
assisted by several committees. The term of the Lok Sabha is 5
years.
(2) STATE
The administrative pattern in the States closely resembles that
of the Union. The States executive consists of a Governor, and a
council of Ministers with a Chief Minister as its head. The
Governor who is the head in each State is appointed by the
President for a term of 5 years. The State Legislature consists of
Vidhan Sabha (Legislative Assembly) and its members are chosen
by direct election. In Some States, there is also an Upper House
known as Vidhan Parishad or Legislative Council. The powers of
the State Legislature have been defined in the Constitution.
The Union territories (e.g. Pondicherry, Andaman and Nicobar
are administered by the President through an Administrator)
(3) LOCAL GOVERNMENT
(a) Urban Areas : In big cities, the local Government
institution is known as Corporation, and in medium and small
towns as Municipal Committee or Council. The Corporations
are headed by elected Mayors. The executive power of the
Corporation vests in the Commissioner. The Corporation deals
with matters concerning public health and sanitation,
maintenance of roads, bridges, markets, playgrounds, parks
and education. Municipalities are headed by elected
Presidents.
(b) Rural Areas : The rural areas are governed by the system
of Panchayati Raj or democratic decentralization.
Democratic decentralization
In democratic societies, the trend is to distribute power as much
as possible to the people themselves so that they may be able to
manage their own affairs. The Panchayati Raj in India is nothing
but democratic decentralization. It is a 3-tier system of Local selfGovernment.
Village level
Block level
District level
...
...
...
Gram Panchayat
Panchayat Samiti
Zilla Parishad
ECONOMICS '.
Total Numbers
Per cen
Primary Sector
I
Cultivators
II
Agricultural Labourers
III
Livestock, forestry, fishing,
plantations and allied activities
IV
Mining and quarrying
Secondary Sector
V
Manufacturing, processing,
serving etc. Of which in household
industry
VI
Construction
107.1
73.8
5.3
1.7
38.4
26.4
1.9
0.6
28.4
6.7
5.4
10.2
2.4
1.9
20.8
7.8
7.5
2.8
28.5
10.2
278.9
100.0
Tertiary Sector
VII Trade and Commerce
VIII Transport, storage and
communications
IX Other services
Total Main Workers
Source : (40)
INDUSTRIALIZATION
During the early years of this century, the major industrie: in
India were cotton mill industry, jute industry and coa mining.
During recent years, there has been considerable industrial
expansion. A number of new industries have come up such as
steel, sugar, cement, glass, chemicals, soap, vanaspati, heavy
electrical and machine tools, etc.
Industries create new conditions of life and new conditions for
adaptation. There is shifting of the population from rural to urban
areas. People are removed from the warm intimacy of village life
to the isolated and impersonal life in towns and cities. The
community health problems arising out of industrialization are
water and air pollution, creation of slums; accidents;
communicable disease problems such as tuberculosis and venereal
diseases; mental health problems such as delinquency;
psychoneurosis and social problems such as alcoholism, drug
dependence, prostitution, gambling and crime.
ECONOMIC LEVELS
National Income
An important background influence is the size and strength of a
country's economy, which is usually expressed in terms of one of
the national aggregates, such as gross national product (GNP) or
gross domestic product (GDP). These aggregates
Life expectancy at
birth
64.0
61.0
63.0
67.0
67.0
57.0
60.0
73.0
69.0
Infant mortality
rate
64
51
74
33
58
77
66
17
24
Source : (43)
Urban
40,001-80,000
(Lower Middle)
80,001-1,20,000
(Middle)
1,20,001-1,60,000
(Upper Middle)
Above 1,60,000
(High)
Total
43.7
(72.3)
15.5
(56.8)
5.6
(44.7)
4.5
(36.6)
51.3
(29.0)
125.2
(71.0)
___________________________________________POVERTY 5V7
STANDARD OF LIVING
Please see page 491 for details.
PER CAPITA INCOME
An index of the standard of living of the people is "per capita
income". Per capita income in India is among the lowest in the
world. According to recent statistics, the per capita income in
India (2000-01) is Rs.16,707 at current prices.
SOCIAL SECURITY
Social security is defined as "security that society furnishes
through appropriate organization, against certain risks to which its
members are exposed". The risks which social security covers in
most countries are sickness, invalidity, maternity, old age and
death. Social security also includes social insurance and social
assistance.
Social security for Industrial workers
The social security measures for industrial workers in India are
contained in the following legislations :
(1)Workmen's Compensation Act, 1923
(2)Central Maternity Benefit Act, 1961
(3)Employees State Insurance Act, 1948
(4)The Family Pension Scheme, 1971
Some of these Acts have been described elsewhere in the text.
60.4
(100.0)
27.3
(100.0)
12.5
(100.0)
12.2
(100.0)
176.5
(100.0)
Source : (40)
TABLE 6
Socio-economic Indicators in South East Asia Countries
Indicator
Year
2002
Source : (44)
Bangladesh Bhutan
Sri Lanka
Thailand
360
590
n/a
480
710
2090
220
230
840
1980
2000-2001
3.3
4.0
n/a
2.7
1.8
4.5
n/a
3.4
1.0
0.9
2000-2001
1.1
n/a
n/a
3.7
11.5
0.6
21.1
2.8
14.2
1.7
0.502
0.511
n/a
0590
0.682
0.751
0.549
0.499
0.730
0.768
72 5
67
89 8
81
48 9
39
89 7
83
61 7
53
81 7
74
48 9
39
47 8
39
40.0
49.4
30.2
106.11
107.57
104.57
53.73
51.70
55.90
47.3
61.1
33.6
n/a
82.00
62.00
n/a
7.00
2.00
100
100
100
n/a
108.00
101.00
n/a
n/a
n/a
62
55 7
8
48
54
57.2
86.8
68.4
91.8
45.4
81.9
100.93 107.89
108.88 109.71
92.39 106.00
49.92
54.88
58.91
56.23
40.22
53.50
96.9
97.0
96.8
133.71
133.22
134.23
42.75
41.36
44.17
84.7
88.9
80.5
90.95
91.39
90.51
34.87
34.92
34.81
41.7
91.6
59.4
94.4
24.0
89.0
126.38 105.91
140.00 107.39
111.74 104.38
53.90
72.12
62.26
69.85
44.86
74.47
95.5
97.1
93.9
93.50
95.72
91.24
78.95
78.06
79.85
2001
2000
2000
2000
2000
2000
2000
1999/2000
1999/2000
1999/2000
1999/2000
1999/2000
1999/2000
24. Brockington, C.F (1967), World Health, Churchill, London. 25'. Bowlby, J.
(1952), Maternal Care and Mental Health, 2nd Ed., WHO Monograph Series No.2
Geneva.
1.Royal College of Physicians, London (1971). Smoking and Health Now, Pitman,
London.
2.Peel, John and Potts, Malcom (1970), Textbook of Contraceptive Practice,
Cambridge University Press.
3.Kappu Swamy, B. (1976). Manual of Socio-economic Status Scale (Urban),
Manasayan, 32, NetajiSubhash Marg, Delhi-6.
4.Kulshreshtha, S.R (1975), Manual for Socio-economic Status Scale, National
Psychological Corporation, Labh Chand Market, Raja Mandi, Agra-2.
5.Willson, Robert, N. (1963), "The Social Structure of a General Hospital" in
Medicine and Society, The Annuals of the American Academy of Political and
Social Science, 346, 67.
6.Roemer, Milton, I (1963), Ibid, 44-56.
7.Fuchs, V.R. (1970), Arch.Intern.Med., 125, 154.
8.Menke, W.G. (1970), Ann.Intern.Med., 72, 943.
9.Hasan, K.A. (1967), The Cultural Frontier of Health in Village India,
Manaktalas, Bombay.
10.Bates, B. (1970), N. Eng. J. Med. 283, 129.
11.WHO (1995), The World Health Report 1995, Bridging the gaps, Report of the
Director-General WHO
12.Bajpai, S.R. (1960). Methods of Social Survey and Research, Kitab Ghar,
Kanpur.
13.Bailey, N.T.J. (1962), "Operational Research" in Society -Problems and
Methods of Study, Eds, Welford, A.T. et. al., Routledge and Kagan Paul, London.
14.WHO (1972), The Use of Operational Research in Health Services, Regional
Office for Europe, Copenhagen.
15.Statistical Outlines of India (2003 -04), TATA Services Ltd. Department of
Economics and Statistics
16.WHO (1984), PubticHealth Papers No.77
17.World Bank (1993), World Development Report
18.UNICEF (2001), State of World's Children 2004
19.WHO (2003), Health Situation in South-East Asia, Basic Indicators 2002
"The study of disease is really the study of man and his environment"
The term environment implies all the external factors -living
and non-living, material and non-material - which surround man.
In its modern concept, environment includes not only the water,
air and soil that form our environment but also the social and
economic conditions under which we live.
For descriptive purpose, environment has been divided into
three components, all closely related :
(i) Physical : Water, air, soil, housing, wastes, radiation, etc.
(ii) Biologic : Plant and animal life including bacteria,
viruses, insects, rodents and animals.
(iii) Social
: Customs, culture, habits, income, occupation,
religion etc.
The key to man's health lies largely in his environment. In fact,
much of man's ill-health can be traced to adverse environmental
factors such as water pollution, soil pollution, air pollution, poor
housing conditions, presence of animal reservoirs and insect
vectors of diseases which pose a constant threat to man's health.
Often man is responsible for the pollution of his environment
through urbanization, industrialization and other human activities.
In 1972 the UN conference on the Human Environment focused
world-wide attention on the environmental hazards that threaten
human beings. To facilitate work in this area, WHO has compiled
a wide-ranging survey of environmental hazards to human health
(1).
The dictionary meaning of the word sanitation is "the science of
safeguarding health." One of the best definitions is that given by
the National Sanitation Foundation of the USA, which is as
follows : 'Sanitation is a way of life. It is the quality of living that
is expressed in the clean home, the clean farm, the clean business,
the clean neighbourhood and the clean community. Being a way of
life it must come from within the people; it is nourished by
knowledge and grows as an obligation and an ideal in human
relations'. The term "environmental sanitation" has been defined
by WHO as "the control of all those factors in man's physical
environment which exercise or may exercise a deleterious effect
on his physical development, health and survival".
In the past, sanitation was centred on the sanitary disposal of
human excreta. Even now, to many people sanitation still means
the construction of latrines. In actual fact, the term sanitation
covers the whole field of controlling the environment with a view
to prevent disease and promote health. Man has already controlled
a number of factors in his environment, e.g., food, water, housing,
clothing, sanitation. These controllable factors are those included
in the "standard of living". It is the control of these factors that has
been responsible for considerable improvement in the health of the
people during the past century in the developed countries.
However, man's mastery over his environment is not complete. As
old problems
TABLE 1
Population with access to safe water and adequate
sanitation in South-East Asia countries 2000
Countries
India
Bhutan
Bangladesh
Indonesia
Maldives
Myanmar
Nepal
Sri Lanka
Thailand
88
62
97
76
100
68
81
83
80
31
69
53
66
56
46
27
83
96
Source : (3)
network for air and water quality monitoring are operational in
more than 60 countries. Surface and ground water quality are
monitored in 350 cities world-wide (2).
Much of the ill-health in India is due to poor environmental
sanitation, that is, unsafe water, polluted soil, unhygienic disposal
of human excreta and refuse, poor housing, insects and rodents. Air
pollution is also a growing concern in many cities. The high death
rate, infant mortality rate, sickness rate and poor standards of
health are in fact largely due to defective environmental sanitation.
Improvement of environmental sanitation is therefore crucial for
the prevention of disease and promotion of health of individuals
and communities. Since more than 74 per cent of the population of
India live in rural areas, the problem is one of rural sanitation. The
first step in any health programme is the elimination through
environmental control of those factors which are harmful to health.
The environmental factors which are basic and fundamental to
individual and community health are discussed in this chapter.
WATER
Much of the ill-health which affects humanity, especially in the
developing countries can be traced to lack of safe and wholesome
water supply. Water that is easily accessible, adequate in quantity,
free from contamination, safe and readily available throughout the
year. There can be no state of positive health and well-being
without safe water. Water is not only a vital environmental factor to
all forms of life, but it has also a great role to play in socioeconomic development of human population. Each country should
develop its own water resources agency which would collect all
pertinent data on water resources, exploitation and hydrogeology.
In 1980, the United Nations General Assembly launched the
International Drinking Water Supply and Sanitation Decade, 19811990 -the aim being to provide all people with adequate supplies of
safe water and sanitation by 1990. In 1981, the 34th World Health
Assembly in a resolution emphasized that safe drinking water is a
basic element of "primary health care" which is the key to the
attainment of "Health for All by the year 2000 AD". Water is also
integrated with other PHC components because it is an essential
part of health education, food and nutrition, and also MCH.
Safe and wholesome water
Water intended for human consumption should be both safe and
wholesome. This has been defined as water that is
a.
free from pathogenic agents
b.
free from harmful chemical substances
c.
pleasant- to the taste, i.e., free from colour and
odour; and
d.
usable for domestic purposes
_____________________________________________WATER 521
1. Rain
Rain is the prime source of all water. A part of the rain water
sinks into the ground to form ground water; part of it evaporates
back into the atmosphere, and some runs off to form streams and
rivers which flow ultimately into the sea. Some of the water in the
soil is taken up by the plants and is evaporated in turn by the
leaves. These events are spoken of as "water cycle".
CHARACTERISTICS : Rain water is the purest water in nature.
Physically, it is clear, bright and sparkling. Chemically, it is very
soft water containing only traces of dissolved solids (0.0005 per
cent). Being soft, it has a corrosive action on lead pipes.
Bacteriologically, rain water from clean districts is free from
pathogenic agents. IMPURITIES : Rain water tends to become
impure as it passes through the atmosphere. It picks up suspended
impurities from the atmosphere such as dust, soot and
microorganisms and gases such as carbon dioxide, nitrogen,
oxygen and ammonia. Gaseous sulphur and nitrogen oxides are
emitted from power plants that use fossil fuels. These gases react
with atmospheric water, forming dilute solution of sulphuric and
nitric acid. The precipitation of these acids (acid rain) has begun
to have serious impacts on surface water quality and on plants etc.
There are very few places in the world like Gibralter which
depend upon rain as a source of water supply.
2. Surface water
Surface water originates from rain water. It is the main source
of water supply in many areas. Examples of surface water include
rivers, tanks, lakes, wadis (water source which are dry, except in
rainy season), man-made reservoirs and sea water. Surface water
is prone to contamination from human and animal sources. As
such it is never safe for human consumption unless subjected to
sanitary protection and purification before use.
The vast majority of Indian cities and towns depend upon
surface water sources, which are (1) Impounding Reservoirs (2)
Rivers and Streams and (3) Tanks, Ponds and Lakes. In general,
surface water supplies possess a high probability of organic,
bacterial and viral contamination.
(1) IMPOUNDING RESERVOIRS
These are artificial lakes constructed usually of earthwork or
masonry in which large quantities of surface water is stored. Dams
built across rivers and mountain streams also provide large reserves
of surface water. The area draining into the reservoir is called
"Catchment area". Cities such as Mumbai, Chennai and Nagpur
derive their water supply from impounding reservoirs. One
disadvantage of storing water for long periods in reservoirs is the
growth of algae and other microscopic organisms, which impart
bad tastes and odours to water. CHARACTERISTICS : Impounding
reservoirs usually furnish a fairly good quality of water. The water
is usually clear, palatable and ranks next to rain water in purity. If
the surrounding hills are covered with peat, the water may acquire
a brownish coloration. The water is usually soft and considered to
be free of pathogenic organisms. IMPURITIES : The upland
surface water derives its impurities from the catchment area, the
sources being human habitations and animal keeping or grazing. It
is therefore very necessary to keep the catchment area free from
human or animal intrusion. The general belief rfiat mountain
streams are very pure water is often untrue. Even if there is no
human habitation or cattle near, there is still a possibility of
contamination caused by wild animals.
(2) RIVERS
Many rivers furnish a dependable supply of water. Cities such
as Delhi, Kolkata and Allahabad rely on river water for their needs.
The chief drawback of river water is that it is
The points of difference between a shallow well and deep well are set
out in Table 2.
3. Ground water
Rain water percolating into ground constitutes ground water. Water used by humans comes mainly from land. It is now realised that there is a limit to
ground water in the world. We should withdraw only quantities of water that can be renewed.
Ground water is the cheapest and most practical means of providing water to small communities. Ground water is superior to surface water, because the
ground itself provides an effective filtering medium. The advantages of ground water are: (1) it is likely to be free from pathogenic agents, (2) it usually
requires no treatment, (3) the supply is likely to be certain even during dry season. (4) It is less subject to contamination than surface water. The
disadvantages are: (1) it is high in mineral content, e.g., salts of calcium and magnesium which render the water hard (2) it requires pumping or some
arrangement to lift the water (7). The usual ground water sources are wells and springs. Wells have been classified into shallow and deep wells, dug and tube
wells.
WELLS
Traditionally wells are an important source of water supply. Even today, they are an important source of water supply in many communities. Technically,
wells are of two kinds -shallow and deep. (1) Shallow wells : Shallow wells tap subsoil water i.e. the water from above the first impervious layer in the
ground. They yield limited quantities of water, and the water is notoriously liable to pollution unless care is taken in well construction, (ii) Deep wells : A
deep well is one which taps water from the water-bearing stratum below the first impervious layer in the ground (Fig. 2). Deep wells are usually machinedug and may be several hundred meters deep. Deep wells furnish the safest water, and are often the most satisfactory sources of water supply.
Most ot the wells in India are ot the shallow type, bpeaking generally, shallow wells are liable to pollution from neighbouring sources of contamination
such as latrines, urinals, drains, cesspools, soakage pits and collections of manure. Shallow wells are therefore a health hazard to the community if they are
not made sanitary. A deep well can also become a health hazard if it is open, poorly constructed and not protected against contamination. ARTESIAN
WELLS are a kind of deep wells in which the water rises above the level of ground water, because it is held under pressure between two impervious strata.
Artesian wells are not common in India.
Saline intrusion : Near the sea, there is danger of infiltration of sea water in to deep wells. This gives a brackish taste to water and may make the water
unfit for domestic use.
Wells may also be classified, according to the method of construction, into dug wells and tube wells. DUG WELLS are by far the commonest type in
India. Two types of dug wells exist in our rural areas: (a) the unlined katcha well and (b) the masonry or pucca well. The katcha well is a hole dug into the
TABLE 2
Differences between a shallow well and deep well
1.
Definition
1.Chemical qualify
2.Bacteriological qualify
3.Yield
_____________________________________________WATER 523
water-bearing stratum. The pucca well is an open well, built of
bricks or stones.(STEP WELLS are a kind of pucca wells which
.are becoming obsolete, fortunately. Steps are constructed into
K these wells to enable people to descend into the well to fetch
f water or quench their thirst. In these wells, there is
(1 considerable personal contact between the user and the water.
Y Some people may even wash their faces, hands and feet which
is a common Indian custom. Guineaworm disease is quite a
public health problem in areas where step wells are in use. The
open dug wells and step wells are a health hazard to the
(community.) /
Improvement of dug wells
The unlined katcha wells may be made sanitary by deepening
the bottom, installing a hand-pump with screen, and filling the
well with coarse sand up to the water level, and with clay above
that level. When the material used for filling is completely
consolidated a platform and drainage may be constructed.
Masonry well improvement consists of making the upper 10
feet or more of the lining water-tight, raising the lining one foot
above the ground, and providing a reinforced concrete slab cover
at the top. One or more hand-pumps may be installed for lifting
the water. Special attention should be paid to the foundation of the
pump to prevent any possible leakage of waste water into the well.
SANITARY WELL
A sanitary well is one which is properly located, wellconstructed and protected against contamination with a view to
yield a supply of safe water (Fig. 3). The following points should
be taken into consideration while constructing sanitary wells: (1)
LOCATION : The first step in well construction is the choosing of
a proper site. If bacterial contamination is to be avoided, the well
should be located not less than 15 m (50 feet) from likely sources
of contamination. The well should be located at a higher elevation
with respect to a possible source of contamination. The distance
between the well and the houses of the users should also be
considered. If the well is situated far away, people may not use it.
It is therefore recommended that the well should be so located that
no user will have to carry water for more than 100 m (100 yards)
(7). (2) LINING : The lining of the well should be built of bricks or
stones set in cement up to a depth of at least 6 m (20 feet) so that
water enters from the bottom and not from the sides of the well.
The lining should be carried 60-90 cm (2-3 feet) above the ground
level. (3) PARAPET :
B. Chemical
Chemical pollutants of diverse nature derived from industrial and
agricultural wastes are increasingly finding their way into public water
supplies. These pollutants include detergent solvents, cyanides, heavy
metals, minerals and organic acids, nitrogenous substances, bleaching
agents, dyes, pigments, sulphides, ammonia, toxic and biocidal organic
compounds of great variety. Chemical pollutants may affect man's health
not only directly, but also indirectly by accumulating in aquatic life (e.g.
fish) used as human food. The present concern about chemical pollutants
in water relates not so much as to their acute toxic effects on human health
as to the possible long-term effects of low level exposure, which are often
non-specific and difficult to detect. Further, some of the new pollutants are
not easily removed by conventional water treatment or purification
processes. In many developed countries where water-borne communicable
diseases have virtually disappeared, more attention is now being paid to
chemical pollution.
In addition to the above, water is associated with the following :
(a) Dental health : The presence of fluoride at about 1 mg/
litre in drinking water is known to protect against dental caries,
but high levels of fluoride cause mottling of the dental enamel;
(b) Cyanosis in infant : High nitrate content of water is
associated
with
methaemoglobinaemia.
This
is
a
rare
occurrence but may occur when surface water from farmland,
treated with a fertilizer, gain access to the water supply.
Even if the source of water supply and its treatment are of a high
standard, water pollution may still occur as often happens, due to corrosion
of pipe lines, leaky joints and cross connections between water supply
pipes and sewage drainage pipes. Surveillance has to be exercised at every
point in the distribution system to ensure supply of safe water to the.
consumer.
Water-related diseases
Man's health may be affected by the ingestion of contaminated water
either directly or through food; and by the use of contaminated water for
purpose of personal hygiene and recreation. The term water-related
diseases include the classical water-born diseases. Developing countries
carry a heavy burden of water-related diseases, the heaviest being the
diarrhoeal diseases. Water-related diseases may be classified as follows :
A. Biological (Water-borne Diseases)
1. Those caused hy the presence of an infective agent:
(a) Viral
: Viral hepatitis A, hepatitis E, poliomyelitis,
rotavirus diarrhoea in infants
(b) Bacterial
: typhoid and paratyphoid fever, bacillary
dysentery, Esch. coli diarrhoea, cholera
(a)Protozoal
: amoebiasis, giardiasis
(a)Snail
(b)Cyclops
: Schistosomiasis
: guineaworm , fish tape worm
FIG. 5
Section of filter bed
Vital layer : When the filter is newly laid, it acts merely as
a mechanical strainer, and cannot truly be considered as
"biological". But very soon, the surface of the sand bed gets
covered with a slimy growth known as "Schmutzdecke", vital
layer, zoogleal layer or biological layer. This layer is slimy
and gelatinous and consists of threadlike algae and numerous
forms of life including plankton, diatoms and bacteria. The
formation of vital layer is known as "ripening" of the filter. It
may take several days for the vital layer to form fully, and
when fully formed it extends for 2 to 3 cm into the top portion
of the sand bed. The vital layer is the "heart" of the slow sand
filter. It removes organic matter, holds back bacteria and
oxidizes ammoniacal nitrogen into nitrates and helps in
yielding a bacteria-free water. Until the vital layer is fully
formed, the first few days filtrate is usually run to waste.
(3) Under-drainage system
At the bottom of the filter bed is the under-drainage
system. It consists of porous or perforated pipes which serve
the dual purpose of providing an outlet for filtered water, and
supporting the filter medium above. Once the filter bed has
been laid, the under-drainage system cannot be seen.
Filter box : The first 3 elements (e.g. supernatant water,
sand bed and under-drainage system) are contained in the
filter box. The filter box is an open box, usually rectangular in
shape, from 2.5 to 4 metres deep and is built wholly or partly
below ground. The walls may be made of stone, brick or
cement. The filter box consists from top to bottom :
Supernatant water
Sand bed
Gravel support
Filter bottom
1 to 1.5 metre
1.2 metre
0.30 metre
0.16 metre
Mixing
Chamber
/
2, \
<
Flocculation
chamber
Sedimentation
Tank
Filters
Consumption
IG. 6 Flow diagram
of a rapid sand
filtration plant
1.Space:
2.Rate of Filtration :
3.Effective size of sand :
4.Preliminary treatment:
5.Washing :
6.Operation :
7. Loss of head allowed: 6-8 feet
q. Removal of turbidity : Good
9j. Removal of colour:
m Removal of bacteria :
STABLE 3^
Comparison of rapid and slow sand filters
>
f[&
\Z*J
c*""~*"" )
Good
98-99 per cent
METHOD OF CHLORINATION
For disinfecting large bodies of water, chlorine is applied either
as (1) chlorine gas (2) chloramine or (3) perchloron. Chlorine gas
is the first choice, because it is cheap, quick in action, efficient and
easy to apply. Since chlorine gas is an irritant to the eyes and
poisonous, a special equipment known as "chlorinating equipment"
is required to apply chlorine gas to water supplies. Paterson's
chloronome is one such device for measuring, regulating and
administering gaseous chlorine to water supplies. In some water
treatment plants, they use chloramine instead of chlorine gas.
Chloramines are loose compounds of chlorine and ammonia. They
have a less tendency to produce chlorinous tastes and give a more
persistent type of residual chlorine. The greatest drawback of
chloramines is that they have a slower action than chlorine and
therefore they are not being used to any great extent in water
treatment. Perchloron or high test hypochlorite (H.T.H.) is a
calcium compound which carries 60-70 per cent of available
chlorine. Solutions prepared from H.T.H. are also used for water
disinfection. As mentioned already, chlorine gas has replaced all
the other chlorine derivatives in the disinfection of urban water
supplies.
BREAK POINT CHLORINATION
The addition of chlorine to ammonia in water produces
chloramines which do not have the same efficiency as free
chlorine. If the chlorine dose in the water is increased, a reduction
in the residual chlorine occurs, due to the destruction of
chloramine by the added chlorine. The end products do not
represent any residual chlorine. This fall in residual chlorine will
continue with further increase in chlorine dose and after a stage,
the residual chlorine begins to increase in proportion to the added
dose of chlorine. This point at which the residual chlorine appears
and when all combined chlorines have been completely destroyed
is the breakpoint and corresponding dosage is the breakpoint
dosage. Breakpoint chlorination achieves the same results as
superchlorination in a rational manner and can therefore be
construed as controlled superchlorination (4).
SUPERCHLORINATION
Superchlorination followed by dechlorination comprises the
addition of large doses of chlorine to the water, and removal of
excess of chlorine after disinfection, this method is applicable Jo.
fcsenyly polluted waters whose quality fluctuates greatly.
ORVHOTOLIDINE (OT) TEST
., ji, t k {&
(prthotolidine test enables both free and combined chlorine in
j water to be determined with speed and accuracy) The test was
developed in 1918. ^fhe reagent consists of analytical grade
O-tolidine, dissolved nrlO per cent solution of hydrochloric acid.
When this reagent is added to water containing chlorine, it turns
yellow and the intensity of the colour varies with the concentration
of the gas. The yellow colour is produced by both free and
combined chlorine residuals. OT reacts with free chlorine
instantaneously but reacts more slowly with combined chlorine
(12).
&
The test is carried out by adding 0.1 ml of the reagent toj 1 ml of
water. The yellow colour produced is matched against suitable
standards or colour discs. Commercial equipment is available for
this purpose. It is essential to take the reading within 10 seconds
after the addition of the reagent to estimate free chlorine in water
(14). The colour that is produced after a lapse, say 15-20 minutes, is
due to the action of both free and combined chlorine. f .
/ORTHOTOLIDINE-ARSENITE (OTA) TEST
This is a modification of the OT test to determine the free
)4r\:
Hi ftt\
(a) BOILING
Boiling is a satisfactory method of purifying water for
household purposes. To be effective, the water must be brought to
a "rolling boil" for 5 to 10 minutes. It kills all bacteria, spores,
cysts and ova and yields sterilized water. Boiling also removes
temporary hardness by driving off carbon dioxide and precipitating
the calcium carbonate. The taste of water is altered, but this is
harmless. While boiling is an excellent method of purifying water,
it offers no "residual protection" against subsequent microbial
contamination. Water should be boiled preferably in the same
container in which it is to be stored to avoid contamination during
storage.
(b) CHEMICAL DISINFECTION
<-r jr> /3
C*
TZ> ( 1 <C\
\(1) Bleaching Powder : Bleaching powder oKjcMorinated lime
(CaOCLJ is a white amorphous powder with a pungent smell of
chlorine. When freshly made, it contains about 33 per cent of
"available chlorine") It is, however, an unstable compound. On
exposure to air, light and moisture, it rapidly loses its chlorine
content. But when mixed with excess of lime,, it retains its strength;
this is called "stabilized bleach.''S Bleaching powder should be
stored in a dark, cool, dry place Tn a closed container that is
resistant to corrosion. The chlorine content of bleaching powder
stocks should be frequently checked.
Appendix III gives in a tabular form the amount of bleaching
powder required to disinfect certain quantities of water. The
principle in chlorination is to ensure a "free" residual chlorine of
0.5 mg/litre at the end of one hour contact. Highly polluted and
turbid waters are not suited for direct chlorination.
(1)Chlorine solution : Chlorine solution may be prepared from
bleaching powder. If 4 kg of bleaching powder with 25 per cent
available chlorine is mixed with 20 litres of water, it will give a
5 per cent solution of chlorine (13). Ready-made chlorine
solutions in different strengths are also available in the market.
Like bleaching powder, the chlorine solution is subject to losses
on exposure to light or on prolonged storage. The solution
should be kept in a dark, cool and dry place in a closed
container.
(2)High test hypochlorite : High test hypochlorite (HTH) or
perchloron is a calcium compound which contains 60 to 70 per
cent available chlorine. It is more stable than bleaching powder
and deteriorates much less on storage. Solutions prepared from
HTH are also used for water disinfection. Appendix III (page
541) shows the amount of HTH needed to disinfect certain
quantities of water.
(4) Chlorine tablets : Under various trade names (viz.,
halazone tablets) are available in the market. They are quite
good for disinfecting small quantities of water, but they are
costly. The National Environmental Engineering Research
Institute, Nagpur has formulated a new type of chlorine tablet
which is 15 times better than ordinary halogen tablets. These
tablets are manufactured in various strengths and are now
available in plenty, in the Indian market at a cheap rate. A
single tablet of 0.5 g is sufficient to disinfect 20 litres of water.
(5) Iodine : Iodine may be used for emergency disinfection
of water. Two drops of 2 per cent ethanol solution of iodine will
suffice for one litre of clear water. A contact time of 20 to 30
minutes is needed for effective disinfection. Iodine does not
react with ammonia or organic compounds to any great extent;
hence it remains in its active molecular form, over a wide range
of pH values and water conditions and persists longer than
either chlorine or bromine. Iodine is unlikely to become a
municipal water supply disinfectant in a broad sense. High
costs and the fact that the element is physiologically active
(thyroid activity) are its major disadvantages (17).
(c) FILTRATION
Water can be purified on a small scale by filtering through
ceramic filters such as Pasteur Chamberland filter, Berkefeld filter
and "Katadyn" filter. The essential part of a filter is the "candle"
which is made of porcelain in the Chamberland type, and of
kieselgurh or infusorial earth in the Berkefeld filter (Fig. 8). In the
Katadyn filter, the surface of the filter is coated with a silver
catalyst so that bacteria coming in contact with the surface are
killed by the "oligodynamic" action of the silver ions, which are
liberated into the water. Filter candles of the fine type usually
remove bacteriae found in drinking water, but not the filter-passing
viruses. Filter candles are liable to be logged with impurities and
bacteriae. They should be cleaned by scrubbing with a hard brush
under running water and boiled at least once a week. Only clean
water should be used with ceramic filters. Although ceramic filters
are effective in purifying water, they are not quite suitable for
widespread use under Indian conditions.
FIG. 8
Berkefeld filter
VJy
i^
B
;-
S^S"
= -=
=,
-"-:
fe
HOLE
T^FW'- ~~ i
=
f BLEACHING
> POWDER &
COARSE SAND '
* -
HOLE 1 CM
wV;
*/;%''*
T -"
DIA"
:
.' '
\jf
% .* *.:..- *. %*.
FIG. 9
Double pot
Constituents or
characteristics
Physical parameters
Colour
Taste and odour
Temperature
Turbidity
15 TC'J
5NTU
Inorganic constituents
Aluminium
Ammonia
Chloride
Copper
0.2 mg/L
1.5mg/L
250 mg/L
1 mg/L
Hardness
Hydrogen sulfide
Iron
Manganese
0.05 mg/L
0.3 mg/L
0.1 mg/L
Dissolved oxygen
pH
Sodium
Sulfate
Total dissolved solids
Zinc
200 mg/L
250 mg/L
1000 mg/L
3 mg/L
appearance
should be acceptable
should be acceptable
appearance; for effective terminal disinfection, median turbidity < NTU,
single sample 5 NTU
depositions, discolouration
odour and taste
taste, corrosion
staining of laundry and sanitary ware (health based provisional
guideline value 2 mg/L)
high hardness : scale deposition, scum formation; low hardness; possible corrosion
odour and taste
staining of laundry and sanitary ware
staining of laundry and sanitary ware (health-based provisional
guideline value 0.5 mg/L)
indirect effects
low pH : corrosion; high pH : taste, soapy feel
preferably < 8.0 for effective disinfection with chlorine
taste
taste, corrosion
taste
appearance, taste
Source : (19)
greater resistance to the forces of natural purification than the water borne
pathogens. If the coliform organisms are present in a water sample, the
assumption J&.Nthe probable presence of intestinal pathogens^ y,,0UQ fe\J
jlf - S'?'fSf)
(2) Faecal streptococci: FaecaTstreptococci regularly occur
in faeces, but in much smaller numbers than E. coli; in doubtful
-> cases/the finding of faecal streptococci in water is regarded as
imporrarff confirmatory evidence of recent faecal pollution of
^NwaterjStreptococci are highly resistant to drying and may be
_3/valtrSole for routine control testing after laying new mains or
repairs in distribution systems or for detecting pollution by
surface run-off to ground or surface waters.
though generally in much smaller numbers than E. coli : The spores are
capable of surviving in water for a longer time than organisms of the
coliform group, and usually resist chlorination at the doses normally used
in waterworks practice. The presence of spores of CI. perfringens in a
natural water suggests that faecal contamination has occurred, and their
presence, in the absence of the coliform group, suggests^that faecal
contamination occurred at some remote timej Its presence in filtered
supplies may indicate deficiency in filtration practice.
The guideline values for bacteriological quality are given in Table 5. It
is only a guide required to ensure bacteriologically safe supplies of
drinking water whether piped, unpiped or bottled.
TABLE 5
Bacteriological quality of drinking-water3
Organisms
All water intended for drinking
E.coli or thermotolerant coliform bacteriabc
Treated water entering the distribution system
E.coli or thermotolerant coliform bacteriab
Total coliform bacteria Treated water entering
the distribution system
E.coli or thermotolerant coliform bacteriab
Total coliform bacteria
a.
b.
c.
Guideline value
Must not be detectable in any 100 ml sample
Must not be detectable in any 100 ml sample Must
not be detectable in any 100 ml sample
these conditions, the national surveillance agency should set medium-term targets for progressive improvement of water supplies.
Concentration of nitrite
+ ---------------------------guideline value of nitrite
=<1
Antimony
Arsenic
Barium
Boron
Cadmium
Chromium
Copper
Cyanide
Fluoride
Lead
Manganese
Mercury (total)
Molybdenum
Nickel
Nitrate (as N03)
0.005 (P)
0.01 (P)
0.7
0.3
0.003
0.05 (P)
2(P)
0.07
1.5
0.01
0.5 (P)
0.001
0.07
0.02
50
3(P)
0.01
Source : (19)
TABLE 7
Guideline values for health related organic constituents
Organic constituents
Chlorinated alkanes
Carbon tetrachloride
Dichloromethane
Chlorinated ethenes
Vinyl chloride
1.1- dichloroethene
1.2- dichloroethene
Aromatic hydrocarbons
Benzene
Toluene
Xylenes
Ethylbenzene
Styrene
Benzolalpyrene
Source : (19)
Polynuclear aromatic hydrocarbons : A large number of
polynuclear aromatic hydrocarbons (PAHs) from a variety of
combustion and pyrolysis sources have been identified in the
environment. The main source of human exposure to PAHs is
food, with drinking water contributing only minor amounts.
Little information is available on the oral toxicity of PAHs,
especially after long-term exposure. Benzo (a) pyrene, which
constitutes a minor fraction of total PAHs have been found to
Acceptable daily intake (ADI) are established for food additives and
pesticide residues that occur in food for necessary technological purposes
or plant protection reasons. For chemical contaminants, which usually
have no intended function in drinking water the term TDI is seen as more
appropriate than ADI, as it signifies permissibility rather than
acceptability.
TABLE 8
Guideline values of certain pesticides
_ ,. . ,
(Ms/litre)
Aldrin/dieldrin
0.03
Chlordane
DDT
2,4-D
Heptachlor and heptachlor epoxide
Hexachlorobenzene
Lindane
Methoxychlor
Pentachlorophenol
0.2
2
30
0.03
1
2
20
9(P)
Source : (19)
P - Provisional value
Factor
1-10
1-10
1-10
1-10
The total uncertainty factor should not exceed 10,000. If the risk
assessment would lead to a higher uncertainty factor, then the resulting
TDI would be so imprecise as to lack meaning. For substances for which
uncertainty factors were greater than 1000, guideline values are
designated as provisional in order to emphasize the high level of
uncertainty inherent in these values (19).
Derivation of guideline value using a TDI approach : TDI can be
calculated by following formula.
TDI =
NOAEL OR LOAEL
-------------------------UF
The guideline value (GV) is then derived from the TDI as follows :
GV =
TDI X bw X P
-----------------------C
2. Sampling
Sampling of water should be done with the thoroughness a
surgical operation, with the observation of similar asepi
precautions, for upon it depends the results of analysis, should be
carried out by competent and trained personnel strict accordance
with the methods and frequency of samplh prescribed in the WHO
guidelines for drinking-water quality the ICMR 'Manual of
Standards of Quality for Drinking Wat Supplies' (21). The methods
of sampling are set out briefly Appendix II.
3. Bacteriological surveillance
The tests usually employed in water bacteriology a:
presumptive coliform test, tests for the detection of faec
streptococci and CI. perfringens and colony count. A comple
bacteriological examination consists of all these tests.
Plate count
after 2 daps
at37 deg C
Plate count
after 3 days
at 22 deg C.
20
10
100
TABLE 9
Classification of hardness in water
Classification
(a)
(b)
(c)
(d)
Soft water
Moderately hard
Hard water
Very hard water
___________________________
Another long clean string should be tied to the end of the sterilized
string, and the bottle lowered into the water and allowed to fill up.
The bottle should be then raised and the stopper with cover
replaced.
Another method of collecting samples from rivers or reservoirs
is to hold the bottle by the bottom and plunge its neck down-wards
below the surface of the water. The bottle is then turned until the
neck points slightly up-wards, the mouth being directed towards
the current. If no current exists, as in a reservoir, a current should
be artificially created by pushing the bottle horizontally forward in
a direction away from the hand. When full, the bottle is raised
rapidly above the surface and the stopper replaced.
If a sample is to be taken from a well fitted with a pump, the
water should be pumped to waste for about 2 minutes and the
sample collected from the pump delivery or from a tap on the
discharge.
Bleaching
Powder
(25-35%) (g)
1
1.2
1.5
2
2.5
3
4
5
6
7
8
10
12
15
20
30
40
50
60
70
80
100
120
150
200
250
300
400
500
2.3
Q
3.5
5
6
7
9
12
14
16
19
23
28
35
50
70
90
120
140
160
190
230
280
350
470
580
700
940
1170
High Strength
Calcium
hypochlorite
(70%) (g)
1
1.2
1.5
2
2.5
3
4
5
6
7
8
10
12
15
20
30
40
50
60
70
80
100
120
150
200
250
300
400
500
Liquid bleach
(5% sodium
hypochlorite)
(ml)
14
17
21
28
35
42
56
70
84
98
110
140
170
210
280
420
560
700
840
980
1100
1400
1700
2100
2800
3500
4200
5600
7000
HARDNESS OF WAT1
APPENDIX IV
WATER CONSERVATION
Declining trend of rainfall and rapid urbanizatioi
industrialization has created increasing demand for Growing
water shortage is already causing problems in $ areas and
available resources like rivers, ponds, lak shrinking, causing
more & more prrssure on sub-soil resources. Already, the rate
of water extraction is exceedi replenishment that takes place
by natural processes - i recharge due to rainfall. This is causing
alarming fall in su water levels which is going down in and
around several Development of agriculture dependent on tube
well further worsened the situation. The underground
resources, therefore, urgently need conservation. The
conservation implies both, protection of water resource: further
building up the precious water reserves.
Conservation of water resources requires
(a)PREVENTION OF WASTAGE : Wide-spread awar
needs to be developed among people about economical i
water. It has to be propagated that people should mal
effort not to waste water, and help in reducing consumpti
the invaluable water reserves. Efficient water managemer
substantially reduce total water requirement of commur
Domestic consumption of water can be reduced by indivic
by cultivating better habits in kitchen and bathroom us
avoid free running of water.
(b)WATER HARVESTING : Simple innovative idea;
water harvesting are extremely important to preserve
buildup underground water reserves in urban and serni-t
areas, where considerable water is drawn out by tube wel
domestic consumption. Vast quantity of rainwater is norr
discharged in to drains. This rainwater can be easily add<
the underground reserves by diversion of rainwater
rooftops and courtyards into soaking pits or trenches, ins of
drains. It is also viable to clean and filter this water divert it
into existing tube wells or wells. Various econ designs are
suggested by agencies like Central Ground W Board
(CGWB), UNICEF etc. Suitably large pit is fills layers
with big stones, followed by gravel and sand. Colle
rainwater from rooftops is brought into the pit by PVC pi
The rainwater filtered through these layers, then travels 1
PVC pipe connecting bottom of the pit into the nearby we
tube well.
References
1.WHO (1972). Health Hazards of the Human Environment, WHO, Geneva.
2.WHO (1995). The World Health Report 1995, Bridging the gaps, P-41.
3.WHO (2002). The Works of WHO in South -East Asia Region, Report
of the
Regional Director 1 July -30 June 2002, New Delhi
4.Govt, of India (1977). Manual on Water Supply and Treatment, Second Edition,
Central Public Health and Environmental Engineering Organization, Ministry of
Works and Housing, New Delhi.
5.Subrahmanyan, K. and Bhaskaran, T.R. (1948). Indian J . Med. Res., 36,211.
6.WHO (1969). The Village Tank as a Source of Drinking Water WHO/
CWS/RD/69-1..
7.Wagner, E.G. and Lanoix, J.N. (1959). Water Supply for Rural Areas and Small
Communities, WHO
14-15 (1984),
11.Huisman, L. and Wood, W.E. (1974). Slow Sand Filtration, WHO, Geneva.
12.WHO (1977). WHO Chronicle, 31, 318
13.Rajagopalan, S. and Shiffman, M.A. (1974). Guide to Simple Sanitary Measures
for the Control of Enteric Diseases, WHO, Geneva
14.American Public Health Association, American Water Works Association and
Water pollution Control Federation (1971). Standard Methods for the Examination
of Water and Waste Water, 13th ed., New York.
15.Cox, C.R. (1964). Operation and Control of Water Treatment Processes, WHO,
Geneva.
Quality
Vol.1
Establishments, WHO
Geneva
AIR
The immediate environment of man comprises of air on which
depends all forms of life. Apart from supplying the life-giving
oxygen, air and atmospheric conditions serve several functions.
The human body is cooled by the air contact; the special senses of
hearing and smell function through air-transmitted stimuli; disease
agents may be conveyed by air. Pollution of air by dust, smoke,
toxic gases and chemical vapours has resulted in sickness and
death. Man's adventure into outer space has broadened our concept
of air environment. Human beings need a continuous supply of air
to exist. The requirement for air is relatively constant (about 1020m3 per day)
Composition
Air is a mechanical mixture of gases. The normal composition
of external air by volume is approximately as follows: Nitrogen78.1 per cent; Oxygen-20.93 per cent; Carbon dioxide-0.03 per
cent. The balance is made up of other gases which occur in traces,
e.g., argon, neon, krypton, xenon and helium. In addition to these
gases, air also contains water vapour, traces of ammonia and
suspended matter such as dust, bacteria, spores and vegetable
debris.
Air is rendered impure by (1) Respiration of men and animals
(2) Combustion of coal, gas, oil, etc. (3) Decomposition of organic
matter and (4) Trade, traffic and manufacturing processes which
give off dust, fumes, vapours and gases. Under ordinary
conditions, the composition of outdoor air is remarkably constant.
This is brought about by certain self-cleansing mechanisms which
operate in nature (1) Wind : Wind dilutes and sweeps away the
impurities by its movement. Because of wind movement,
impurities do not accumulate in any one place; (2) Sunlight : The
atmospheric temperature and sunlight play their own part by
oxidizing impurities, and killing bacteria; (3) Rain : It cleanses the
atmosphere by removing the suspended and gaseous impurities; (4)
Plant life : The green plants utilise the carbon dioxide and generate
oxygen; this process is reversed during the night time. When the
rate of pollution becomes too high or when the cleansing process
becomes ineffective, it constitutes a health hazard.
The Air of occupied room
Human occupancy and activity vitiate air in occupied rooms and
give a sense of discomfort to the occupants. The changes in air that
take place in confined places are both chemical and physical, (a)
CHEMICAL CHANGES : The air becomes progressively
contaminated by carbon dioxide and the oxygen content decreases
due to metabolic processes. An average person at rest gives off 0.7
eft. of carbon dioxide per hour; this may increase up to 2 eft.
during physical activity. In a mixed gathering comprising all age
groups, the per capita output of carbon dioxide is taken as 0.6 eft.
per hour, (b) PHYSICAL CHANGES : The most important changes
that occur due to human occupancy are the physical changes. These
are (i) Rise in temperature : The indoor temperature tends to rise as
a result of the emanation of body heat. A man at rest gives off
approximately 400 Btu per hour. One Btu (British Thermal Unit) is
the quantity of heat required to raise the temperature of one pound
of water by 1 deg. F. Under conditions of physical exertion, the
heat output may go up to 4,000 Btu. (ii) Increase of humidity :
There is an increase in the relative humidity due to moisture
evaporated from the skin and lungs. The expired air contains about
6 per cent of water vapour. An adult person at rest releases an
average 700 gms. of water vapour per 24 hours in the form of
perspiration. It has been calculated that a human being releases
18.4 gms of water vapour per hour when sleeping and upto 175
gms of water vapour when engaged in really vigorous exercise (1).
(iii) Decrease in air movement: In crowded places, the natural
movement of air is impeded, (iv) Body odours : Unpleasant odours
arise from foul breath, perspiration, bad oral hygiene, dirty clothes
and other sources. The production of body odours depends upon
the social status, age and personal hygiene of the people, (v)
Bacterial pollution : The exhaled air contains microorganisms in
suspension. These are principally saprophytic bacteria and may
include pathogenic bacteria. These organisms are discharged into
the air during conversation, coughing, sneezing and loud talking.
Unless the vitiated air is replaced by fresh air, it may adversely
affect the comfort, health and efficiency of the occupants. It is
known that a feeling of suffocation or
(2TTS
1.Comfort zone
2.Just tolerable
3.Intolerable
AIR POLLUTION
Sources
Tobacco smoke
Stove
Carbon Monoxide
Nitrogen dioxide
Sulphur dioxide
Carbon dioxide
Formaldehyde
Other organic vapours
(benzene, toluene, etc.)
Ozone
Radon and "daughters"
Asbestos
Mineral fibres
Aerosol sprays
Combustion equipment, Stove,
Gas heaters
Gas cookers, cigarettes
Coal combustion
Combustion, respiration
Particle board, carpet adhesives,
insulation
Solvents, adhesives, resin products,
aerosol sprays
Electric arcing, UV light sources
Building material
Insulation, fireproofing
Appliances
Source : (9).
Monitoring of air pollution
The best indicators of air pollution are sulphur dioxide, smoke and
suspended particles. These are monitored on a daily basis over several
sites. The results are then collected by a central agency, (a) Sulphur
dioxide : This gas is a major contaminant in many urban and industrial
areas. Its concentration is estimated in all air pollution surveys, (b) Smoke
or Soiling index : A known volume of air is filtered through a white filter
paper under specified conditions and the stain is measured by photoelectric
meter. Smoke concentration is estimated and expressed as
micrograms/cubic metre of air as an average level over a period of time, (c)
Grit and dust measurement : Deposit gauges collect grit, dust and other
solids. There are analysed monthly, (d) Coefficient of haze : A factor used,
particularly in the USA in assessing the amount of smoke or other aerosol
in air. (e) Air pollution index : It is an arbitrary index which takes into
account one or more pollutants as a measure of the severity of pollution.
For example, the following index has been used in USA : 10 times the
sulphur dioxide concentration plus twice the carbon monoxide
concentration (both in ppm by volume) plus twice the coefficient of haze.
It was considered to be a cause for alarm when the value of this index rose
from its value of about 12-50 or more.
The WHO (1987) in its publication "Air quality guidelines for Europe"
has described approved methods of determining the concentration of
common air pollutants and their health hazards. The emphasis in the
guideline is placed on exposure, since this is the element that can be
controlled to lessen the dose and hence lessen response. The starting point
for the derivation of guideline value was to define the lowest concentration
at which adverse effects are observed. On the basis of the body of scientific
evidence and judgements of protection (safety) factors, the guideline
values were established. The regulatory approach to controlling air
pollution differs from country to country as several sources of air
pollutants having unique national components are best subject to national
control procedures. The approach taken in the preparation of the air quality
guidelines was to evaluate data on health effects of individual compounds.
As part of this approach, each chemical is considered in isolation.
Inevitably, there is little emphasis on such factors as interaction between
pollutants that might lead to synergistic effects and on the environmental
fate of the pollutants. For some of the substances, a direct relationship
between concentrations in air
Substance
Cadmium
Carbon disulphide
Time-weighted
average
1 -5 ng/m3 1020 ng/m3
100 ng/m3
3
Averaging time
1 year (rural areas 1
year (urban area:
24 hours
Carbon monoxide
100 mg/m
60 mg/m3 30
mg/m3 10
mg/m3
1.2 -Dichloroethane
0.7 mg/m3
24 hours
Dichloromethane
(Methylene chloride)
3 mg/m3
24 hours
100 ug/m3
150 ng/m3
30 minutes
24 hours
0.5-1.0 ng/m3
1 ng/m3
1 year
1 year
1 year
1 hour 24
hours
Ozone
150-200 ng/m3
100-120 ng/m3
1 hour 8
hours
Styrene
800 ng/m3
Sulphur dioxide
500 ng/m3
350 ng/m3
Formaldehyde
Hydrogen sulphide
Lead
Manganese
Mercury
Nitrogen dioxide
15 minutes
30 minutes
1 hour
8 hours
24 hours
10 minutes 1
hour
5 mg/m3
24 hours
Toluene
Trichloroethylene
8 mg/m
1 mg/m3
24 hours
24 hours
Vanadium
1 ng/m3
24 hours
Tetrachloroethylene
Source : (2)
Air pollution monitoring in India
The National Air Quality Monitoring Programme, sponsor by the
Central Pollution Control Board (CPCB) since 1990, r generated
database over last 14 years in 10 major Indian citi viz. Ahemedabad,
Mumbai, Kolkata, Delhi, Hyderabad, Jaip Kanpur, Kochi, Chennai and
Nagpur. The programi facilitates evaluation of long-term air quality
trends for healt related criteria pollutants such as inhalable dust, sulpl
dioxide, nitrogen dioxide, lead, hydrogen sulphide, ammoi and PAH.
The trend analysis showed that suspend Particulate Matter (SPM)
exceeds the CPCB standards in cities most of the time throughout the
year. The concentrati ratio of < P10 fraction (human respirable
particles) to the tc SPM varies between 30 to 60 per cent, with coastal
cit showing higher percentages. The concentration of respira1
Sources
.,
Adverse effects
Oxides of
nitrogen
Automobile exhaust,
gas stoves and heaters,
wood-burning stoves,
kerosene space heaters
Lung cancer
Ozone
Automobile exhaust,
high altitude aircraft
cabins
Sulphur
dioxide
Lead
Automobile exhaust
using leaded gasoline
Impaired neuropsychological
development in children
VENTILATION
The modern concept of ventilation implies not only the
replacement of vitiated air by a supply of fresh outdoor air, but also
control of the quality of incoming air with regard to its
temperature, humidity and purity with a view to provide a thermal
environment that is comfortable and free from risk of infection.
Standards of ventilation
The fixing of standards of ventilation is a matter of much
difficulty. Most of the standards of ventilation have been based on
the efficiency of ventilation in removing body odour. (1) Cubic
Space : Different workers have advocated standards for the
minimal fresh air supply ranging from 300 to 3,000 eft. per hour
per person (1). The widely quoted standard is that of De Chaumont
who advocated a fresh air supply of 3,000 eft. per person per hour
on the following grounds: It was observed that so long as the
amount of carbon dioxide due to respiration was not more than 2
parts in 10,000 parts of air, the air of the rooms seemed fresh and
did not sensibly differ from outdoor air. Assuming that an average
person expires 0.6 eft. of carbon dioxide per hour, and that 0.0002
eft. of C02 in one eft. of air as the "permissible impurity", it was
calculated that 0.6/0.0002 or 3,000 eft. of air would be required by
a man at rest per hour. This standard of ventilation is no longer
followed. (2) Air Change : It is now established that the carbon
dioxide theory is not quite correct because even if the C02 content
of air is raised to over 5 per cent and the 02 content reduced to 18
per cent, there were no deleterious effects so long as the "cooling
power" of the air was satisfactory. Air change is more important
than the cubic space requirement. It is recommended that in the
living rooms, there should be 2 or 3 air changes in one hour; in
work rooms and assemblies 4 to 6 air changes. If the air is changed
more frequently, i.e., more than 6 times in one hour, it is likely to
produce a drought which should be avoided. Based on this concept,
it is now considered that a space of 1,000 to 1,200 eft. per person is
quite sufficient. The number of air changes per hour is calculated
by dividing the total hourly air supply to the room by the cubic
capacity of the room (1). (3) Floor Space : Floor space per person
is even more important than cubic space. Heights in excess of 10 to
12 feet are ineffective from the point of view of ventilation, as the
products of respiration tend to accumulate in the lower levels.
Therefore, in calculating cubic space requirements, heights over 10
to 12 feet are not taken into account. The optimum floor space
requirements per person vary from 50 to 100 sq.ft.
Types of ventilation
1. NATURAL VENTILATION
Natural ventilation is the simplest system of ventilating small
dwellings, schools and offices. In this method, reliance is placed on
certain forces which operate in nature. These are: (1) THE WIND :
The wind is an active force in ventilation. When it blows through a
room, it is called perflation. When there is an obstruction, it
bypasses and exerts a suction action at its tail end - this is called
aspiration. Doors and windows facing each other provide "cross
ventilation". Back to back houses do not permit cross ventilation
and therefore, their construction is not allowed. (2) DIFFUSION :
Air passes through the smallest openings or spaces by diffusion.
This is a slow process and therefore, is not relied upon as the sole
means of ventilation. (3) INEQUALITY OF TEMPERATURE :
Air flows from high density to low density; it rises when slightly
heated and escapes from openings provided high up in the room.
The outside air which is cooler and more dense will enter the room
through inlets placed low. The greater the temperature difference
between outside and inside air, the greater the velocity of the
incoming air. In the tropics the outside air may be hotter than the
inside and the reverse may take place (2). These properties of air
are utilised to best advantage by the proper location of windows,
doors, ventilators and skylights. The chief drawback of natural
ventilation is that it is not possible to regulate the velocity of the
incoming air nor to adjust its temperature or humidity.
2. MECHANICAL VENTILATION
Mechanical or artificial ventilation may be of the following
types :
(1) Exhaust Ventilation (2) Plenum Ventilation (3) Balanced
Ventilation (4) Air Conditioning.
(1) EXHAUST VENTILATION : In this system, air is
extracted or exhausted to the outside by exhaust fans usually driven
by electricity. As air is exhausted, a vacuum is created which
induces fresh air to enter the room through windows, doors and
other inlets. Exhaust ventilation is generally provided in large halls
and auditoria for removal of vitiated air. The exhaust fans are
housed in apertures in the external walls, high up near the roof
which facilitate removal of the upper layers of the heated light air.
The ventilation may be regulated by adjusting the speed of the
fans. Local exhaust ventilation is widely used in industries to
remove dusts, fumes and other concentrated contaminants at their
source. (2) PLENUM VENTILATION : In this system, fresh air is
blown into the room by centrifugal fans so as to create a positive
pressure, and displace the vitiated air. Plenum or propulsion system
is used for supplying air to air-conditioned buildings and factories.
Air is delivered through ducts at desired points. This system is of
limited utility. (3) BALANCED VENTILATION: This is a
combination of the exhaust and plenum systems of ventilation. The
blowing fan must balance the exhaust fan. When this system is
employed, the natural system of ventilation is entirely dispensed
with (4) AIR CONDITIONING : Air conditioning is defined as
"the simultaneous control of all, or at least the first three of those
factors affecting both the physical and chemical conditions of the
atmosphere within any confined space or room. These factors
include temperature, humidity, air movement, distribution, dust,
bacteria, odours and toxic gases,
LIGHT 5'
most of which affect in greater or lesser degree the human health
and comfort". Air conditioning is popular in large institutions,
hospitals, industries and dwellings. Its use in operation theatres is
of particular value in control of pathogenic organisms in the air.
The air is filtered when drawn into an airconditioner system from
the room. Excess humidity is removed and the air is circulated
back into the room after heating or cooling it, to bring room
temperature to required comfort zone. Mixing some percentage of
fresh air with recirculated air is regulated. Large institutions or
hospitals often install central airconditioning system for entire
building, instead of installing equipments for individual rooms.
Better controls and economy is achieved in central airconditioning.
Where the temperature difference is large between outside
atmosphere and airconditioned room, "transition room" is
sometimes provided, which maintains temperature in between the
two, so as to prevent sudden exposure to high or low temperature.
Measurement of light
What we perceive as light is a narrow wavelength band <
electromagnetic radiation from about 380 to 780 nm (nar metre).
Light containing all visible waves is perceived as whit There is
considerable confusion about units of ligl measurement. There
are four measures of importance. F< each of these four measures
again, there are a number of tern and also a great variety of
names. These are given in Table The four measures are : (1)
Luminous intensity, which is tr "power" of a light source
considered as a point radiating in z directions; this is measured as
candelas or candle pow (2) Luminous flux, which is the flow of
light related to a unit < solid angle measured in lumens (3)
Illumination or illuminanc which is the amount of light reaching
a surface measured in k per unit area; and (4) Brightness or
luminance which is tr amount of light reflected from a surface
measured in lamberts
References
1.Bedford, T (1964). Basic Principles of Ventilation and Heating. Lewis, London.
2.Wilkie, W. (1965), Jordan's Tropical Hygiene and Sanitation, Bailliere Tindall &
Co.
LIGHT
The requirements of good lighting
Good lighting is essential for efficient vision. If the lighting
conditions are not ideal, the visual apparatus is put to strain which
may lead to general fatigue and loss of efficiency. For efficient
vision, the following light factors are essential : (1)
SUFFICIENCY: The lighting should be sufficient to enable the eye
to discern the details of the object as well as the surroundings
without eye strain. An illumination of 15 to 20 foot candles is
accepted as a basic minimum for satisfactory vision. The
illumination requirements vary from as little as 5 foot candles in
stairways and corridors to 100 foot candles in some industries. (2)
DISTRIBUTION : The distribution of light should be uniform,
having the same intensity, over the whole field of work. If there are
contrast differences in light, it will strain the eyes and affect
adversely the visual acuity. Proper dispersal of light, without the
production of shadows is therefore necessary for efficient vision.
(3) ABSENCE OF GLARE : Glare is excessive contrast. The best
example of glare is the automobile headlights at night, the same
lights during daylight would not cause glare owing to the absence
of excessive contrast. Glare may be a direct glare from a light
source or reflected glare from sources such as table tops and
polished furniture. Glare causes annoyance. The eye cannot tolerate
glare because it causes acute discomfort and reduces critical vision.
(4) ABSENCE OF SHARP SHADOWS : Slight shadows are
inevitable, but sharp and contrasting shadows are disturbing. Like
glare, shadows cause confusion to the eye and therefore should not
be present in the field of vision. (5) STEADINESS : The source of
light should be constant. It should not flicker because flickering
causes eye strain and may lead to accidents. (6) COLOUR OF
LIGHT : The colour of light is not very important so long as the
intensity is adequate. Since natural light has a soothing effect on
the eye, the artificial light should as far as possible approximate the
daylight colour. (7) SURROUNDINGS : When a black object is
viewed against a dark background, recognition is difficult. High
levels of illumination will be required where there is little colour
contrast. For efficient vision, colour schemes in rooms are
important. Ceilings and roofs should have a reflection factor of 80
per cent; walls 50 to 60 per cent; furniture 30 to 40 per cent. There
should not be much reflection from the floor, not more than 15 to
20 per cent. Contrasting colours are often used to prevent accidents,
e.g., culverts, bridges, etc.
TABLE 1
Light measurement units
Description
1. Brightness of
point source
Quantity
measured
Name
Recommend
Unit*
Luminous
intensity
Luminous flux
Illumination
Illuminance
Candela
2. Flow of light
3. Amount of light
reaching
surface
4. Amount of light Brightness
remitted by surface Luminance
Lumen
Lux
Lambert
d
Other Units
3
Candle powe
Foot candle
Lumen/Cm2
(Phot)
Foot lambert
Candles/Cm
Natural lighting
Natural lighting is derived partly from the visible sky an partly
from reflection. In fact, much light comes to the roorr by
reflection from light coloured objects. Efficient utilisation c
natural light calls for careful design, location and orientation c
buildings and relationship between buildings (town planning
Natural lighting also depends upon the time of the day, seasor
weather and atmospheric pollution. Since natural light i
accompanied by radiant heat, all attempts should be made t
exclude radiant heat while admitting daylight.
Suggestions for Improving Daylight Illumination : Th
following general principles are taken into consideration i
planning for the best utilisation of daylight. (1) ORIENTATION
The brightness of the sky is not constant on the east and wes and
therefore the illumination is subject to variation in building facing
east or west. Further, the direct penetration of sunligh from the
east or west may heat up the rooms unduly in th tropics, especially
during summer. Buildings are therefor oriented, wherever
possible, towards north or south for uniforr illumination. This is
particularly important in respect of schools factories and
laboratories where uniform lighting is required ii all the rooms.
This rule may not be strictly observed with regan to dwelling
houses, as uniform lighting is not required in all thi rooms. When
a building faces east and west, window shade are provided to
protect against the direct penetration o sunlight. (2) REMOVAL
OF OBSTRUCTIONS : Removal o obstructive items either
wholly or partially is likely to give thi most effective single
improvement in lighting. (3) WINDOWS Windows should be
properly planned, as the natural lightinj within any room is
influenced by the amount of visible sky, th( size, shape and
arrangement of the window openings. A tal window gives greater
penetration of light; a broad windov gives greater diffusion of
light. The rule that window are; should not be less than 10 per cent
of the floor area is now outdated. In modern practice, window area
is correlated to th<
---------------1--------------------------------------------------------
X 100
Lighting standards
The eye responds to a range of illumination ranging from 0.1
lux (full moonlight night) to 100,000 lux (bright sunshine). There
is considerable confusion about standards because of the
adaptability of the eye. Many standards have been published but
these standards are arbitrary. The visual efficiency increases with
the increase of illumination, but the curve flattens out at higher
levels. The law of diminishing return applies. A useful rule of
thumb is that the illumination level should be 30 times higher than
the level at which the task can just be done. It is worth repeating
there are no exact lighting standards and it is usually better to err
on the side of too much light, provided glare can be avoided. For
practical situations and various activities, the following values (in
lux) have been suggested by the Illuminating Engineer Society (1).
TABLE 2
Recommended illumination (the IES Code)
Visual task
Illumination (lux)
Casual reading
General office work
Fine assembly Very
severe tasks Watch
making
100
400
900
1300-2000
2000-3000
NOISE
Noise is often defined as "unwanted sound", but thi: definition
is subjective because of the fact that one man': sound may be
another man's noise. Perhaps a better definitior of noise is :
"wrong sound, in the wrong place, at the wronc time". Man is
living in an increasingly noisy environment. Th< 20th Century has
been described as the "Century of Noise" Noise has become a very
important "stress factor" in the environment of man. The term
"Noise Pollution" has beei recently coined to signify the vast
cacophony of sounds that an being produced in the modern life,
leading to health hazards.
Sources : The sources of noise are many and varied. Thesi are
automobiles, factories, industries, air-crafts etc. Noisi levels are
particularly acute near railway junctions, traffi round-abouts, bus
terminuses and airports. Use of pressur horns, recreational noise
of loudspeakers with full volume during festivities particularly at
night are other sources of nois< production. The domestic noises
form the radios, transistors T.V sets - all add to the quantum of
noise in daily life.
Properties : Noise has two important properties : loudnes or
intensity; and frequency.
(1) LOUDNESS : Loudness or intensity depends upon th
amplitude of the vibrations which initiated the noise. Th
NOISE 551
Mechanical damage
n 150
Jf
l4
Threshold of pain
\-'
13
u
!* 1 20
S
H" ^ " O
U- 100
n" 90
U-
80
Printing press
H-
70
"c
U.
Normal conversation
1/5
P- 50
.n
Quiet library
30
Whispering
y. 20
The effects of noise exposure are of two types : auditory and nonauditory. (1) AUDITORY EFFECTS, (a) Auditory fatigue . It
FIG.l
appears in the 90 dB region and greatest at 4000 Hz. It mav, be
associated with side effects such as whistling and buzzing ir the ears,
Community noise levels
(b) Deafness : The most serious pathological effect is deafness or
It has been observed that the human ear responds in a non- hearing loss. The victim is generally unaware of il in early stages.
uniform way to different sound-pressure levels, that is, it responds The hearing loss may be temporary or permanent. Temporary
not to the real loudness of a sound, but to the perceived intensity. A hearing loss results from a specific exposure to noise; the disability
weighting curve, called curve A has been constructed which takes disappears after a period ol time up to 24 hours following the noise
into account the subjective effects of that sound. Sound-pressure exposure. Most temporary hearina Jpss occurs in frequency range
levels are therefore expressed in dB (A), that is in decibels between 4,000 to 6,000 Hz|_Repeated or continuous exposure to
conforming to the weighting curve A, because this reflects the noise V around 100 decibels may result in a permanent hearing loss;
perception of that sound emission by the normal human ear. in 'Tjhis, the inner ear damage may vary from minor changes in the
C!j*ir ce'l endings to complete destruction of the organs of Corti.
Acceptable noise levels are as given in Table 1. V-^
TABLE 1
^ When this occurs as a result of occupation in industries, it is called
'occupational hearing loss'. Exposure to noise above 160 dB may
Acceptable noise levels (dBA)
rupture the tympanic membrane and cause permanent loss of
Residential:
Bed room
25
,/ hearing7/(2) NON-AUDITORY EFFECTS ) These are : (a)
Interference with speech : Noise interferes with speech
Living room
40
communication. In everyday life, the frequencies causing most
Commercial :
Office
35-45
disturbance to speech communication lie in the 300-500 Hz range.
Conference
40-45
Such frequencies are commonly present in noise produced by road
Restaurants
40-60
and air traffic. For good speech intelligibility, it is considered that
Industrial :
Workshop
40-60
the speech sound level must exceed the SIL (Speech Interference
Laboratory
40-50
Level) by approximately 12 dB. (b) Annoyance : This is primarily a
Educational :
Class room
30-40
psychological response. Neurotic people are more sensitive to noise
Library
35-40
than balanced people. Workmen exposed to higher intensity of noise
Hospitals :
Wards
20-35
in occupational capacities, were often irritated, short tempered and
impatient and more likely to resort to agitation and disrupt
Source : (1)
production, (c) Efficiency : Where mental concentration is to be
(2) FREQUENCY : The frequency is denoted as Hertz (Hz.) undertaken, a low level of noise is always desired. Reduction in
One Hz is equal to one wave per second. The human ear can hear noise has been found to increase work output, (d) Physiological
frequencies from about 20 to 20,000 Hz, but this range is reduced changes : A number of
with age and other subjective factors. The range of vibrations
below 20 Hz are infra-audible; and those above
I 10
TABLE 1
Sources of radiation exposure
Natural
(1)
Cosmic rays
(1)
(2)
Environmental:
(a) Terrestrial
(b) Atmospheric
(2)
(3)
RADIATION
Sources of radiation exposure
Radiation is part of man's environment. The sources of radiation to
which man is exposed are divided into two groups (Table 1) :
Internal:
Potassium-40
Carbon-14
(3)
(4)
Man-made
Medical and dental:
X-rays, Radioisotopes
Occupational
exposure
Nuclear:
radioactive fallout
Television sets
Radioactive dial
watches, Isotope
tagged products,
Luminous markers.
RADIATION 553
Types of radiation
The term "ionizing radiation" is applied to radiation which has
the ability to penetrate tissues and deposit its energy within them.
Ionizing radiation may be divided into two main groups :
(1)electromagnetic radiations - X-rays and gamma rays, and
(2)corpuscular radiations - alpha particles, beta particles
(electrons) and protons. Some common types of environmental
radiations are as given in Table 2.
TABLE 2
Some common environmental radiations
Type of radiation
Tissue
Alpha particles
4 cm
0.05 mm
Beta particles
Gamma rays
X-rays
Cosmic rays
6-300 cm
400 metres
120-240 metres
0.06-4.0 mm
50 cm
15-30 cm
some
components
very high
0.005-0.3 mm
40 mm
0.3 mm
Source : (1)
Alpha particles are 10 times as harmful as X-rays, beta particles
or gamma rays. Alpha particles, luckily, have little penetrating
force. On the other hand, they are quite dangerous if radioactive
substance has entered the body (by inhalation or through a wound).
Gamma rays and X-rays have short wave lengths; they are deep
penetrating radiations. X-rays are manmade, while gamma rays are
emitted spontaneously by radioactive elements during their
disintegration. Otherwise there is no material difference between
gamma rays and X-rays. Cosmic rays also contain ionizing
radiations.
The term "non-ionizing radiation" refers to several forms of
electromagnetic radiation of wavelengths longer than those of
ionizing radiation. As wavelength elongates, the energy value of
electromagnetic radiation decreases. So all non-ionizing forms of
radiation have less energy than cosmic, gamma, and X-radiation
have. In order of increasing wavelength, nonionizing radiation
includes ultraviolet (UV) radiation, visible light, infrared radiation,
microwave radiation and radio frequency radiation.
Radiation units
The activity of a radioactive material is the number of nuclear
disintegration per unit of time. The unit of activity is a becquerel
(Bq); 1 Bq is equal to 1 disintegration per second. Formerly, the
unit of activity was curie (Ci) and 1 Bq corresponds approximately
to 27 picocuries.
The potency of radiation is measured in three ways : (1)
Roentgen: Roentgen is the unit of exposure. It is the amount of
radiation absorbed in air at a given point, i.e., number of ions
produced in 1 ml of air (2) Rad : Rad is the unit of absorbed dose.
It is the amount of radioactive energy absorbed per gram of tissue
or any material, lmrad - 0.001 rad (3) Rem : Rem is the product of
the absorbed dose and the modifying factors. The rem indicates the
degree of potential danger to health. The radiation to which the
average citizen is exposed is made up almost of the fast moving,
highly penetrating X-rays and gamma rays, where rem and rad are
equal (2).
The radiation units (viz roentgen, rad, rem) are being replaced
by the new SI Units (International System of Units) which are : (a)
Coulomb per kilogram (C/Kg) replacing the roentgen. 1 roentgen is
equal to 2.58 x 10~4 C kg-1. It is the unit for exposure. There is no
special name for this, (b) Gray (Gy) replacing the rad. It is the unit
of absorbed dose, defined as the dose of ionizing radiation that
impart 1 joule of energy to 1 kg of
absorbing material. 1 rad is equal to 0.01 Gy. (2), and (c) Sievert
(Sv) replacing the rem. It is the SI unit of dose equivalent. The
dose equivalent of 1 sievert is equal to 100 rems.
Dose equivalent (H) : As all types of radiation do not produce
the same biological effect per unit of energy absorbed, the concept
of dose equivalent has been introduced. The dose equivalent, M
(Sieverts) is equal to the absorbed dose, D (grays), multiplied by a
quality factor Q which depends upon the density of ionization
produced in the tissue by the radiation.
H = DQ
The factor Q for X-rays and Y-rays and electrons is equal to 1,
whereas for a particles it is 20 (11).
Biological effects of radiation
The biologic effects of ionizing radiation may be divided into
two separate groups (2,4,5,6)
(1) SOMATIC EFFECTS : A dose of 400 to 500 roentgens on
the whole body is fatal in about 50 per cent of cases, and 600 to
700 in practically every case. A dose of 25 to 50 roentgens to the
whole body was found to affect the white blood corpuscles and to
produce mild lassitude and softening of the muscles (2). The
delayed effects take time to develop : the latent period may vary
from a few weeks to years. It is now fairly well established that
delayed effects are mainly of three kinds : leukaemia, malignant
tumours and shortening of life.
Immediate (1) Radiation
sickness (2) Acute radiation
syndrome Delayed :
(1) Leukaemia
(1)Carcinogenesis
(2)Foetal developmental abnormalities
(3)Shortening of life
<
{
METEOROLOGICAL ENVIRONMENT
The elements which comprise the meteorological environment
are: (1) atmospheric pressure (2) air temperature (3) humidity (4)
rainfall (5) direction and speed of wind and (6) movement of
clouds and character of weather (1). The term "climate" is a
geographical concept representing a summation of the whole range
of meteorological phenomena.
Atmospheric pressure
The atmospheric pressure at earth's surface close to the sea level
averages 760 mm of Hg. This is called "one atmosphere of
pressure". Man is physiologically adapted to live at 760 mm of Hg
pressure or close to it. The atmospheric pressure falls as altitude
increases, and rises as altitude decreases. Thus, at an altitude of
100,000 feet above mean sea level, the atmospheric pressure is less
than 10 mm. of Hg. The pressure increases at the rate of "one
atmosphere" for each 33 feet depth below sea level.
Measurement
The instruments used for measuring atmospheric pressure are
known as barometers of which there are three well-known kinds :
Fortin's Barometer; the Kew Pattern Station Barometer and the
Barograph. The 'Kew Pattern' Station Barometer is widely used by
the Indian Meteorological Department for measuring the
atmospheric pressure. Barograph is an instrument for obtaining a
continuous record of atmospheric pressure. It is a circular box, the
walls of which collapse or distend when the atmospheric pressure
rises or falls.
No thermal stress
Moderate to mild heat strain
Severe heat strain
Very severe heat strain
Upper limit of heat tolerance
(c) Predicted four hour sweat rate : The rate at which a man
sweats is a good index of the heat stress to which he is subjected. A
sweat rate of 4.5 litres in 4 hours is the upper limit of tolerance in
health for work in hot environment. A sweat rate of 2.5 litres in 4
hours is considered optimal for a working man. P4Sr is applicable
only in the situation where sweating occurs.
Effects of heat stress
As many as 14 disorders resulting from exposure to heat
have been recognised and documented (8). The important ones
are : (1) Heat stroke : This is attributed to failure of the heat
regulating mechanism. It is characterised by very high body
temperature which may rise to 110F (43.3C) and profound
disturbances including delirium, convulsions and partial or
complete loss of consciousness. The skin is dry and hot.
Classically, sweating is absent or diminished, but many victims
of clear-cut heat stroke perspire profusely. The outcome is often
fatal, even when patients are brought quickly to medical
attention; death/case ratios of 40 per cent or more have been
reported. The treatment consists of rapidly cooling the body in
ice water bath till the rectal temperature falls below 102F
(38.9C). The rectal temperature should be monitored
continuously, both to monitor the efficacy of hypothermia^
treatment and to guard against the development of clinically
significant hypothermia, which can occur if cooling is continued
too long. Further treatment is supportive and directed towards
the
many
potential
complications
of
hyperthermia.
Hypovolaemia,
hyperkalaemia,
rhabdomyolysis,
hypocalcaemia and bleeding diathesis may require intensive
supportive treatment. The patient should be kept in bed for several
days until the temperature control becomes stable. (2) Heat
hyperpyrexia : This is attributed to impaired functioning of the
heat-regulating mechanism but without characteristic features of
heat stroke. It is arbitrarily defined as a temperature above 106F
(8). It may proceed to heat stroke.
___________________________________________HUMIDITY 5
Global warming
Emission of green-house gases into the atmosphere have been
increasing ever since the beginning of the industrial revolution. A
major component of emission of carbon dioxide is from the
combustion of fossil fuels. It is generally conceded that the main
effects of this include an increase of about 3C in the average
global surface temperature by the year 2030, a rise in the sea level
of 0.1-0.3 meters by 2050, and an increase in the occurrence of
extreme climatic events such as cyclones, heatwaves and draughts
(12). The temperature rise could overwhelm the capacity of many
species to adapt. A change of this magnitude would affect local,
regional and global ecosystem, sea levels and ocean currents,
prevailing winds, fresh water supplies, agriculture, forests,
fisheries, industry, transport, urban planning, demographics and
human health. Some effects are mutually reinforcing, so a small
additional change in the existing trend could have massive
consequences, in accordance with the mathematics of catastrophe
theory (13).
Changes in the configuration of jet streams, prevailing winds
and ocean currents could alter the distribution of rainfall in many
regions, making some wetter, others drier. The summers are
becoming hotter. Temperate zone warming induces a decline in soil
moisture that impairs grain production. This will also change the
distribution of vegetation. The distribution of insect vectors of
disease will change. The "heat island" phenomenon that makes
cities warmer than surrounding rural areas will lead to longer and
more severe heat waves than we are accustomed to now (13).
early morning and are near the minimum value in the afternoc at
about 15.00 hours. For accurate readings of the wet bu
thermometer, the air should pass over the bulb with a speed
about 800 ft/min. The sling psychrometer (described belo\
achieves this when rotated rapidly.
SLING PSYCHROMETER
The sling or whirling psychrometer (Fig. 3) consists 2 mercury
thermometers (wet and dry) mounted side by sid on a suitable
wooden frame, and provided with a handle f< rotating the
instrument. The underlying principle is that t rotating, the bulbs
are exposed to air at a definite velocity. TI wet bulb is first
moistened with distilled water and tr instrument is whirled or
rotated standing with the back to tr sun, for about 15 seconds at
the rate of 4 revolutions pi second, so as to obtain the desirable
air speed of about metres per second. The reading of the wet bulb
is then note< The instrument is again whirled for about 10
seconds and th wet bulb reading is noted. This is repeated several
times till successive readings of the wet bulb are identical. The
readin of the dry bulb is then noted. By use of suitable tables c
charts, the relative humidity of the air may be obtained froi the
readings of the psychrometer.
HUMIDITY
Humidity or moisture is always present in the atmosphere. The
amount of moisture which air can hold depends upon its
temperature. If the air is cooled, the excessive moisture precipitates
for the particular temperature. This is called Dew Point. Humidity
may be expressed as absolute humidity or relative humidify, (a)
ABSOLUTE HUMIDITY is the weight of water vapour in a unit
volume of air. It is expressed as grammes per kilogram or grammes
per cubic metre of air. (b) RELATIVE HUMIDITY is the
percentage of moisture present in the air, complete saturation being
taken as 100. The greater the relative humidity, the nearer the air to
saturation. Relative humidity is more commonly employed than
absolute humidity to express the moisture content of air. There is
no evidence that humidity has an effect on physical health although
it definitely has an effect on comfort. If the RH exceeds 65 per
cent, the air inside the room feels sticky and uncomfortable. Better
ventilation serves to lower such humidity. RH below 30 per cent is
also unpleasant. Permanent exposure to such low humidities can
cause drying of the nasal mucosa which may predispose to
infection (viz sore-throat, cough).
Measurement
There are several instruments which may be used for measuring
humidity. The ones commonly used are described below :
DRY AND WET BULB HYGROMETER
This is the most widely used instrument for measuring humidity.
The instrument consists of two similar thermometers - a dry bulb
thermometer and a wet bulb thermometer, which are mounted side
by side on a stand. The dry bulb measures the air temperature
(DBT). The bulb of the second one is covered with a gauze or wick
and is kept moist. The wet bulb reading (WBT) is usually lower
than the DBT. If both the readings are the same, it indicates that the
atmosphere is 100 per cent saturated with moisture, which never
occurs in reality. After obtaining the readings of the dry and wet
bulb thermometers, the corresponding RH can be found from
specially constructed psychrometric charts or slide rule. Humidity
values are high in
Sling psychrometer
ASSMANN PSYCHROMETER
This is a portable instrument specially designed to giv( accurate
measurement of the wet and dry bulb temperature o the air. In this
instrument, air is d^awn at a speed higher than I metres per second
by a clock-work fan. The bulbs of the thermometer are protected
from the effects of solar radiation sc that the instrument can be
used even in strong sunshine.
PRECIPITATION
The term precipitation is the collective term used for rain, snow,
hail, dew and frost - that is, all forms of water precipitated from the
atmosphere. It is measured by rain-gauges. The rain-gauge
prescribed by the Government of India for use at rainfall
measuring stations in India is known as the "Symon's Rain-gauge".
The funnel for receiving the rainfall has a diameter of 5 inches.
Great care is exercised in selecting a suitable site for the erection
of rain-gauge. The Rain-gauge should be set on a level ground,
away from trees, buildings, or other obstructions. The rule which
must be strictly adhered to in the erection of a Rain-gauge is that
its rim should be exactly horizontal, and one foot above the ground
level, the instrument having been fixed in a masonry or concrete
foundation. The rainfall is measured in millimetres per a time unit
(mm/day; mm/month).
AIR VELOCITY
Air velocity
The air velocity is measured by an instrument called the
anemometer. It consists of four hemispherical cups, attached to the
ends of 2 crossed metal arms. There is a vertical spindle which is
attached to the 'anemometer box'. The velocity of the
defined as the physical structure that man uses and the environs of
the structure including all necessary services, facilities, equipment
and devices needed or desired for the physical and mental health
and the social well -being of the family and the individual (1). The
immediate surroundings of residential building are often referred to
as the neighbourhood or microdistrict.
Social goals of housing
Goals are statements about desirable or projected conditions.
The generally accepted goals of housing are :
(1) Shelter : That the house should provide a sanitary shelter,
which is a basic need. (2) Family life: That the house should
provide adequate space for family life and related activities, viz
preparation and storage of food, meeting, sleeping, individual
activities and other basic activities. The adequacy of housing at
this level has been found to have a direct impact on such things
as worker productivity and family stability. (3) Access to
community facilities : A third element of housing is accessibility
to community services and facilities such as health services,
schools, shopping areas, places of worship etc. (4) Family
participation in community life : Family is part of the wider
community. Community is important to family in many ways it can offer help in times of need; it is an important source of
friends. Communities are able to pool their efforts and improve
their living conditions. (5) Economic stability : Housing is a
form of investment of personal savings. It provides for
economic stability and well being of the family.
The implementation of social goals in housing requires that
government should (1) introduce social housing schemes;
(2) establish both minimum and maximum standards;
(3) create financial and fiscal institutions geared to helping low
income people obtain credit for building or improving their
houses.
CRITERIA FOR HEALTHFUL HOUSING :
An Expert Committee of the WHO (3) recommended the
following criteria for healthful housing similar to the Basic
Principles of Healthful Housing published by the American Public
Health Association (4) :
1.Healthful housing provides physical protection and shelter;
2.provides adequately for cooking, eating, washing, and
excretory functions;
3.is designed, constructed, maintained and used in a manner
such as to prevent the spread of communicable diseases;
4.provides for protection from hazards of exposure to noise
and pollution;
5.is free from unsafe physical arrangements due to
construction or maintenance, and from toxic or harmful
materials; and
6.encourages personal and community development,
promotes social relationships, reflects a regard for ecological
principles, and by these means promotes mental health.
Housing standards
With the broadening concept of housing, the concept of housing
standards has also changed. The standards are no longer confined
to narrow health criteria like per capita space and floor space.
Social and economic characteristics such as family income, family
size and composition, standard of living, life style, stage in life
cycle, education and cultural factors must be taken into
consideration in determining housing standards. Because of
cultural diversity and other factors such as climate and social
traditions, standards of housing must vary from country to country
and from region to region. In short there cannot be rigid, uniform
standards.
___________________________________________HOUSING 559
However, minimum standards are still maintained by building
regulations, the aim being improvement of housing and
environmental conditions for the majority of families within the
limits set by available resources and objectives. The standards in
India are those recommended by the EHC (1947). These are as
below :
SITE : (a) The site should be elevated from its surroundings so
that it is not subject to flooding during rains (b) the site should have
an independent access to a street of adequate width (c) it should be
away from the breeding places of mosquitoes and flies (d) it should
be away from nuisances such as dust, smoke, smell, excessive
noise and traffic (e) it should be in pleasing surroundings (f) the
soil should be dry and safe for founding the structure and should be
well drained. "Made-soil", i.e., ground that is levelled by dumping
refuse is very unsatisfactory for building purposes for at least 20 to
25 years. The subsoil water should be below 10 feet.
SET BACK : For proper lighting and ventilation, there should
be an open space all round the house - this is called "set back". In
rural areas it is recommended that the built-up area should not
exceed one-third of the total area; in urban areas where land is
costly, the built-up area may be upto two-thirds. The set back
should be such that there is no obstruction to lighting and
ventilation.
FLOOR : The floor should be pucca and satisfy the following
criteria : (a) it should be impermeable so that it can be easily
washed and kept clean and dry. Mud floors tend to break up and
cause dust; they are not recommended, (b) the floor must be
smooth and free from cracks and crevices to prevent the breeding
of insects and harbourage of dust, (c) the floors should be dampproof, (d) the height of the plinth should be 2 to 3 feet.
WALLS : The walls should be (a) reasonably strong (b) should
have a low heat capacity i.e., should not absorb heat and conduct
the same (c) weather resistant (d) unsuitable for harbourage of rats
and vermin (e) not easily damaged and (f) smooth. These standards
can be attained by 9-inch brick-wall plastered smooth and coloured
cream or white.
ROOF : The height of the roof should not be less than 10 feet in
the absence of air-conditioning for comfort. The roof should have a
low heat transmittance coefficient.
ROOMS : The number of living rooms should not be less than
two, at least one of which can be closed for security. The other may
be open on one side if that side is a private courtyard. The number
and area of rooms should be increased according to size of family,
so that the recommended floor space per person may be
madrjivailable.
FLOOR AREAfjhe^oor tsefe of a living room should be at least
120 sq.ft. fororcupancy by more than one person and at least 100
sq.ft. for occupancy by a single person. The floor area available in
living rooms per_person should not be less than 50 sq.ft; the
optimum is 100 sq.ftl w _iq^ fj#S
CUBIC SPACE : Unless means are prWfded for mechanical
replacement of air the height of rooms should be such as to give an
air space of at least 500 eft. per capita, preferably 1,000 eft.
WINDOWS : (a) Unless mechanical ventilation and artificial
lighting are provided, every living room should be provided with at
least 2 windows, and at least one of them should open directly on
to an open space, (b) the windows should be placed at a height of
not more than 3 feet above the ground in living rooms (c) window
area should be l/5th of the floor area. Doors and windows
combined should have 2/5th the floor area.
LIGHTING : The daylight factor should exceed 1 per cent over
half the floor area.
Overcrowding
Overcrowding refers to the situation in which more people are
living within a single dwelling than there is space for, so that
movement is restricted, privacy secluded, hygiene impossible, rest
and sleep difficult (8). In general the risks as regards physical
health are clear enough - infectious diseases spread rapidly under
conditions of overcrowding. The effects on psychosocial health are
not so clear-cut, viz. irritability, frustration, lack of sleep, anxiety,
violence and mental disorders. Children are said to be more
affected. In short, it is a psychosocial stress, leading to unhappiness
and very probably to psychosomatic and mental disorders.
Overcrowding is a health problem in human dwellings. It may
promote the spread of respiratory infections such as tuberculosis,
influenza and diphtheria. High morbidity and mortality rates are
observed where housing conditions are substandard. The accepted
standards with respect to overcrowding are as below :
(1) PERSONS PER ROOM : The degree of overcrowding
can best be expressed as the number of persons per room, i.e.,
number of persons in the household divided by the number of
rooms in the dwelling. The accepted standards are :
1room
2rooms
3rooms
4rooms
5or more rooms
..
..
..
..
..
2 persons
3 persons
5 persons
7 persons
10 persons (additional 2 for
each further room)
(2) FLOOR SPACE : The accepted standards are :
110 sq.ft. or more
..
2 persons
90-100 sq.ft.
..
172 persons
70-90 sq.ft.
..
1 person
50-70 sq.ft.
..
V2 person
Under 50 sq.ft
..
nil
(A baby under 12 months is not counted; children between
1 to 10 counted as half a unit).
SEX SEPARATION : Overcrowding is considered to exist if
2 persons over 9 years of age, not husband and wife, of
opposite sexes are obliged to sleep in the same room.
Indicators of housing
In recent years the use of indicators has become widespread for
the measurement of quality of life. The indicators for housing may
be classified as :
(1)Physical : These are based on floor space, cubic space, room
height, persons per room, rooms per dwelling, environmental
quality (e.g., air, light, water, noise, sewage disposal, etc)
(2)Economic indicators : These are cost of the building, rental
levels, taxes, expenditure on housing, etc.
(3)Social indicators : The following were proposed at an interregional seminar on the Social Aspects of Housing, organized
by the UN in 1975.
(a) Indicators related to prevention of illness :
(1)Frequency of illness due to inadequate sewage and
garbage collection.
(2)Frequency of illness associated with contaminated water
source.
(3)Frequency of insect borne diseases
(4)Frequency of illness due to overcrowding.
household
DISPOSAL OF WASTES
Disposal of wastes is now largely the domain of sanitarians and
public health engineers. However, health professionals need to
have a basic knowledge of the subject since improper disposal of
wastes constitutes a health hazard. Further the health professional
may be called upon to give advice in some special situations, such
as camp sanitation or coping with waste disposal problems when
there is a disruption or breakdown of community health services in
natural disasters. These aspects are considered in this section.
SOLID WASTES
The term "solid wastes" includes garbage (food wastes) rubbish
(paper, plastics, wood, metal, throw-away containers, glass),
demolition products (bricks, masonry, pipes), sewage treatment
residue (sludge and solids from the coarse screening of domestic
sewage), dead animals, manure and other discarded material.
Strictly speaking it should not contain nightsoil. In India and
similar other countries, it is not uncommon to find nightsoil in
collection of refused. The output of daily waste depends upon the
dietary habits, life styles, living standards and the degree of
urbanization and industrialization. The per capita daily solid waste
produced ranges between 0.25 to 2.5 kg in different countries.
Solid waste, if allowed to accumulate, is a health hazard
because:
a. it decomposes and favours fly breeding
b. it attracts rodents and vermin
c. the pathogens which may be present in the solid waste
may be conveyed back to man's food through flies
and dust.
d. there is a possibility of water and soil pollution, and
e. heaps of refuse present an unsightly appearance and
nuisance from bad odours.
There is a correlation between improper disposal of solid wastes
and incidence of vector-borne diseases. Therefore, in all civilized
countries, there is an efficient system for its periodic collection,
removal and final disposal without risk to health."
Sources of refuse
(1) Refuse that is collected by the street cleansing service or
scavenging is called street refuse. It consists of leaves, straw,
paper, animal droppings and litter of all kinds. (2) Refuse that is
collected from markets is called market refuse. It contains a large
proportion of putrid vegetable and animal matter.
(1)Refuse that is collected from stables is called stable litter. It
contains mainly animal droppings and left-over animal feeds.
(2)Industrial refuse comprises a wide variety of wastes ranging
from completely inert materials such as calcium carbonate to
highly toxic and explosive compounds. (5) The domestic refuse
consists of ash, rubbish and garbage. Ash is the residue from fire
used for cooking and heating. Rubbish comprises paper, clothing,
bits of wood, metal, glass, dust and dirt. Garbage is waste matter
arising from the preparation, cooking and consumption of food. It
consists of waste food, vegetable peelings and other organic
matter. Garbage needs quick removal and disposal because it
ferments on storage.
Storage
The first consideration should be given to the proper storage of
refuse, while awaiting collection. The galvanized steel dust bin
with close fitting cover is a suitable receptacle for storing refuse.
The capacity of a bin will depend upon the number of users and
frequency of collection. The output of refuse per capita per day in
India is estimated to vary from V10 to V20 eft. For a family of 5
members, a bin having a capacity of 5/10 or 1/2 eft. would be
needed. If collection is done once in 3 days, a bin having a capacity
of 1 V2 or 2 eft. would be adequate. A recent innovation in the
western countries is the "paper sack." Refuse is stored in the paper
sack, and the sack itself is removed with the contents for disposal
and a new sack is substituted. Public Bins : Public bins cater for a
larger number of people. They are usually without cover in India
because people do not like to touch them. They are kept on a
concrete platform raised 2 to 3 inches above ground level to
prevent flood water entering the bins. In bigger municipalities, the
bins are handled and emptied mechanically by lorries fitted with
cranes.
Collection
The method of collection depends upon the funds available.
House-to-house collection is by far the best method of collecting
refuse. In India, there is no house-to-house collection system.
People are expected to dump the refuse in the nearest public bin,
which is usually not done. Refuse is dispersed all along the street,
and some is thrown out in front and around the house. As a result,
an army of sweepers is required for sweeping the streets in addition
to the gang for collecting the refuse from public bins. The refuse is
then transported in refuse collection vehicles to the place of
ultimate disposal. Dead animals are directly transported to the
place of disposal.
The collection methods normally practised in this country need
drastic revision and improvement in the interest of better hygiene.
The Environmental Hygiene Committee (1949) recommended that
municipalities and other local bodies should arrange for collection
of refuse not only from the public bins but also from individual
houses (4). A house-to-house collection will result in a
simultaneous reduction in the number of public bins (5). The open
refuse cart should be abandoned and replaced by enclosed vans.
Mechanical transport should be used wherever possible as it is
more practical and economical than the 19th century methods.
There is a wide variety of refuse collection vehicles of all shapes
and sizes. The latest arrival in the western countries is the
"Dustless Refuse Collector" which has a totally enclosed body.
Methods of disposal
There is no single method of refuse disposal which is equally
suitable in all circumstances. The choice of a particular method is
governed by local factors such as cost and availability of land and
labour. The principal methods of refuse disposal are :-
(a)Dumping
(b)Controlled Tipping or Sanitary Land-fill
(c)Incineration
(d)Composting
(e)Manure Pits
(f)Burial
(a) Dumping
Refuse is dumped in low lying areas partly as a method of
reclamation of land but mainly as an easy method of disposal of dry
refuse. As a result of bacterial action, refuse decreases considerably
in volume and is converted gradually into humus. Kolkata disposes
of its refuse by dumping and the reclaimed land is leased out for
cultivation. The drawbacks of open dumping are : (1) the refuse is
exposed to flies and rodents, (2) it is a source of nuisance from the
smell and unsightly appearance, (3) the loose refuse is dispersed by
the action of the wind and (4) drainage from dumps contributes to
the pollution of surface and ground water. A WHO Expert
Committee (1967) condemned dumping as "a most insanitary
method that creates public health hazards, a nuisance, and severe
pollution of the environment. Dumping should be outlawed and
replaced by sound procedures (6).
(b) Controlled tipping
^? \&A
Controlled tipping or sanitary landfill is the most satisfactory
method of refuse disposal where suitable land is available. It differs
from ordinary dumping in that the material is placed in a trench or
other prepared area, adequately compacted, and covered with earth
at the end of the working day^The term "modified sanitary landfill"
has been applied'^ to those operations where compaction and
covering are accomplished once or twice a week (7).
Three methods are used in this operation : the trench method,
the ramp method and the area method (7,8).
(1)The trench method : Where level ground is available, the
trench method is usually chosen. A long trench is dug out - 2 to
3 m (6-10 ft.) deep and 4 to 12 m, (12-36 ft.) wide, depending
upon local conditions. The refuse is compacted and covered
with excavated earth. Where compacted refuse is placed in the
fill to a depth of 2 m (6 ft.), it is estimated that one acre of land
per year will be required for 10,000 population (7).
(2)The ramp method : This method is well suited where the
terrain is moderately sloping. Some excavation is done to secure
the covering material.
(3)The area method : This method is used for filling land
depressions, disused quarries and clay pits. The refuse is
deposited, packed and consolidated in uniform layers up to 2 to
2.5 m (6-8 ft.) deep. Each layer is sealed on its exposed surface
with a mud cover at least 30 cm (12 inches) thick. Such sealing
prevents infestation by flies and rodents and suppresses the
nuisance of smell and dust. This method often has the
disadvantage of requiring supplemental earth from outside
sources.
Chemical, bacteriological and physical changes occur in buried
refuse. The temperature rises to over 60 deg. C within 7 days and
kills all the pathogens and hastens the decomposition process. Then
it takes 2 to 3 weeks to cool down. Normally it takes 4 to 6 months
for complete decomposition of organic matter into an innocuous
mass. The tipping of refuse in water should not be done as it creates
a nuisance from odours given off by the decomposition of organic
matter. The method of controlled tipping has been revolutionized
by mechanisation. The bulldozer achieves the tasks of spreading
trimming and spreading top soil.
(c) Incineration
Refuse can be disposed of hygienically by burning or
incineration. It is the method of choice where suitable land is not
available. Hospital refuse which is particularly dangerous is best
disposed of by incineration. Incineration is practised in several of
the industrialized countries, particularly in large cities due to lack
of suitable land. Incineration is not a popular method in India
because the refuse contains a fair proportion of fine ash which
makes the burning difficult. A preliminary separation of dust or
ash is needed. All this involves heavy outlay and expenditure,
besides manipulative difficulties in the incinerator. Further,
disposal of refuse by burning is a loss to the community in terms of
the much needed manure. Burning, therefore, has a limited
application in refuse disposal in India.
\d) Composting Ij^KferTs
" Composting is a rhethaailof combined disposal of refuse and
nightsoil or sludge^It is a process of nature whereby organic matter
breaks down under bacterial action resulting in the formation of
relatively stable humus-like material, called the compost which has
considerable manurial value for the soi% The principal by-products
are carbon dioxide, water and heaf The heat produced during
composting - 60 deg C or higher, over a period of several daysdestroys eggs and larvae of flies, weed seeds and pathogenic agents.
The end-product -compost - contains few or no disease producing
organisms, and is a good soil builder containing small amounts of
the major plant nutrients such as nitrates and phosphates(9j. The
following methods of composting are now used :
(1)Bangalore Method (Anaerobic method)
(2)Mechanical Composting (Aerobic method)
(1) BANGALORE METHOD (Hot fermentation process)
As a result of investigations carried out under the auspices of
the Indian Council of Agricultural Research at the Indian Institute
of Science, Bangalore, a system of anaerobic composting, known
as Bangalore method (hot fermentation process) has been
developed. It has been recommended as a satisfactory method of
disposal of town wastes and nightsoil (10).
Trenches are dug 90 cm (3 ft.) deep, 1.5 to 2.5 m (5-8 ft.) broad
and 4.5 to 10 m (15-30 ft.) long, depending upon the amount of
refuse and nightsoil to be disposed of. Depths greater than 90 cm (3
ft.) are not recommended because of slow decomposition. The pits
should be located not less than 800 m (1/2 mile) from city limits.
The composting procedure is as follows : First a layer of refuse
about 15 cm (6 in) thick is spread at the bottom of the trench. Over
this, nightsoil is added corresponding to a thickness of 5 cm (2 in).
Then alternate layers of refuse and nightsoil are added in the
proportion of 15 cm (6 in) and 5 cm (2 in) respectively, till the
heap rises to 30 cm (1 ft.) above the ground level. The top layer
should be of refuse, at least 25 cm (9 in) thickness. Then the heap
is covered with excavated earth. If properly laid, a man's legs will
not sink when walking over the compost mass (10).
Within 7 days as a result of bacterial action considerable heat
(over 60 deg.C) is generated in the compost mass. This intense heat
which persists over 2 or 3 weeks, serves to decompose the refuse
and nightsoil and to destroy all pathogenic and parasitic organisms.
At the end of 4 to 6 months, decomposition is complete and the
resulting manure is a well decomposed, odourless, innocuous
material of high manurial value ready for application to the land.
The Environmental Hygiene Committee (1949) did not recommend
composting by municipalities with a population of over 100,000
(4). Bigger municipalities should install underground sewers to
transport human excreta.
(2) MECHANICAL COMPOSTING
Another method of composting known as 'Mechanical
References
1.WHO (1971). Techn. Rep. Ser., No.484
2.National Environmental Engineering Research Institute, Nagpur
EXCRETA DISPOSAL
Public health importance
Human excreta is a source of infection. It is an important cause
of environmental pollution. Every society has a responsibility for
its safe removal and disposal so that it does not constitute a threat
to public health. The HEALTH HAZARDS of improper excreta
disposal are : (1) soil pollution, (2)
water pollution,
(3)
contamination of foods and
(4) propagation of flies. The resulting diseases are typhoid and
paratyphoid fever, dysenteries, diarrhoeas, cholera, hookworm
disease, ascariasis, viral hepatitis and similar other intestinal
infections and parasitic infestations. These diseases are not
only a burden on the community in terms of sickness, mortality
and a low expectation of life, but a basic deterrent to social and
economic progress. Proper disposal of human excreta,
therefore, is a fundamental environmental health service
without which there cannot be any improvement in the state of
community health.
International cooperation
An organization was formed - the International Solid Wastes
and Public Cleansing Association (ISWA) in 1970, to assist
countries in the general endeavour to improve sanitary services. A
WHO International Reference Centre has also been set up in
Switzerland to collect, evaluate and disseminate information on
wastes-disposal practices and to foster research (9).
Public education
Refuse disposal cannot be solved without public education.
People have very little interest in cleanliness outside their homes.
Many municipalities and corporations usually look for the
cheapest solution, especially in regard to refuse disposal. What is
needed is public education on these matters, by all known methods
of health education, viz., pamphlets, newspapers, broadcasting,
films etc. Police enforcement of the laws may also be needed at
times.
(3) PAN
The pan (Fig. 7) receives the nightsoil, urine and wasr water.
The length of the pan is 42.5 cm (17 in.). The width o the front
portion of the pan has a minimum of 12.5 cm (5 in. and the width
at its widest portion is 20 cm (8 in.). There is e uniform slope from
front to back of the pan. The pan is given i smooth finish.
(1) LOCATION
The safe distance between the latrine and a source of water
supply will depend upon the porosity of the soil, level of ground
water, its slope and direction of flow. In general, it may be stated,
that latrines of any kind should not be located within 15 m (50 ft)
from a source of water supply, and should be at a lower elevation
to prevent the possibility of bacterial contamination of the water
supply. Where possible, latrines should not be located in areas
usually subject to flooding.
(2) SQUATTING PLATE
The squatting plate or slab (Fig. 6) is an important part of a
latrine. It should be made of an impervious material so that it can
be washed and kept clean and dry. If kept dry, it will not facilitate
the survival of hookworm larvae. In recommending squatting
plates, due consideration should be paid to the habits of Indian
people who defecate in the squatting position and use water for
anal washing. The slab of the RCA latrine has been designed to
meet the above needs. It is made of cement concrete with minimum
dimensions of 90 cm (3 ft) square and 5 cm (2 in.) thickness at the
outer edge. There is a slope 1/2 inch towards the pan. This allows
drainage into the latrine of the water used for ablution or cleansing
purposes. A circular squatting plate of 90 cm (3 ft.) diameter and of
5 cm (2 in.) uniform thickness, has also been found satisfactory.
For the convenience of the users, raised footrests are included in
the squatting plate.
(4) TRAP
The trap (Fig. 8) is a bent pipe, about 7.5 cm (3 in.) ir diameter
and is connected with the pan. It holds water anc provides the
necessary 'water seal'. The water seal is th< distance between the
level of water in the trap and the lowes point in the concave upper
surface of the trap. The depth o the water seal (AB) in the RCA
latrine is 2 cm (3/4 in.) (Fig. 8) The water seal prevents the access
by flies and suppresses th< nuisance from smell.
FIG.
8
Trap
(5) CONNECTING PIPE
When the pit is dug, away from the squat plate, the trap i
connected to the pit by a short length of connecting pipi 7.5 cm (3
in.) in diameter and at least 1 m (3 ft.) in length witl a bend at the
end (Fig. 9).
A latrine of this type is called the Indirect type because thi pit
is sited away from the squatting plate. In the direct typi there is no
need for a connecting pipe (Fig. 5). The direct typi is best suited
for areas where the ground is hard and does no
easily cave in. The direct type is cheaper and easier to construct and occupies less space (1). An advantage with the indirect type is that
when the pit fills up, a second pit can be put into operation by merely changing the direction of the connecting pipe. Therefore, the
for men and women. The earth from the trench should be piled up
at the side. People should be instructed to cover faeces with earth
each time they use the latrine. However, these instructions may not
be carried out, and it will be necessary to post sweepers in
attendance to do this work. Ablution water should be provided.
The shallow trench is a rudimentary arrangement for a short period
(up to one week). When the trench is filled to 30 cm (12 in.) below
ground level, it must be covered with earth, heaped above ground
level and compacted; if necessary, a new trench must be dug (8).
DEEP TRENCH LATRINE
This type of latrine is intended for camps of longer duration,
from a few weeks to a few months. The trench is 1.8 to 2.5 m (6-8
ft.) deep and 75-90 cm (30-35 in.) wide. Depending upon the local
customs, a seat or a squatting plate is provided. A superstructure is
built for privacy and protection. Other requirements are the same
as for shallow trench latrine (8).
WATER CARRIAGE SYSTEM
FIG. 11
Aqua privy
Night soil undergoes purification by anaerobic digestion. Since
there is evolution of gases, a vent should be provided for the escape
of gases into the atmosphere, the vent should be open above the
roof of dwellings. The effluent is far from innocuous. It contains
finely divided faecal matter in suspension and may carry parasitic
and infective agents. It should be treated in the same manner as the
effluent from a septic tank by sub-soil irrigation or absorption. The
digested sludge which accumulates in the tank should be removed
at intervals.
SULABH SHAUCHALAYA
The "Sulabh Shauchalaya" model, the invention of a Patnabased firm, is a low cost pour-flush, water-seal type of latrine,
which is now being used in many parts of India. Basically it is an
improved version of the standard handflush latrine (e.g., RCA
type). It consists of a specially designed pan and a water-seal trap.
It is connected to a pit 3 feet square and as deep. Excreta undergoes
bacterial decomposition and is converted to manure (compost). The
method requires very little water.
Sulabh International, the investors, not only build but also
maintain the system of Sulabh Community Latrines. Their usual
structure is a lavatory block of several dozen seats, with a bathing
block adjoining. The system is to charge Rs. 1 per user (who is
given soap powder by the Sulabh attendant after use). Recently
Delhi has opted for this system in all its slums. This system has
drawn praise from ecologists and planners.
CHEMICAL CLOSET
It has very limited use under Indian conditions. The closet
consists of a metal tank containing a disinfectant fluid. The active
ingredients of the fluid are formaldehyde and quaternary
ammonium compounds. In addition, a harmless water dye and a
deodorizing substance are usually incorporated (6). A seat with a
cover is placed directly over the tank. Nothing except the toilet
paper should be thrown into the chemical closet.
SHALLOW TRENCH LATRINE
This is simply a trench dug with ordinary tools. The trench is
. 30 cm (1 ft.) wide and 90-150 cm (3-5 ft.) deep. Its length
depends on the number of users : 3-3.5 m (10-12 ft.) are
necessary for 100 people. Separate trenches should be provided
2 House drain
be classified as high level, low level and integrated depending
upon the height of location above the water closet bowl or pan.
The Indian squatting type W.C. pans are used with a high level
flushing cisterns.
_______________________________________
SEWAGE 569
Composition of sewage
jCVl^ewage contains 99.9 per cent of water. The solids which
Comprise barely 0.1 per cent are partly organic_^rTd_partly
inorganic; they are partly in suspension and partly in solution. The
offensive nature of the sewage is mainly due to the organic matter
which it contains"!) The organic matter decomposes according to
the laws of nature during which process it gives off offensive
odours. In addition, sewage is charged with numerous living
organisms derived from faeces, some of which may be agents to
disease. It is estimated that one gram of faeces may contain about
1,000 million of E. coli, 10 to 100 million of faecal streptococci, and
1 to 10 million spores of CI. perfringens besides several others. The
average adult person excretes daily some 100 grams of faeces.
Aim of Sewage Purification
Raw sewage or inadequately treated sewage should not be
discharged into rivers, sea or other sources of water supply. This is
because, the oxygen in the water supply is used up by the
numerous aerobic bacteria found in the sewage. Depletion of
oxygen may lead to the death of the plant and animal life in water.
Furthermore, the water may yield an offensive smell because of the
release of hydrogen sulphide.
The aim of sewage treatment is to "stabilize" the organic
matter so that it can be disposed off safely; and, to convert the
sewage water into an effluent of an acceptable standard of
purity which can be disposed of in to land, rivers or sea. A
standard test which is an indicator of the organic content of the
sewage is biochemical oxygen demand (BOD).
%of The "strength" of the sewage is expressed in terms of
W BIOCHEMICAL OXYGEN DEMAND (BOD) : It is the most
/.important test done on sewage. It is defined as the amount of
oxygen absorbed by a sample of sewage during a specified
^period, generally 5 days, at a specified temperature, generally
j/20 deg.C for the aerobic destruction or use of organic matter
by living organisms (10). BOD values range from about 1 mg
per litre for natural waters to about 300 mg per litre for
untreated domestic sewage. If the BOD is 300 mg/1 and above,
sewage is said to be "strong"; if it is 100 mg/1, it is said to be
"weak" (b) CHEMICAL OXYGEN DEMAND (COD) : The COD
test measures the oxygen equivalent of that portion of the
organic matter in a sample which is susceptible to oxidation by
a strong chemical oxidiser. If wastes contain toxic substances,
this test may be the only practical method for determining the
organic load, (c) SUSPENDED SOLIDS : The suspended solids
are yet another indicator of the "strength" of sewagej The
amount of suspended solids in domestic sewage may vaiy from
Secondary Treatment
Primary Treatment
Screen
Sewage
Primary
Sedimentation
Tank
Grit
Chamber
f
1
1
Biological
Treatment
1
1
Final
Sedimentation
Tank
Chlorine
Effluent Disposal
"T
oxygen and can cause pollution of soil or water. It is subjected to further treatment, aerobic oxidation, by one of the following methods :
(a)Trickling Filter Method
(b)Activated Sludge Process
(a) TRICKLING FILTER
The trickling filter or percolating filter is a bed of crushed stones or cinker, 1 to 2 m (4-8 ft.) deep and 2 to 30 m (6-100 ft.) in diameter,
depending upon the size of the population. The effluent from the primary sedimentation tank is sprinkled uniformly on the surface of the
bed by a revolving device. The device consists of hollow pipes each of which have a row of holes. The pipes keep rotating, sprinkling the
effluent in a thin film on the surface of the filter. Over the surface and down through the filter, a very complex biological growth consisting
of algae, fungi, protozoa and bacteria of many kinds occurs. This is known as the "zoogleal layer". As the effluent percolates through the
filter bed, it gets oxidized by the bacterial flora in the zoogleal layer. The action of the filter is thus purely a biological one, and not one of
filtration as the name suggests. The term "filter" is a misnomer. The trickling filters are very efficient in purifying sewage. They do not
need rest pauses, because wind blows freely through the beds supplying the oxygen needed by the zoogleal flora. The biological growth or
zoogleal layer lives, grows and dies. The dead matter sloughs off, breaks away and is washed down the filter. It is a light green, flocculent
material and is called "humus". The oxidized sewage is now led into the secondary sedimentation tanks or humus tanks.
(b) ACTIVATED SLUDGE PROCESS
^NlAjctivated sludge process (Fig. 14) is the modern method of rifying sewage, in place of the trickling filter. The "heart" of the activated
sludge process is the aeration tank. The effluent from the primary sedimentation tank is mixed with sludge drawn from the final settling
tank (also known as activated sludgeoxreturn sludge; this sludge is a rich culture of aerobic bacteriaj^The proportion of activated sludge to
the incoming effluent is of the order of 20 to 30 per cent. The mixture is subjected to aeration in the aeration chamber for about 6 to 8 hours
(10).\The aeration is accomplished either by mechanical agitation or by forcing compressed air continuously from the bottom of the aeration
tank. This latter method, also known as 'diffuse aeration' is considered a better method of aeration. During the process of aeration, the
organic matter of the sewage gets oxidized into carbon dioxide, nitrates and water with the help of the aerobic bacteria in the activated
sludge. The typhoid and cholera organisms are definitely destroyed, and the coliforms greatly reduced) Activated sludge plants occupy less
space, require skilled operations. One acre of activated sludge plant does the work of 10 acres of percolating filter. Activated sludge process
is therefore, best suited for
larger cities and the percolating filter for smaller towns because they are cheaper to install and easier to operate.
Secondary sedimentation
The oxidized sewage from the trickling filter or aeration chamber is led into the secondary sedimentation tank where it is detained for
2-3 hours. The sludge that collects in the secondary sedimentation tank is called 'aerated sludge' or activated sludge, because it is fully
aerated. It differs from the sludge in the primary sedimentation tank in that it is practically inoffensive and is rich in bacteriae, nitrogen and
phosphates. It is a valuable manure, if dehydrated. Part of the activated sludge is pumped back into the "aeration tanks" in the activated
sludge process and the rest pumped into the sludge digestion tanks for treatment and disposal.
Sludge digestion
One of greatest problems associated with sewage treatment is the treatment and disposal of the resulting sludge. One million gallons of
sewage produces 15-20 tons of sludge. The sludge is a thick, black mass containing 95 per cent of water, and it has a revolting odour.
There are a number of methods of sludge disposal : (a) Digestion : Modern sewage treatment plants employ digestion of sludge as the
method of treatment. If sludge is incubated under favourable conditions of temperature and pH, it undergoes anaerobic auto-digestion in
which complex solids are broken down into water, carbon dioxide, methane and ammonia. The volume of sludge is also considerably
reduced. It takes 3-4 weeks or longer for complete sludge digestion. The residue is inoffensive, sticky and tarry mud which will dry readily
and form an excellent manure. Sludge digestion is carried out in special tanks known as "sludge digestion tanks". Methane gas, which is a
byproduct of sludge digestion, can be used for heating and lighting purposes, (b) Sea Disposal: Sea coast towns and cities can dispose of
sludge by pumping it into the sea (c) Land : Sludge can be disposed of by composting with town refuse.
Disposal of effluent
(a) Disposal by dilution : Disposal into water courses such as rivers and streams is called 'disposal by dilution'. The effluent is diluted
in the body of water and the impurities are oxidized by the dissolved oxygen in water. The diluting capacity of the river or the receiving
body of water and its dissolved oxygen contents, are important considerations before discharging the effluent into a river or any body of
water. Since people use river water for drinking purpose, the effluent must be rendered free from pathogenic organisms by adequate
chlorination. The Royal Commission in England in its Fifth Report (1908) recommended that an effluent from a sewage treatment plant
should not have more than 30 mg/litre of suspended solids and the 5 day B.O.D. of the effluent including the suspended matter, should
not exceed 20 mg/litre. These standards
13
by
of
day
the
The
may
In
to
Raw sewage should never be discharged into rivers. The present day practice is to purify the sewage before it is discharged into
rivers. How far the sewage should be purified depends upon the dilution the river provides to carry on
and water. The algae, with the help of sunlight, utilise the carbon dioxide, water and inorganic minerals for their growth, Thus there is a
mutually beneficial biological balance between the algae and bacteria in oxidation ponds. Oxygen that is needed for oxidation is derived to
a small extent from the atmosphere but mostly from the algae which liberates oxygen under the influence of sunlight. Consequently,
sunlight is an important factor in the proper functioning of oxidation ponds. Cloudy weather definitely lowers the efficiency of the process.
The oxidation ponds are predominantly aerobic during sunshine hours as well as some hours of the night. In the remaining hours of the
night, the bottom layers are generally anaerobic. Thus the sewage purification in oxidation ponds is brought about by a combination of
aerobic and anaerobic types of bacteria. The effluent may be used for growing vegetable crops (land irrigation) or may be discharged into a
river or other water courses after appropriate treatment. Mosquito nuisance is avoided by keeping weed growth in the neighbourhood of
oxidation ponds to a minimum and the water line free from marginal vegetation. There is no odour nuisance associated with these ponds
when they are properly maintained. Oxidation ponds have become an established method of purifying sewage for small communities.
(e) Oxidation ditches
Other methods recommended are (1) oxidation ditches and (2) aerated lagoons. These methods make use of mechanical rotors for
extended aeration. For treatment of the wastes of a population between 5,000 to 20,000 an oxidation ditch requires an area of one acre as
compared to 22 acres for an oxidation pond and 2.5 acres for an aerated lagoon. These are low-cost treatment methods for the purification
of sewage.
SOCIAL ASPECTS OF EXCRETA DISPOSAL IN INDIA
India is a land of villages and about 74 per cent of its population lives in villages. The problem of sanitation therefore is one of "Rural
sanitation". Surveys have shown that 90 per cent of the population "go to the open fields" for defecation. This habit of indiscriminate
fouling of the surroundings with human excrement is generations-old, and rooted firmly in the cultural behaviour of the Indian village
people.
In urban areas, the latrine is considered a necessary part of a house. In rural areas, by and large, people have not accepted latrines with
any enthusiasm, and even when installed only a few used them regularly. The problem in rural sanitation is how to overcome the resistance
of the village people, and induce them to use sanitary latrines. Research studies have indicated that there is only one way to solve the
problem, i.e., through health education. Social scientists have listed the reasons why villagers do not accept latrines. Some of the reasons
found in the surveys are : (1) latrines are associated with bad smell (2) they are the breeding places of flies (3) they are something foul and
dirty so that one should not have them close to houses
(1)latrines are costly and beyond their means to install, and
(2)they do not know how faecal-borne diseases are spread. In short, people have a bad "image" of latrines in their minds. Secondly, using a
latrine goes against a DAILY habit pattern of going to the fields. The use of latrines involves a drastic change in the day to day behaviour
of a large number of people.
The solution to the problem lies in teaching the people first the reasons why latrines are important. The teaching should be undertaken
by all known methods of health education - direct discussion, group discussion, latrine demonstration, and use of visual aids and above all
service facilities. The ultimate goal of health education will be to motivate the rural people towards acceptance and use of sanitary latrines.
MEDICAL ENTOMOLOGY
Arthropods comprise the most numerous and varied of the living things
in the environment of man. Some of them are man's allies helping in the
fertilisation of flowers, but the majority of arthropods, in general, are either
of no use to man or his most dangerous enemies. They destroy man's crops
and his food reserves; and some which live close to man act as vectors or
carriers of disease. A study of the arthropods of medical importance is
known as medical entomology which is an important branch of preventive
medicine.
G\3
1. Mosquitoes:
Anophelines
Culicines
1.Flies:
Houseflies
Sandflies
flies
mite
1. Ticks:
Hard ticks
Soft ticks
(JZ
Diseases transmitted
1.
Mosquito
2.
Housefly
3.
Sandfly
s^f^^
Arthropod
TABLE 1
Class:
Insecta
vXTABLry^
Class:
Crustacea
1. Cyclops
2. Mites (Chiggers):
Leptotrombidium
and trombiculid Tsetse
mites; Blackflies
Itch
1.Tsetse fly
Sleeping sickness
2.Louse
6.
Rat flea
1.Blackfly
Onchocerciasis.
4.Reduviid bugs
2.Reduviid bug
Chagas disease.
3.Hard tick
1.Soft tick
Distinctive characters
The distinctive characters of the above arthropods are as given in Table
2.
TABLE 2
Distinctive characters of arthropods of medical importance
1. Body
divisions
Insecta
Arachnida
Head,
thorax
abdomen
Cephalothorax
Cephalothorax
and abdomen (no and abdomen
division) in some
cases
2.Trombiculid mite
Crustacea
2. Legs
3 pairs
4 pairs
5 pairs
3. Antennae
1 pair
None
2 pairs
4. Wings
One or two
pairs; some
are wingless
None
None
5. Where found
On land
On land
In water
Arthropod-borne diseases
Arthropod-borne diseases constitute a major health problem in
India. Malaria continues to be an important vector-borne disease with an
annual morbidity of 4 to 5 million cases^j Filaria is another important
arthropod-borne disease with anr estimated 236 million people living in
filaria-endemic areas.
3.Itch-mite
Scabies.
4.Cyclops
14.
Enteric pathogens.
Cockroaches
(4) Genetic control: Much progress has taken place in recent years
in the theoretical and applied aspects of genetic control of
arthropods. The WHO/ICMR Research Unit at New Delhi has
contributed massively to the techniques of genetic control of
mosquitoes (3). Techniques such as sterile male technique,
cytoplasmic incompatibility and chromosomal translocations have
been found to be effective in small field trials. In conclusion, it
may be stated that these methods are nowhere near the stage where
they can be used large-scale in an effective way. (5) Newer
methods : New and innovative methods are being sought for pest
control. These are (a) insect growth regulators (b) chemosterilants,
and (c) sex attractants or pheromones (4).
Integrated approach
Since no single method of control is likely to provide a solution
in all situations, the present trend is to adopt an "integrated
approach" for vector control combining two or more methods with
a view to obtain maximum results with the minimum effort and to
avoid the excessive use of any one method (5).
MOSQUITO
General description
Mosquitoes constitute the most important single family of
insects from the standpoint of human health. They are found all
over the world. The four important groups of mosquitoes in India
which are related to disease transmission are the Anopheles, Culex,
Aedes and Mansonia.
The body of a mosquito consists of three parts : head, thorax
and abdomen, (a) HEAD : The head is semi-globular in outline,
and bears the following structures :- (i) a pair of large compound
eyes (ii) a long needle-like structure, called the proboscis with
which the mosquito bites (iii) a pair of palpi, each a four-jointed
structure, situated on either side of the proboscis and (iv) a pair of
antennae or feelers. The antennae are bushy in the male, and not
quite so in the female. They provide an easy means of
distinguishing the male from the female (b) THORAX : The thorax
is large and rounded in appearance and bears :- (i) a pair of wings
dorsally (ii) three pairs of legs ventrally. The wings of the mosquito
are characterised by a fringe of scales on the posterior border and
the first, third and sixth veins on the wings are not branched. When
the mosquito is at rest, the wings are folded. The buzzing noise
which the mosquitoes produce is due to the beating of their wings,
and not to "singing", (c) ABDOMEN : The abdomen is long and
narrow and is composed of 10 segments, the last two of which are
modified to form the external genitalia.
Life history
There are four stages in the life history of mosquitoes (Fig. 1):
egg, larva, pupa and adult. Metamorphosis is complete.
(1) EGG : Eggs are laid on the surface of water, 100-250 at a
time. The Anopheles lays her eggs singly; the eggs are boat-shaped
and possess lateral floats. The Culex lays her eggs in small clusters
or rafts; the eggs do not possess lateral floats. The Aedes lays her
eggs singly; the eggs are cigar-shaped and do not possess lateral
floats. The Mansonia lays her eggs in star-shaped clusters attached
to the under-surface of the leaves of certain aquatic plants, notably
the pisita plant. Under favourable conditions, the egg stage of
mosquitoes lasts for 1-2 days. The period that elapses from the
moment a blood meal is taken until the eggs are laid is called the
"gonotrophic cycle", it is about 48 hours in hot and humid tropical
areas.
(1)LARVA : The larva is a free swimming creature with an elongated body divisible into head, thorax and abdomen. It feeds on algae,
bacteria and vegetable matter and passes through four stages of growth called "instars" with moulting between each stage. The larva of the
Anopheles floats horizontally in the water, and has no siphon tube at the tip of its abdomen. The Culicine (e.g., Culex, Aedes, and
Mansonia) larvae, in contrast, are suspended in water with their heads downwards; they all possess a siphon tube, which is situated on the
8th abdominal segment. The larvae of the Mansonia are peculiar in the respect they are attached to the rootlets of certain aquatic plants by
their siphon tubes; they obtain air from the plant rootlets. The larval stage occupies 5-7 days.
(2)PUPA : The pupa is comma-shaped in appearance, with a large rounded cephalothorax and a narrow abdomen. Two small respiratory
tubes or trumpets project from the upper surface of the thorax. The pupa represents the resting stage in the life history of the mosquito; it
does not feed but prefers to stay quiet at the water surface. But when disturbed it swims rapidly downwards into the water. The pupal stage
lasts for 1 -2 days.
(3)ADULT : When the development is complete, the pupal skin splits along the back and the adult mosquito or imago emerges. It rests for
a while on the pupal skin to allow its wings to expand and harden and then flies away. Under favourable conditions of temperature and
food supply the life cycle from the egg to adult is complete in 7-10 days. Normally the adult mosquito lives for about 2 weeks. The males
are generally short-lived.
Differentiation between anophelines and culicines
There are two main tribes of mosquitoes - Tribe Anophelini and Tribe Culicini. The tribe anophelini contains only one genus, Anopheles.
The tribe Culicini is represented in India by 15 genera of which the important ones are Culex, Aedes and Mansonia. The main points of
difference between the two tribes, Anophelini and Culicini ate as given in Table 4 (See Fig. 2).
(1) Anopheles
Some 45 species of anopheles mosquitoes have been found in India but only a few of them have been incriminated as vectors or carriers of
malaria. They are (1) An. culicifacies
(2) An.
fluuiatilis
(3)
An.
minimus
(4)
An.
philippinensis
(5)
An.
stephensi
(6)
An.
sundaicus
and
(7)
An.
leucosphyrus.
The
areas
of
distribution
of
these
mosquitoes
are
different:
An.
fluuiatilis
and
An.
minimus
are
found
in
the
foot-hill
regions;
An.
sundaicus
and
An.stephensi
are
found
in
the
coastal
regions;
and
,
An.
culicifacies
and
An.
philippinensis
are
found
in
the
plains.
An
accurate
guide
to
the
identification
of
the
known
species
of
anopheles mosquitoes in India may be found in Health Bulletin
NoAO entitled : "Synoptic Table for the Identification of the
Anopheles Mosquitoes in India (6)."
TABLE 4
Differentiation between anophelini and culicini
Tribe
Genus
Anophelini Anopheles
EGGS
MOSQUITO 57
37
facilitate and the total number of houses examined in that area" (8 This index
s
/itsis kept at zero at all ports.
eradicati
on^
(4) Mansonia
Under
The mosquitoes of this genus are big, black or brow mosquitoes
the
with speckling on their wings and legs. Th common Indian species
WHO are : M. annulifera, M. uniformis, JV indiana and M. longipalpis.
Internati The mansonoides mosquitoes ai peculiar in their breeding habits.
onal
They breed in ponds an lakes containing certain aquatic plants,
Health especially the floatin types like Pistia stratiotes and water hyacinth.
Regulati The eggs are lai in star-shaped clusters on the under-surface of the
ons
leaves c these aquatic plants. The larvae and pupae are found
(IHR), attache to the rootlets of these plants by their siphon tubes; they
all
obtai their air supply from these rootlets. When about to becom
internati adults, the pupae come to the surface of water and the full formed
onal
adults emerge and escape. The control of mansonoide mosquitoes is
airports easy by the removal or destruction of the aquati host plants by
and
herbicides.
seaports
are kept
free
from all
types of
mosquit
oes for a
distance
of 400
metres
around
the
perimete
r of the
ports.
Under
the
Internati
onal
Health
Regulati
ons,
Aedes
aegypti
index is
defined
as "the
ratio,
expresse
d
as
percenta
ge,
between
the
number
of
houses
in
a
limited
welldefined
area on
the
premises
of which
actual
breeding
of Ae.
aegypti
are
found,
Mosquito-borne diseases
Apart from their pestiferous nature, mosquitoes play an important role
in the transmission of human disease. They act as vectors of many
diseases in India : (Table 5).
TABLE 5
Mosquito-borne diseases in India
Type of mosquito
Disease
1.
Anopheles
Malaria
Filaria (not in India)
2.
Culex
Bancroftian filariasis
Japanese encephalitis
West Nile fever Viral
arthritis
(epidemic/polyarthritis)
3.
Aedes
4. Mansonoides
1. ANTI-LARVAL MEASURES
(a) Environmental control
The most important step in reducing the numbers of mosquitoes is to
eliminate their breeding places. This is known as "source reduction", and
comprises minor engineering methods such as filling, levelling and
drainage of breeding places; and water management (such as intermittent
irrigation). These are proven methods of larval control. Source reduction
also implies rendering the water unsuitable for mosquito breeding, as for
example, changing the salinity of water. Source reduction requires an
accurate knowledge of the breeding habits of mosquitoes. If Culex
mosquitoes are a problem, there should be a programme for the abolition
of domestic and peridomestic sources of breeding such as cesspools and
open ditches; and arrangements should be made for adequate collection,
removal and disposal of sewage and waste water. If Aedes mosquitoes are
a problem, the environment should be cleaned up and got rid of water
holding containers such as discarded tins, empty pots, broken bottles,
coconut shells and similar other artificial collections of water. If
Anopheles mosquitoes are a problem, their breeding places should be
looked for and abolished by appropriate engineering measures such as
filling and drainage. If Mansonia mosquitoes are a problem, the aquatic
plants to which the larvae attach themselves should be removed or
destroyed by herbicides. Source reduction methods generally produce
results that are permanent.
(b) Chemical control
The commonly used larvicides are :
(i)
Mineral oils
Dosage (g/ha)
Abate
56-112
Malathion
Fenthion
Chloropyrifos
224-672
22-112
11-16
Biological control
A wide range of small fish feed readily on mosquito larvae. The
best known are the Gambusia affinis and Lebister reticulatus
(sometimes known as Barbados Millions). These fish can be used
in burrow pits, sewage oxidation ponds, ornamental ponds, cisterns
and farm ponds. In recent years, there has been a revival of interest
in the biological control of mosquitoes through the use of fish (11).
It is however recognised that biological control can be effective
only when used in conjunction with other methods.
Ill fa\
. ANTI-ADULT MEASURES
ri (a) Residual
frV sprays
TABLE 7
Toxicants suitable against malaria vectors as residual spray
applications
Toxicant
Dosage in g/m2
Average Duration of
effectiveness
(months)
DDT
Lindane
Malathion
OMS-33
lto2
0.5
2
2
6 to 12
3
3
3
(\c) Repellents
fj^iM ^(nty
colour. The body is divided into head, thorax and abdomen. (1)
HEAD : The head bears a pair of antennae, a pair of large
compound eyes and a retractile proboscis, which is adapted for
sucking liquid foods. The eyes of the male are close together; those
of the female are set apart widely. (2) THORAX : The thorax is
marked with 2 to 4 dark longitudinal stripes, which is characteristic
of the genus, musca. The thorax bears a pair of wings and three
pairs of legs. Each leg is provided with a pair of pads which enable
the fly to walk on highly polished surfaces. The legs and the body
are covered with numerous short and stiff hairs, called the tenent
hairs which secrete a sticky substance. (3) ABDOMEN : The
abdomen is segmented and shows light and dark markings.
Life history
The housefly undergoes a complete metamorphosis with four
stages in its life cycle : egg, larva (maggot), pupa and adult (Fig.3).
(1) EGG : The female lays from about 120 to 150 eggs at one
sitting in moist decaying organic matter such as human and animal
excreta, manure heaps, garbage and vegetable
The fly lays from 600 to 900 eggs during her life time. The eggs
hatch in 8 to 24 hours; during summer, in India, they may hatch
within 3 hours. (2) LARVA : The larvae or maggots measure 1 to 2 mm
in length at birth. They are white, segmented and footless with a narrow anterior end,
and a broad posterior end. They eat voraciously and moult twice in the course of
development. The full grown /arva may measure up to 12 mm in length. The
larvae resent light; they bury
Habits
The habits of housefly make it eminently suited for the spread
of disease. (1) BREEDING HABITS : The most important
breeding places of flies in order of importance are (a) fresh horse
manure (b) human excreta fc) manure of other
(f) rubbish dumps containing organic matter and (g) ground where
liquid wastes are spilled. (2) FEEDING HABITS : The housefly
does not bite. It is attracted to food by its sense of smell. It cannot
eat solid foods; it vomits on solid food to make a solution of it and
sucks in a liquid state. Adult flies delight in sputum, faeces,
discharges from wounds and open sores. (3) RESTLESSNESS :
The fly is a restless insect and moves back and forth between food
and filth. This helps in the spread of infection mechanically. (4)
VOMIT DROP : The fly vomits frequently. The "vomit drop" is
often a culture of disease agents. (5) DEFECATION : The housefly
has the habit of defecating constantly all the day. Thus it deposits
countless bacteria on exposed food. (6) RESTING HABITS : Flies
have a tendency to rest on vertical surfaces and hanging objects. They have a
tendency to fly towards light. (7) DISPERSAL : Normally houseflies remain
close to their breeding places, but they disperse frequently up to 4
miles, and sometimes even more from the point of their origin.
Transmission of disease
Flies are potential vectors of many diseases : typhoid and
_________________________________________HOUSEFLIES
581
5. Health education
It is difficult to achieve fly control without the willing cooperation of the people. A "fly consciousness" should be created
among the people, through health education. Fly control
campaigns require organised individual and community effort
which is the basis of a successful public health programme. It is
only through health education that people can be motivated with a
desire to get rid of flies permanently.
SANDFLIES
Sandflies are small insects, light or dark-brown in colour. They
are smaller than mosquitoes, measuring 1.5 to 2.5 mm in length
with their bodies and wings densely clothed with hair. Some 30
species of sand-flies have been recorded in India. The important
ones are : Phlebotomus argentipes, P. papatasii, P. sergenti, and
Sergentomyia punjabensis. Our knowledge of the Indian sandflies
is meagre, and needs more studies (19).
General characters
The body of a sandfly is divided into head, thorax and
abdomen, (1) HEAD : The head bears a pair of long, slender and
hairy antennae; palpi and a proboscis. Only the females bite, the
males live on vegetable juices. (2) THORAX : The thorax bears a
pair of wings and three pairs of legs. The wings are upright,
lanceolate in shape and densely hairy. The second longitudinal
vein on the wings branches twice, the first branching takes place in
the middle of the wing. This is a characteristic feature of the genus,
Phlebotomus. The legs are long and slender and out of proportion
to the size of the body. (3) ABDOMEN : The abdomen has 10
segments and is covered with hair. In the female, the tip of the
abdomen is rounded; in the male, there are claspers, which are
conspicuous and attached to the last abdominal segment.
Sandflies may be distinguished from mosquitoes by the
following characteristics : (1) Size : Sandflies are smaller than
mosquitoes. (2) Wings : The wings of the sandfly are up-right and
lanceolate in shape; the second longitudinal vein branches twice,
the first branching taking place in the middle of the wing. (3) Legs
: The legs of the sandfly are longer compared with the size of the
body. (4) Hairs : Sandfly is a hairy insect. (5) Hopping: Sandflies
hop about, and do not fly by choice.
Life history
The life history of the sandfly is characterised by complete
metamorphosis, having four stages : egg, larva, pupa and adult
(Fig. 4).
(1) EGG : The eggs are laid in damp dark places in the vicinity
of cattle sheds and poultry. The eggs are comparatively large, and
torpedo-shaped with longitudinal wavy lines on the outside. The
eggs hatch within 7 days. (2) LARVA : The larvae are hairy
maggots with a distinct head, thorax and abdomen. The last
abdominal segment carries two pairs of long stout hairs; one pair is
remarkably long. The larva feeds on decaying organic matter and
becomes a pupa in about 2 weeks. (3) PUPA : The pupal stage lasts
for about 1 week. (4) ADULT : The average life of a sandfly is
about 2 weeks.
Habits
Sandflies are' troublesome noctural pests. Their bite is irritating
and painful, while their presence is scarcely observed. They infest
dwellings during night, and take shelter during day in holes and
crevices in walls, holes in trees, dark rooms, stables and store
rooms. The females alone bite, as they require a blood meal every
third or fourth day for oviposition. Sandflies are incapable of
flying over long distances; they merely hop about from one place
to another. Sandflies are generally confined to within 50 yards of
their breeding places.
FIG. 5
Tsetse fly
Diseases transmitted
SPECIES
Phlebotomus argentipes
Phlebotomus papatasii
Phlebotomus sergenti
S. punjabensis
DISEASES CARRIED
Kala-azar
Sandfly fever
Oriental sore
Oriental sore
Sandfly fever
Control of sandflies
Sandflies are easily controlled because they do not move long
distances from the place of their breeding. (1) INSECTICIDES :
Resistance to DDT has not been demonstrated. A single
application of 1 to 2 g/m2 of DDT or 0.25 g/m2 of lindane has been
found effective in reducing sandflies. DDT residue may remain
effective for a period of 1 to 2 years, and lindane only for a period
of 3 monthsflZ,). Spraying should be done in the human dwellings,
cattle sheds and other places. (2) SANITATION : Sanitation
measures such as removal of shrubs and vegetation within 50 yards
of human dwellings, filling up cracks and crevices in walls and
floors, and location of cattle sheds and poultry houses at a fair
distance from human habitations should receive attention.
TSETSE FLIES
Tsetse flies or the Glossinae are bloodsucking flies, which
present a general resemblance to the common housefly. They are
yellow or dark-brown in colour, and measure about half an inch
long. Their wings, when folded, overlap each other like the blades
of a scissors. They have a proboscis which is rigid and nonretractile and adapted for piercing the skin and sucking blood.
Tsetse flies are only found in African continent. Regions infested
with tsetse flies are called "fly belts". For centuries, the tsetse fly
has ravaged vast areas of tropical Africa, and hampered economic
and social progress; it continues to be a menace even today.
Life history
The life history of the tsetse fly is somewhat abnormal. The
female does not lay eggs, but gives birth to a living larva, one at a
time, at 10-day intervals. The female produces only a few
LICE
Lice are small wingless ectoparasites of mammals and birds.
They bite severely and are annoying pests. The lice that infest man
are of three kinds : head louse (Pediculus capitis), body louse
(Pediculus corporis), and pubic or crab louse (Phthirus pubis).
Human lice occur in all parts of the world wherever standards of
hygiene are low, but people in colder climates are affected more
frequently than those in warmer regions. Infestation by lice is
called pediculosis.
Head and body lice
The head and body lice differ very little in structure except in
their habitat. The head lice inhabit the hairs of the scalp, and the
body lice occur mainly in the seams of clothing and on the bodies
of the hosts. The body of a louse is flattened dorso-ventrally, and
is divided into head, thorax and abdomen. (1) HEAD : The head is
pointed in front and bears a pair of 5-jointed antennae. The mouth
parts are adapted for sucking blood. (2) THORAX : The thorax is
a fused mass and is shaped somewhat like a square. Three pairs of
legs are attached ventrally to the thorax. The legs are strongly
developed and are provided with claws which help the insect to
cling to the hair and clothing. (3) ABDOMEN : The abdomen is
elongated and consists of 9 segments. The last abdominal segment
is pointed in the case of males, and bilobed in the case of females.
Life history
There are three stages in the life history of lice : egg, larva and
adult. Metamorphosis is gradual (Fig. 7).
(1) EGG : The eggs, called "nits" are laid singly or in groups,
firmly attached to the hair or seams of clothing by a cementing
substance. The eggs are small, white ovoid bodies, pointed at one
end and truncated and pitted at the other end. A female lays up to
300 eggs at the rate of 4 to 9 a day. Under favourable conditions
of temperature, the eggs will hatch in 6 to 9 days. The eggs will
not hatch if the temperature is below 22 deg. C (71.6 deg.F). (2)
LARVA OR NYMPH : The larva looks very much like an adult,
except for its smaller size. It feeds on the host and develops into
an adult after passing through 3 moults. The larval stage may take
10 to 15 days. (3) ADULT : The entire life cycle from the laying
of an egg to the appearance of the adult louse takes about 15 to 17
days under favourable conditions. Adult lice live from 30 to 50
days.
Dissemination
(1) DIRECT CONTACT : Lice are disseminated by close
contact with lousy or infested persons. Overcrowding provides an
excellent opportunity for the direct transference of lice from one
person to another. Children get easily infested at school when their
heads come together at work or play. (2) INDIRECT CONTACT :
Lice may also be acquired from clothing, bedding, combs or
brushes used by lousy persons. Lice have been seen to be blown by
puffs of wind from heavily infested persons. Lice tends to leave the
host whose temperature rises above or falls below the normal.
, Lice and disease
MfAH^ n$]
Lice are vectors of the following disuses :
DISEASE
1.Epidemic typhus
2.Relapsing fever
3.Trench fever
4.Dermatitis
CAUSATIVE AGENT
Rickettsia prowazeki
Borrelia recurrentis
Rickettsia quintana
Due to scratching and
secondary infection
Crab louse
The crab louse or pub ic louse (Phthirus pubis) is generally
found in the pubic and perineal region, but at times it may occur in
the other parts of the body as well. It adheres close to the skin, and
its removal is a matter of difficulty. The crab louse has a
characteristic body form, and is readily recognised by (1) its small
size and square body, (2) head impacted on the thorax, (3) the
relatively enormous and powerful legs and claws, (4) the first pair
of legs slenderer than others and, (5) its extreme inertness. It does
not move very much from the site of its birth. The life cycle of crab
louse is similar to that of head or body louse. The crab louse has
not been proved to carry any disease (Fig. 8).
Rat Fleas:
(Oriental)
1.Rat Fleas
(Temperate zone)
2.Human Fleas
3.Dog and Cat Fleas
5.
Xenopsylla cheopis
XenopsyUa astia
XenopsyUa braziliensis
Nosopsylla fasciatus
Pulex irritans
Ctenocephalus canis
Ctenocephalus felis
Tunga penetrans
Sand Fleas
(Jigger or Chigoe fleas)
The rat fleas are of greatest importance because they are vectors
of plague and typhus. Nosopsylla fasciatus is rare in
Habits
Fleas are found on their normal hosts and in the nests, burrows
and lairs of their hosts. They are also found in the dwellings, on the
ground, in cracks and crevices, and under carpets. Both the sexes
bite and suck blood. They feed at frequent intervals, usually once a
day and sometimes more often. Fleas cannot fly, but "they are
capable of making vertical jumps of about 4 inches when starved,
and about 3 inches when gorged. The distance they can cover by
horizontal jumps is less than 6 inches. Fleas are passively
transported by (a) their hosts (b) transport vehicles (c) humans - on
the person or in the luggage, and (d) the movement of goods like
grain, raw cotton, gunny bags, rags and hides.
Flea indices
The following indices are used in flea surveys : (1) GENERAL
FLEA INDEX : It is the average number of fleas of all species per
rodent. (2) SPECIFIC FLEA INDEX : (X.cheopis index; X.astia
index, etc.) It is the average number of fleas of each species, found
per rodent. (3) PERCENTAGE INCIDENCE OF FLEA SPECIES
: It is the percentage of fleas of each species, found per rodent. (4)
RODENT INFESTATION RATE : It is the percentage of rodents
infested with the various flea species.
Flea indices do not in themselves indicate an imminent plague
epidemic. But flea indices serve as useful indicators of the
potential explosiveness of the situation, should a plague outbreak
occur in an endemic area (23). Specific flea indices are more
significant than are overall flea indices.
Fleas and human disease
Fleas are known to transmit the following diseases : (1) Plague
(bubonic), (2) Endemic or murine typhus, (3) Chiggerosis and (4)
Hymenolepis diminuta
MODE OF TRANSMISSION : Fleas convey disease by (1)
Biting : The chief method of transmission, in the case of plague, is
by the bite of hungry 'blocked' fleas. Some fleas which ingest
plague bacilli become blocked due to the multiplication of plague
bacilli in their proventriculus or stomach. Fleas affected in this
way are called 'blocked' fleas. The blockage of the food passage
renders the flea unable to obtain further blood feeds. Because of
hunger, the flea begins to bite more ferociously and makes frantic
efforts to suck blood. Each time it bites, instead of sucking blood,
it injects plague bacilli into the wound. Such 'blocked' fleas play a
great role in the spread of plague. (2) Mechanical Transmission :
Mechanical transmission takes place from the proboscis of the
fleas, which had recently fed on an infected rodent. (3) Faeces :
The fleas are apt to defecate while feeding. The faecal drop of
infected fleas may contain numerous bacilli. When the host
scratches over the flea-bitten area, there is direct inoculation of the
infective agent into the angry spot.
Control of fleas (17, 18)
(1) INSECTICIDAL CONTROL : The cheapest and most
widely used formulation has been 10 per cent DDT dust. As the
rodents pass over the dust, they pick it up on their fur where it
kills the fleas. In a number of plague areas, the rat fleas have
developed resistance to DDT and/or to gamma-HCH and dieldrin.
In such areas, carbaryl or diazinon (2%) or malathion (5%) should
prove effective (9). The sprays should be applied to floors and
walls up to a height of about 1 ft. Patch dusting with insecticides
has also been found to be an effective method of controlling fleas.
The insecticidal powder is dusted over rat runs, under gunny bags,
and other harbourage areas. The insecticidal dust should also be
blown into the rodents' burrows with the help of dust-blowers at
about 30 g. per burrow. Animal hosts like cats and dogs and their
quarters and
REDUVIID BUGS
Reduviid bugs, also known as cone-nose bugs, are vectors of
Chagas' disease in Mexico and Central and South America. All are
of large size, about an inch or more in length. Adults have wings.
These bugs live exclusively on the blood of animals including man
and transmit Trypanosoma cruzi, the causative agent of Chagas'
disease. These bugs occur in India (21), but are not incriminated in
the transmission of any disease. These bugs frequently attack man
and their bites may cause intense itching, nausea, flushed face,
palpitation of the heart, etc. (Fig. 11).
cycle from egg to adult is about 2 months in the case of hard ticks, and
from 9 to 10 months in the case of soft ticks. Adult ticks may live for a
year or more. Soft ticks live longer than hard ticks.
Public health importance
Vj^Hard ticks transmit the following diseases :
r^*- (a) Tick typhus (Rocky Mountain spotted fever)
;.. J
(b) Viral encephalitis (e.g., Russian spring-summer
encephalitis)
(a)Viral fevers (e.g., Colorado tick fever)
(b)Viral haemorrhagic fevers (e.g. KFD in India)
(c)Tularaemia
(d)Tick paralysis
/^&\
(e)Human babesiosis . -\ uCFy
(.Soft ticks transmit:
j5
ty0 (a) Q fever 0\ (b)
Relapsing fever KJ^ (c) KFD \
The tick attaches itself to its host by means of its mouth parts. The
rostrum is burrowed into skin to enable it to suck blood. At the same time
saliva is secreted, which contains a neurotoxin. Mature ticks, especially
gravid female ticks, may remain attached for a comparatively long time
but the male usually drops off the body after a few days. As the tick feeds,
it gradually becomes engorged with blood.
Ticks transmit disease by biting; The larva and nymph are also
capable of transmitting disease by biting (i.e., infection is maintained
trans-stadially). Experiments have also shown transovarian transmission
of infection through successive generations!} V. ' % ^ ^\
Hard and soft ticks compared
TABLE 8
Comparison of hard and soft ticks
Hard Ticks
(Ixodidae)
1. Scutum
2. Head
3. Spiracles
4. Eggs
Life history
There are four stages in the life history of ticks; egg, larva, nymph and
adult. (1) EGG : Hard ticks lay eggs in a few hundreds or even thousands,
all at one time, after which the female is exhausted and dies. The soft ticks
lay eggs in batches of 20 to 100 over a long period. The eggs are deposited
on the ground and hatch in 1 to 3 weeks. (2) LARVA : The larva of the
tick possesses 3 pairs of legs. It lies in wait among grass and herbiage till a
suitable host appears to which it attaches itself. After a blood meal, it
drops off, and in course of time it moults to become a nymph. The
duration of the larval stage may vary from 3 to 13 days. (3) NYMPH : The
nymph resembles the adult in having 4 pairs of legs, but it has no genital
pore. The nymphs are all blood suckers, and they attach themselves to
suitable hosts for a blood meal. There are 5 nymphal stages in the life
history of soft ticks. (4) ADULT : The duration of the life
Soft Ticks
(Arqasidae)
5. Nymphal
stages
Lies ventrally;
not seen from above
Situated between III
and IV coxa
Laid in batches
of 20-100 over a long
period
Five
6. Habits
Dermacentor andersoni
Haemophysalis
spinigera
Ornithodorus moubata
ITCH MITE
The discovery in 1687 of the itch mite marks scabies as the first
disease of man with known cause (26). The itch mite {Sarcoptes
scabiei or Acarus scabiei) is an extremely small, globular
arthropod just visible to the naked eye. The female parasite
burrows into the epidermis where it breeds and causes the
condition known as scabies or itch. Species of the genus sarcoptes
also infest animals such as dog, cattle and horse. The human
acarus is morphologically indistinguishable from the animal
variety but it is quite distinct physiologically. Therefore, animal
scabies cannot flourish on the human skin.
General description
The itch mite is just visible to the naked eye, measuring 0.4 mm
in size and has a body shaped like a tortoise, rounded above and
flattened below. The body shows no demarcation into
cephalothorax or abdomen. The body surface is thrown into folds
and is covered with short bristles. The parasite has two pairs of
legs in front, and two pairs behind. The front legs end in long
tubular processes known as suckers and the hind legs end in long
bristles. The male has suckers on all the legs excepting the third
pair, which distinguishes it from female (Fig. 15).
Life history
There are four stages in the life history of an itch mite : egg,
larva, nymph and adult. (1) EGG : The female burrows within the
stratum corneum, and lays eggs in the burrow. A single female
may lay up to 30 eggs at the rate of 2 to 3 per day, and ultimately
dies at the end of the burrow. The eggs hatch into larvae in 3 to 4
days. (2) LARVA : The larvae are three-legged. They leave the
burrows, come to the surface and bore into the hair follicles where
vesicles form. The larvae mature into nymphs in about 3 days. (3)
NYMPH : The nymphs develop into adults in 6 to 8 days. (4)
ADULT : The life cycle from egg to adult may take 10 to 15 days.
The adult mites live for 1 to 2 months.
Mode of spread
(1) CLOSE CONTACT : Scabies is usually transmitted by
close contact with an infested person. This is often due to sleeping
in the same bed or by children playing with each other or nursing
an infested person. Because of close contact, the disease tends to
spread through families. Scabies is therefore called a familial or
household infection. (2) CONTAMINATED CLOTHES : the
disease may be acquired sometimes from contaminated clothes and
bed linen.
Site of lesions
The disease classically affects the hands and wrist (63%), The
extensor aspect of elbows being next (10.9%). The axillae,
buttocks, lower abdomen, feet and ankles, palms in infants are all
common sites of infestation. The disease also affects the breasts in
women and the genitals in men.
Diagnosis of scabies
The main diagnostic features of scabies are : (1) the patient
complains of itching which is worse at night, (2) examination
reveals follicular lesions at the affected site, (3) secondary
infection leads to crusted papules and pustules, (4) the diagnosis is
probable if the other members of the household are affected, (5)
confirmation of the diagnosis may be made by searching for the
parasite in the skin debris under microscope.
Control of scabies
In the control of scabies, it is essential to treat all members of
the affected household simultaneously whether or not they appear
to be infested. Before commencing the treatment the patient is
given a good scrub with soap and hot water. (1) BENZYL
BENZOATE : Benzyl benzoate (25 per cent) is an effective
sarcopticide. It should be applied with a paint brush or shaving
brush to every inch of the body below the chin including the soles
of the feet and allowed to dry. In the case of babies, the head must
also be treated, The application should be repeated after 12 hours,
and after a further 12 hours a bath given and all underclothes,
clothes and sheets changed and washed. Not more than two
applications of benzyl benzoate should be given per week as
excessive use can cause an irritant dermatitis (27). (2) HCH : 0.5 to
1.0 per cent strength of gamma-HCH (lindane) in coconut oil or
any vegetable oil or vanishing cream is an efficient sarcopticide.
The preparation should be rubbed on the affected parts of the skin
on one or two occasions separated by an interval of 2 to 3 days. (3)
TETMOSOL : A 5 per cent solution of tetmosol is also an efficient
sarcopticide, three daily applications are recommended (4)
SULPHUR OINTMENT : 2.5 to 10 per cent daily for 4 days is a
cheap remedy.
CYCLOPS
Cyclops or water flea is a crustacean present in most collections
of fresh water. It is a tiny arthropod, not more than 1 mm in length
and just visible to the trained eye. It has a pear-shaped semitransparent body, a forked tail, 2 pairs of antennae, 5 pairs of legs
and a small pigmented eye (Fig. 16). It swims in water with
characteristic jerky movements. The average life of a cyclops is
about 3 months.
Group II
Group III
_______________________________________________________________________________________________________INSECTICIDES 589
Insecticides
_______________________________I------------------------------------------------.
Contact Poisons
Natural
Synthetic
Stomach Poisons
Fumigants
Paris green -^
.-...
r-. ,
Sodium Fluoride
i----------------------- '
-------------------------Hydrogen cyanide
Pyrethrum ^
Rotenone
Derris
Methyl bromide
Sulphur dioxide
Carbon disulphate
Nicotine
Mineral Oils
Organo-Chlorine
Compounds
DDT
Methoxychlor
HCH (BHC) (f^WAvufjt; **)
Lindane
Chlordane
Heptachlor
Dieldrin
Aldrin
Toxaphene
Kepone
Mirex
______________________I
______________________
Repellents----------------- Gardona
-------------------------------Meta-diethyltoluamide
Benzyl benzoate
lndalone
Dimethl phthalalate
Ethyl hexanediol
-----------
Organo-Phosphorus
Insecticides
Chlorthion
Diazinon
Dioxathion
Demethoate
EPN
Malathion (OMS-1) J
Fenthion (OMS-2)
Methyl parathion
Parathion
Ronnel
Trichlorfon
Dichlorvos
Abate (OMS-786)
Naled
Carbamates
Carbaryl
Dimetilan
Pyrolan
Propoxur (OMS-33)
.------------------------------Synthetic Pyrethroids
Resmethrin
Bioresmethrin
Pothrin
Chlorpyrifos
Fenitrothion (OMS-43)
Dicapthon (OMS-214)
JZTi---- W 0'
___________________________________________RODENTS 591
The use of paris green was largely responsible for the eradication
of A. gambiae from Brazil in 1940, and the near-eradication of the
same species in Egypt in 1944.
INSECTICIDE RESISTANCE
The widespread use of synthetic insecticides has given rise to
the serious problem of insecticide resistance practically all over
the world. The magnitude of the problem can be appreciated from
the fact that, whereas in 1946 resistance to insecticides was
reported in only 2 species of insects of public health importance,
in 1962, the number rose to 81 species and in 1980 to 134.
Evidence has accumulated to show that resistance in many vectors
has been caused as a side effect of agricultural pesticide usage.
Resistance has been defined by WHO (1957) as "the
development of an ability in strain of insects to tolerate doses of
toxicants which would prove lethal to the majority of individuals
in normal population of the same species" (34). Resistance is due
to biochemical and genetic factors. In the former, the toxicant is
converted into a non-toxicant form in the body of the insect by
various enzymes; in the latter, resistance is transmitted through
genes, single or multiple.
A knowledge of insecticide resistance is important from the
point of view of proper selection of insecticides. Generally
speaking, organochlorine insecticide resistance is divided into two
groups : resistance to DDT and its analogues; and the other to
HCH-dieldrin group of insecticides. Resistance to DDT amounts
to resistance to a number of DDT analogues such as
methoxychlor, but not to HCH-dieldrin group. Similarly resistance
to HCH amounts to resistance to dieldrin but not to DDT. Many
insects now have developed "double resistance", that is, resistance
to the two groups of organochlorine insecticides. When an insect
develops resistance to DDT and HCH, the only effective action
that can be taken is to change over to organophosphorus and
carbamate insecticides. The change to organophosphorus and
carbamate compounds involves substantial increase in cost, as
these are all costly insecticides. Furthermore, cases of resistance
towards them have already appeared. There is cross resistance
between most carbamates and most organophosphorus
compounds. To sum up, the problem of insecticide resistance
which is growing in magnitude, is no doubt, steadily diminishing
the choice of effective insecticides for vector control.
TOXICITY OF INSECTICIDES
1. Organo-chlorine compounds
DDT and its chemical relations are all nerve poisons. They
increase the nervous excitability, and cause tremors and
convulsions. Of the three commonly used compounds namely
DDT, HCH and dieldrin, DDT is the least toxic. The median lethal
dose for the humans is about 250 mg per kg. of body weight.
Gamma-HCH is about twice as toxic as DDT, and dieldrin is
about 5 to 8 times as toxic as DDT. Dieldrin poisoning is met with
more frequently than DDT or HCH poisoning : the reason is,
dieldrin is absorbed through the skin whereas DDT and HCH are
not absorbed through the skin in the solid state. TREATMENT :
Poisoning with chlorinated hydrocarbons is treated with
barbiturates, specially phenobarbitone. Stomach washouts are
generally necessary, purgative may be useful but no oils or fats
should be given.
2. Organo phosphorus compounds and carbamates
These insecticides interfere with the mechanism of transmission
of nerve impulses. They act by inhibiting cholinesterase, the
enzyme which catalyses the degradation of acetyl choline in the
synapse of striated muscle. Consequently there is accumulation
of acetyl choline. The effects of
R. Norvegicus
(Sewer Rat)
1. Body
2. Muzzle
3. Tail
4. Ears
5. Eyes
Large
Big and prominent
Small
Small
___________________________________________RODENTS 591
The use of paris green was largely responsible for the eradication
of A. gambiae from Brazil in 1940, and the near-eradication of the
same species in Egypt in 1944.
INSECTICIDE RESISTANCE
The widespread use of synthetic insecticides has given rise to
the serious problem of insecticide resistance practically all over
the world. The magnitude of the problem can be appreciated from
the fact that, whereas in 1946 resistance to insecticides was
reported in only 2 species of insects of public health importance,
in 1962, the number rose to 81 species and in 1980 to 134.
Evidence has accumulated to show that resistance in many vectors
has been caused as a side effect of agricultural pesticide usage.
Resistance has been defined by WHO (1957) as "the
ievelopment of an ability in strain of insects to tolerate doses )f
toxicants which would prove lethal to the majority of ndividuals
in normal population of the same species" (34). iesistance is due
to biochemical and genetic factors. In the jrmer, the toxicant is
converted into a non-toxicant form in le body of the insect by
various enzymes; in the latter, >sistance is transmitted through
genes, single or multiple.
A knowledge of insecticide resistance is important from the
Dint of view of proper selection of insecticides. Generally
leaking, organochlorine insecticide resistance is divided into
'o groups : resistance to DDT and its analogues; and the other
HCH-dieldrin group of insecticides. Resistance to DDT
lounts to resistance to a number of DDT analogues such as
sthoxychlor, but not to HCH-dieldrin group. Similarly
;istance to HCH amounts to resistance to dieldrin but not to
)T. Many insects now have developed "double resistance",
it is, resistance to the two groups of organochlorine
ecticides. When an insect develops resistance to DDT and
'H, the only effective action that can be taken is to change
>r to organophosphorus and carbamate insecticides. The
nge to organophosphorus and carbamate compounds
?lves substantial increase in cost, as these are all costly
icticides. Furthermore, cases of resistance towards them
e already appeared. There is cross resistance between most
>amates and most organophosphorus compounds. To sum
the problem of insecticide resistance which is growing in
nitude, is no doubt, steadily diminishing the choice of
:tive insecticides for vector control.
TOXICITY OF INSECTICIDES
rgano-chlorine compounds
3T and its chemical relations are all nerve poisons. They
ise the nervous excitability, and cause tremors and
ilsions. Of the three commonly used compounds namely
HCH and dieldrin, DDT is the least toxic. The median
dose for the humans is about 250 mg per kg. of body
t. Gamma-HCH is about twice as toxic as DDT, and
in is about 5 to 8 times as toxic as DDT. Dieldrin
ling is met with more frequently than DDT or HCH
ling : the reason is, dieldrin is absorbed through the skin
as DDT and HCH are not absorbed through the skin in
lid state. TREATMENT : Poisoning with chlorinated
:arbons is treated with barbiturates, specially
Darbitone.s Stomach washouts are generally necessary,
ve may be useful but no oils or fats should be given.
ano-phosphorus compounds and carbamates
;e insecticides interfere with the mechanism of ssion of
nerve impulses. They act by inhibiting sterase, the enzyme
which catalyses the degradation of fioline in the synapse
of striated muscle. Consequently i accumulation
of
acetyl choline. The effects of
R. Norvegicus
(Sewer Rat)
1. Body
2. Muzzle
3. Tail
4. Ears
5. Eyes
Large
Big and prominent
Small
Small
Rattus rattus
3. Rodenticides: Rodenticides are of two main types - singledose (acute) and multiple-dose (cumulative). The former are lethal
to the rat after a single feeding, while the latter require repeated
feedings over a period of 3 more days (17).
An Expert Committee of the WHO (37) grouped the "acute"
rodenticides as below :
1. Those requiring ordinary care :
Red squill
PNorbromide Zinc phosphide
2. Those requiring maximal precaution :
Sodium fluorocetate
Fluoroacetamide
Strychnine
3. Too dangerous for use :
Arsenic trioxide
Phosphorus
Thallium sulphate
ANTU Gophacide
The commonly used poisons in this country are : (i) Barium
carbonate : This is a white tasteless powder, and is very cheap. It is
mixed with wheat or rice flour in the ratio of 1 part to 4 parts of
flour. The mixed material is moistened with water and made into
small round marbles. The poisoned baits are placed near the rat
burrows and in dark, secluded places. On eating the pills, rats are
killed in 2 to 24 hours. Barium carbonate is a weak rodenticide of
uneven performance, and probably easily detected by rats in many
baits. In the opinion of many workers, in view of the availability of
more efficient rodenticides, barium carbonate should not be used
any more (38). (ii) Zinc phosphide : Zinc phosphide is an efficient
rodenticide. When moist, the chemical slowly gives off phosphine
whose garlic odour is repellent to man and domestic animals, but
seems to have no adverse effect on rats. Zinc phosphide is now
extensively used in India. It is used in the ratio of 1 part to 10 parts
of wheat or rice flour and mixed with a few drops of edible oil in
order to render it more attractive to rats. Rats are
______________________________________________ZOONOSES 593
killed in about three hours. The use of rubber gloves is recommended in
handling zinc phosphide as it is highly poisonous. Special bait boxes have
been designed for the administration of very toxic compounds such as
zinc phosphide to eliminate the risk to man and domestic animals.
Because of its good safety record, low cost and reasonably high
effectiveness, Zinc phosphide is recommended for large scale use against
rats (38).
TABLE 1
Yr^.
\P )
----------------------------------- ^K.------------------------------------------------------------------------
Disease in man
Anthrax
Brucellosis
Ornithosis
Q fever
Leptospirosis
Tuberculosis
Plague
B. Viral infections
Cowpox
Cattle
Monkeypox
Monkeys, rodents
Easternequine encephalitis Horses, rodents
Ross river fever
Horses, cattle, goats, sheep, dogs,
rats, bats, pigs
Yellow fever
Monkeys
Japanese encephalitis
Wild birds
Lassa fever
Multimammate rat
Rabies
Dog, fox, shunk, mongoose, bat and
jackal
C. Protozoan infections
Leishmaniasis
Dogs, cats, swine
Toxoplasmosis
Cats, mammals, birds
Trypanosomiasis
Game animals, cattle
Babesiosis__________________Cattle_____________________________
D. Helminthic infections
Clonorchiasis
Fasciolopsis
Schistosomiasis
Echinococcosis
Taeniasis
Trichinellosis
Source : (41, 42)
Control of zoonoses
The principal components of control are : (a) Control in
animals : The measure comprise diagnosis of the zoonotic
condition, treatment, destruction, quarantine and immunization, (b)
Control of vehicles of transmission : These include establishment
of food hygiene practices, ensuring safety of animal products such
as wool, hides, horn, bones, fat, etc.; proper disposal of animal
carcasses and wastes, and disinfection procedures, (c) Prevention
and treatment in man : This involves protection of high risk
groups, by immunization, chemoprophylaxis, monitoring of health
status including occupational health programmes, prevention of
spread by man, early diagnosis and treatment of the condition in
man, health education, prevention of environmental contamination,
prevention of food contamination, and improvement of diagnostic
facilities (42).
During the past 50 years, the concept of environment has
become broad-based. Modern ecologists use the term in its widest
sense. The concept of environment covers first the general
environment, for instance water and air pollution, to which an
individual is exposed. Secondly, it refers to the personal
environment created by the individual himself -including such
cultural habits as cigarette smoking, alcohol, drug addiction. This
has been described as "chemical environment". The concept that
the general everyday chemical environment could also be
dangerous to human health developed slowly. Evidence is
accumulating that environmental factors, especially factors in the
chemical environment, play a major role in carcinogenesis, and
that many cancers may be theoretically preventable (43).
It is now current jargon to advocate an "integrated" approach to
the environmental problems where all aspects of a given problem
are looked at from all angles. It implies an unprecedented
cooperation between different services and disciplines. The United
Nations Environmental Programme (UNEP), UNESCO's Man and
Biosphere (MAB) Programme, WHO's Environmental Health
Criteria Programme, and the UN's International Drinking Water
Supply and Sanitation Decade, 1981-1990 are efforts in the
direction to promote health in the human environment.
References
1.Singh, K.R.P. (1976). J. Com. Dis., 8,147-153.
2.Smith, R.E (1973). Bull. Wld. Hlth. Org., 48.686.
3.Rao, T.R. (1974). J. Com. Dis., 6.57.
4.WHO (1974). Techn. Rep. Ser., No. 586.
-g Q
M f^
Hospital Waste
Management
Let the wastes of "the sick" not contaminate the lives of "the healthy"
Incineration
Incineration is a high temperature dry oxidation process, that
reduces organic and combustible waste to inorganic incombustible
matter and results in a very significant reduction of waste-volume
and weight. The process is usually selected to treat wastes that
cannot be recycled, reused or disposed off in a land fill site.
The flow diagram of incinerator is as shown in Fig. 1.
Incineration requires no pretreatment, provided that certain
waste types are not included in the matter to be incinerated.
Characteristics of the waste suitable for incineration are : (a) low
heating volume - above 2000 kcal/kg for single -chamber
incinerators, and above 3500 kcal/kg for pryolytic double-chamber
incinerators; (b) content of combustible matter above 60 per cent;
(c) content of noncombustible solids below 5 per cent; (d) content
of noncombustible fines below 20 per cent; and (e) moisture
content below 30 per cent (2).
Waste types not to be incinerated are : (a) pressurized gas
containers; (b) large amount of reactive chemical wastes;
(a)silver salts and photographic or radiographic wastes;
(b)Halogenated plastics such as PVC; (e) waste with high mercury
or cadmium content, such as broken thermometers, used batteries,
and lead-lined wooden panels; and (f) sealed ampules or ampules
containing heavy metals (2).
TYPES OF INCINERATORS
Incinerators can range from very basic combustion unit that
operates at much lower temperature to extremely
sophisticated, high temperature operating plants. It should be carefully chosen on the basis of the available resources, the local situation,
and the risk- benefit consideration.
Three basic kinds of incineration technology are of interest for treating health-care waste :
(a) Double-chamber pyrolytic incinerators which may be especially designed to burn infectious health-care waste;
(a)Single-chamber furnaces with static grate, which should be used only if pyrolytic incinerators are not affordable; and
(b)Rotary kilns operating at high temperatures, capable of causing decomposition of genotoxic substances and heat-resistant chemicals.
II Chemical disinfection
Chemicals are added to waste to kill or inactivate the pathogens it contains, this treatment usually results in disinfection rather than
sterilization. Chemical disinfection is most suitable for treating liquid waste such as blood, urine, stools or hospital sewage. However, solid
wastes including microbiological cultures, sharps etc. may also be disinfected chemically with certain limitations.
III Wet and dry thermal treatment
WET THERMAL TREATMENT : Wet thermal treatment or steam disinfection is based on exposure of shredded infectious waste to
high temperature, high pressure steam, and is similar to the autoclave sterilization process. The process is inappropriate for the treatment of
anatomical waste and animal carcassess, and will not efficiently treat chemical and pharmaceutical waste.
SCREW-FEED TECHNOLOGY : Screw-feed technology is
the basis of a non-burn, dry thermal disinfection process in which waste is shredded and heated in a rotating auger. The waste is reduced by
80 per cent in volume and by 20-35 per cent in weight. This process is suitable for treating infectious waste and sharps, but it should not be
used to process pathological, cytotoxic or radioactive waste.
IVMicrowave irradiation
Most microorganisms are destroyed by the action of microwave of a frequency of about 2450 MHz and a wave length of 12.24 cm. The
water contained within the waste is rapidly heated by the microwaves and the infectious components are destroyed by heat conduction. The
efficiency of the microwave disinfection should be checked routinely through bacteriological and virological tests.
VLand disposal
MUNICIPAL DISPOSAL SITES : If a municipality or medical authority genuinely lacks the means to treat waste before disposal, the
use of a land fill has to be regarded as an acceptable disposal route. There are two types of disposal land-open dumps and sanitary landfills.
Health-care waste should not be deposited on or around open dumps. The risk of either people or animals coming into contact with
infectious pathogens is obvious.
Sanitary landfills are designed to have at least four advantages over open dumps : geological isolation of waste from the environment,
appropriate engineering preparation before the site is ready to accept waste, staff present on site to control operations, and organized
deposit and daily coverage of waste.
measures :
TABLE 3
Main advantages and disadvantages of treatment and disposal options
Treatment /
disposal method____________________Advantages
Disadvantages High
Rotary kiln
Pyrolytic
incineration
Single-chamber
incineration
Drum or brick
incinerator
Chemical
disinfection
Wet thermal
treatment*
Environmentally sound,
Mircowave
irradiation
Encapsulation
Safe burying
Low costs.
Relatively safe if access to site is restricted and where
natural infiltration is limited.
Inertization
Relatively inexpensive.
TABLE 4
Schedule I Categories of BioMedical Waste in India
i Option
I----------------- ,
Category No. 1
Category No. 2
Category No. 3
Category No. 4
Category No. 5
Category No. 6
Category No. 7
Category No. 8
Category No. 9
Waste Category
Category No. 10
@@
Chemical treatment using at least 1% hypochlorine solution or any other equipment chemical reagent. It must be ensured that
chemical treatment ensures disinfection. ##
Multilation / shredding must be
such so as to prevent unauthorized reuse.
@
There will be no chemical pretreatment before incineration. Chlorinated plastics shall not be incinerated.
2
Deep burial shall be an option available only in towns with population less than five lakhs and in rural areas.
TABLE 5
Schedule II Colour coding and type of container for disposal of bio-medical
wastes
Colour coding
Type of container
Waste category
Yellow
Plastic bag
Incineration/deep burial
Red
Disinfected container/
plastic bag
Cat. 3, Cat. 6,
Cat. 7
Blue / White
translucent
Plastic bag/puncture
proof container
Cat. 4, Cat. 7.
Autoclaving/Microwaving/Chemical
Treatment
Autoclaving/Microwaving/Chemical
Treatment and Destruction/Shredding
Black
Plastic bag
Notes :
1.Colour coding of waste categories with multiple treatment options as defined in Schedule I, shall be selected depending on the treatment option
chosen, which shall be as specified in Schedule I.
2.Waste collection bags for waste types needing incineration shall not be made of chlorinated plastics.
3.Categories 8 and 10 (liquid) do not require containers / bags.
4.Category 3 if disinfected locally need not be in containers / bags.
References
1.Sharma, A.K., Bio-Medical Waste (Management & Handling) Rules,
Source : (2)
There are many types of disasters such as earthquakes,
cyclones, floods, tidal waves, land-slides, volcanic eruptions,
_____________________________DISASTER
MANAGEMENT 601
DISASTER MANAGEMENT
There are three fundamental aspects of disaster management:
a. disaster response ;
b. disaster preparedness ; and
c. disaster mitigation.
These three aspects of disaster management correspond to
different phases in the so - called "disaster cycle" as shown in
Fig. 2.
Triage (5)
(^ ^^ ^
/fjj)
_. ,
,
Earthquakes
Death3
Many
Severe injuries
requiring extensive
treatment
Increased risk of
communicable
diseases
Damage to health
facilities
Many
Damage to
water systems
Food shortage
(
Major population
movements
Severe
(structure and
equipment)
Severe
High winds
(without flooding)
Tidal waves /
flash floods
Slow - onset
floods
Landslides
Volcanoes /
Lahars
Few
Many
Few
Many
Many
Moderate
Few
Few
Few
Few
Rare
may occur due to economic and logistic factors)
Rare (may occur in
heavily damaged urban areas'
Severe
Common
major disasters
and deteriorating sanitation)
Severe
(equipment
only)
Light
Common
Severe but
localized
Severe but
localized
Rare
Severe
(structure and
equipment)
Severe
Rare
simulation
excercises
that
test
response
State
Andhra
Pradesh
Type of
disaster
9001
1 s
Villages
c iffecte affected
d
Heavy rains
18
4522
/floods
Population Human
affected
life lost
(000)
29.35
257
Arunachal
Pradesh
Heavy rains/
floods/ land
slides
30
0.42
26
Assam
Heavy rains
/floods
19
3474
36.09
32
Bihar
Heavy rains
/floods
33
11696
79.72
273
Gujarat
Floods/
earthquake
10
24
389
4.08
116
16480
Uttar
Pradesh
Heavy rains
/floods
Heavy rains
/floods
49
6893
48.40
400
1412
218.18
1320
West
Bengal
Source : (6)
In the federal structure of India, the state governments are
VCX
annoyance and visual fatigue. Intense direct glare may also result
in blurring of vision and lead to accidents. There should be
sufficient and suitable.lighting, natural or artificial, wherever
persons are working.
(1)NOISE: Noise is a health hazard in many industries. The
effects of noise are of two types: (i) Auditory effects which
consist of temporary or permanent hearing loss (ii) Non- '
auditory effects which consist of nervousness, fatigue,
interference with communication by speech, decreased
efficiency and annoyance. The degree of injury from exposure to
noise depends upon a number of factors such as intensity and
frequency range, duration of exposure and individual
susceptibility. r~X/& CT)
(2)VIBRATION J Vibration',"especially in the frequency range
10 to 500 Hz, may be encountered in work with pneumatic
tools such as drills and hammers. Vibration usually affects the
hands and arms. After some months or years of exposure, the
fine blood vessels of the fingers may become increasingly
sensitive to spasm (white fingers). Exposure to vibration may
also produce injuriesjif the joints of the hands, elbows and
shouldersTfj. \C^/$y
(3)ULTRAVIOLET RADIATION : Occupational exposure to
ultraviolet radiation occurs mainly in arc welding. Such
radiation mainly affects the eyes, causing intense conjunctivitis
and keratitis (welder's flash). Symptoms are redness of the eyes
and pain, these usually disappear in a few days with no
permanent effect on the vision or on the deeper structures of the
eye (9).
(6) IONIZING RADIATION : Ionizing radiation is finding
increasing application in medicine and industry, e.g., X-rays and
radio active isotopes. Important radio-isotopes are cobalt 60 and
phosphorus 32. Certain tissues such as bonemarrow are more
sensitive than others and from a genetic standpoint, there are
special hazards when the gonads are exposed. The radiation
hazards comprise genetic changes, malformation, cancer,
leukaemia, depilation, ulceration, sterility and in extreme cases
death. The International Commission of Radiological Protection
has set the maximum permissible level of occupational exposure
at 5 rem per year to the whole body (10).
b. Chemical hazards
There is hardly any industry which does not make use of
chemicals. The chemical hazards are on the increase with the
introduction of newer and complex chemicals. Chemical agents act
in three ways : local action, inhalation and ingestion. The ill-effects
produced depend upon the duration of exposure, the quantum of
exposure and individual susceptibility.
(1)LOCAL ACTION : Some chemicals cause dermatitis,
eczema, ulcers and even cancer by primary irritant action;
some cause dermatitis by an allergic action. Some chemicals,
particularly the aromatic nitro and amino compounds such as
TNT and aniline are absorbed through the skin and cause
systemic effects. Occupational dermatitis is a big problem in
industry. Rao and Banerji (1952) were the first to draw
attention in India to the prevalence of occupational dermatitis
due to machine oil, rubber, X-rays, caustic alkalies and lime
(7).
(2)INHALATION : (i) DUSTS : Dusts are finely divided solid
particles with size ranging from 0.1 to 150 microns. They are
released into the atmosphere during crushing, grinding,
abrading, loading and unloading operations. Dusts are produced
in a number of industries - mines, foundry, quarry, pottery,
textile, wood or stone working industries. Dust particles larger
than 10 microns settle down from the air rapidly, while the
smaller ones remain suspended indefinitely. Particles smaller
than 5 microns are directly inhaled into the lungs and are
retained there. This fraction of the dust is called
__________________________________PNEUMOCONIOSIS 609
/^(&*)
PNEUMOCONIOSIS
[ Dust within the size range of 0.5 to 3 micron is a health
hazard producing, after a variable period of exposure, a lung
disease known as pneumoconiosis, which may gradually
cripple a man by reducing his working capacity due to lung
fibrosis and other complications. The hazardous effects of dusts
on the lungs depend upon a number of factors such as
(a) chemical composition (b) fineness (c) concentration of dust
in the air (d) period of exposure and (e) health status of the
person exposed. Therefore, the threshold limit values for
different dusts are different. In addition to the toxic effect of the
dust on the lung tissues, the super-imposition of infections like
tuberculosis may also influence the pattern of pneumoconiosis.
The important dust diseases are silicosis, anthracosis,
byssinosis, bagassosis, asbestosis and farmer's lung. As no cure
for the pneumoconiosis is known, it is essential to prevent these
diseases from arising. A brief account of these conditions is
given below:
-,
V*
1. Silicosis
v~
I fry
Among the occupational diseases, [silicosis is the major cause
of permanent disability and mortality. It is caused by inhalation of
dust containing free silica or silicon dioxide (Si02). It was first
reported in India from the Kolar Gold Mines (Mysore) in 1947.
Ever since, its occurrence has been uncovered in various other
industries, e.g., mining industry (coal, mica, gold, silver, lead,
zinc, manganese and other metals), pottery and ceramic industry,
sand blasting, metal grinding, building and construction work,
{npk mining, iron and steel industry and several others"} k-"
o)
In the mica mines of Bihar, out of 329 miners examined, 34.1
per cent were found suffering from silicosis. In a ceramic and
pottery industry, the incidence of silicosis was found to be 15.7 per
cent (12). The incidence of silicosis depends upon the chemical
composition of the dust, size of the particles, duration of exposure
and individual susceptibility. The higher the concentration of free
silica in the dust, the greater the hazard. Particles between 0.5 to 3
micron are the most dangerous because they reach the interior of
the lungs with ease. The longer the duration of exposure, the
greater the risk of developing silicosis. It is found that the
incubation period may vary from a few months up to 6 years of
exposure, depending upon the above factors.
The particles are ingested by the phagocytes which accumulate
and block the lymph channels. Pathologically,
yiilicosis is characterised by a dense "nodular" fibrosis, the _ 0 nodules
ranging from 3 to 4 mm in diameter. Clinically theV' onset of the
disease is insidious. Some of the early manifestations are
irritant cough, dyspnoea on exertion andy'* pain in the chest. With
more advanced disease, impairment of total lung capacity (TLC) is
commonly present. An X-ray of the
JYhest shows "snow-storm" appearance in the lung fields. Silicosis
is progressive and what is more important is that silicotics are
prone to jDuhnonary tuberculosis, a condition called
"silicotuberculosis/jln recent years doubts have been raised,
whether silico-tuberculotics are really tubercular or purely
silicotics. It is because, sputum in silico-tuberculotics rarely shows
tubercle bacilli; children and women of silico-tuberculotics do not
develop tuberculosis; post-mortems on silico-tuberculotics failed to
prove the existence of tuberculosis disease, but showed them to be
cases of pure silicosis. The radiological evidence in the two
conditions is so similar that one is apt to mistake a case of silicotic
to be a case of tuberculosis of lungs (13). The final answer to this
question is still awaited.
There is no effective treatment for silicosis. Fibroticxhanges
that have already taken place cannot be reversed.^ The only way
that silicosis can be controlled (if not altogether
>
Undesirable conditions
Anaemia, hypertension, nephritis,
peptic ulcer
Asthma; skin, bladder and kidney
diseases; precancerous lesions
Liver and kidney disease, dermatitis,
alcoholism
Healed or active tuberculosis of
lungs, chronic lung disease
Signs of ill-health, especially any
blood disease
Pre-placement examination will also serve as a useful benchmark for future comparison. It may be mentioned that in most
countries, many workers start employment without the benefit of a
pre-employment medical examination. This is particularly true of
workers in small-scale industries and mines and those engaged in
construction and agricultural work in the developing countries.
2. Periodical examination
Many diseases of occupational origin require months or even
years for their development. Their slow development, very often,
leads to their non-recognition in the early stages and this is
harmful to the worker. This is the reason why a periodical medical
check-up of workers is very necessary when they handle toxic or
poisonous substances.
The frequency and content of periodical medical
____________________________________________LEGISLATION 617
(1)Maternity benefit
(2)Disablement benefit
(3)Dependant's benefit
(4)Funeral expenses
(5)Rehabilitation allowance
1. Medical benefit
Medical benefit consists of "full medical care" including
hospitalization, free of cost, to the insured persons in case of
sickness, employment injury and maternity. The services comprise
: (1) out-patient care (2) supply of drugs and dressings (3)
specialist services in all branches of medicine (4) pathological and
radiological investigations (5) domiciliary services (6) antenatal,
natal and postnatal services (7) immunization services (8) family
planning services (9) emergency services (10) ambulance services
(11) health-education and (12) in-patient treatment. In complicated
cases where specialized treatment is necessary, patients are sent
for institutional treatment even outside their State at the expense of
the ESI Corporation.
Medical care is provided either directly through the agency of
ESI hospitals and dispensaries, or indirectly through a panel of
private medical practitioners (panel system) appointed as
"insurance medical practitioners". DIRECT PATTERN : (1) In
areas having a concentration of 1,000 or more employees' family
units, service dispensaries are established with full-time medical
and para-medical personnel. On an average, a doctor will attend to
about 80 cases in the out-patient department per day, and makes
one home visit a day. (2) In areas where the employees are less
than 750, part-time ESI dispensaries are established. (3) If the
residential concentration of employees is scattered over a long
distance, mobile dispensaries are established. INDIRECT
PATTERN: This is known as "panel system". Registered medical
practitioners designated as Insurance Medical Practitioners are
appointed to provide medical care. They are paid remuneration
quarterly, according to the number of family units attached to
them. An Insurance Medical Practitioner is allowed a maximum of
750 family units. The existing doctor-population ratio under the
ESI Scheme is 1:585 as against the national average of 1:2148.
Medical care is also extended to families of workers where
requisite arrangements could be made. A start has been made by
providing "restricted medical care", i.e., only out-patient care.
Where facilities are available "expanded medical care i.e., full
medical care short of hospitalization is given. The ESI has 26849
beds available as on 31.3.03. There are 322 specialist centres and
more than 687 centres. ESI Dispensaries are 1447.
OTHER MEDICAL FACILITIES :(1) Dentures, spectacles and
hearing aids are provided free to patients who are incapacitated
due to employment injury (2) Artificial limbs are provided free to
insured persons who lose their limbs in employment injury or
otherwise (3) Special appliances such as hernia belts, walking
callipers, surgical boots, spinal braces and jackets are provided as
prescribed by specialists.
COST OF MEDICAL BENEFIT: The per capita cost of
medical benefit under the ESI Scheme has been steadily
increasing. It was Rs.23.79 in 1961-62 Rs.58.91 in 1969-70 and
Rs.67.53 in 1973-74, Rs.406.78 in 1992-93 and Rs.905 in 200102, and has been rising further since then.
2. Sickness benefit
It consists of periodical cash payment to an insured person in
case of sickness, if his sickness is duly certified by an Insurance
Medical Officer or Insurance Medical Practitioner. The benefit id
payable for a maximum period of 91 days, in any continuous
period of 365 days, the daily rate being about 50% of the average daily wages. A person receiving the sickness benefit is required to remain
under medical treatment provided under the Act.
EXTENDED SICKNESS BENEFIT: In addition to 91 days of sickness benefit, insured persons suffering from certain long-term
diseases are entitled to Extended Sickness Benefit as shown below:
34 diseases for which Extended Sickness Benefit with effect from 1.1.2000 is payable for upto 309 days, in case where the insured
person has been in continuous employment for 2 years :
I. Infectious Diseases
1.Tuberculosis
2.Leprosy
3.Chronic empyema
4.AIDS
II. Neoplasms
5. Malignant diseases
III. Endocrine, Nutritional and Metabolic Disorders
6. Diabetes mellitus with proliferative retinopathy/
Diabetic foot/Nephropathy
3. Maternity benefit
The benefit is payable in cash to an insured woman for
confinement/miscarriage or sickness arising out of pregnancy/
confinement or premature birth of child or miscarriage. For
confinement, the duration of benefit is 12 weeks, for miscarriage 6
weeks and for sickness arising out of confinement etc. 30 days.
The benefit is allowed at about full wages.
4. Disablement benefit
The Act provides for cash payment, besides free medical
treatment, in the event of temporary or permanent disablement as a
result of employment injury as well as occupational diseases. The
rate of temporary disablement benefit is about
References
1.WHO (1950). Unpublished Working Document, WHO/Occ. Health/2,
Geneva, 1950
2.Dastur, H.P. (1960). A Doctor's Approach to Industrial Medicine, Tata
Institute of Social Sciences, Bombay.
3.WHO (1962). Techn. Rep. Ser.,No. 246
4.WHO (1969). WorldHealth, March 1969.
5.Chanda, S.L. (1971). In: Report on the Symposium on Academic,
Education and Training in Occupational Health and Hygiene, WHO/
SEA/Occ/Hlth.6
6.WHO (1960). WHO Chronicle, 7, 279
7.Rao, M.N. and Lundgren. N.P.V. (1955). A Review of Occupational
Health Research in India, ICMR, New Delhi
8.Chakraborty, M.K. (1967). Ind. J. Indust. Med., 13, 121
9.WHO (1962). Health Hazards of the Human Environment, Geneva
10.Nagaratnam, A. (1968). Ind. J. Industr. Med., 14, 212
11.Shivram, C. et al (1970). Ind. J. Industr. Med., 16, 20-24
12.Thacker, RV. (1967). Souvenir, Indian Public Health Association, 12th
Annual conference, Poona, p. 65
13.Ghosh, P.K. (1969). Ind. J. Industr. Med., 15, 1
14.Sen, J.R. (1968). Ind. J. Industr. Med., 14, 186
15.Wyatt, J.R (1971). Amer. J. Pathology, 64, 197
16.Gupta, M.N. (1969). Indian J. Med. Res. ,57, 1776-1789
17.Gupta, M.N. (1970). Technical Review on Pneumoconiosis in India,
ICMR, Spl.Rep.Ser.,No,4 New Delhi
18.Editorial (1970). Brit. Med. J., 2 : 496
19.Editorial (1973). Brit. Med. J., 4, 312
20.Banerji, D.R (1968). Ind. J. Industr. Med., 14, 157
21.Gilson, J.C. (1973). Proceedings of the Royal Society of Medicine, 66,
395.
22.Quinlan, J.J. etal (1969). Canad.J. Public Health, 60, 15
23.Editorial (1970). Brit. Med. J., 2,496
24.Coyer, R.A. (1971). Amer. J. of Pathology, 64, 167
25.Barltrop, D. (1968). Post Graduate Med.,J. 44, 537
26.Govt, of India (1965). Occupational Diseases, A Guide to Recognition
and Notification, Chief Adviser Factories, Ministry of Labour and
Employment, New Delhi.
27.WHO (1975). Techn.Rep.Ser., No.571
28.Bhansali, K.N. (1967)./nd. J. Industr. Med., 13, 45
29.Donald Hunter (1959). Health in Industry, Pelican Book,
30.Mendonca, Lobo (1970). The Antiseptic,67', 455.
31.WHO (1976). WHO Chronicle,30, 318
32.Gupta, M.N. (1961). Swasth Hind, 5, 74
33.Sabnis, C.V. and Rao, M.N. (1961). Swasth Hind, 5, 81
34.ILO (1967). Accident Prevention, A Worker's Education Manual,
Geneva.
35.Wanchoo, N.N. (1969). Swasth Hind, 13, 90
36.Govt, of India (1969). SioasthHind, 13, 109
37.Banerji, B. and Chakraborty, S. (1969). Ind. J. Industr. Med., 15, 85
38.WHO (1953). Techn. Rep. Ser., No.66
39.Lobo-Mendonca, R. (1965). Protecting the Indian Worker,Society for
the Study of Industrial Medicine, Bombay
40.ESI Corporation (1974). Annual Report 1992-93 of the Director
General, New Delhi.
I f^
:
The basic principles of genetics were laid down by Mendel and
Galton towards the close of the 19th century. But it is only during
the past few years the science of genetics including human genetics
has made rapid progress. The discovery of the biological role of
nucleic acids, the uncovering of the structure of genetic
information and its role in regulating life processes are discoveries,
the importance of which can hardly be over estimated.
With increasing control of communicable diseases and infant
mortality, inherited abnormalities are assuming a proportionately
greater importance in medical practice. Over 2300 hereditary
diseases have been identified and more are added to the list every
year. According to many authors, genetically conditioned diseases
or diseases with a clear genetic component account for 25-40 per
cent of all cases treated by the health services (1).
Human genetics is much more than the study of mere hereditary
diseases. It has emerged as a basic biological science for
understanding the endogenous factors in health and disease and the
complex interaction between nature and nurture. Owing to rapid
specialization, several branches in genetics have come into being,
e.g., cytogenetics, biochemical genetics, clinical genetics,
pharmacogenetics, immunogenetics, microbial genetics, population
genetics and so on. Achievements in these fields have created a
basis for effective medical and preventive intervention in many
diseases, and also possibly of "genetic engineering", i.e., of
controlling the traits of an individual.
Cytologic facts
In 1956, Tjio and Levan surprised the scientific world by
reporting that they could find only 46 chromosomes in the normal
human karyotype. This was immediately confirmed by other
workers. There is now universal agreement that the normal human
body cell (except the sex cells) contains 46 chromosomes, i.e., 22
pairs of autosomes and a pair of sex chromosomes, XX in the
female and XY in the male. The chromosomes vary in length, the
longest being about 5 times as long as the smallest. Each pair of
chromosomes is homologous. The autosomes are numbered
according to their length, the first pair being the longest and the
last pair the shortest. The sex chromosomes are not included in the
numbering, but are merely termed X and Y. Barr and his group
discovered that the normal female cell nucleus contains in addition
a dark-staining area at the periphery of cell nucleus, called a Barr
body or "sex chromatin" body which is not present in normal
males.
The autosomes have been classified and divided on the basis of
length and certain morphological similarities into 7 groups as
follows :
Group A
1 to 3
pairs
Group B
4 and 5
pairs
Group C
6 to 12
pairs
Group D
13 to 15
pairs
Group E
16 to 18
pairs
Group F
19 and 20 pairs
Group G
21 and 22 pairs
The X chromosome is included in Group C with chromosomes
6-12, and the Y chromosome is included in Group G with
chromosomes 21 and 22.
Mitosis
During ordinary cell division, each chromosome divides
lengthwise into two sister chromosomes called chromatids. The
chromatids are joined together for a short time at a point called
centromere. Then the chromatids separate, one goes to one
daughter cell and one to the other daughter cell. In this manner,
each daughter cell inherits the same number and kind of sister
chromosomes. This process of nuclear division is called mitosis.
Meiosis
The reproductive cells (sperms and ova) are produced in a
different manner. There are two nuclear divisions and only one
chromosome division. This form of division is called 'reduction
division' or meiosis. A detailed description of meiosis is
unnecessary here. Broadly, the main events in meiosis are (1) The
homologous chromosomes first come together. This is called
"pairing". (2) The chromosomes then replicate - each doubling into
two chromatids which are held together at centromere. (3) At this
stage there is "crossing over" and a redistribution of genetic
material. (4) Then the homologous chromosomes separate - one
goes to one pole of the nucleus and the other to the other pole. The
chromosome number is thus reduced to half, i.e., 23. (5) The cell
divides and the nucleus of each daughter cell contains 23
chromosomes. (6) The second meiotic division follows : the
centromeres divide and the chromatids move apart. (7) The cell
divides again so that the daughter cells each contain 23
chromosomes. During fertilization, the two half-sets come together
and restore the full compliment of 46. The full compliment of 46
chromosomes is called the diploid number, and the half set of 23 is
called the haploid number.
Chromosomes
Chromosomes are rod-like condensations of chromatin. They
become visible in the nucleus only during cell division. They occur
in pairs - one member of each pair comes from the father, and
other from the mother. The largest chromosome measures about 7
n and is about five times the length of the shortest. Biochemically,
the chromosomes are made up of
TABLE 1
JXtf
Phenotype
(Blood Group)
Approximate frequency
in Indian population
00
40 per cent
AA
AO
BB
BO
AB
A
A
B
B
AB
22 per cent
33 per cent
5 per cent
Source : (13)
Gene O is recessive; the red blood cells of a person whose blood group
is O have no antigens. Genes A and B are co-dominant; when both are
present, the red blood cells carry antigen-A and antigen-B. Blood groups
provide valuable evidence in cases where there is a question of true
parentage; they are also extensively used to determine whether the twins
are identical or not:
RHESUS SYSTEM
The Rhesus system depends upon three genes which are designated by
the letter C, D and E and their alleles by the small letters c, d and e. The
Rh antigens develop very early and have been demonstrated in a 38-day
old foetus. It had been established that the Rh antigens are present only on
the surface of red cells (14).
The possible genotypes in the rhesus system will be CDE, CDe, cDE,
cdE, cDe and cde. The diploid individual inherits any two of these units,
e.g., CDe/cde. Of the rhesus antigens, the most potent is the antigen D; so
much so, the term "Rhesus positive" has come to mean possessing this
antigen and "Rhesus negative" lacking it. In India, it is found that about 93
per cent of the population are Rhesus positive as compared to 85 per cent
in countries of Northern Europe and North America (11). The importance
of the rhesus system in preventive medicine is exemplified in the fatal
disease in the newborn, Erythroblastosis foetalis.
Erythroblastosis foetalis
If the foetus is Rh positive and the mother Rh negative, certain
consequences are likely. Some of the foetal red cells cross the placenta
and enter the maternal circulation where they act as foreign antigen and
the production of Rh antibodies.
The Rh antibodies are of two main types : (a) the "strong" or saline
antibodies and (b) the "weak" or albumin antibodies. The latter are small
7S gamma globulins which cross the placental barrier and pass back into
the blood circulation of the foetus. When this happens, the RBC of the
foetus are destroyed. If the damage is severe, the foetus is killed in utero
and results in miscarriage; if the damage is less severe, the infant may be
born with jaundice, anaemia and oedema. This symptom complex is
known as Rh haemolytic disease or erythroblastosis foetalis.
2. Specific protection
Increasing attention is now being paid to the protection of
individuals and whole communities against mutagens such as Xrays and other ionizing radiations and also chemical mutagens.
Patients undergoing X-ray examination should be protected against
unnecessary exposure of the gonads to radiation. X-ray
examination of the pregnant uterus to determine the presence of
twins or the lie of the foetus is to be strongly deprecated. Rh
haemolytic disease of the newborn which is a genetically
determined immunological disorder is now preventable by
immunization by anti- D globulin.
3. Early diagnosis and treatment
(a) Detection of genetic carriers : It is now possible to
identify the healthy carriers of a number of genetic disorders,
especially the inborn errors of metabolism. The female carriers
of Duchenne type of muscular dystrophy, an X-linked disorder,
can now be detected by elevated levels of serum creatine
kinase in 80 per cent of carriers. In some conditions, carriers
can be recognized with a high degree of certainty (e.g.,
acatalasia); in some only a proportion of carriers can be
detected (e.g., haemophilia, PKU, galactosaemia); in other
conditions, no method has yet been found which will
distinguish carriers (e.g., alkaptonuria) (20).
(b) Prenatal diagnosis : Amniocentesis in early pregnancy
(about 14-16 weeks) has now made it possible for prenatal
diagnosis of conditions associated with chromosomal
anomalies (e.g., Down's Syndrome); many inborn errors of
metabolism (e.g., Tay-Sach disease, galactosemia, Maple syrup
urine disease, Alpha-thalassemia and neural tube defects). The
indications for prenatal diagnosis are listed in Table 3.
TABLE 3
Indications for prenatal diagnosis
a. Advanced maternal age,
previous child with
Cytogenetics (amniocentesis,
chorionic villus sampling)
chromosome aberration,
intrauterine growth delay
b. Biochemical disorders
c. Congenital anomaly
d. Screening for neural tube
defects and trisomy
Source : (9)
Amniocentesis : Examination of a sample of amniotic fluid
makes possible the prenatal diagnosis of chromosomal anomalies
and certain metabolic defects. The procedure can be used as early
as 14th week of pregnancy when abortion of the affected fetus is
still feasible. The diagnosis of chromosomal anomalies is made by
culture and Kryotyping of fetal cells from the amniotic fluid, and
of metabolic defects by biochemical analysis of the fluid.
Amniocentesis is called for in the following circumstances if the
parents are prepared to consider abortion.
1.A mother aged 35 years or more (because of high risk of
Down's syndrome with advanced maternal age).
2.Patients who have had a child with Down's syndrome or other
chromosomal anomalies.
TABLE 4
Established genetic population-screening services
Type of
Conditions
Preventive or screening action
service
Primary
Rhesus haemolytic Post-partum use of Anti-D
prevention disease
globulin
Congenital rubella Immunization of girls
Congenital
Addition of folic acid to the
malformations
maternal diet (may prevent
neural tube defects) Control of
maternal diabetes; Avoidance of
mutagens and teratogens such as
alcohol, certain drugs and
possibly tobacco
Antenatal
Congenital
Ultrasound foetal anomaly scan,
screening
malformations
maternal serum alphafetoprotein estimation
Chromosomal
Noting maternal age and
abnormalities
maternal serum factor levels
Checking family history
Inherited disease
Carrier screening for
haemoglobinopathies, TaySachs disease
Neonatal
Congenital
Examination of the newborn for
screening
malformations
early treatment (e.g., of
congenital dislocation of the
hip)
Phenylketonuria,
Biochemical tests for early
congenital
treatment
hypothyroidism,
sickle-cell disease
Source : (5)
Agent factors
Dependence-producing drug
A dependence-producing drug is one that has the capacity to
produce dependence, as described above. The specific
characteristics of dependence varies with the type of drug
involved. ICD-10 recognizes the following psychoactive drugs, or
drug classes, the self administration of which may produce mental
and behavioural disorders, including dependence :
1.Alcohol
2.Opioids
3.Cannabinoids
4.Sedatives or hypnotics
5.Cocain
6.Other stimulants including caffeine
7.Hallucinogens
8.Tobacco
9.Volatile solvents
10.Other psychoactive substances, and drugs from
different classes used in combination
Although the dependence-producing properties and public
health problems caused by tobacco were recognized since long, its
acute effects on behaviour were minimal. The WHO Expert
Committee on drug dependence at its meeting in Sept. 1992 felt
that tobacco and other forms of nicotine use warranted their
inclusion in the report. Furthermore, it recommended that WHO
should consider expanding the Committee's term of reference to
include substances such as anabolic steroids, which are used
because of their performance-enhancing effects. Anabolic steroids
are being abused by people who wish to increase muscle mass for
cosmetic reasons or for greater strength. In addition to the medical
problems, the practice is associated with significant mood swings,
aggressiveness, and paranoid delusions. Alcohol and stimulant use
is higher in these individuals. Withdrawal symptoms of steroid
dependency include fatigue, depressed mood, restlessness, and
insomnia (14). This form of use is described in ICD-10 under the
category F-55, "Abuse of non-dependence-producing substances".
The development of other performance enhancing drugs may
present new types of drug use problems in the future.
The drugs which are in common use today are (6, 10, 11, 12,
13) :
(1) AMPHETAMINES AND COCAINE : Amphetamines are
synthetic drugs, structurally similar to adrenaline. In medical
practice, they are used to treat obesity, mild depression, narcolepsy
and certain behaviour disorders in children. The ordinary
therapeutic dose is 10-30 mg a day. There are various brands of
amphetamines: the common names are Benzedrine, Dexedrine,
Methedrine, etc. These drugs act on the central nervous system.
They produce mood elevation, elation, a feeling of well-being and
increased alertness and a sense of heightened awareness. Because
they give a tremendous boost to self-confidence and energy, while
increasing endurance, they are called "superman" drugs. The use
of these drugs results in psychic dependence. With large doses,
such dependence, is often rapid and strong.
Cocaine is derived from the leaves of the coca plant. It was
formerly used in medical practice as a potent local anaesthetic.
Cocaine is a central nervous stimulant. It produces a sense of
excitement, heightened and distorted awareness and hallucinations.
Unlike amphetamines, it produces no tolerance. There is a 'no
physical dependence; no withdrawal symptoms', per se. The
chewing of coca leaves is a very common practice in Bolivia and
Peru in South America.
636
MENTAL HEALTH
C /. i>
Withdrawal
4.Presence
home.
t
Environmental factors
attributed to
developments
drug
with
^I'm&tomf:
r- - - .
-tissie^iFi ,
hfciUfctUI
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;
>=^,
*,.
,=
= -
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certain occupations
(tourism, drug production or sale)
-areas with high rates of crime or
vice
-areas where there are drug
-using gangs
-areas where delinquency is
common
Source : (6)
Prevention
No.836
8.WHO (1975). A Manual on Drug Dependence., Edited by J.F. Ktamer and D.C.
Cameron.
Health information is an integral part of the national health system. It is a basic tool of management and a key input for the progress of
any society. A health information system is defined as :
"a mechanism for the collection, processing, analysis and transmission of information required for organizing and operating health services, and also
for research and training" (1,2).
The primary objective of a health information system is to provide reliable, relevant, up-to-date, adequate, timely and reasonably
complete information for health managers at all levels (i.e., central, intermediate and local), and at the sharing of technical and scientific
(including bibliographical) information by all health personnel participating in the health services of a country; and also to provide at
periodic intervals, data that will show the general performance of the health services and to assist planners in studying their current
functioning and trends in demand and work load.
Unfortunately, it is still very difficult to get the information where it matters most - i.e., at the community level. It is conceded that no
country at the present time has such a thoughtfully constructed system of health information in operation, but the concept is receiving
much attention. The whole science of health statistics has undergone considerable changes in the past two decades (3). In 1973, the World
Health Assembly stressed the need for complete reconstruction of the health information systems.
Distinction between data and information
There is more than a subtle semantic difference between "data", "information" and "intelligence". Data consist of discrete observations
of attributes or events that carry little meaning when considered alone; data as collected from operating health care systems or institutions
are inadequate for planning. Data need to be transformed into information by reducing them, summarising them and adjusting them for
variations, such as the age and sex composition of the population so that comparisons over time and place are possible. It is the
transformation of information through integration and processing with experience and perceptions based on social and political values that
produces intelligence (4).
Data that are not transformed into information, and information that is not transformed into intelligence to guide decision-makers,
policy makers, planners, administrators and health care personnel themselves, are of little value.
Requirements to be satisfied by health information systems
A WHO Expert Committee (5) identified the following requirements to be satisfied by the health information systems :
(1) The system should be population-based
[x(l., Census
The census is an important source of health information. It is
taken in most countries of the world at regular intervals, usually of
10 years. A census is defined by the United Nations as "the total
process of collecting, compiling and publishing demographic, gjhhe Central Births and Deaths Registration Act, 1969
7\ Uu. an effort to improve the civil registration system, the
economic and social data pertaining at a, specified.time or times, to
" JBovt. of India promulgated the Central Births and Deaths
all persons in a country or delimited; territory"/ 7). Census is a
Registration Act in 1969. The Act came into force on 1 April
massive undertaking to contact every member of the population in a
1970. The Act provides for compulsory registration of births
given time and collect a variety of information. It needs
and deaths throughout the country, and compilation of vital
considerable organization, a vast preparation and several years to
statistics
in the States so as to ensure uniformity and
analyse the results. This is the main drawback of census as a data
comparability of data. The implementation of the Act required
source - i.e., the full results are usually not available quickly.
aaoption of rules Torwhich also, model guidelines have been
~!K frhe first regular census in India was taken in 1881, andd
provided. The AcJ^lso fixes the responsibility for reporting
w others took place at 10-year intervals. The last census was held .
births and deaths.'While the public (e.g., parents, relatives) are
i in March 2001J The census is usually conducted at the end of
/to report events occurring in their households, the heads ofN
the first quarter of the first year in each decade, the reason
hospitals, nursing homes, hotels, jails or dharmashalas are to
being, most people, are usually resident in their own homes
report events occurring in such institutions to the concerning
during that period.(The legal basis of the census is provided by
__Rflfl'gtyarlXhe time limit for registering the event of births is 14
3
the Census Act of 1948. The supreme officer who directs,
, days and mat of deaths is 7 days. In case of default a fine up to
f guides^and operates the census is the Census Commissioner for '
,, Rs.50 can be imposed^The Act makes the beginning of a new
India.^)
. era in the history of vital statistics registration in India.
v<3
L /Although the primary function of census is to provide (
a demographic information such as total count of population and its"/$breakdown into groups and subgroups such as age and sex
distribution, it represents only a small part of the total information
collected/The census contains a mine of information on subjects
not only demographic, but also social and economic
characteristics of the people, the conditions under which they live,
how they work, their income and other basic information. These
data provide a frame of reference and base line for planning,
action and research not only in the field of medicine, human
ecology and social sciences but in the entire governmental
system. Population census provides basic data (such as
population by age and sex) needed to compute vital statistical
rates, and other health, demographic and socio-economic
\|) indicators/Without census data, it is not possible to obtam
S quantified health, demographic and socio-economic indicators.")
2. Registration of vital events
Whereas census is an intermittent counting of population,
registration of vital events (e.g., births, deaths) keeps a continuous
check on demographic changes. If registration of vital events is
complete and accurate, it can serve as a reliable source of health
information. Much importance is therefore given to the registration
of vital events in all countries. It is the precursor of health
statistics. Over the years, it has dominated the health information
system.
The United Nations defines a vital events registration system as
including "legal registration, statistical recording and reporting of
the occurrence of, and the collection, compilation, presentation,
analysis and distribution of statistics pertaining to vital events,
i.e., live births, deaths, foetal deaths, marriages, divorces,
adoptions, legitimations, recognitions, annulments and legal
separations" (7). Registration of vital events has been the
foundation of vital statistics.
India has a long tradition of registration of births and deaths. In
1873, the Govt, of India had passed the Births, Deaths and
Marriages Registration Act, but the Act provided only for
voluntary registration. Subsequently, individual States like Tamil
Nadu, Karnataka and Assam passed their own Acts.
Lay reporting
'KP/ r
(_^5'
Because of slow progress in the development of a
comprehensive vital registration system, some countries have
attempted to employ first-line health workers (e.g., village health
guides) to record births and deaths in the community. Indeed, one
of the important functions of a primary health worker is to collect
and record data on vital events and other health information in his
or her community.
In order to obtain this information, a new approach has been
developed in several countries. This approach is known as "lay
reporting of health information" (9). Lay reporting is defined as the
collection of information, its use, and its transmission to other
levels of the health system by nonprofessional health workers (10).
In large majority of countries properly functioning vital events
registers do not exist and it is necessary to resort to demographic
surveys, etc. as an alternative source. The demographic survey,
however, can never lead to the desired goal of complete recording
of all vital events in a country. Thus, where a vital events
registration system is not functioning, the demographic survey
should be regarded as a temporary substitute rather than a
replacement (7).
3. Sample Registration System (SRS)
Since civil registration is deficient in India, a Sample
Registration System (SRS) was initiated in the mid-1960s to
provide reliable estimates of birth and death rates at the National
and State levels. The SRS is a dual-record system, consisting of
continuous enumeration of births and deaths by an enumerator and
an independent survey every 6 months by an investigatorsupervisor. The half-yearly survey, in addition to serving as an
independent check on the events recorded by the enumerator,
produces the denominator required for computing rates.
The SRS now covers the entire country. It is a major source of
health information. Since the introduction of this system, more
reliable information on birth and death rates, age-specific fertility
and mortality rates, infant and adult mortality, etc. have become
available.
4. Notification of diseases
Historically notification of infectious diseases was the first
health, information sub-system to be established. The primary
purpose of notification is to effect prevention and/or control of the
disease. Notification is also a valuable source of morbidity data
i.e., the incidence and distribution of certain specified diseases
which are notifiable.
Lists of notifiable diseases vary from country to country, and
also within the same country between the States and between urban
and rural areas. Usually diseases which are considered to be serious
menaces to public health are included in the list of notifiable
diseases. Notification system is usually operative through certain
legal Acts (e.g., Madras Public Health Act, 1930). Some State
Governments in India do not have any specific Act, except
invoking the Epidemic Diseases Act of 1897, and extending the
same from year to year. The notification system is linked up with
the vital statistics machinery and the reporter is often the village
chowkidar or headman. With the introduction of village Health
Guides and multipurpose workers, the reporting responsibility is
now shifted from the village chowkidar to the health workers.
Since the legal provision is an essential prerequisite for any
notification system, the enactment of a uniform Act similar to the
Registration of Births and Deaths Act, 1969 is deemed necessary
for any improvement in the notification system in India.
At the international level, the following diseases are notifiable
to WHO in Geneva under the International Health Regulations
(IHR), viz. cholera, plague and yellow fever. A few others - louseborne typhus, relapsing fever, polio, influenza, malaria, rabies and
salmonellosis are subject to international surveillance. This
information is published by WHO on a world-wide basis. The
Expert Committee on Health Statistics in its third Report (11)
recommended that yearly data of notification should be detailed by
age and sex.
Although notification is an important source of health
information, it is common knowledge that it suffers from serious
limitations : (a) notification covers only a small part of the total
sickness in the community (b) the system suffers from a good deal
of under-reporting (c) many cases especially atypical and
subclinical cases escape notification due to non-recognition, e.g.,
rubella, non-paralytic polio, etc. The accuracy of diagnosis and
thereby of notification depends upon the availability of facilities for
bacteriological, virological and serological examination. The lack
of such facilities in the rural areas of India also works against the
correct reporting of the causes of sickness.
In spite of the above limitations, notification provides valuable
information about fluctuations in disease frequency. It also
provides early warning about new occurrences or outbreaks of
disease. The concept of notification has been extended to many
non-communicable diseases and conditions notably cancer,
congenital malformations, mental illness, stroke and handicapped
persons.
5. Hospital records
In a country like India, where registration of vital events is
defective and notification of infectious diseases extremely
inadequate, hospital data constitute a basic and primary source of
information about diseases prevalent in the community. The eighth
report of the WHO Expert Committee on Statistics (12)
recommended that hospital statistics be regarded in all countries as
an integral and basic part of the national statistical programme.
The main drawbacks of hospital data are : (a) they constitute
only the "tip of the iceberg" - i.e., they provide information on only
those patients who seek medical care, but not on a representative
sample of the population. Mild cases may not attend hospitals;
subclinical cases are always missed (b) the admission policy may
vary from hospital to hospital;
TABLE 2
Population of India*
'
Population
238,396,000
251,321,000
685,185,000
843,930,000
1027,015,247
i*v ,
(frequency) which occur in each group is shown in the adjacent
column.
Example : The following figures are the ages of patients
admitted to a hospital with poliomyelitis. Construct a frequency
distribution table.
8, 24, 18, 5, 6, 12, 4, 3, 3, 2, 3, 23, 9, 18, 16, 1, 2, 3, 5, 11, 13;
15, 9, 11, 11, 7, 10 6, 9, 5, 16, 20, 4, 3, 3, 3, 10, 3, 2, 1, 6, 9, 3, 7,
14, 8, 1, 4, 6, 4, 15, 22, 2, 1, 4, 7, 1, 12,3, 23, 4, 19, 6, 2, 2, 4, 14,
2, 2, 21, 3, 2, 9, 3, 2, 1, 7, 19
The data given above may be conveniently analysed as shown
below :
Age group
Frequency
o~4
mmmwmmm
35
5-9
m m-m 111
is
10-14 m m 1
11
15-19
m III
8
20-24 ~m 1__________________________6______
The data, analysed above, is prepared in the form of a
frequency table as shown below :
TABLE 3
Age distribution of polio patients
In the above example, the age is split into groups of five. These
are known as class intervals. The number of observations in each
group is called frequency. In constructing frequency distribution
tables, the questions that arise are : Into how many groups the data
should be split ? And what class intervals should be chosen ? As a
practical rule, it might be stated that when there is large data, a
maximum of 20 groups, and when there is not much data, a
minimum of 5 groups, could be conveniently taken. As far as
possible, the class intervals should be equal, so that observations
could be compared. The merits of a frequency distribution table
are, that it shows at a glance how many individual observations are
in a group, and where the main concentration lies. It also shows
the range, and the shape of distribution.
CHARTS AND DIAGRAMS
Charts and diagrams are useful methods of presenting simple
statistical data. They have a powerful impact on the imagination of
people. Therefore, they are a popular media of expressing
statistical data, especially in newspapers and magazines. The
impact of the picture depends on the way it is drawn. A few
general remarks need be mentioned about charts and diagrams.
Diagrams are better retained in the memory than statistical tables.
The data that is to be presented by diagrams ought to be simple.
Then there is no risk that the reader will misunderstand. However,
simplicity may be obtained only at the expense of details and
accuracy. That is, lot of details of the original data may be lost in
the charts and diagrams. If we want the real study, we have to go
back to the original data.
1. Bar Charts
^Bar charts are merely a way of presenting a set of numbers by Ihe
length of a bar - the length of the bar is proportional to the
magnitude to be representedT^ar charts are a popular media of
presenting statistical daTarJecause they are easy to prepare, and
enable values to be compared visually. The following are some
examples of bar charts.
*#-------------- f.-------------------------------
AM
FIG. 4
India : Growth of population 1901 to 2001
3. Pie Charts
Instead of comparing the length of a bar, the areas of segments
of a circle are compared. The area of each segment depends upon
the angle. Pie charts are extremely popular with the laity, but not
with statisticians who consider them inferior to bar charts. It is
often necessary to indicate the percentages in the segments (Fig. 8)
as it may not be sometimes very easy, virtually, to compare the
areas of segments.
FIG. 8 World
Population
4. Pictogram
Pictograms are a popular method of presenting data to the "man
in the street" and to those who cannot understand orthodox charts.
Small pictures or symbols are used to present the data. For
example, a picture of doctor to represent the population per
physician (Fig. 9). Fractions of the picture can be used to represent
numbers smaller than the value of a whole symbol. In essence,
pictograms are a form of bar charts.
STATISTICAL MAPS
When statistical data refer to geographic or administrative
areas, it is presented either as "Shaded Maps" or "Dot maps"
according to suitability. The shaded maps are used to present data
of varying size. The areas are shaded with different colours, or
different intensities of the same colour, which is indicated in the
key.
jgcaQer diagram shows the relationship between two
varia5l^}e.g., Fig. 10 shows a positive correlation between the
intakes of fat and sugar in the average diets of 41 countries.
Populations with more income are known to consume
more protein, fat and also sugar (Source : Yudkin, J. (1964) : Lancet, 2, 5)
FIG. 10
Relation between average fat intake and sugar intake in 41 countries
!/*yf rthe dots cluster round a straight line, it shows evidence of ^\ a relationship of a linear nature. If there is no such clusterjit is J probable
that there is no relationship between the variables7|
adding together is called 'summation' and is denoted by the sign X or S. The individual observation is denoted by the sign r\ and the
mean is denoted by the sign x (called "X bar").
The mean (x) is calculated thus : the diastolic blood pressure of 10 individuals was 83, 75, 81, 79, 71, 95, 75, 77, 84, 90. The total was
810. The mean is 810 divided by 10 which is 81.0.
The advantages of the mean are that it is easy to calculate and understand. The disadvantages are that sometimes it may be unduly
influenced by abnormal values in the distribution. Sometimes it may even look ridiculous; for instance, the average number of children born to
a woman in a certain place was found to be 4.76, which never occurs in reality. Nevertheless, the arithmetic mean is by far the most useful of
the statistical averages.
The Median
The
median
is
an
average
of
a
different
kind,
not
depend
upon
the
total
and
number
of
items.
To
median,
the
data
is
first
arranged
in
an
descending
order
of
magnitude,
and
then
the
value
middle
observation
is
located,
which
is
called
the
example,
the
diastolic
blood
pressure
of
9
individuals
follows
:
(Fig. 11).
The median is 79, which is the value of the middle observation (Fig. 12).
Diastolic Blood
Pressure
83
75
81
79
71
95
75
77
84
FIG. 11
Data unarranged
which
obtain
ascending
of
median.
was
does
the
or
the
For
as
Diastolic Blood
Pressure
71
75
75
77
79 Median
81
83
84
J____95
FIG. 12
Data arranged in
order of magnitude
If there are 10 values instead of 9, the median is worked out by taking the average of the two middle values. That is, if the number of items
or values is even, the practice is to take the average of the two middle values. For example, the diastolic blood pressure of 10 individuals was :
Fig. 13.
In the example given, the median will be 79 + 81 divided by 2 which is 80 (Fig. 14).
E(x }
n
Example : The diastolic blood pressure of 10 individuals was as
follows : 83, 75, 81, 79, 71, 95, 75, 77, 84 and 90. Find the mean
deviation.
Answer (Mean deviation)
Diastolic B.P.
Arithmetic Mean
83
75
81
79
71
95
75
77
84
90
Total = 810
81
81
81
81
81
81
81
81
81
81
Deviation from
the Mean (x - x)
2
-6
0
2
-10
14
-6
-4
3
9
V------- \
(wv
^"^
.*
jf (a) First of all, take the deviation of each value from the
arithmetic mean,
&,
y
-i, ) /
(b)
(c)
(a)Divide the result by the number of observations r| : [or (n, 1) in case the sample size is less than 30]
(b)Then take the square root, which gives the standard
deviation.
Example : The diastolic blood pressure of 10 individuals was as
follows : 83, 75, 81, 79, 71, 95, 75, 77, 84, 90. Calculate the
standard deviation.
FIG.
15
^ffifyi,
Pyf^TS
/
Normal Curve,,
V-f I *?)
(Supposing we are considering the 95 per cent confidence limits
(3c 2 a). When we say this, we mean that 95 per cent of the area
of the normal curve, and hence 95 per cent of the values in the
distribution will be included between the limits x 2 a . Therefore,
the probability of a reading falling outside the 95 per cent
confidence limits is 1 in 20 (P = 0.05U
= V 53.55
= 7.31
0.00
.0000
0.50
.1915
1.00
.3413
1.50
.4332
2.00
.4772
3.00
.4987
4.00
.49997
5.00
.4999998
1
\y
Source : (20)
Estimation of Probability (Example)
Let us suppose, the pulse of a group of normal healthy males
was 72, with a standard deviation of 2. What is the probability that
a male chosen at random would be found to have a pulse of 80 or
more ?
The relative deviate (z)
= ------------a
80-72
= ---------- = 4
2
x-u
a /yjr\
Significance
N.D. > 2
P < 0.05
Significant at 5 per cent level
N.D. = 2
P = 0.05
Just significant at 5 per cent level
N.D. < 2
P > 0.05
Not significant at 5 per cent level
TESTS OF SIGNIFICANCE
We have observed till now that standard error indicates how reliable
an estimate of the mean is likely to be. The concept of standard error is
applied with appropriate formulate to all statistics, i.e., mean, standard
deviation, etc. It is proposed to consider briefly the following :(a)Standard Error of the Mean
(b)Standard Error of Proportion
(c)Standard Error of Difference
(d)Standard Error of Difference between two Proportions.
(a) Standard Error of the Mean
We have already considered in some detail the meaning of the
"standard error of the mean" which is also called simply the standard
error, and the distribution of the sample means about the true mean of the
universe. In actual practice, we don't take repeated samples usually from a
population. We take only one sample from the universe and calculate the
mean and standard deviation. The questions that arise are : How accurate
is the mean of our sample ? What can be said about the true mean of the
universe ? In order to answer these questions, we calculate the standard
error of the mean and set up 'confidence limits' within which the mean (ji),
of the population (of which we have only one sample) is likely to lie.
Example : Let us suppose, we obtained a random sample of 25 males,
age 20-24 years whose mean temperature was 98.14 deg. F with a
standard deviation of 0.6. What can we say of the true mean of the
universe from which the sample was drawn ?
We use the standard error as the yard stick : S.E.x =
S/VCn) = 0.06/^(25) = 0.12
We now set up confidence limits on the basis of the normal curve
distribution. If the limits are set out at twice the standard error from the
mean (95 per cent confidence limits) the range of the population mean
would be 98.14 (2 x 0.12) = 97.90 deg. F. to 98.38 deg. F. The chances
will be only 1 in 20 (P = 0.05) that the population mean would be outside
these limits.
Very often we come across in scientific terminology the word
'significant'. When we say that "this difference is significant", we mean
that it is unlikely to be merely due to chance. It has become customary to
regard as significant, when P<0.05 (1 in 20) and more significant, when P
< 0.01 (1 in 100).
(b) Standard Error of Proportion
Let us suppose, the proportion of males in a certain village was 52 per
cent. A random sample of 100 people was taken, and the proportion of
males was found to be only 40 per cent. What conclusions could be drawn
from the sample ? What possible range of males could we expect in a
sample of 100, within 95 per cent confidence limits ?
In an example of this kind, we are not dealing with means but with
proportions in a sample and its universe. We may designate these
proportions as p and q and proceed to calculate the standard deviation
round that expected 52 per cent. This is called the standard error of
proportion and is given by the formula :
/ PQ
S.E. (Proportion)
=\
52
* 48
=5.0 \
100
Mean
12
318
Control group
Experimental group
12
10.2
difference, i.e., 2x6. We infer that there was no strong evidence of any
difference between the efficacy of the two vaccines. Therefore, the
observed difference might be easily due to chance.
24.1
Standard
Deviation
370
\
1
s
i
'(10.2)
(24.1)
+
12
^8.67
CHI-SQUARE TEST
|Chi-square (%2) Test offers an alternate method of testing the
significance of difference between two proportions. It has the advantage
that it can also be used when more than two groups are to be compared?)
Let us considerme previous example : we were making a trial of 2
whooping cough vaccines. The results of the field trial were as below:
Attacked
Not
Attacked
22
68
90
24.4%
14
72
86
16.2%
36
140
176
12
4 -
48.4
Attack
Rate
Vaccine
2
Total
Total
^ 57.07
7.5
The standard error of difference between the two means is 7.5. The
actual difference between the two means is (370-318) = 52, which is more
than twice the standard error of difference between the two means, and
therefore "significant". We conclude that the treatment affected the kidney
weights.
(d) Standard Error of Difference Between Proportions
Instead of means, sometimes we may have to test the significance of
difference between two proportions or ratios to find out if the difference
between the two proportions or ratios have occurred by chance. In this
case, we calculate the standard error of difference between two
proportions.
Let us suppose, we are making a trial of 2 whooping cough vaccines.
The results of the field trial were as follows :
Vaccine
No.
Vaccinated
No. of
Exposures
2,400
2,300
Attack
Rate
90
No. of
cases
22
24.4%
86
14
16.2%
Melee
between two
proportions
_5lfi.
n
+
n
Attacked
^i
24.4x75.6
9~
0 = 22
18.36
rf
+ 3.64
0 = 68
71.55
0 = 14
o = 72
B
16.2x83.8
Not Attacked
3.55
17.54
68.37
- 3.54
+ 3.63
86
V 20.49 + 15.78
----------V 36.27 = 6.02
The standard error of difference is 6 whereas the observed difference
(24.4 - 16.2) was 8.2. In other words, the observed difference between the
two groups is less than twice the S.E. of
(3.64)2
18.36
(3.55)2
71.55
0.71+0.19 =
17.54
1.79
(3.54)2
+
68.37 =
(3.63)2 X =
0.72 + 0.17 +
(c-l)(r-l)
(2 - 1) (2 - 1) = 1 J
S(x-x)(y -y) r =
VS(x-x)2 S(y-y)2
TABLE OF x2
Probability (P)
D.F._____________150______________L10______________.05______________.02______________.01______________.005_____________.001
1.0.45
2.1.39
3.2.37
4.3.36
5.4.35
6.5.35
7.6.35
8.7.34
9.8.34
10.9.34
76
47
10
00
07
20
31
98
24
01
50
90
46
47
12
23
65
37
2.71
4.61
6.25
7.78
9.24
10.65
12.02
13.36
14.68
15.99
58
56
80
95
28
26
56
40
33
31
78
78
72
21
73
54
76
55
30
91
21
01
37
36
34
07
45
60
13
50
60
61
73
20
36
85
3.84
5.99
7.82
9.49
11.07
12.59
14.07
15.51
16.92
18.31
83
29
38
31
07
31
19
17
77
10
69
05
18
88
99
83
95
78
64
34
84
76
61
62
09
81
58
39
36
62
77
32
12
85
90
78
5.41
7.82
9.84
11.67
13.39
15.03
16.62
18.17
19.68
21.16
87
05
90
17
11
68
79
22
80
53
37
77
55
27
49
23
18
01
29
87
56
16
16
69
57
45
45
58
68
79
66
80
99
86
48
48
6.64
9.21
11.34
13.28
15.09
16.81
18.48
20.09
21.67
23.21
25
31
35
29
36
86
92
44
67
47
53
13
12
30
57
66
27
41
58
06
03
56
27
95
36
84
93
70
37
57
62
21
94
99
45
19
84
95
09
63
03
44
59
11
82
93
31
44
11
60
82
07
68
10
86
12
43
38
78
84
14
24
75
85
71
59
08
10
96
36
27
35
7.88
10.60
12.64
14.86
16.75
18.55
20.28
21.96
23.59
25.19
50
45
12
78
86
95
93
62
70
81
26
60
99
92
88
37
23
19
60
57
74
94
72
48
87
20
16
56
35
10
55
35
57
34
65
54
10.83
13.82
16.27
18.47
20.51
22.46
24.32
26.13
27.88
29.59
00
09
49
49
04
46
81
42
08
39
03
39
64
36
17
92
30
07
25
09
14
81
95
45
40
31
24
38
71
66
57
12
91
09
72
73
*Taken from Table XXXIII of : Fisher, R.A. & Yates, F. Statistical tables for biological, agricultural and medical research, 6th ed., Longman
Group Ltd., London, 1974.
References
where
y
"y
x
=
=
=
y+b ( x - x )
meanofyry2 y3.......................yn
mean of x x,, x,................. x
E ( x - x ) (y-y)
E(x-x)2
&
(source)
(audience)
(content)
(medium)
(effect)
1. Sender
The sender (communicator) is the originator of the message. To
be an effective communicator, he must know:
-his objectives, clearly defined
-his audience : it's interests and needs
-his message
-channels of communication
-his professional abilities and limitations
The impact of the message will depend on his own social status
(authority), knowledge and prestige in the community.
2. Receiver
All communications must have an audience, this may be a
single person or a group of people. Without the audience,
communication is nothing more than mere noise. It is this element
of audience and their frame of mind (e.g., opinions, attitudes,
prejudices) which lends meaning to all the different types of
communication.
The audience may be of two types : the controlled and the
uncontrolled. A controlled audience is one which is held together
by a common interest. It is a homogeneous group. An uncontrolled
or "free" audience is one which has gathered together from motives
of curiosity. This type of audience poses a challenge to the ability
of the educator. The more homogeneous the audience is, the
greater are the chances of an effective communication.
3. Message
A message is the information (or "technical know - how") which the communicator transmits to his audience to receive, understand,
accept and act upon. It may be in the form of words, pictures or signs. Health communication may fail in many cases, if its message is not
adequate.
A good message must be :
-in line with the objective (s)
-meaningful
-based on felt needs
-clear and understandable
-specific and accurate
-timely and adequate
-fitting the audience
-interesting
-culturally and socially appropriate
Transmitting the right message to the right people at the right time is a crucial factor in successful communication.
4. Channels of Communication
By channel is implied the "physical bridges" or the media of communication between the sender and the receiver.
Media systems
The total communication effort is based on three media systems :
a. Interpersonal communication
b. Mass media
c. Traditional or folk media
a. Interpersonal communication
The most common channel of communication is the interpersonal or face - to - face communication. Being personal and direct it is more
persuasive and effective than any other form of communication. Interpersonal communication is particularly important in influencing the
decisions of the undecided persons. The superiority of interpersonal communication over mass media for creation of motivational effect has
been well documented (4).
When the message relayed via mass media gets diffused in the community, it is picked up by the interpersonal and informal networks.
The message is then subject to debate and discussion by interpersonal communications. On the basis of this scrutiny a consensus is
gradually built up in the community whether to accept or reject the message (5).
b. Mass media
In mass communication, the channel is one or more of the
following "mass media", viz TV, radio, printed media, etc/74ass
^media have the advantage of reaching a relatively larger
i population in a shorter time than is possible with other means.
Being one - way channels of communication, mass media carry
\ messages only from the centre to the periphery ; feedback
mechanisms are poorly organized. Being impersonal media,
they are usually not effective in changing established modes of
behaviourj
c. Folk media
Every community has its own network of traditional or folk media such as folk dances, singing, dramas, Nautanki in Uttar Pradesh,
Burrakatha in Andhra Pradesh and Harikatha in Western India besides informal group gatherings, caste or religious meetings. These are
important channels of communication close to the cultural values of the rural population. They have been the principal instruments of
preserving the cultural heritage. Health messages may b communicated through these traditional media.
Every channel of communication has its advantages an limitations. For instance, knowledge of surgery cannot b effectively transmitted
by verbal communicatior demonstrations are needed. The proper selection and use c channels results in successful communication. Since
effectiv communication is seldom achieved through the use of om method alone, an attempt should be made to combine < variety of
methods to accomplish the educational purpose Health education uses a variety of methods to help peopl< understand their own situations
and choose actions that wil improve their health.
5. Feedback
It is the flow of information from the audience to the sender It is the reaction of the audience to the message. If the message is not clear or
otherwise not acceptable the audience may reject it outright. The feedback thus provides an opportunity tc the sender to modify his message
and render it acceptable. In interpersonal communication the feedback is immediate. In mass communication it takes some time to get
feedback. Feedback is generally obtained through opinion polls, attitude surveys and interviews. It can rectify transmission errors.
TYPES OF COMMUNICATION
1. One - way communication (Didactic Method)
The flow of communication is "one-way" from the communicator to the audience. The familiar example is the lecture method in class
rooms. The drawbacks of the didactic method are :
-knowledge is imposed
-learning is authoritative
-little audience participation
-no feedback
-does not influence human behaviour
2. Two - way communication (Socratic Method)
The Socratic method is a two - way method of communication in which both the communicator and the audience take part. The audience
may raise questions, and add their own information, ideas and opinions to the subject. The process of learning is active and "democratic". It
is more likely to influence behaviour than one - way communication.
3. Verbal communication
The traditional way of communication has been by word of mouth. The advent of written and printed matter are of comparatively recent
origin. Direct verbal communication by word of mouth may be loaded with hidden meanings. It is persuasive. Non - direct or written
communication may not be as persuasive as the spoken word.
4. Non - verbal communication
Communication can occur even without words. It includes a whole range of bodily movements, postures, gestures, facial expressions
(e.g., smile, raised eye brows, frown, staring, gazing etc.). Silence is non - verbal communication. It can speak louder than words.
5. Formal and informal communication
Communication has been classified into formal (follows lines of authority) and informal (grape-vine) communication. Informal network
(e.g., gossip circles) exists in all organizations. The informal channels may be more active, if the formal channels do not cater to the
information needs.
-increase awareness of the people to the point that they are able
to perceive their health needs ; and
-influence people to the extent that unfelt needs become felt
needs, and felt needs become demands.
The government, the media and health providers have an
important social responsibility to provide factual and balanced
health and health related information to the people and awaken
their interest on the basis of which they can make informed
decisions. But, the assumption that the acquisition of information
will mean a change in an individual's behaviour and attitudes is
fallacious. Most people make important decisions regarding their
health only after much thought -perhaps over a period of time and
after serval educational contacts. The cultural values, beliefs and
norms of the people influence their acceptance of health
information. Correct information is a basic part of health
education.
2. Education
Education of the general public is an integral part of a
prevention - oriented approach to health and disease problems;
and, the basis of all education is communication. Education can
help to increase knowledge. It is often assumed that knowledge
determines attitudes and attitudes determine behaviour (7).
Health education can bring about changes in life styles and risk
factors of disease. Most of the world's major health problems and
premature deaths are preventable through changes in human
behaviour at low cost (8). But education alone is insufficient to
achieve optimum health. The target population must have access to
proven preventive measures or procedures.
3. Motivation
It is the power that drives a person from within to act. One of
the goals of health communication is to motivate individuals to
translate health information into personal behaviour and life - style
for their own health. Motivation includes the stages of interest,
evaluation and decision making. Health communication assists the
individual in passing from the state of awareness and interest to the
final stage of decision making and adoption of the new idea or
programme. Motivation may not be long - lasting; it may diminish
with lapse of time. The best channels of success involve
programmes directed at individuals who already have some strong
motivation, in patients with chronic illness or a disability, those
facing acute crisis such as surgery or childbirth. This suggests that
probably the quickest pay off will come in the area of patient
education.
4. Persuasion
Persuasion is the art of winning friends and influencing people.
It is an art that does not employ force or deliberate manipulation.
The sole purpose of communication is to influence. Persuasion is
"a conscious attempt by one individual to change or influence the
general beliefs, understanding, values and behaviour of another
individual or group of individuals in some desired way".
Persuasive communication is more effective than coercion or
authoritative communication. Persuasion can change life style and
modify the risk factors of disease.
When persuasive communication is deliberately employed to
manipulate feelings, attitudes and beliefs, it becomes "propaganda"
or "brain washing" (1).
5. Counselling
Counselling is a process that can help people understand better
and deal with their problems and communicate better with those
with whom they are emotionally involved. It can improve and
reinforce motivation to change behaviour. It can provide support at
times of crisis. It helps them face up to their problems and to
reduce or solve them.
_________________________________HEALTH EDUCATION
657
disease in his community, as for example vaccination in an
emergency. Secondly in areas involving personal choice (e.g., diet,
exercise, smoking) no government can pass legislation to force
people to eat a balanced diet or not to smoke. It amounts to taking
away some of the rights of the individual. The disastrous
sterilization campaign of 1976 in India which led to the Congress
defeat in the 1977 elections is a case in point. The lesson learnt is
that it is difficult to enforce a law unless the majority of people are
in favour of it and if it does not interfere with the rights of the
individual.
However, laws may be useful in times of emergency or in
limited situations such as control of an epidemic disease or
management of fairs and festivals. Even in cases where it is the
duty of the government to make laws to prevent the spread of
disease (e.g., AIDS) it is difficult to enforce laws without a vast
administrative infrastructure and considerable expenditure. To a
degree, the people must be ready to accept a law. In short, the
coercive approach runs counter to the basic tenet of health
education, that is, in health education, we do not force people to
change. In specific situations, legislation can be used to reinforce
the pressure to change collective behaviour.
2. Service approach
This approach was tried by the Basic Health Services in 1960's.
It aimed at providing all the health services needed by the people
at their door steps on the assumption that people would use them to
improve their own health. This approach proved a failure because
it was not based on the felt-needs of the people. For example,
when water-seal latrines were provided by the government, free of
cost, many people in the rural areas did not make use of them
because it was not their habit to use latrines. The lesson is simple the people will not accept a programme or service, even if it is
offered free of cost, unless it is based on their felt-needs.
3. Health education approach
There are many problems (e.g., cessation of smoking, use of
safe water supply, fertility control) which can be solved only
through health education. It is a general belief in western
democracies that people will be better off if they have autonomy
over their own lives, including health affairs on which an informed
person should be able to make decisions to protect his own health.
These are the higher goals of health education. However, if the
necessary behaviour changes are to take place, people must be
educated through planned learning experiences what to do, and be
informed, educated and encouraged to make their own choice for a
healthy life. This approach is consistent with democratic
philosophy which does not "order" the individual. The results are
slow, but enduring. The mass media and social organizations must
be mobilized to help introduce new attitudes and new habits
without conflicting with the masses and the collective reaction to
particular change.
Since attitudes and behavioural patterns are formed early in life.
We must move back in time and start health education with young
population. The assumption is that behaviour is more easily
controlled or developed in young population than adults (16).
4. Primary health care approach
This is a radically new approach starting from the people with
their full participation and active involvement in the planning and
delivery of health services based on principals of primary health
care, viz community involvement and intersectoral coordination.
The underlying objective is to help individuals to become selfreliant in matters of health. This, in turn, can be done if the people
receive the necessary guidance from health care providers in
identifying their health problems and finding workable solutions.
This approach is a fundamental shift from the earlier approaches.
Interest
Evaluation
Decision - making
Adoption or acceptance
FIG. 2
Adoption Model
TABLE 1
Health education and propaganda
Health Communication
I---------------------------------------------------------- 1---------------------------------------------------------- 1
Individual
Group
approach
approach
Mass approach
I
1. Personal contact
2 Home visits
3. Personal Letters
I
1. Lectures
2. Demonstrations
3. Discussion methods
-Group discussion
-Panel discussion
-Symposium
-Workshop
-Conferences
-Seminars
-Role play
FIG. 3 Methods in Health
Communication
I
Television
Radio
News paper
Printed material
Direct mailing
Posters
Health museums
and exhibitions
8. Folk methods
9. Internet
1.
2.
3.
4.
5.
6.
7.
2.
3.
4.
Personal communication
(Interpersonal and group methods)
1. Capitalizes on warmth and understanding
and knowledge of communication
2. Provides the opportunity for involvement,
for asking questions, expressing fears,
and learning more
3. Can get people to make changes in personal
habits more readily, when discussion presents
reasonable explanations for these changes.
4. More influential with average and below
average educational level.
(1) Chalk and talk (Lecture)
A lecture may be defined as carefully prepared oral presentation
of facts, organized thoughts and ideas by a qualified person. The
"chalk" lends the visual component. The chalk and talk
communication has still a very important place in small group
education. Its effectiveness depends to a large extent on the
speaker's ability to write legibly and to draw with chalk on a black
board. The talk should be based on a topic of current interest or
health needs of the group. The group should not be more than 30
and the talk should not exceed 15 to 20 minutes. If the talk is too
long people may become bored and restless.
The lecture method can be made more effective by combining
with suitable audio-visual aids such as :
(a)Flipcharts : They consist of a series of charts (or posters), about
25 by 30 cms or more, each with an illustration pertaining to the
talk to be given. They are meant to be shown one after another.
Each chart is "flashed" or displayed before a group as the talk is
being given. The message on the charts must be brief and to the
point. These charts are primarily designed to hold attention of the
group and help the lecture to proceed.
(b)Flannelgraph : A piece of rough flannel or khadi fixed over a
wooden board provides an excellent background for displaying
cut-out pictures, graphs, drawings and other illustrations. The cutout pictures and other illustrations are provided with a rough
surface at the back by pasting pieces of sand paper, felt or rough
cloth and they adhere at once when put on the flannel.
Flannelgraph offers the advantage that pre-arranged sequence of
pictures displayed one after another helps maintain continuity and
adds much to the presentation. The other advantages are that the
flannelgraph is a very cheap medium, easy to transport and
promotes thought and criticism (c) Exhibits : Objects, models,
specimens, etc. convey a specific message to the viewer. They are
essentially'mass media of communication, which can also be used
in group teaching, (d) Films and charts : These are mass media of
communication. If used with discrimination, they can be of value
in educating small groups.
(Lectures can be faulted on a number of grounds. Theiij^j
disadvantages include the following : students are involved to a
minimum extent; learning is passive; do not stimulate thinking^ or
problem-solving capacity; the comprehension of a lecture^ varies
with the student; and the health behaviour of the listeners is not
necessarily affected.")
(2) Demonstrations
A demonstration is a carefully prepared presentation to show
how to perform a skill or procedure. Here a procedure (e.g. lumber
puncture, disinfection of a well) is carried out step by step before
an audience or the target group, the demonstrator ascertaining that
the audience understands how to perform it. The demonstrator
involves the audience in discussion.
M3)
1
1
FIG. 4 A good group
discussion
Limitations : Group discussion is not without limitations. Those
who are shy may not take part in the discussions. Some may
10.TRS 7661988
11.NIHAE : A Guide
23.Kelley E.C. (1950). The Workshop Way of Learning, Harper & Row, N.Y.
2
0
"Plan ahead - it was not raining when Noah built the ark"
Planning and management are relatively new subjects. Planning
is for tomorrow, and management is for today. These subjects have
acquired great importance during the past two decades. The
purpose of planning is (1) to match the limited resources with
many problems; (2) to eliminate wasteful expenditure or
duplication of expenditure; and (3) to develop the best course of
action to accomplish a defined objective. The increasing demand
for medical and health care services, in the face of limited
resources, has brought out the need for careful planning and
management of health services. Planning and management are
considered essential if higher standards of health and health care
are to be achieved (1).
Planning in its broadest sense includes three steps:
(a)Plan formulation
(b)Execution; and
(c)Evaluation
Planning is a matter of team work and consultation. The
planning team consists of not only specialists within the field, but
also specialised in other fields, viz. economics, statistics,
sociology, management, etc.
DEVELOPMENT PLANNING
Every country has its own plan for national development. The
purpose of national planning is to achieve a rapid, balanced,
economic and social development of the country as a whole. The
National Development Plan of a country is a combination of
sectoral plans which comprise the following sectors, viz. food and
agriculture, education, health and family planning, industry,
transport and communications, housing, power, social welfare, etc.
All these sectors compete for national resources (2).
In this context, National Development Planning has been
defined as "continuous, systematic, coordinated, planning for the
investment of the resources of a country (men, money and
materials) in programmes aimed at achieving the most rapid
economic and social development possible (3).
HEALTH PLANNING
Health planning is a concept of recent origin. It is part of
national development planning. Health planning is necessary for
the economic utilisation of material, man-power and financial
resources. The purpose of health planning is to improve the health
services.
In this context/National Health Planning has been defined
as "the orderly ^process of defining community health
problems, identifying unmet needs and surveying the resources
to meet them, establishing priority goals that are realistic and
population.
2. Establishment of objectives and goals
Objectives and goals are needed to guide efforts. Unless objectives are established, there is likely to be haphazard activity, uneconomical use of funds and poor performance. Objectives must be established at all levels, down to the smallest organizational unit. At
upper levels, objectives are general; at successively lower levels, they become more specified and detailed. The objectives may be shortterm or long-term. In setting these objectives, time and resources are important factors. Objectives are not only a guide to action, but also
a yard-stick to measure work after it is done. Modern management techniques such as "cost-benefit" analysis, and "input-output" study of
health services are being used for defining goals, objectives and targets in more definite terms than hitherto.
3. Assessment of resources
The term resources implies the manpower, money, materials, skills, knowledge and techniques needed or available for the
implementation of the health programmes. These resources are assessed and a balance is struck between what is required and what is
available, or likely to be available in terms of resources.
4. Fixing priorities
Once the problems, resources and objectives have been determined, the next most important step in planning is establishment of
priorities in order of importance or magnitude, since the resources always fall short of the total requirement. In fixing priorities, attention
is paid to financial constraints, mortality and morbidity data, diseases which can be prevented at low cost, saving the lives of younger
people in whom there has been considerable social investment; and also political and community interests and pressures.
Once priorities have been established, ALTERNATE PLANS for achieving them are also formulated and assessed in order to
determine whether they are practicable and feasible. Alternate plans with greater effectiveness are chosen.
5. Write-up of formulated plan
The next major step in the planning process is the preparation of the detailed plan or plans. The plan must be complete in all respects
for the execution of a project. For each proposed health programme, the resources (inputs) required .are related to the results (outputs)
expected. Each stage of the plan is defined and costed and the time needed to implement is specified. The plan must contain working
guidance to all those responsible for execution. It must also contain a "built-in" system of evaluation. It will be left to the central planning
authority and the government to consider modifications of the plan relating to allocation of resources.
6. Programming and implementation
Once the health plan has been selected and approved by the policy making authorities, programming and implementation are begun.
Plan execution depends upon the existence of effective organization. The organizational structure' must incorporate well-defined
procedures to be followed and sufficient delegation of authority to and fixation of responsibility of different workers for achieving the
predetermined objectives during the period prescribed. It is at the implementation stage that shortcomings often appear in practice. Many
well considered plans have fallen down because of delays in critical supplies, inappropriate use of staff, and
similar factors. The main considerations at the implementation ' stage include: (a) definition of roles and tasks (b) the selection, training,
motivation and supervision of the manpower involved (c) organization and communication and (d) the efficiency of individual institutions
such as hospitals or health centres.
7. Monitoring
Monitoring is the day-to-day follow-up of activities during their implementation to ensure that they are proceeding as planned and are
on schedule. It is a continuous process of observing, recording, and reporting on the activities of the organization or project. Monitoring,
thus, consists of keeping track of the course of activities and identifying deviations and taking corrective action if excessive deviations
occur.
8. Evaluation
The purpose of evaluation is to assess the achievement of the stated objectives of a programme, its adequacy, its efficiency and its
acceptance by all parties involved. While monitoring is confined to day-to-day or on-going operations, evaluation is mostly concerned
with the final outcome and with factors associated with it. Good planning will have a built-in evaluation to measure the performance and
effectiveness and for feed-back to correct deficiencies or fill up gaps discovered during implementation. In the words of the WHO Expert
Committee on National Health Planning in Developing Countries, evaluation "measures the degree to which objectives and targets are
fulfilled and the quality of the results obtained. It measures the productivity of available resources in achieving clearly-defined
objectives. It measures how much output or cost-effectiveness is achieved. It makes possible the reallocation of priorities and of
resources on the basis of changing health needs" (6).
MANAGEMENT (7)
The term "management" is used in many senses. It is sometimes confused with administration; sometimes with organization. Some
equate the terms, management and administration. Others view it as a technique of leadership. The widely prevalent view is that
administration broadly means "getting things done" and management as "the purposeful and effective use of resources - manpower,
materials and finances - for fulfilling a pre-determined objective". In theory, management consists of four basic activities :
(i) planning: determining what is to be done.
(ii) organizing: setting up the framework or apparatus and making it possible for groups to do the work.
(iii) communicating: motivating people to do the work.
(iv) monitoring (controlling): checking to make sure the work is progressing satisfactorily.
Management techniques are familiar in business, industry, defence and other fields. The current emphasis by WHO and many
governments is on improving the efficiency of the health care delivery systems through the application of modern management methods
and techniques.
MANAGEMENT METHODS AND TECHNIQUES (1, 8, 9)
$0% (Management techniques are many. They are based on principles of behavioural sciences as well as quantitative methods)These
techniques have been developed by experts of management science to help the managers of any organization to achieve the stated goals
more efficiently. Efforts are being made by the WHO for making these techniques more popular for application in the health field. A
brief account of these techniques is given below :
______________________________________MANAGEMENT 669
Methods based on behavioural sciences
1. ORGANIZATIONAL DESIGN
Poor organization results in waste of resources. It is a theory of
management that organization must be suited to its current^
situation and the needs to be serviced. The organization or health
services should, therefore, be designed so as to meet the health
needs and demands of the people. Further, the organizational design
should be reviewed every few years because of changing concepts
or purpose, changing problems and changing technology. Efficient
delivery of health services depends upon the existence of an
effective organization.
2. PERSONNEL MANAGEMENT
This is skilful use of human resources. Proper methods of
selection, training and motivation; division of responsibility;
distribution of roles; elimination of "square pegs in round holes"
(i.e., professional staff not suited to administration, either through
training, selection or natural inclination, should not bev entrusted
with administrative and management burdens); incentive for better
work; opportunities for promotion and professional advancement;
effective design of "health teams" are all fundamental techniques of
personnel management which could contribute to the efficiency of
health service delivery.
3. COMMUNICATION
Better communication contributes to effective functioning of an
organization. Communication roadblocks exist at various levels:
between the doctor and the patient; doctor and nurse; between the
senior officials and juniors; between the directorate and the health
ministry; between the health ministry and other ministries and rest
of the government. Communication barriers are responsible for
delays in regular reporting and notification; delays in the
compilation of statistics; delays in the release of supplies and
salaries; delays in the institution of prompt remedial measures. In
fact, these are some of the major weaknesses in health ministries.
One of the tasks of health management is to solve the
communication problems by establishing suitable vertical and
horizontal communication channels.
4. INFORMATION SYSTEMS
Information is needed for day-to-day management of the health
system. Information comes from many sources - both, formal and
informal. The information system should be tailored according to
the management needs of the individual health services. The
functions of an information system consist of collection,
classification, transmission, storage, retrieval, transformation and
display of information. A good information system provides data
for monitoring and evaluation of health programmes and gives the
requisite feed-back to health administrators and planners at all
levels. Computers can play a great role in improving the health
information system.
0^4
/
(Quantitative Methods
oibs^
1
Quantitative methods are derived from the field Vief
economics, operation research and budgeting. Some of these
techniques have a great role in the management of health
services :)
/"\ ,, .X*\
\*P'\\
H (Ju)
calculate the time by which each activity mustjje 1completed, and to identify those activities that are criticaTTJThis simple technique provides a basic
discipline by which aflconcerned in a project can know what is expected of them and to minimise any delays or crises in the implementation of the plan.
Y* (PERT is a useful management technique which can be ^applied to a great variety of projects. It aids in planning, .scheduling and monitoring the project;
it allows better * communication between the various levels of management; it identifies potential problems; it furnishes continuous, timely progress
reports; it forms a solid foundation upon which to build an evaluation and checking system.;., JQ\O
1(b) CRITICAL PATH METHOD (CPM) : The longest path of the network (Fig. 2) is called "critical path". If any activity along the critical path is
delayed, the entire project will be
de,av""IU
t PLANNING-PROGRAMMING-
<\V*N
BUDGETING SYSTEM (PPBS) : \/The Planning-Programming-Budgeting System (PPBS) is primarily a system to help decision makers to allocate resources so that the available resources
of an organization are used in the most effective way in achieving its objectives. The PPBS does not call for changes in the existing organization. It calls foj
grouping of activities into programmes related to each objectiue.jAnother\ approach is known as the 'Zero Budget Approactf*7 i.e., all ' budgets start at zero
and no one gets any budget that he cannot; specifically justify on a year-to-year basis.
f 9. WORK SAMPLING : (^ w (J ^ ^ (*?V
It is systematic observation and recording of activities of one or more individuals, carried out at predetermined or random intervals. It provides
quantitative measurement of the various activities^ The major parameters that are analysed are the type of activities performed and the time needed to do
specified jobs. Work sampling studies have been done on doctors, nurses, pharmacists and laboratory technicians. Work sampling permits judgments to
the appropriateness of current staff, job description and training. It helps in standardising the methods of performing jobs and determining the manpower
needs in any organization.
10. DECISION MAKING :
Decision making is just like the basic discipline of differential diagnosis in medical practice. It is an adage that decisions should be made at the level
where the best decisions can be made; it does not follow that the best decision is always made at the top of an organization. Decisions should not be made
with incomplete data. In the health sector, decisions have to be made about development of resources, optimum work load for medical and paramedical
workers, strategies for providing health care, etc.
2005
2005
2010
2015
2007
2010
2010
2010 \
2010
2005
2010
2010
2005
2010
1.
2.
3.
4.
5.
6.
Subcentres
Community health centres
Total beds
Medical colleges
Annual admissions
in medical colleges
Dental colleges
Allopathic doctors
Nurses
ANMs
Health visitors
Health Workers (F)
(in position) March 2001
Health Workers (M)
(in position) March 2001
Village Health Guides (2002)
7.
8.
9.
10.
11.
12.
13.
14.
TABLE 2
Achievements during the Plan periods
1st Plan
1951-56
10th Plan
2002-2007
725
229,367
NA
125,000
42
3,500
138,368
3076
908,168 (2001)
222
19,000
7
65,000
18,500
12,780
578
-
142
575,600 (2001)
839,862
502,503
40,536
137,407
71,053
3.23 lakh 1
(1) ORGANIZATION
The Union Ministry of Health and Family Welfare is headed by
a Cabinet Minister, a Minister of State and a Deputy Health
Minister. These are political appointments. Currently, the Union
Health Ministry has the following departments: (1) Department of
Health and (2) Department of Family Welfare. The Health
Department is headed by a Secretary to the Government of India as
its executive head, assisted by joint secretaries, deputy secretaries
and a large administrative staff. The Department of Family
Welfare was created in 1966 within the Ministry of Health and
Family Welfare. The Secretary to the Govt, of India in the Ministry
of Health and Family Welfare is in overall charge of the
Department of Family Welfare. He is assisted by an Additional
Secretary & Commissioner (Family Welfare), and one Joint
Secretary.
12) FUNCTIONS
vjhe functions of the Union Health Ministry are set out in the
seventh schedule of Article 246 of the Constitution of India under
(a) the Union list and (b) the Concurrent list.
(a) Union list: The functions given in the Union list are: (1)
International health relations and administration of port quarantine
(2) Administration of central institutes such as the All India
Institute of Hygiene and Public Health, Kolkata;
!
Total Plan
Investment
Health
Family
Welfare
1960.00
65.20
0.1
NA
4672.00
8576.00
6625.40
15,778.80
39,322.00
11,650.00
97,500.00
180,000.00
61,518.10
72316.80
798000.00
859200.00
921291.00
140.80
225.00
140.20
335.50
682.00
268.20
1821.05
3,392.89
960.90
1185.50
7575.92
10818.40
9253.00
2.20
24.90
70.50
284.40
497.40
116.20
1010.00
3,256.26
784.90
749.00
6500.00
15120.20
27125.00
NA
10.70
102.70
458.90
971.00
429.50
3922.02
6,522.47
1876.80
2514.40
16711.03
-
the Aryans around 1,400 B.C. It was probably during this period,
the Ayurveda and the Siddha systems of medicine came into
existence. Ayurveda or the Science of Life developed a
comprehensive concept of health. The Manu Samhita prescribed
rules and regulations for personal health, dietetics and hygienic
ritual at the time of birth and death, and also emphasised the unity
of the physical, mental and spiritual aspects of life (47). Sarve Jana
Sukhino Bhavatu (May all men be free from disease and may all be
healthy) was an ancient saying of the Indian sages. This concept of
happiness has its roots in the ancient Indian philosophy of life,
which conceived the oneness and unity of all people, wherever
they lived.
The Post-Vedic period (600 B.C-600 A.D.) was dominated by
the religious teachings of Buddhism and Jainism. Medical
education was introduced in the ancient universities of Taxila and
Nalanda, leading to the titles of Pranacharya and Pranavishara
(47). A hospital system was developed during the reign of Rahula
Sankirtyana (son of the Buddha) for men, women and animals and
the system was continued and expanded by King Ashoka.
The next phase in Indian history (650-1850 A.D.) witnessed the
rise and fall of the Moghul empire The Muslim rulers introduced
into India around 1,000 A.D. the Arabic system of medicine,
popularly known as the Unani system, the origin of which is traced
to Greek medicine. The Unani system since then became part of
Indian medicine. With changes in the political conditions in India,
the torch which was lighted thousands of years ago by the ancient
sages grew dim, medical education and medical services became
static, and the ancient universities and hospitals disappeared.
2. Public Health in British India (14, 15, 47, 48, 49)
By the middle of the 18th Century, the British had established
their rule in India which lasted till 1947. The significant events in
the history of public health during this period are given below in
chronological order :
1757 The British had established their rule in India. The civil and
military services were established.
1825
The Quarantine Act was promulgated.
1859 A Royal Commission was appointed to investigate the causes
of the extremely unsatisfactory condition of health in the
British Army stationed in India. The Commission
recommended the establishment of a 'Commission of
Public Health' in each presidency and pointed out the
need for the protection of water supplies, construction of
drains and prevention of epidemics in the civil
population for safeguarding the health of the British
Army.
1864 Sanitary Commissioners were appointed in the three major
provinces-Bombay, Madras and Bengal. The Civil
Surgeons/District Medical Officers became ex-officio
District Health Officers.
1869 A Public Health Commissioner and a Statistical Officer were
appointed with the Government of India.
1873
A Birth and Death Registration Act was promulgated.
1The Vaccination Act was passed.
2The first Indian Factories Act was passed; the first all-India
Census was taken.
1885
The Local Self-Government Act was passed; Local
Bodies came into existence. 1888
The Government
of India directed that sanitation
should be looked after by the local bodies, but no
local public health staff was created to look after
sanitation.
1896
A severe epidemic of plague occurred in India which
of Health,
Ministry of Health and Family Welfare, New Delhi
13.Rao, S.K. (1969). NIHAE Bulletin, 2, No.3, pp. 5-19
14.Govt, of India (1946). Report of the Health Survey and Development
Committee, Govt, of India Press, Simla.
15.Govt, of India (1962). Report of the Health Survey and Planning Committee,
Ministry of Health. New Delhi.
16.Chadha, M.S. (1963). Report of the Special Committee on the preparation for
entry ofthe NMEP into the Maintenance Phase, Ministry of Health. Govt, of India.
17.Mukherjee. B. (1966). Report on Reorganization of Family Planning Services
Administration and Basic Health Services. Ministry of Health. Govt, of India.
2
1
Health Care of
the Community
"The needs of the many must prevail over those of the few"
Health has been declared a fundamental human right. This
implies that the State has a responsibility for the health of its
people. National governments all over the world are striving to
expand and improve their health care services. The current
criticism against health care services is that they are (a)
predominantly urban-oriented (b) mostly curative in nature, and
(c) accessible mainly to a small part of the population. The present
concern in both developed and developing countries is not only to
reach the whole population with adequate health care services, but
also to secure an acceptable level of Health for All, through the
application of primary health care programmes.
Concept of health care
Since health is influenced by a number of factors such as
adequate food, housing, basic sanitation, healthy lifestyles,
protection against environmental hazards and communicable
diseases, the frontiers of health extend beyond the narrow limits of
medical care. It is thus clear that "health care" implies more than
"medical care". It embraces a multitude of "services provided to
individuals or communities by agents of the health services or
professions, for the purpose of promoting, maintaining,
monitoring, or restoring health"(2J.
The term "medical care" is not synonymous with "health care".
It refers chiefly to those personal services that are provided
directly by physicians or rendered as the result of physicians's
instructions. It ranges from domiciliary care to resident hospital
care. Medical care is a subset of health care system.
Health care is a public right, and it is the responsibility of
governments to provide this care to all people in equal measure.
These principles have been recognized by nearly all governments
of the world and enshrined in their respective constitutions. In
India, health care is completely or largely a governmental
function.
Health system
Health services are designed to meet the health needs of the
community through the use of available knowledge and , resources.
It is not possible to define a fixed role for health services when the
socio-economic pattern of one country differs so much from
another. The health services are delivered by the "health system",
which constitutes the management sector and involves
organisational matters.
Two major themes have emerged in recent years in the delivery
of health services : (a) First, that health services should be
organised to meet the needs of entire populations and not merely
selected groups. Health services should cover the full range of
preventive, curative and rehabilitation
services. Health services are now seen as part of the basic social
services of a country (2); (b) Secondly, it is now fully realised that
the best way to provide health care to the vast majority of
underserved rural people and urban poor is to develop effective
"primary health care" services supported by an appropriate referral
system. The social policy throughout the world was to build up
health systems based on primary health care, towards the policy
objective of Health for All by 2000 AD.
Community participation is now recognized a major component
in the approach to the whole system of health care-treatment,
promotion and prevention. The stress is on the provision of these
services to the people-representing a shift from medical care to
health care and from urban population to rural population.
Levels of health care
It is customary to describe health care service at 3 levels, viz.
primary, secondary and tertiary care levels. These levels represent
different types of care involving varying degrees of complexity.
1. Primary care level
It is the first level of contact of individuals, the family and
community with the national health system, where "primary health
care".("essential" health care) is provided. As a level of care, it is
close to the people, where most of their health problems can be
dealt with and resolved. It is at this level that health care will be
most effective within the context of the area's needs and limitations
(3).
In the Indian context, primary health care is provided by the
complex of primary health centres and their subcentres through the
agency of multipurpose health workers, village health guides and
trained dais. Besides providing primary health care, the village
"health teams" bridge the cultural and communication gap between
the rural people and organised health sector. Since India opted for
"Health for All" by 2000 AD, the primary health care system has
been reorganized and strengthened to make the primary health care
delivery system more effective.
2. Secondary care level
The next higher level of care is the secondary (intermediate)
health care level. At this level more complex problems are dealt
with. In India, this kind of care is generally provided in district
hospitals and community health centres which also serve as the
first referral level (4).
3. Tertiary care level
The tertiary level is a more specialized level than secondary
care level and requires specific facilities and attention of highly
the people, placing people's health in people's hands (11). The ends
of the primary health care approach are the same as those of earlier
approaches (i.e., attainment of an acceptable level of health by
every individual), but the means adopted are different (12), that is,
more equitable distribution and nationwide coverage, more
intersectoral coordination and more community involvement in
health related matters. In short, primary health care goes beyond
the conventional health services. It forms part of the larger concept
of Human Resources and Development.
HEALTH FOR ALL
In 1977, it was decided in the World Health Assembly to
launch a movement known as "Health for All by the year 2000".
The fundamental principle of HFA strategy is equity, that is, an
equal health status for people and countries, ensured by an
equitable distribution of health resources. The Member countries
of WHO at the 30th World Health Assembly defined Health for
All as :
"attainment of a level of health that will enable every
individual to lead a socially and economically
productive life."
In 1978, the Alma-Ata International conference on Primary
Health Care reaffirmed Health for All as the major social goal of
governments, and stated that the best approach to achieve the goal
of HFA is by providing primary health care, especially to the vast
majority of underserved rural people and urban poor. It was
envisaged that by the year 2000, at least essential health care
should be accessible to all individuals and families in an
acceptable and affordable way, with their full participation.
The Alma-Ata Conference called on all governments to
formulate national policies, strategies and plans of action to launch
and sustain primary health care as part of a national health system.
It is left to each country to develop its norms and indicators for
providing primary health care according to its own circumstances.
In 1981, a global strategy for UFA was evolved by WHO (13).
The global strategy provides a global framework that is broad
enough to apply to all Member States and flexible enough to be
adapted to national and regional variations of conditions and
requirements. This was followed by individual countries
developing their own strategies for achieving HFA, and synthesis
of national strategies for developing regional strategies.
The WHO has established 12 global indicators (13) as the basic
point of reference for assessing the progress towards HFA, as for
example, a minimum life expectancy of 60 years and maximum
IMR of 50 per 1000 live births.
National strategy for HFA/2000
As a signatory to the Alma-Ata Declaration in 1978, the
Government of India was committed to taking steps to provide
HFA to its citizens by 2000 AD. In pursuance of this objective
various attempts were made to evolve suitable strategies and
approaches. In this connection two important reports appeared : (i)
Report of the Study Group on "Health for All-an alternative
strategy", sponsored by ICSSR and ICMR, and (ii) Report of the
Working Group on "Health for All by 2000 AD" sponsored by the
Ministry of Health and Family Welfare, Govt, of India (14, 15).
Both the groups considered in great detail the various issues
involved in providing primary health care in the Indian context.
These reports formed the basis of the National Health Policy
formulated by the Ministry of Health and Family Welfare, Govt, of
India in 1983 (16) which commited the Government and people of
India to the achievement of HFA.
HFA
goals
dates
to be
(1)
TABLE 1
Health-related Millennium Development Goals in India
Indicator
Year
India
Goal 1 : Eradicate extreme poverty and hunger
Target 2 : Halve, between 1990 and 2015,
the proportion of people who suffer from hunger
Gl.T2.14 - Prevalence of underweight children
1990
(under-five years of age)
2001
G1.T2.I5-Proportion (%) of population below
1991
minimum level of dietary energy consumption
1999
Goal 4 : Reduce child mortality
Target 5 : Reduce by two-thirds, between 1990
and 2015, the under-five mortality rate
G4.T5.I13-Under-five mortality rate
(probability of dying between birth and age 5)
G4.T5.U4-Infant mortality rate
G4.T5.I15 - Proportion (%) of 1 year-old 1990
children immunized for measles
Goal 5 : Improve maternal health
Target 6 : Reduce by three-quarters, between 1990
and 2015, the maternal mortality ratio
G5.T6.I16-Maternal mortality ratio
G5.T6.I17 - Proportion (%) of births attended
by skilled health personnel
1990
2002
1990
2000
53.4
47.0
25
24
2001
112.0
90.9
80.0
68.0
32.7
56.0
1990
2001
1990
2001
420
407
89/36
42.3
under
age
in
malaria
risk
NA
using insecticide-treated bed nets
G6.T8.I22 - Proportion (%) of population
under age 5 with fever being treated
with antimalarial drugs
G6.T8.I23-Tuberculosis death
rate per 100,000
G6.T8.I23 - Tuberculosis prevalence
rate per 100,000
G6.T8.I24 - Proportion (%) of smear-positive
pulmonary tuberculosis cases detected and put
under directly observed treatment short course
(DOTS)
G6.T8.I24-Proportion (%) of smear-positive
pulmonary tuberculosis cases" detected cured under
directly observed treatment short course (DOTS)
areas
2000
1990
NA
2000
1990
2002
1990
2002
1990
NA
NA
40.4
NA
426
NA
2001
22.7
1990
2000
NA
84
Contd.
Year
India
THE MODEL:
A number of models have been developed for the delivery of
health care services (21). One of the simplest models is shown in
Fig. 1.
In actual practice the model is more detailed and complex. The
INPUTS are the health status or health problems of the
community; they represent the health needs and health demands of
the community. Since resources are always limited to meet the
many health needs, priorities have to be set. This envisages proper
planning so that resources are not wasted. An account of the health
planning has already been given in the preceding chapter. The
HEALTH CARE SERVICES are designed to meet the health
needs of the community through the use of available knowledge
and resources. The services provided should be comprehensive and
community-based. The resources must be distributed according to
the needs of the community. The HEALTH CARE SYSTEM is
intended to deliver the health care services; in other words, it
constitutes the management sector, and involves organisational
matters. The final outcome or the OUTPUT is the changed health
status or improved health status of the community which is
expressed in terms of lives saved, deaths averted, diseases
prevented, cases treated, expectation of life prolonged, etc. Models
such as these are being employed for improving health care
services. A discussion of the application of the model (Fig. 1) in
the Indian context is given in the following pages :
HEALTH STATUS AND HEALTH PROBLEMS
An assesment of the health status and health problems is the
first requisite for any planned effort to develop health care
services. This is also known as Community Diagnosis. The data
required for analysing the health situation and for defining the
health problems comprise the following :
1.Morbidity and mortality statistics.
2.Demographic conditions of the population.
3.Environmental conditions which have a bearing on health.
4.Socio-economic factors which have a direct effect on
health.
5.Cultural background, attitudes, beliefs, and practices which
affect health.
6.Medical and health services available.
7.Other services available.
An analysis of the health situation in the light of the above data
will bring out the health problems and health needs of the
community. These problems are then ranked according to
1. Demographic profile
A major concern today is population explosion. The
demographic profile is characterised by:
a. large population base
b. high fertility both in terms of birth rate and family size
c. low or declining mortality
d. "young" population (about 35.35 per cent of the
population) is below the age of 15 years
e. the proportion of illiterate population is close to 34.62
per cent: this explains why the decline in birth rate has
been so slow
f. dependency ratio of 62 per 100; that is, every
economically productive member has to support almost
one dependent
Table 1 summarises the most recent demographic
information available.
TABLE 1
India: Demographic profile
Total population (2002)
Crude birth rate (2002)
Crude death rate (2002)
Annual growth rate % (2001)
Population doubling time (at current growth rate)
Population rural % (2002)
Adult literacy rate % (2001)
Density of population per sq.km (2001)
Sex ratio female per 1000 male (2001)
Population below 15 years % (2001)
Population above 60 years % (2000)
Average family size (2002)
Age at marriage, female (1998)
Annual per capita GNP
(at current prices 2001 -02)
1049 million
25
8.1
1.93
30 years
72
65.38
324
933
35.35
6.77
3.1
19.5 years
Rs. 17978
2. Mortality profile
During the last few decades, there has been a notable
improvement in the health status of the population. The death
rate has steadily declined from 21 (1965) to 8.1 (2002). The
life expectancy at birth has gone up considerably since 1951,
recording an estimated 65.3 years during 2001-02. The
mortality rates for a number of infectious and communicable
diseases have also registered a decline (e.g., cholera, malaria).
However, a deeper study reveals distressing situation.
India's health standards are still low compared to those in
developed countries. While in the world as a whole, the IMR is
about 60 per 1000 live births, and in the developed countries as
low as 6, in India it is as high as 67 (22). Our life expectancy of
about 65.3 years lags behind by almost 12-15 years
compared to that in developed countries where it is currently
between 76 and 80 years.
The mortality profile in terms of age-sex distribution is
presented in Table 2. It shows wide variations in death rate
between rural and urban areas. The current urban death rate
(during 1999) was 6.3 and the rural death rate 9.4 per 1000 of
population. There were also considerable interstate variations
in death rate, as for example, during 2000 the death rate in
Uttar Pradesh was 10.2 as compared to the national average of
8.7 and 6.4 in Kerala. Among the states, Kerala had the lowest
IMR of 14 per 1000 live births and Orissa had the highest IMR of
96 per 1000 live births (23).
Table 2 shows that the death rate is the highest in the age
group 0-4 years. This is as a result of malnutrition and
infection. About 21 per cent of total deaths are estimated to be in
the age group 0-1 year. 15 to 25 per cent of total deaths are
attributed to infectious and parasitic diseases.
:
Health Problems
The HEALTH PROBLEMS of India may be conveniently
grouped under the following heads :
1.Communicable disease problems
2.Nutritional problems
3.Environmental sanitation problems
4.Medical care problems
5.Population problems
TABLE 2
Estimated Age-Specific Death Rate By Sex : India (1999) per 1000 population
Age Group
0-4
5-9
10-14
15-19
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85+
All Ages
(Crude Death
Rate)
Source : (23)
Rural
Urban
Combined
Total
22.9
Male
21.9
Female
23.9
Total
11.7
Male
12.2
Female
11.2
Total
20.4
Male
19.8
Female
21.1
2.1
1.4
2.2
2.9
2.9
3.3
4.0
5.3
7.3
1.8
1.3
1.9
2.7
2.9
3.7
4.8
6.3
8.8
2.4
1.5
2.4
3.1
3.0
3.0
3.0
4.3
5.6
8.8
1.0
0.7
1.2
1.8
2.6
2.4
3.4
4.1
6.4
8.1
0.9
0.7
1.1
1.3
2.9
3.0
4.5
5.0
1.1
0.7
1.3
2.2
2.4
1.9
2.3
3.1
4.5
6.8
9.9
1.8
1.2
1.9
2.6
2.9
3.1
3.8
5.0
7.0
1.6
1.2
1.7
2.3
2.9
3.5
4.8
5.9
8.5
2.1
1.3
2.1
2.8
2.8
2.7
2.8
4.0
5.3
8.3
' 7.9
9.3
11.0
16.8
24.7
37.9
58.7
83.0
107.2
167.4
13.2
19.6
28.9
41.5
62.4
92.3
116.1
175.8
14.0
20.8
34.4
55.4
74.2
98.9
159.6
14.8
17.2
33.1
47.9
64.4
90.4
160.9
19.0
21.0
38.4
49.9
66.5
87.8
158.2
9.4
9.7
9.1
6.3
6.7
13.3
28.1
46.0
62.6
92.7
163.0
10.2
16.3
22.9
36.8
56.2
78.6
103.2
165.8
12.1
19.4
27.0
40.8
59.5
86.3
109.4
171.8
13.0
19.1
33.0
33.0
71.3
97.4
160.5
5.7
8.7
8.9
8.2
_____________________________________________RESOURCES 693
graduates and 12260 Homoeopathic graduates (27).
Health manpower
TABLE 3
Suggested norms for health personnel
Category of personnel
Norms suggested
1.Doctors
2.Nurses
3.Health worker
1.Trained dai
2.Health assistant
6. Health assistant
(male and female)
1.Pharmacists
2.Lab. technicians
Source : (28)
Although the averages are satisfactory on a national basis, they vary
widely within the country. There is also maldistribution of health
manpower between rural and urban areas. Studies in India have shown
that there is a concentration of doctors (up to 73.6 per cent) in urban areas
where only 26.4 per cent of population live. This maldistribution is
attributed to absence of amenities in rural areas, lack of job satisfaction,
professional isolation, lack of rural experience and inability to adjust to
rural life.
The national averages of doctor-population ratio, population-bed ratio
and nurse to doctor ratio in some countries are shown in Table 4.
TABLE 4
Health manpower in some countries 1999-2001
Country
Doctors per
100000
population
Beds per
10000
population
Nurses and
midwives
per 100000
population
India
56
9.3
78
Nepal
1.5
26.7
25.1
41
30
30
3.36
29
22.3
6.3
14.0
112
162
25
Bangladesh
Sri Lanka
Thailand
Myanmar
Source : (23, 29)
limited resources.
1.ANM
2.MPW (Male)
3.Health Assistant (Female)/ LHV
4.Health Assistant (Male)
5.Doctors in PHCs
137407
70153
10855
19927
25724
6.Specialists :
(a)Surgeon
781
(b)Gynaecologist and Obstetrician
780
(c)Physician
7047
(d)Paediatrician
440 Total Specialists at CHC
4124
1.Radiographer
1643
2.Pharmacist
21118
3.Lab. Technician
13262
4.Nurse Midwife
27336
5.BEE_________________________________________ 5708
Source : (30)
2. Sub-centre level
\ The sub-centre is the peripheral outpost of the existing
"-.health delivery system in rural areas. They are being
^^established on the basis of one sub-centre for every 5000
^population in general and one for every 3000 population in
hilly, tribal and backward areas"lAs on 31st March 2003,
138368 sub-centres were established in the country (37); the
total requirement is estimated to be 1.34 lakh (37).
Each sub-centre is manned by one male and one female
multipurpose health worker. At present the functions of a subcenter are limited to mother and child health care, family planning
and immunization. It is proposed to extend the facilities at all subcentres for IUD insertion, and simple laboratory investigations like
routine examination of urine for albumin and sugar. Creation of
these facilities would go a long way in securing greater acceptance
of IUD and early detection of complications of pregnancy. The
work at sub-centres is supervised by male and female health
assistants. According to the revised norm, one female HA will
supervise the work of 6 female HWs. The job descriptions of these
workers have been published as Manuals by the Rural Health
Division of the Ministry of Health and Family Welfare.
Staffing pattern
\ At present in each community development block, there are one
or more PHCs each of which covers 30,000 rural population. In
the new set-up each PHC will have the following staff :
At the PHC level:
Medical officer
1
Pharmacist
1
Nurse mid-wife
1
Health worker (female )/ANM
1
Block Extension Educator
1
Health assistant (male)
1
Health assistant (female)/LHV
1
U.D.C.
1
L.D.C.
1
Lab. technician
1
Driver (subject to availability of vehicle)
1
Class IV
4
15
At the sub-centre level:
Health worker (female)/ANM
Health worker (male)
Voluntary worker
(paid Rs.50 per month as honorarium)
1
1
1
f\
X-~r
^
\0
V,
3
Notwithstanding the strong criticism of primary health centres
it must be emphasized that their establishment is a valuable
national asset. Their establishment is the fruit of many years of
great efforts to increase the outreach of the health services (39).
_______-V^e
death in 1944, the Fund was raised with the main object of
improving the lot of women, especially in the villages, through
gram-sevikas. The trust has nearly a crore of rupees and is actively
engaged in various welfare projects in the country.
8. Family Planning Association of India
The Family Planning Association was formed in 1949 with its
headquarters at Mumbai. It has done pioneering work in
propagating family planning in India. The Association has
branches all over the country. These branches are running family
planning clinics with grants-in-aid from the Government. The
Association has trained several hundred doctors, health visitors
and social workers. One of the activities of the Headquarters is to
answer enquiries on family planning by correspondence or by
personal interviews.
1?
JLiAll India Women's Conference
It is the only women's voluntary welfare organisation in the
country. Established in 1926, it has now branches all over the
country. Most of the branches are running M.C.H. Clinics,
Medical centres, andadult education centres, milk centres and
family planning clinics7\ . fi^J^\
10. The All-India Blind Relief Society
V The All-India Blind Relief Society was established in 1946 with a
view to coordinate different institutions working for the blind. It
organises eye relief camps and other measures for the relief of the
blind.
11. Professional bodies
The Indian Medical Association, All India Licentiates
Association, All India Dental Association, The Trained Nurses
Association of India are all voluntary agencies of men and women
who are qualified in their respective specialities and possess
registerable qualifications. These professional bodies conduct
annual conferences, publish journals, arrange scientific sessions
and exhibitions, foster research, set up standards of professional
education and organise relief camps during periods of natural
calamities.
12. International agencies
The Rockefeller Foundation, Ford Foundation, and CARE
(Cooperative for American Relief Everywhere) are examples of
voluntary international health agencies.
HEALTH PROGRAMMES IN INDIA
Since India became free, several measures have been
undertaken by the National Government to improve the health of
the people. Prominent among these measures are the NATIONAL
HEALTH PROGRAMMES, which have been launched by the
Central Government for the control/ eradication of communicable
diseases, improvement of environmental sanitation, nutrition,
control of population and rural health. Various international
agencies like WHO, UNICEF, UNFPA, World Bank, as also a
number of foreign agencies like SIDA, DANIDA, NORAD and
USAID have been providing technical'and material assistance in
the implementation of these programmes. A brief account of these
programmes which are currently in operation is given in chapter 7.
References
1.Last J.M. ed (1993). A Dictionary of Epidemiology, Oxford University
Press. New York.
2.WHO (1971) Techn Rep Ser., 472.
3.WHO (1984). Public Health Paper No. 80.
4.WHO (1987). Seventh Rep. World Health Situation. Vol. 1.
5.WHO (1987). Techn Rep. Sen, No. 746.
6.WHO (1984). Glossary of Terms, HFA Series 1-8.
7.UNICEF//WHO (1975). Joint Committee on Health Policy
8.Ashish Bose (1984). In : Practising Health for All, David Morley et al (eds),
17.WHO (2003), The World Health Report 2003, Shaping the future.
18.UNDP (2003), Human Development Report 2003, Millennium
Development Goals : A Compact among nations to end human poverty.
1.Govt,
13.http://esic.nic.in
14.Govt, of India (2000),
Basic
Health Needs in Developing countries.
18.Gunn, S.M. and Piatt, RS. (1945). Voluntary Health Agenies, The Ronald Press,
New York.
19.Leavell, H. and Clark, E.G. (1958). Preventive Medicine for the Doctor in his
Community, Mc Graw Hill.
20.Govt, of India (1961). Voluntary Health Organizations and India's Health
Programmes, Central Health Education Bureau, New Delhi.
c)
^ 1. PREVENTION AND CONTROL OF SPECIFIC DISEASES
Almost all communicable diseases are or have been at
sometime the subject of WHO activities. The global eradication of
smallpox is an outstanding example of international health
cooperation. With the same energy and commitment with which
WHO eradicated smallpox, it is now directing the global battle
against AIDS.
An important activity of WHO is epidemiological surveillance
of communicable diseases. The WHO collects and disseminates
epidemiological information on diseases subject to International
Health Regulations and occasionally other communicable diseases
of international importance through an Automatic Telex Reply
Service (ATRS) and the "Weekly Epidemiological Record"
(WER). The latter contains more complete details and brief
reviews of communicable diseases of international importance (7).
Member States can also make use of the "WHO Emergency
Scheme for Epidemics" whenever necessary (8). The aim of
International Health Regulations is to ensure maximum security
against international spread of diseases with the minimum
interference with world traffic.
The WHO has also paid attention in its programme of work to
non-communicable disease problems such as cancer,
cardiovascular diseases, genetic disorders, mental disorders, drug
addiction and dental diseases.
The activities of WHO have also branched out into the fields of
vector biology and control, immunology, quality control of drugs
and biological products, drug evaluation and monitoring and health
laboratory technology as these activities are relevant to the control
of both communicable and non-communicable diseases.
Immunization against common diseases of childhood
(Expanded Programme on Immunization) is now a priority
programme of the WHO. The 30th World Health Assembly
adopted a resolution aimed at ensuring immunization of all
children by 1990 (10).
2. DEVELOPMENT OF COMPREHENSIVE
HEALTH SERVICES
WHO's most important single function is to promote and
support national health policy development and the development of
comprehensive national health programmes. This broad field of
endeavour encompasses a wide variety of activities such as
organizing health systems based on primary health care, the
development of health manpower and utilization, building of longterm national capability, particularly in the areas of health
infrastructure development, and managerial capabilities (including
monitoring and evaluation) and health services research.
Appropriate Technology for Health (ATH) is another new
programme launched by the WHO to encourage self-sufficiency in
solving health problems. The new programme is part of WHO's
efforts to build up primary health care. WHO's main activities in
1980 were towards promoting national, regional and global
strategies for the attainment of Health for All by 2000 AD.
3. FAMILY HEALTH
Family health is one of the major programme activities of WHO
since 1970, and is broadly subdivided into maternal and child
health care, human reproduction, nutrition and health education.
The chief concern is improvement of the quality of life of the
family as a unit.
4. ENVIRONMENTAL HEALTH
Promotion of environmental health has always been an
important activity of WHO. WHO advises governments on
national programmes for the provision of basic sanitary services.
Recent activities are directed to protection of the quality of air,
water and food; health conditions of work, radiation protection and
early identification of new hazards originating from new
technological developments. A number of programmes have been
developed such as the 'WHO Environmental Health Criteria
Programme' and 'WHO Environmental Health Monitoring
Programme' towards improving environmental health. The WHO
is committed to attain the target adopted by Habitat, the UN
Conference on Human Settlements, that was to have "Water for
All by 1990" (10).
5. HEALTH STATISTICS
From its earliest days in 1947, WHO has been concerned with
the dissemination of a wide variety of morbidity and mortality
statistics relating to health problems. The data is published in the
(a) Weekly Epidemiological Record (b) World Health Statistics
Quarterly and (c) World Health Statistics Annual. Readers
interested in current data may obtain it from the Chief Statistician,
Dissemination of Statistical Information, WHO, Geneva. In order
that statistics from different countries may be comparable, WHO
publishes 'International Classification of Diseases' which is
updated every 10th year. The Tenth Revision of ICD came into
effect from 1 January 1993. Assistance is also given to countries in
the improvement of their medical records, and in the planning and
operating national health information systems.
6. BIO-MEDICAL RESEARCH
The WHO does not itself do research, but stimulates and
coordinates research work. It has established a world-wide
network of WHO collaborating centres, besides awarding grants to
research workers and research institutions for promoting research.
There are Regional Advisory Committees on health research
which define regional health research priorities and a Global
Advisory Committee, which in close collaboration with the
regional committee deals with policy issues of global import. Six
tropical diseases (malaria, schistosomiasis, trypanosomiasis,
filariasis, leishmaniasis and leprosy) are the target of the WHO
Special Programme for Research and Training in Tropical
Diseases to develop new tools, strengthen research institutions and
training workers in the countries affected.
7. HEALTH LITERATURE AND INFORMATION
WHO acts as a clearing house for information on health
problems. Its publications comprise hundreds of titles on a wide
variety of health subjects. The WHO library is one of the satellite
centres of the Medical Literature Analysis and Retrieval System
(MEDLARS) of the U.S. National Library of Medicine.
MEDLARS is the only fully computerised indexing system
covering the whole of medicine on an international basis. The
WHO has also a public information service both at headquarters
and each of the six regional offices.
8. COOPERATION WITH OTHER ORGANIZATIONS
WHO collaborates with the UN and with the other specialized
agencies, and maintains various degrees of working relationships.
Besides, WHO has also established relations with a number of
international governmental organizations.
Structure
The WHO consists of three principal organs : the World Health
Assembly, the Executive Board and the Secretariat.
Regions
In order to meet the special health needs of different areas,
WHO has established six regional organizations. (Table 1).
TABLE 1
WHO Regional Organizations
Headquarters
Region
1.
2.
3.
4.
5.
6.
Member country
SEARO
1972
1982
1948
1950
1973
1965
1948
1953
1948
1947
Bangladesh
Bhutan
India
Indonesia
Korea (Dem. People's Rep.)
Maldives Islands
Myanmar
Nepal
Sri Lanka
Thailand
Population 2002
(million)
143.8
2.2
1049.5
217.4
22.5
0.3
48.9
24.6
18.8
62.2
care of children, both within and outside their homes through such
means as parent education, day-care centres, child welfare and
youth agencies and women's clubs. These services are carried out
not as separate projects but as part of health, nutrition and
education or home economics extension programmes.
(d) Education -formal and non-formal : In collaboration with
UNESCO, UNICEF is assisting India in the expansion and
improvement of teaching science in India. Science laboratories'
equipment, workshop tools, library books, audiovisual aids are
being made available to educational institutions. Emphasis is
placed on the kind of schooling relevant to the environment and
future life of the children.
/Currently, UNICEF is promoting a campaign known as GOBI
campaign to encourage 4 strategies for a "child health revolution"
-G for growth charts to better monitor child development >
-O for oral rehydration to treat all mild and moderate'j
dehydration
V^
-B for breast feeding, and
-I for immunization against measles, diphtheria, polio,
pertussis, tetanus and tuberculosis *\
Since 1976, UNICEF has been participating in Urban Basic
Services (UBS). The aim of the UBS projects is to upgrade basic
services (e.g., health, nutrition, water supply, sanitation and
education) - especially for children and women - in selected cities
and towns. The overall objective is to improve the degree and
quality of survival and development of the children of urban lowincome families.
In short, UNICEF activities cover programmes assisting in
child survival, protection and development; interventions like
immunization, improved infant feeding practices; child growth
monitoring, homebased diarrhoea management, drinking water,
environmental sanitation, birth spacing, education of girls and
income-generating activities for women.
As full partners in primary health care, UNICEF and WHO
have been developing joint strategies in support of its
implementation at country level.
UNDP
The United Nations Development Programme (UNDP) was
established in 1966. It is the main source of funds for technical
assistance. The member countries - rich and poor - of the United
Nations meet annually and pledge contributions to the UNDP.
The basic objective of the UNDP is to help poorer nations
develop their human and natural resources more fully. The UNDP
projects cover virtually every economic and social sector agriculture, industry, education and science, health, social welfare,
etc.
UN Fund for Population Activities
The United Nations Fund for Population Activities (UNFPA)
has been providing assistance to India since 1974. In addition to
funding national level schemes, Area Projects for intensive
development of health and family welfare infrastructure and
improvement in the availability of services in the rural areas have
been under implementation in eleven districts of Bihar and 4
districts of Rajasthan.
The UNFPA inputs are designed to develop national capability
for the manufacture of contraceptives, to develop population
education programmes, to undertake organized sector projects, to
strengthen programme management as well as to improve output
of grass-root level health workers and introduction of innovative
approaches to family planning and MCHcare(16j.
INTERNATIONAL HEALTH
___________________________________________________
Deration of the Rockefeller Foundation. The Foundation's
gramme included the training of competent teachers and
arch workers; training abroad of candidates from India
lugh fellowships and travel grants; the sponsoring of visits
a large number of medical specialists from the USA;
viding grants-in-aid to selected institutions: development
nedical college libraries; population studies; assistance to
2arch projects and institutions (e.g., National Institute of
alogy at Pune and more recently the setting up of a field
nonstration area (Ballabhgarh) in connection with a
Dartment of preventive and social medicine, as well as to the
India Institute of Medical Sciences. At present the
undation is directing its support to the improvement of
riculture, family planning and rural training centres as well as
medical education (5).
ird Foundation
Whereas the Rockefeller Foundation earlier concentrated
ost of its assistance on universities and post-graduate
stitutions, on professional education and on research, the
Drd Foundation has been active in the development of rural
aalth services and family planning (5). The Ford Foundation
as helped India in the following projects : (1) Orientation
aining centres : The orientation training centres at Singur,
oonamalle and Najafgarh were set up with help from the Ford
oundation. The centres provide training courses in public
ealth for medical and paramedical personnel from all over
ndia (2) Research-cum-action projects : These projects were
limed at solving some of the basic problems in environmental
anitation, e.g., designing and construction of hand-flushed
icceptable sanitary latrines in rural areas (3) Pilot project in
ural health services, Gandhigram (Tamilnadu) : Among a rural
population of 100,000 people, an attempt was made to
develop and operate a coordinated type of health service
which will provide a useful model for health administrators in
the country (4) Establishment of N1HAE: In the last few years,
the Ford Foundation has supported the establishment of the
National Institute of Health Administration and Education at
Delhi. The Institute provides a senior staff-college type training
for health administrators (5) Calcutta water supply and
drainage scheme : The Foundation has helped in the
preparation of a master plan for water supply, sewerage and
drainage for the city of Calcutta in collaboration with other
international agencies. (6) Family planning programme : The
Foundation is supporting research in reproductive biology and
in the family planning fellowship programmes.
CARE
CARE (Co-operative for Assistance and Relief Everywhere)
was founded in North America in the wake of the Second World
War in the year 1945. It is one of the world's largest independent,
non-profit, non-sectarian international relief and development
organization. CARE provides emergency aid and long term
development assistance.
CARE began its operation in India in 1950. Till the end of
1980s, the primary objective of CARE - India was to provide food
for children in the age group of 6-11 years. From mid 1980s,
CARE-India focused its food support in the ICDS programme and
in development of programmes in the areas of health and income
supplementation. It is helping in the following projects : Integrated
Nutrition and Health Project; Better Health and Nutrition Project;
Anaemia Control Project; Improving Women's Health Project;
Improved Health Care for Adolescent Girl's Project; Child Survival
Project; Improving Women's Reproductive Health and Family
Spacing Project; Konkan Integrated Development Project etc.
CARE-India works in partnership with the Government of
India, State Governments, NGOs etc. Currently it has projects
Abate, 590
Abortion, 371
Abortion rate, 357
Abstinence, 372
Accidents, 323
Acculturation, 491
Act
Central Births and Deaths
Registration, 1969, 515
Central Maternity benefit, 1961, 515
Charitable Endowment, 1980, 409
Child Labour (Prohibition
Regulation) 1986, 431
Child Marriage Restraint, 1978, 432
Children, 1960, 432, 513
Consumer Protection, 1986, 511
Dock Labourers, 1948, 615
Employees State
Insurance, 1948, 515,517,617
Epidemic diseases, 1897, 515
Factories Act, 1948, 617
Hindu Adoptions and
maintenance, 1956, 432
Indian Factories, 1948, 515
Juvenile Justice, 1986, 432, 515
Medical Termination of
Pregnancy, 1971, 371,515
Model Public Health, 1955, 479
Prevention of Food
Adulteration, 1954, 481, 515
Water (Prevention and Control
of Pollution), 1974, 524
Workmen's Compensation, 1923, 620
Acid
Ascorbic, 448
Nicotinic, 446
Pantothenic, 447
Folic, 447
Acids
Amino, 439, 460
Essential amino, 439, 460
Essential fatty, 440, 469
Fatty, 440, 454, 469
Linoleic, 440
Activated sludge process, 571
Active immunity, 93
Active Immunization, 102
Acute diarrhoea, 183
Acute respiratory infections, 139
Acute respiratory disease control, 141, 345
Adjusted rates, 53
Adult intelligence, 498
Aedes aegypti, 557
Aedes aegypti index, 227
Aflatoxins, 479
Age and sex composition, 351
Age at marriage, 355
Aged, Health Status of, 435
Agent, 32
Agent factors, 32
Age pyramids, 352
Age - specific fertility rate, 356
Age - specific maternal fertility rate, 356
AIDS, 160, 271
Air, 542
change, 548
composition, 542
conditioning, 548
discomfort, 543
disinfection, 547
of occupied room , 544
pollution, 544
temperature, 543, 554
velocity, 557
Air-borne transmission, 91
Alcohol, 108, 457, 470, 635
Alcohol abuse, 513, 634
Alcoholic beverages, 457
Altitudes, 554
Alma Ata
Declaration, 10, 21, 28, 656, 687, 656
Alzheimer's disease, 40
Amantadine, 132
Amino acids, 460
Amniocentesis, 424, 630
Amoebiasis, 192
Anaemia
Diagnosis of, 450
Iron deficiency, 450
Megaloblastic, 447
Nutritional, 450, 465, 692
Pernicious, 448
Sickle cell, 626
Analytical epidemiology, 64
Ancylostomiasis, 195
Anganwadi worker, 411, 434, 482, 695
'
Calcium, 448
Cancer, 302, 470, 611
breast, 308
bladder, 611
Causes of, 304
Control, 305
Industrial, 611
Classification of disease, 44
Clinical medicine, 489
Clinical trials, 77
Cobalt, 452
Coding system, 44
Coherence of association, 84
Cohort study, 69
Coitus interruptus, 372
Cold chain, 98
Colombo Plan, 709
Colostrum, 393
Combined injectable contractive, 370
Combined pill, 367
Commensal rodents, 234
Communicable disease, 86
Communicable period, 92
Communication
Barriers of, 655
channels of, 654
formal and informal, 654
health, 655
types of, 654
two-way, 654
verbal, 654
Community, 490, 506
development, 677
diagnosis, 43, 84
health, 41, 489
health centres, 697
medicine, 9, 42
participation, 20
responsibility, 20
services, 514
treatment, 43 Community need
assessment approach, 378 Community
nutrition proramme, 481 Comparability, 66
Comparison studies, 80 Composting, 562
Concept
Biomedical, 12
Changing, 12
Ecological, 12
Health a relative, 15
Holistic, 13
Psychosocial, 13
in nutrition, 438
in sociology, 490
of aetiology and cure, 504
of child abuse, 430
of cohort, 69
of control, 35
of correlation, 80
of defined population, 48, 57
of disability, 39
of disease, 29, 35, 115
of disease causation, 29
of disease eradication, 6
of health, 12
of health services research, 29
of iceberg phenomenon, 35
of IQ, 428, 498
of "lead time", 113
of mental age, 498
of normality, 399
of prevention, 36
of primary health care, 27, 28
of primary health centre, 696
of well-being, 15
of welfare, 360
Condom,362 Condom
promotion, 338 Conflicts,
496 Confounding factor, 66
Confounding variable, 81
Congenital
abnormalities, 423
anomaly, 423
defect, 424
dislocation of hip, 395
disorders, 424
hypothyroidism, 395
malformations, 423
rubella, 128
syphilis, 394 Consanguinity, 424,
629 Consistency of association, 83
Constitution of India, 21 Consumer
Protection Act 1986, 511 Contact tracing,
267 Contagious disease, 86
Contamination, 85 Contraceptive
methods, 361 Contraception and
adolescence, 376 Control
Concept of, 35
Evaluation of, 36
Controlled tipping, 562
Convalescent-carrier, 88
Copper, 452
Copper T, 363
Coronary heart disease, 287
Correlation, 651
Cost accounting, 669
Cost benefit analysis, 669
Cost effectiveness, 669
Couple protection rate, 360
Crab louse, 583
Cresol, 107
Cretinism, 451
Cross-over trials, 77
Cross-sectional studies, 63
Crude death rate 23, 51, 350, 357, 358
Culex, 576
Culture, 491
Cultural factors in health and disease, 504
Customs, 491
Cyclic trend, 60
Cyclops, 588
Cysticercus cellulose, 242
Cystic fibrosis, 626
DALYs, 24
Dapsone, 260
Dark ages of medicine, 4
DDT, 589
Death rates
Age-specific, 23
Crude, 23, 48
SoGcific 52 Death rates 23, 51, 52,
350, 357, 358 Defence mechanisms, 497
Definition
abortion, 371
abortion rate, 357
abortion ratio, 357
accident, 323
age-specific fertility rate, 356
age-specific marital fertility rate, 356
anti-septic, 106
arthropod-borne viruses, 227
battered baby syndrome, 430
bias, 67
birth rate, 350, 357, 358
blood pressure, 293
carrier, 88
case, 65, 88
census, 639
child death rate, 422
child mortality rate, 23, 422
child-woman ratio, 357
cohort, 69
communicable disease, 86
communicable period, 92
community development, 642
community diagnosis, 43
community health, 41
community medicine, 42
community treatment, 43
confounding factor, 66
congenital anomaly, 424
congenital disorders, 424
congenital malformations, 423
contagious disease, 86
contamination, 85
data, 638
deodorant, 106
disease specific mortality, 23
diet, 461
dietetics, 438
disability, 39, 428
disease, 29
disinfectant, 106
drug, 634
drug abuse, 634
drug dependence, 634
ecology, 19
eligible couples, 360
endemic, 86
environment, 519
epidemic, 58, 86
epidemic curve, 59
epidemiology, 47
epizootic, 87
eradication, 87
evaluation, 36
exotic, 86
family planning, 358
fertility, 355
foetal death, 415
food borne disease, 479
food factor, 438
general fertility rate, 356
general marital fertility rate, 356
generation time, 92
gross reproduction rate, 357
growth and development, 399
handicap, 39, 428
Pyridoxin, 446
Q fever, 241 Quality
of life, 16
Quarantine, 102
Rabies, 217
Radiation, 107, 387, 552
Radiation hazards, 553, 612
Rapid sand filter, 526
Random numbers, 651
Randomization, 76
Randomized controlled trial, 74,77, 483
Rate, 49
Ratio, 50
Red cross, 710
Refuse, 561
Registration of births and deaths, 639
Regression, 651
Repeatability, 115
Rehabilitation, 39, 263
Relative risk, 67, 72, 82
Reservoir of infection, 87
Responsibility for health, 20
Retrospective cohort studies, 70
Revised national tuberculosis control programme, 335
RH status, 388
Rhesus system, 625
Rheumatic heart disease, 299
Riboflavin, 446
Rice, 452
Rickets, 444
Rickettsial diseases, 239
Right to health, 20, 500
Risk approach, 34, 386, 410
Risk factors, 34, 115, 295, 396
Risk factor trials, 78, 292
Risk groups, 34
Road traffic accidents, 325
Road-to-health chart, 402
Rodent control, 592
Rodenticides, 592
Role play, 663
Rooming-in, 389
Rubella, 128
Rubeola, 124
Rural Health Scheme, 672
Sabin vaccine, 164
Safe period, 372
Salk vaccine, 164
Sample Registration System, 639
Sampling, 648
Sandflies, 581
Sand flea, 585
Sandfly fever, 230
Sanitary latrines, 564
Sanitary well, 523
Scatter diagram, 644
Schick test, 134
School health service, 425
Screening for disease, 113
Scrub typhus, 240
Secondary attack rate, 55, 92
Secondary health care, 28
Secondary prevention, 37,291,297,302,305,307,429
Secular trend, 60
Selenium, 452
Self care, 20
Sensitivity, 117
Sentinel Surveillance, 36
Septic tank, 567
Serial interval, 92
Serum cholesterol, 276
Sewage, 569
Sewage purification, 569
Sex ratio, 352
Sexually transmitted diseases, 265
Shrivastav Committee, 672
Sickle cell anaemia, 626
Sickness benefit, 618
Significance tests, 649
Silicosis, 609
Slow sand filter, 525
Small family norm, 360
Small-for-dates babies, 395
Smallopox, 121
Social agents, 32
agencies, 514
and behavioural science, 489
case study, 492
class and health, 508
class, 63, 506
communication, 493
concepts in, 490
control mechanism, 491
defence, 493
differentiation, 507
factors influencing health, 488
indicators, 25
institutions, 491
medicine, 7, 42
mobility, 506
organization, 500
obstetrics, 383
paediatrics, 384
pathology, 492
problems, 492, 513
psychology, 499
sciences, 489
security, 517
stress, 492
structure of a hospital, 508
surveys, 492 Socialism, 491
Socialization, 491,503 Social
welfare programmes, 432 Society,
490
Socio-economic indicators, 517
Sociology, 490, 491 Sociology of family
planning, 379 Sodium, 449 Solid
wastes, 561 Source of infection, 87
Soyabean, 454 Specific death rates, 52
Specific defences, 93 Specificity, 117
Specificity of association, 83 Specific
protection, 38 Spectrum of disease, 35
Spectrum of health, 17 Spermicides, 363
Spleen rate, 207 Sporadic, 86 Standard
deviation, 646 Standard error, 648
Standard of living, 15, 491 Standardized
rates, 53 Standardized mortality ratio,
52 Statistics, 604 Still-birth rate, 415
Strength of association, 82 Stroke, 298
Subclinical case, 88 Subdermal
implants, 370 Subject variation, 77, 116
Suicides, 313 Sulabh shauchalaya, 568
Sullivan's index, 24
Supplementary feeding programmes, 481
Surveillance, 36, 87, 105 Surveillance of
drinking water quality, 537 Surveillance
sentinel, 36 Survival rate, 53 Successful
parasitism, 91 Susceptible host, 91
Syndrome X, 311 Syndrome identification,
85 Syphilis, 266, 388
Taeniasis, 242 Temporal
association, 82 Temporary carrier,
89 Target couples, 360 Targetted
interventions, 338 Termination of
pregnancy, 373 Tertiary health
care, 28, 685 Tertiary prevention,
37, 315 Tests of significance, 649
Tetanus, 248, 343, 388 Tetanus
neonatorum, 249, 250 Thalidomide
tragedy, 69 Thalassemia, 626
Thiamine, 445 Ticks, 586
Time distribution, 58 Torch
agents, 90 Total fertility rate, 356
Toxoids, 96 Trace elements, 448
Transmission dynamics, 87
Trachoma, 247 Trench fever, 242
Treponematoses, 269 Triage, 601
Trickling filter, 571 Triglycerides,
469 Tsetse flies, 582 Tuberculosis,
146 Type A personality, 290
Typhoid fever, 187 Twenty-point
programme, 348
Uncontrolled trials, 79, 119 Underfives clinic, 408 Under-fives mortality
rate, 23, 422 UNICEF, 707
Contents
suggestions and advice, the author is
nal Institute of Virology, Pune; Dr. G.
1 of National Institute of Cholera and
iristian Medical College, Vellore, Prof.
Institute, Mumbai; Prof. M.D. Mathur,
SCT Medical Centre, Trivandrum;
Laboratories, Mumbai.
Part I
1.Historical Introduction
2.Morphology and Physiology of Bacteria
3.Sterilisation and Disinfection
4.Culture Media
5.Culture Methods
6.Identification of Bacteria
7.Bacterial Taxonomy
8.Bacterial Genetics
Part II
9.
Infection
1.Immunity
2.Antigens
3.Antibodies-Immunoglobulins
4.Antigen-Antibody Reactions
5.Complement System
6.Structure and Functions of the Immune System
7.Immune Response
8.Immunodeficiency Diseases
9.Hypersensitivity
10.Autoimmunity
11.Immunology of Transplantation and Malignancy
12.Immunohematology
Part III
1.Staphylococcus
2.Streptococcus
3.Pneumococcus
4.Neisseria