MALARIA-IN

BELGAUM-2008
Dr.J.Nuchin. M.D.,M.B.A.
Epidemiologist
Belgaum
MALARIA
 By the end of session, you would be
expected to be able to describe:

 Problem statement
Life cycle of parasite
Type of vector
Clinical features
8 important CFs of severe complicated
malaria
Treatment
Diagnosis
 Introduction…
 A protozoan disease caused by a parasite plasmodium
 A major parasitic cause of death in man
 One of the oldest recorded diseases
 Malaria was well known to the Ancient Greeks and
Romans.
 The Romans thought the disease was caused by bad
air (mal-aria) from swamps, which they drained to
prevent the disease.
 A tropical disease-considered as ‘king of tropical
diseases’
 Problem statement
-World
 Has been a scourge of
mankind for the centuries
 Total death toll due to malaria
is more than that due to any
other diseases or even wars
 Endemic in 91 countries
covering about 40% of global
population
 Burden – 300-500 million cases
and 2-3 million deaths
 African countries contribute
90% of the total burden
Malaria in Africa
• Kills a child every 10 to
15 seconds or 8000
children per day

• 90 percent of global
incidence of malaria
occurs in Africa

• Nine of 10 deaths
globally are among sub-
Saharan children under
age 5
 Indian scenario
 Has always been a home ground for malaria
 Before 1947 (preDDT era)- malaria was a major
cause of death
 In 1908, an outbreak in UP and Punjab killed
more than 3 lakh people in just a span of 2
months
 In 1947, India had about 75 million cases and
>50% of total deaths were due to Malaria
alone
 Contnd…
• All the aspects of life were
affected directly or
indirectly
• Industrial and agricultural
production was very low
• At present, 2-2.5 million
cases are being reported
with 1000 deaths every
year
Current situation analysis of malaria in
India
• 1 Billion population at risk of malaria
• 10 Million population under sp treatment
• 2 Million cases reported
• 800-1000 malaria deaths reported
• 6 Major vectors-resistant, exophilic and or endophilic
behavior
• New malaria ecotypes identified
• Spraying produces transient control
• Widespread mono-drug resistance, multi-drug
resistance in p. falciparum
• Inadequate resources
• 1 billion us dollars loss due to malaria
Major malaria ecotypes found in
India

• Rural malaria
• Urban malaria
• Forest malaria
• Irrigation malaria
• Project malaria
• Migration malaria
• Border malaria
Factors responsible for the increase in
VBDs

Poverty and rapid population growth

Irrigation
Urbanization and improper sanitation
Industrialization
Migration and rapid population movement
Natural disasters
Resistance
Global warming
Political instability
Inadequate health infrastructure
1.1 billion people live on
less than $1 a day.

2.7 billion people live on

less than $2 a day.
 IRRIGATION IN INDIA
100

91.02
80
Million Hectares

78.12

60
56.81
52.02
40
41.21
37.1
29.12 30.57
20 22.6
26.25

0
Pre 1st IInd IIIrd Annual IVth Vth Annual VIth VIIth
1951-56 1956-61 1961-66 1966-69 1969-74 1974-78 1978-80 1985-90 1990-95
 Karnataka
 A major CMD in the state.
 7 districts namely DK,K,R,G,T and Belgaum
together contributed >65% of the total burden
in the state in 2006
 The P.f cases are being increased.
 Double resistance has been recorded
Karnataka in 2006- 62864 cases

Dakshina
kannada
21%
Others
32%

Kolar
13%
Belgaum
7%
Raichur
Tumkur Gulbarga 12%
7% 8%
Geographically the district has been
divided into 3 parts
1) Hilly region-
Khanapur
2) (South) Semi
Malnad – Savdatti,
Hukkeri, Bailhongal
and Belgaum
3) (North) Tropical
Region- Athani,
Raibagh, Gokak,
Ramdurga and
Chikkodi Taluks
 Belgaum district
• Taluks-10
• GHs-9
• CHCs-16
• PHCs-140
• SCs-660
• M.O.s-165, HWs-745,LTs-121
• Villages-1160
• Rural population-3201814 (2001 census)
• Urban population-1012691
• Total population-4214505
• Density-314 per sq mtr
• The average rain fall in the district is 808mm
every year.
• Krishna, Malaprabha and Ghata prabha being
the major rivers in the districts, it also has five
small rivers namely Markhandeya, Hiranyakeshi,
Mahadaayi, Vedaganga and Dudhaganga. Navilu
Tirtha dam is built for Malaprabha river in
Savadatti taluka and Hidkal dam for
Ghataprabha river in Hukkeri taluka. These two
huge dams provide irrigation facilities through
canals for the 8 taluks of the district
• With many historical places to its credit
and plenty of Jatraas, the district attracts
travelers from the near by districts and
neighboring states all through the year
 Trend of Malaria in the District- 1987-2008

1987 1251
1988 2066
1989 1576
1990 879
1991 633
1992 1490
1993 574
1994 400
1995 692
1996 601
1997 2102
1998 6334
1999 4343
2000 2689
2001 989
2002 352
2003 869
2004 1674
2005 2859
2006 4149
2007 3908
2008 2226
 Trend of Malaria in the District-1987-2008

7000

6000

5000

4000

3000

2000

1000

0
 Talukwise malaria incidence-2007

Soundatti Bailhongal
10% 5%
Ramdurg
13%

Gokak
68%

T alukwise Malaria incidence-2008

Ba ilhonnga l
4%
Sa vda tti Be lga um
18% 4%

Ramdurg
13%

Goka k
59%
 Malaria incidence-2006 month wise-Total Cases- 4149

678

589
551
Malaria cases

386 392
363 374

246 237

160

93
80

1
Jan to Dec
 Monthwise Malaria incidence-2007

560

421 429 419

401

299 305
279
250
210
181
154

Jan Feb Mar Apr May June July Aug Sept Oct Nov Dec
 Monthwise incidence-2004 to 2007

2000
1849
1498 1483
1500 1358 1334
1072
960
1000 776 836
643
408 373
500

0
January to December
 Monthwise Malaria incidence-2007

560

421 429 419

401

299 305
279
250
210
181
154

Jan Feb Mar Apr May June July Aug Sept Oct Nov Dec

Monthwise Malaria incidence-2008

355
332

242
208 208
183 175
139
127 124

76
57

Jan Feb Mar Apr May June July Aug Sept Oct Nov Dec
 Trend of Pf incidence rate in the district

2004 45.2

2005 39.5

2006 30.1

2007 28.0

2008 21

2008 2007 2006 2005 2004

Series1 21 28.0 30.1 39.5 45.2
PHCs which reported malaria in 2008
• Belgaum taluk- Except Sulebhavi and Yallur
• Bailhongal-Except Dodwad
• Chikkodi- Jainapur and Soundalaga have and others
not
• Gokak-Except Melavanki and Thukkanatti
• Hukkeri-Ammanagi, Daddi, Hulloli, Kot & Paschapur
have reported
• Khanapur- Except Halashi &Itagi
• Ramdurg- Except Katakol & Ramdurga GH
• Soudatti- Except Sutagatti,Muragod,
Madlur,Imanhongal,Hirekumbi and Asundi
• Athani and Raibagh- No cases
What’s the Good News?

• Every one of these deaths is

preventable!!!
• Just a 3 day course of treatment can cure the
disease
• No stigma associated with malaria
• No morality debates
• No “Save the Mosquito” groups
Endemicity and immunity to malaria

Endemicity
Malaria is said to be endemic when there is a constant
incidence of cases over a period of many successive years.
Endemic malaria may be present in various degrees.
There are four grades
A. Hypoendemicity – There is a little transmission and the
disease has little effect on the population.
B. Mesoendemicity - varying intensity of transmission;
typically found in the small, rural communities of the sub-
tropics.
C. Hyperendemicity - intense but seasonal transmission;
immunity is insufficient to prevent the effects of malaria on all
age groups.
 contnd…
D. Holoendemicity - intense transmission occurs
throughout the year.
- As people are continuously exposed to malaria
parasites, they gradually develop immunity to the
disease.
- In these areas, severe malaria is mainly a disease of
children from the first few months of life to age 5
years.
- Pregnant women are also highly susceptible
Although seasonal variations in transmission may occur in
holoendemic areas, malaria transmission occurs all year round.
Therefore, people acquire natural immunity and epidemics are
unlikely.
Contnd…
Depending on the intensity of transmission, malaria can be
stable or unstable, reflecting different epidemic scenarios.
Stable malaria: Sustained incidence over several years.
Seasonal fluctuations in transmission may occur but epidemics
are unlikely.

Unstable malaria: Marked variations in the incidence of

malaria over time. Population does not develop immunity and
people of all ages are susceptible to severe disease when
transmission increases.
Agent –Parasite-Plasmodium
• Unicellular
• 140 types are there of which only 4 can infect
man(P.vivax, falciparum, ovale and malariae)
• Malaria also affects other animals like primates,
rodents, birds, bats and even cold blooded
animals like lizards
• Some parasites infecting primates can also
infect man- eg,-P.knowelesi, P.brasilianum and
P.cyanomalgi
Figure 11.30

Plasmodium Sporozoite
Different species
P.vivax- all 60-70% BTM Mild
over world-less Anaemia, splenic
common in rupture rarely
Africa

P.falciparum- 25-35% MTM High degree

tropics and sub- parasitaemia, all
tropics deaths

P.malariae <1% BQM NS

P.ovale-very NF BTM OM
rare
 Mode of transmission

1. By bite of female anopheles mosquitoes

2. By blood- Blood transfusion and contaminated
syringes and needles
3. Mother to foetus.
Congenital malaria
• Occurs in 5% of the babies borne to mothers who
were MP positive during pregnancy
• Transplacental infection
– Can occur in all 4 species
– Commonly seen P.v. and P.f. in endemic areas
– P.m. infections in nonendemic areas due to long
persistence of species
• Neonate can be diagnosed with parasitemia within 7
days of birth
• Fever, irritability, feeding problems, anemia,
hepatosplenomegaly, and jaundice
Life cycle of plasmodia
• The parasite 2 cycles of development- the
Human cycle (asexual cycle) and Mosquito
cycle (sexual cycle)

• Man is the intermediate host harbouring the

larval stages

• Mosquito is the definitive host harbouring the

adult stages
 Asexual cycle or Human cycle
• Begins with the injection of
sporozoites following the bite
of infected mosquito
• Three phases are observed
Phase 1-Hepatic phase (pre
or exo erythrocytic or
tissue)-
 Sporozoites disappear from
the circulation within 45-60
mins
Many of them are
destroyed by
phagocytes and
some reach the liver
cells
After 1-2 weeks of
development
( depending upon the
species) they become
hepatic schizoints
Hepatic schizoint
Hepatic schizoint

Pre-erythrocytic schizonts
 Contnd…
These hepatic
schizoints
eventually
rupture,
releasing
showers of
merozoites
which attack
RBCs
The number
of merozoites
released vary
according to
the type of
parasite
In case of P.f, as many as 40,000 and in
others 2000-15,000 merozoites are
released
In case of P.f, the intrahepatic schizoints
rupture almost simultaneously and there is
no persistent tissue- no secondary exo
erythrocytic stage
Contnd…
On the contrary, the intrahepatic schizoints of
other plasmodia do not burst all at the same
time.
Some intrahepatic schizoints persist and remain
dormant (hypnozoites) for considerable periods
and later they cause relapses
Once the parasites enter RBCs, they do not
reinvade the hepatic cells
Phase 2- Erythrocytic
phase (erythrocytic
schizogony)
 Many of the merozoites
are quickly destroyed and
significant number of
merozoites bind and
enter the RBCs
 Then they pass through
the stages of trophozoites
and schizoints
 Each parasite spends two
days in a red blood cell
consuming the
hemoglobin and
reproducing.
Erythrocytic Schizogony
• nuclear division =
begin schizont stage
• 6-40 nuclei
• budding merozoites =
segmenter
• erythrocyte rupture
releases merozoites
erythrocytic schizogony
• 48 hr in Pf, Pv, Po
• 72 hr in Pm

gametocytes
Erythrocytic forms (signet)

Young ring form trophozoites

RBCs rupture releasing merozoites which infect
the fresh RBCs

 16 new parasites burst out to infect other red

blood cells from each merozoite

The sporozoites first invade liver cells and

asexually reproduce to produce huge numbers
of merozoites which spread to red blood cells
where more merozoites are produced through
more asexual reproduction.
 Contnd…

Duration of erythrocytic phase is constant for

species to species
It is 48 hrs in case of P.v, P.f and P.o whereas
72 hrs in P.m
The cycle may be repeated many times and
may end with complications or be slowed down
by immunity of the host
Contnd…
Phase 3- Gametogony
 Some of the
erythrocytic forms do
not divide but become
male (smaller) and
female (longer)
gametocytes
These are infective to
mosquitoes
Characteristics of different species

Species Duration of Incubation Number of Red cells

tissue period merozoites invaded
phase (days) / cell
(days)
P. 5.5 – 7 8 - 11 40,000 cells of all
falciparum ages

P. vivax 6-8 10 - 17 10,000 reticulocytes

P. ovale 9 10 – 17 15,000 reticulocytes

P. malariae 12-16 18 - 40 2,000 mature

cells
 Sexual or mosquito cycle
 These infective gametocytes are
ingested by the anopheles
mosquitoes
 Then develop and undergo
stages of fertilisation- zygote,
ookinate, oocyst and sporozoites
 Sporozoites enter the salivary
gland from the gut and are
infective to man
 Once in the mosquito,
Plasmodium needs about 8-10
days to produce sporozoites that
are ready to be injected into a
human.
Plasmodia in Anopheles
Malaria Life
Cycle Oocyst
Sporozoites

Mosquito Salivary
Zygote Gland

Gametocyte Liver stage

s

Red Blood
Cell Cycle
Life Cycle
Sporozoite Liver Schizont

Trophozoite
Oocyst
RBC
Merozoite

Ookinete

Gametocytes
 Types of Infections
• Recrudescence
– exacerbation of persistent undetectable parasitemia, due to
survival of erythrocytic forms, no exo-erythrocytic cycle (P.f.,
P.m.)
• Relapse
– reactivation of hypnozoites forms of parasite in liver,
separate from previous infection with same species (P.v. and
P.o.)
– P.v and P.o continue to relapse for 2-3 years and P.m may
persist for as long as 45 years

• Recurrence or reinfection
– exo-erythrocytic forms infect erythrocytes, separate from
previous infection (all species)
• Can not always differentiate recrudescence from
reinfection
An.culicifacies Breeding Sites
 Host factors
• Malaria affects all ages, but rare in newborn due to
presence of foetal haemoglobin and maternal
immunity
• Common in males because of outdoor activities and
clothing pattern (816 F -45% and 1014 M-55% out of
1830 in Belgaum till August 2008)
• Duffy negative people are resistant to P.v. Most of the
Africans are Duffy negative, this explains why P.v is
not so common in Africa
• Patients of SC trait ( Hb AS), G6PD and thalasseamia
are less likely to be affected by malaria
High risk group
• Pregnant mothers- have an increased risk of severe malaria
especially in primigravidae, as the immunity to the malaria is
impaired in pregnancy.
• Pregnant women attract twice the number of
mosquitoes than non-pregnant women
• There is a greater susceptibility to P. falciparum than P.
vivax during pregnancy

Children - Malaria affects cognitive development and

learning abilities of children
• Malaria is a risk factor of neuro-sensory and behavioral
development in children

Immigrants from Europe- as they lack natural immunity

Immunity

• Occurs only after repeated exposure to the disease

• Influenced by
– Genetics
– Age
– Health condition
– Pregnancy status
– Intensity of transmission in region
– Length of exposure
– Maintenance of exposure
 Incubation period
It is the length of time between the bite of
infected mosquito and appearance of first
clinical feature (ie,fever). It is about 10-12 days
in P.f and 10-14 days in other species

Prepatent period
This is the length of time between the bite of
infected mosquito and appearance of parasites
in peripheral blood
 Clinical course

• Following a bite by an infected mosquito,

many people do not develop any signs of
infection. If infection does progress, the
outcome is one of three depending on the
host and parasite factors enumerated in the
previous slides:
– Asymptomatic parasitaemia (“clinical
immunity”)
– Acute, uncomplicated malaria
– Severe malaria
Asymptomatic parasitaemia

• This is usually seen in older children and adults who

have acquired natural immunity to clinical disease as a
consequence of living in areas with high malaria
endemicity.
• There are malaria parasites in the peripheral blood but
no symptoms.
• These individuals may be important reservoirs for
disease transmission.

• Some individuals may even develop anti-parasite

immunity so that they do not develop parasitaemia
following infection.
 Simple, uncomplicated malaria

• This can occur at any age but it is more likely to be

seen in individuals with some degree of immunity to
malaria. The affected person, though ill, does not
manifest life-threatening disease.

• Fever is the most constant symptom of malaria. It

may occur in paroxysms when lysis of red cells
releases merozoites resulting in fever, chills and
rigors (uncontrollable shivering).
 The periodicity of malaria fever
• The first febrile attack corresponds to the development
of parasites in the RBCs.
• The fever may be continuous or remittent before it
becomes classically intermittent
• Intermittent nature of the fever is due to cyclical
release of merozoites following rupture of infected RBCs
• It is once in 48 hours in case of P.v, P.f (36 hrs- sub-
tertian) and P.o whereas 72 hours in P.m
(erythrocytic schizogony is the time taken for
trophozoites to mature into merozoites before release
when the cell ruptures).
 Contnd…
• A typical attack involves 3 distinct stages (in a
person from non-endemic area).
Cold stage
Begins with feeling of cold, shivering and
headache
Patient covers himself with blankets, BT
reaches 39-410C
It may continue for 15 mins to 1 hour
Parasites are demonstrable in the blood
Contnd
…

Hot stage
 The fever raises so high so the patient feels
burning hot and takes off the clothes
The patient feels intense headache with nausea
and vomiting
Pulse is of bounding type, patient feels thirsty
and it may continue for 2-6hrs
 Sweat stage
 Fever comes down with profuse sweating
He goes usually into deep sleep
Lasts for 2-4 hours
Febrile herpes is very common
Malaria- one clinical febrile episode of
malaria consumes 5,000 k Cal.
 Note how the frequency of spikes of fever differ
according to the Plasmodium species.
In practice, spikes of fever in P. falciparum, occur
irregularly - probably because of the presence of
parasites at various stages of development.
Other features of simple,
uncomplicated malaria include:
Malaria is a multisystem disease. Other common clinical
features are:
o Vomiting
o Diarrhoea – more commonly seen in young children and,
when vomiting also occurs, may be misdiagnosed as viral
gastroenteritis
o Convulsions – commonly seen in young children. In an
endemic area, cerebral malaria should be ruled out if any child
fails to regain consciousness within an hour after an episode of
febrile convulsion.
o Pallor – resulting mainly from the lysis of RBCs. Malaria also
reduces the synthesis of red blood cells in the bone marrow.
o Jaundice – mainly due to haemolysis.
Contnd…

o Anorexia
o Cough
o Headache
o Malaise
o Muscle aches
o Splenomegaly
o Tender hepatomegaly

These clinical features occur in “mild” malaria. However,

the infection requires urgent diagnosis and management
to prevent progression to severe disease.
Hepatosplenomegaly
Severe and complicated malaria
• Although severe malaria is both preventable
and treatable, it is frequently a fatal disease.

• 0.5 -2% of the total P.f malaria develop

complications and of which 50% are fatal

• The following are 8 important severe

manifestations of malaria
1. Severe malaria anaemia
2. Cerebral malaria
3. Hypoglycaemia
4. Metabolic acidosis
5. Acute renal failure
6. Pulmonary oedema
7. Circulatory collapse, shock or “algid malaria”
8. Blackwater fever

Note: It is common for an individual

patient to have more than one severe
manifestation of malaria!
Anaemia in malaria

It is severe in P.f

infections as it attacks
20-35% of total RBCs
whereas only 1% is
affected in other
plasmodia
Immediate blood
transfusion is required
in majority of patients
Contnd…

Causes
Haemolysis of infected RBCs
Haemolysis of uninfected RBCs
Dyserythropoiesis
Splenomegaly-erythrocyte sequestration
Depletion of folate stores
Cerebral
malaria
• The most well-known
severe manifestation
of malaria
• Defined as:
– unarousable coma
persisting for more
than one hour
– with asexual forms
of P. falciparum in
the peripheral
blood
– other common
causes of
encephalopathy
excluded
(WHO1999)
• Common in P.f
infections where the
erythrocytic
schizogony takes
place in the smaller
capillaries of the
internal organs
• Results in the
blockage of capillaries
by parasitized RBCs
A young girl with cerebral
malaria. Note the abnormal,
decerebrate posturing
Cerebral malaria
A 4 year old boy who
was deeply comatose
and had persistent
deviation of the eyes
Cerebral malaria

• Occurs most commonly in young children

although non-immune adults are also at
risk
• Cerebral malaria can rapidly progress to
death, even with appropriate treatment.
Case fatality is between 20-50%.
Cerebral malaria

• The illness may start with drowsiness and confusion

and then progress to coma.
• The loss of consciousness is often preceded by
repeated convulsions.
• Retinal haemorrhages may be seen on fundoscopy.
• In survivors, resolution of coma usually occurs within
1-2 days in children and within 2-4 days in adults but
may be complicated by neurological sequelae in ~5%
adults and >10% of children.
 3. Hypoglycaemia

• Blood sugar <2.5 mmol/L

• Increases the risk of mortality and sequelae in children
with cerebral malaria; may present with convulsions or
a deterioration in level of consciousness.
• Results from a combination of factors:
– reduced glycogen stores because of reduced food
intake
– increased metabolism due to fever and repeated
convulsions
– glucose consumption by malaria parasites
– cytokine or quinine-stimulated hyperinsulinaemia
4. Metabolic acidosis
• Lactic acidosis is a major contributor and
probably results from tissue anoxia and
anaerobic glycolysis

• Presents with deep, rapid respirations (as in

diabetic ketoacidosis)
5. Acute renal failure

• occurs almost exclusively in adults and older

children in areas of unstable malaria

• affected patients are usually oliguric (urinary

output <400 ml/day) or anuric (<50 ml/day)

• serum creatinine levels are elevated

Nephrosis

P. Malariae
quarten nephrosis
6. Acute pulmonary oedema
This is a grave and usually fatal
manifestation of severe
falciparum malaria and occurs
mainly in adults.
Hyperparasitaemia, renal failure
and pregnancy are recognised
predisposing factors and the
condition is commonly
associated with hypoglycaemia
and metabolic acidosis.
 7. Circulatory collapse, shock,
“algid malaria”
• Features of circulatory collapse (cold/clammy
skin, hypotension, peripheral cyanosis,
weak/thready pulses) may be seen in patients
with severe P. falciparum malaria.

• “Algid malaria” is characterised by hypotension,

vomiting, diarrhoea, rapid respiration and
oliguria. This condition is associated with a poor
prognosis.
8. Haemoglobinuria or “Blackwater
Fever”
• Characterized by rapid, severe intravascular
haemolysis
• It is associated with infection by P.f, most
commonly seen in a non-immune person who
has resided in the endemic country for the last
6 months to 1 year and inadequately treated by
quinine
• In these cases, quinine is a precipitating factor
• It is triggered by exposure to cold, sun, fatigue,
trauma, pregnancy, X-rays etc,.
Contnd…

The condition presents with severe pallor,

jaundice and passage of dark urine due to
haemoglobinuria.
It may be associated with acute renal
failure.
A 3 year old boy with severe anaemia (Hb% 3.3
g/dl) and dark urine (shown in the container)
Diagnosis
Malaria is a multisystem disease.
 It presents with a wide variety of non-specific
clinical features.
 None of the clinical features are
pathognomonic.
Many patients have fever, general aches and
pains and malaise and are initially
misdiagnosed as having “flu”.
P. falciparum malaria can be rapidly
progressive and fatal.
Diagnosis
• A good history
– Residence or a recent visit (in the preceding 3 months) to a
malaria endemic area
– History of fever
– Recognise significance of non-specific clinical features such
as vomiting, diarrhoea, headache, malaise
• Physical examination
– Identify signs consistent with malaria: fever, pallor,
jaundice, Splenomegaly
– Exclude other possible causes of fever (e.g. signs of viral
and bacterial infections)

The diagnosis of malaria should be

considered in any unwell person who has
been in a malarious area recently
 Laboratory Investigations

Blood Film Examination

Thick and thin blood films (or “smears”) have remained the gold
standard for the diagnosis of malaria. The films are stained and
examined by microscopy.

Thick blood film - Used for detecting malaria: a larger volume

of blood is examined allowing detection of even low levels of
parasitaemia. Also used for determining parasite density and
monitoring the response to treatment.
Thin blood film – Gives more information about the parasite
morphology and, therefore, is used to identify the particular
infecting species of Plasmodium.
Appearance of P. falciparum in thin blood
films. Ring forms or trophozoites; many red cells
infected – some with more than one parasite
Other methods of diagnosis of malaria

These are not routinely used in clinical practice.

a) Antigen capture kits. Uses a dipstick and a

finger prick blood sample. Rapid test - results
are available in 10-15 minutes. Expensive and
sensitivity drops with decreasing
parasitaemia.
b) PCR based techniques. Detects DNA or
mRNA sequences specific to Plasmodium.
Sensitivity and specificity high but test is
expensive, takes several hours and requires
technical expertise.
Contnd…
c) Fluorescent techniques- Relatively low
specificity and sensitivity. Cannot identify the
parasite species. Expensive and requires skilled
personnel.

d) Serologic tests- Based on immunofluorescence

detection of antibodies against Plasmodium
species. Useful for epidemiologic and not diagnostic
purposes.
The treatment of malaria Treatment
depends on a number of
factors
• Severity of the infection:
whether simple,
uncomplicated or severe,
complicated malaria.
• Parasite factors: species,
drug sensitivity
• Patient factors: age,
pregnancy, prior
chemoprophylaxis, known
allergies, likelihood of drug
compliance.
 Chloroquine

 A 4-aminoquinoline, orally- well absorbed.

 Has rapid blood schizointicidal activity against all species
 Has gametocidal activity against P.v, but not against Pf
 No action on liver schizoints, hence it cannot clear the
parasite
 Safe in pregnancy
 Therapeutic concentration-plasma-30 mins-oral
 Low margin of safety in children
 Dosage -25mg/kgbw given over 3 days for treatment and
5mg/kgbw weekly once for chemoprophylaxis
 Given after food, cheapest, rapid action, symptomatic relief
 Pruritus may be seen in dark skinned people
 Cardiovascular toxicity with hypotension and arrhythmias-
death
2) Primaquine

An 8-aminoquinolone, readily absorbed orally

Highly active against gametocytes of all human
malaria parasites and hypnozoites of P.v
Haemolysis occurs in G6PD deficiency people
and in infants with foetal haemoglobin
It crosses placental barrier, not to be given in
pregnancy
Also causes methaemoglobinaemia and
suppression of myeloid activity
3) Quinine-
Since 1638 malaria has been treated with an extract
from the bark of the cinchona tree, known as quinine.
DOC to treat severe malaria and uncomplicated
malaria resistant to chloroquine, S-P and mefloquine.
Severe side effects, extremely bitter, long regimen,
therefore not often used as oral treatment.
Use restricted for CRPF infection
 Intravenous treatment suitable for treating pregnant
women and children
10mg/kgbw,slow infusion IV in isotonic soln or 5%
dext
4) Sulfa drug/Pyrimethamine
combination (SP)

 Highly active against blood schizoints of P.f but less

effective against P.v.
 No gametocidal activities
 Use restricted for CRPF infection which is not
complicated
 Active in a single dose of 3 tablets (adults)
 Not used in pregnancy, lactation and infancy
 Hypersensitivity involving skin and mucous membrane
(SJ syndrome)
 Resistance to S-P has also been found
 5) Mefloquine

a 4-quinoline methanol chemically related to

quinine
Potent long acting blood schizonticide active
against all species
Use restricted to multi-resistant P.f infections
Not safe in pregnancy
Not available in India, to be imported
6) Artemisenin and its derivatives:

 Artemisenin, Artesunate and Artemether used to treat

complicated malaria of CRPF, S-P and Mefloquine.
 Indicated when quinine is not advisable
 It acts on the broadest range of parasite stages, gives
the most rapid cure, has the least side effects.
 Artesunate 4mg/kgbw for 3 days. Available strength is
50mg tabs
 Arteether inj. I.M.- 3mg/KG B.Wt. daily for 3 days.
Available as 150mg/ ampoule
Site of Action

Primaquine

Chloroquine
Quinine, SP
Artemisinin

Quinine &
Chloroquine in P.V.
and Primaquine in
P.F.
Drug Sporozoite Primary Asexual Gametocyt Hypnozoit
s tissue parasite e e
phase

Quinine NA NA A A-P.v NA

Chloroquine NA NA A A-P.v NA

Primaquine A A A A A
in toxic dose
SP Less A Little A on Incomplete NA NA
P.f
Mefloquine NA NA A NA NA

NA-not active, A-active,

 Avoid these combinations
• Most antimalarial drugs have a long plasma half-life. Therefore,
adding similar drugs half way through the treatment will only
add to the adverse effects and not to the therapeutic benefit.
The following combinations should therefore be avoided,
concurrently or within a short interval:
(1.) Chloroquine + Quinine
(2.) Chloroquine + Mefloquine
(3.) Quinine + Mefloquine
(4) Quinine + Primaquine
(5.) Quinine + Halofantrine
(6.) Mefloquine + Primaquine
(7.) Administration of Primaquine on the same day is also not
advisable.
Both sulpha and primaquine can precipitate hemolytic crisis in
patients with Glucose 6-phosphate dehydrogenase deficiency.
Treatment of uncomplicated malaria
Presumptive treatment: It is given to
1. All fever cases with H/O fever during past 15 days
2. All fever cases irrespective of age and sex
3. No Primaquine to infants and pregnant women.
4. Each Chloroquine tab available as 150 mg and
Primaquine tab as 2.5 mg & 7.5 mg.
Radical Treatment:
1. Given after microscopic confirmation
2. No Primaquine to infants and pregnant women.
3. Each Chloroquine tab available as 150 mg and
Primaquine tab as 2.5 mg & 7.5 mg.
Treatment in low risk areas
Presumptive treatment- only one day
tab Chloroquine(10mb/kgbw) 600mg
Radical treatment- 1 day in P.f and 14days in P.v
infections
P.V. infections - tab Chloroquine(10mb/kgbw)
600mg single dose, with Primaquine
(0.25mg/kgbw) 15mg daily for 14 days
P.F. cases-tab Chloroquine(10mg/kgbw) 600mg
with Primaquine (0.75mg/kgbw) 45mg single dose.
Treatment in high risk areas
• For P.V.- Here, as we have already given
chloroquine base (1500mg) spread over 3 days
and 45mg Primaquine (adult dose), chloroquine
need not be given again, but Primaquine
0.25mg daily (15mg/day- adult) must be given
for 14 days.
• For P.F.- R.T. with Primaquine is not required
as we have already given required dose.
In Chloroquine resistant P.F. cases (HRAs)

- 236 PHCs in 19 states are identified as

Chloroquine resistant.
- Sulfadoxine(25mg/kgbw) and Pyrimethamine
(1.25mg/kgbw) available as 500mg tab and
25mg tabs given as single dose for Presumptive
treatment.
- For radical treatment- Primaquine 0.75mg as
single dose.
 Criteria for high risk area

Subcentre is the basic unit considered for

selection of HRA.
Criteria for identification of high risk areas are:
• Deaths due to malaria recorded during any of
the last three years
• Average SPR of last three years is 5% or more
• Doubling of SPR during last three years
provided the SPR in second and third reaches
4% or more
• Pf proportion is 30% or more provided SPR is
3% or more during the last three years
• An area having a focus of Chloroquine resistant
foci.
• Tropical segregation of labour in project areas
Based on the above criteria, Karnataka had 64
PHCs and Belgaum had 5 PHCs in the year 2006
and 10 PHCs in 2007 &2008
MOH has to calculate- 3 years data-SC wise
Mass drug administration
• Recommended in API>5 per 1000 popn (WHO)
• Not for under 5 children
Chemoprophylaxis
- Use of anti-malarial drugs to prevent the
development of malaria is known as
chemoprophylaxis.
- Unreliable with development of drug resistance
- Started 1 week before arrival in the malarious area
and continued for atleast 4 weeks, preferably 6
weeks after leaving a HRA.
- Should be complemented by personal protection and
other VCMs
Chemoprophylaxis

- Recommended for
1.Travellers from non endemic areas
2.As a short measure for soldiers, police
and labours serving in highly endemic
areas
3.All ANCs in HRAs- initiated in II semester
Contnd…
• Start with a loading dose of 10mg/kgbw and
followed by a weekly dose of 5 mg/kgbw till 1
month after delivery and in travellers till one
month after return from HRA.
• Not recommended for >3 years with
Chloroquine- cumulative toxicity
• In CRAs, chemoprophylaxis is recommended
with Chloroquine 5mg/kgbw weekly and
Proguanil 100mg daily.
Treatment of Complicated Malaria
• All the patients are to be hospitalised
• Choice of antimalarial is quinine injection
• 10mg/kg BW.IV in 5% dextrose 8th hourly till
the patient regains consciousness
• Switch over to oral dose as early as possible-
Oral quinine 600mg tds for 7-10 days
• Total duration of treatment -7 days including
both parenteral and oral dose
• Corrections of other associated metabolic
disorders
 MALARIA TREATMENT COST OF

AN ADULT IN INDIA
Drugs Cost (Rs.)
 Chloroquine 3.50-10.00
Chloroquine injection + fluids 200.00
Sulfadoxine Pyrimethamine 7.00-30.00
Mefloquine 240.00-300.00
Artemether injections 390.00-1000.00
Arteether injections 275.00
Artesunate injections 1120.00
Quinine tables + Tetracycline 270.00-210.00
Quinine injections+IV fluid+Tetracycline 800-910  
*Antipyretics @ Rs. 5.00-10.00 per treatment
Pregnant women and their fetus/newborn

• HIV does make malaria in pregnancy

worse
– More and higher density malaria, more illness, more
anemia, more low birth weight
• Malaria may make HIV worse
– Higher HIV viral load
– ? impact on Mother-to-Child Transmission (MTCT)
 The Worlds Priorities? Annual Expenditure
Global Reduction in Malaria $ 1 billion
Basic education for all $ 6 billion
Cosmetics in the US $ 8 billion
Safe water and sanitation $ 9 billion
Ice cream in Europe $ 11 billion
Reproductive health for all women $ 12 billion
Perfumes in Europe and the US $ 12 billion
Basic health and nutrition $ 13 billion
Pet food in Europe and the US $ 17 billion
Business entertainment in Japan $ 35 billion
Cigarettes in Europe $ 50 billion
Alcoholic drinks in Europe $ 105 billion
Narcotic drugs in the world $ 400 billion
Military spending in the world $ 780 billion

Source-Favaloro et al Circulation 1999

• Prevention and Control of
Malaria
Thank you
Any ????