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Microorganism causes of

Gastro-Intestinal Infection
(1)

Oleh :

Efrida Warganegara
GIT Infections
I. Diarrhoeal Disease
I. Bacterial causes of Diarrhoea
2. Antibiotic-associated Diarrhoea
3. Viral Diarrhoea
4. Food Poisoning

II. Systemik Infection Initiated in the GIT


1. Enteric Fever (Typhoid and Paratyphoid)
2. Hepatitis
I. Bacterial causes of Diarrhoea
1. Escherichia coli
Characteristic are : gram-negative-rod; motile;
capsule +/-; facultatif anaerobe; bile-tolerant;
capable of grwoth at 44o C; growth readily on
routine lab. media and on bile-containing
selective media; lactose fermenter.
Some strain are important member of the
normal gut flora in human and animal, whereas
others posses virulence factors which enable
them to cause infection in the intestinal tract or
at other sites, particularly urinary tract
1. Escherichia coli Pathogenesis
Escherichia coli that posses virulence
factors which enable them to cause
infection in the intestinal tract are :
ETEC, EPEC, EIEC, EHC/VTEC and EAgEC
A). Enterotoxigenic Escherichia coli
(ETEC) :
posses colonization factors bind the
bacteria to spesific receptors on the GIT
memb. where m.o. produce powerful
enterotoxin
1. Escherichia coli Pathogenesis
Heat-labile enterotoxin (LT) is very
similar in structur and mode of action
to cholera toxin (by Vibrio cholerae),
and infection with these strain can
mimic cholera, particularly in young
and malnourished children
Other ETEC strain produce heat-stable
enterotoxins (ST) in addition to, or
instead of, LT.
Escherichia coli
2. ETEC (Enterotoxigenic E.coli)
* Penyebab umum dr "Traveler's diarrhea
* Sangat penting sbg penyebab diare pada
negara sedang berkembang
* Berkolonisasi menempel pd sel epitel usus kecil
* Bbp strain menghasilkan eksotoksin tdk tahan
panas (LT) st kompleks protein, BM
besar, imunogenik, gen pengkode pd plasmid
- LT : bersifat antigenik, reaksi silang dgn
eksotoksin dr V.cholerae
- LT t.d. : 1 subunit polypeptide A
5 subunit polypeptide B
Escherichia coli
Sub unit B melekat pd sel epitel,
Memfasilitasi masuknya sub unit A kedalam sel
Mengaktivasi adenyl cyclase

Konsentrasi cAMP lokal

Hipersekresi yg intens dan berkepanjangan
dari air dan khlorida
Menghambat reabsorbsi Natrium

Lumen usus mengembang karena cairan,
Hipermotilitas dan diare
1. Escherichia coli Pathogenesis
STs have a similar but distict mode of
action to that of LT
STA : activated guanylate cyclase activity
causing an increase in cyclic guanosine
monophosphate, which result in
increased fluid secretion.
STB : mechanism of action is unknown

Like LT, the ST are not immunogenic and


therefore cannot be detected by
immunological tests
1. Escherichia coli Pathogenesis
B). Enterohaemorrhagic Escherichia coli
(EHEC) :
Other E. coli strains produce a verotoxin
(VT), so called because it is toxic to tissue
culture of vero cells, or Shiga-like toxin
After attachment to the intestinal mucosa
by an attaching-effacing mechanism, the
m.o. elaborate verotoxin, which has a
direct effect on intestinal epithelium
resulting in diarrhoae
1. Escherichia coli Pathogenesis
Two disease of previously unknown
aetiology : Haemorrhagic Colitis (HC)
and haemolytic Uraemic Syndrome
(HUS), have recently been associated
with verotoxin-producing E. coli
strains
InHC there is destruction of the
mucosa and consequent haemorrhage;
this may be followed by HUS.
1. Escherichia coli Pathogenesis
Verotoxin receptors have been
identified on renal epithelium and
may account for the kidney
involvement.
The association between
haemorrhage and verotoxin-
producing E. coli has lead to the
acronim EHEC
Enterohaemorrhagic Escherichia coli
1. Escherichia coli Pathogenesis
C). Enteropathogenic Escherichia coli
(EPEC) :
The first group of E. coli intestinal pathogen
to be described but their mechanism of
pathogenicity remain unclear.
They do not appear to produce any toxin but
have a particular mechanism of adhesion
(attaching-effacing as with VTEC) to
enterocytes which appears to destroy the
microvilli
1. Escherichia coli Pathogenesis
D). Enteroinvasive Escherichia coli
(EIEC) :
EIEC attach spesifically to the mucosa
of the large intestine and invade the
cells by being taken in by endocytosis.
Inside
the cell they lise endocytic
vacuole, multiply and spread to
adjacent cells, causing tissue
destruction and consequently
inflammation
1. Escherichia coli Pathogenesis
E). Enteroaggregative Escherichia
coli (EAggEC) :
the term enteroadherent E. coli refers
to E.coli strain do not produce LT/ST,
not invasive, and not grouped
according to O:H serotypes as ETEC,
EPEC, EIEC, or EHEC.
EAggEC is the best study
enteroaadherent E. coli
Strain Pathogenic Mechanism Enteric Infection(s) Common Clinical Presentation

ETEC LT and ST Diarrhea; Traveler's Profuse watery diarrhea, cramps,


diarrhea Nausea, dehydration

EPEC Adherence factor; Accute diarrhea Watery diarrhea, fever, vomiting,

Attachment to and affacement mucus in stool

of intestinal epithelium
Dysentry; scant stool; blood,
EIEC Invasion and destruction of Dysentry similar to mucus

intestinal mucosa and leucocytes in stoo; fever;


epithelium Shigella dysenthry cramp

Diarrhea; Diarrhea (no leucocytes);


EHEC Shiga-lika toxin haemorrhagic abdominal

colitis cramp; blood in stool; fever, HUS


may or may not be present

EAggEC Unknown Chronic and acute Watery diarrhea, vomiting


diarrhea
1. Escherichia coli Labor. Diagnosis;
Treatment and Prevention
Epidemiology and Laboratorium diagnosis of
Pathogenic E.coli - fig. 6
Treatment : Specific antibacterial therapy is not
indicated; fluid replacement may be necessary,
especially in young children; For HUS is urgent and
may involve dialysis
Prevention : Provision of a pure water and adequate
system for sewage disposal are fundamental.
Food and unpasteurized milk may be important
vehicle of infection, especially for EIEC and EHEC
2. Salmonella Pathogenesis
All Salmonella except S.typhi and S.paratyphi are found
in animal as well as human. There is a large animal
reservoir of infection which is transmitted to man via
contaminated food. Waterborne infection is less
frequent
Pathogenesis of Salmonella diarrhoea : diarrhoea is
produce as a result of invasion by the salmonella of
epithelial cells in the terminal portion of the small
intestine
The bacteria migrate to the lamina propria layer of the
ileocaecal region multiplication stimulates an
inflamation response infection to GIT mediate
the release of prostaglandins in turn activate cyclic
AMP and fluid secretion diarrhoea
2. Salmonella Clinical features and
laboratorium diagnosis
Salmonella cause an acute but self-liiting diarrhoea,
but in the young and elderly symptoms may be
more severe. Incubation 6 hours 2 days
Duration 3 days-3 weeks.Vomiting is rare and fever
is usually a sign of invasive disease
Diarrhoea caused by salmonella cannot distinguish
from other causes without culturing faecal
specimens on selective media
Preliminary identification without culturing faecal
specimens on selective media can be made rapidly
but, complete result, including serotype 48 hours
2. Salmonella Treatment
Diarrhoea is usually self-limiting and resolves
without treatment
Fluid and electrolyte replacement msy be required
particularly in the very young and the elderly
Unless there is evidence of invasion and
septicemia, antibiotic positivelydiscouraged
because they do not reduce the symptom or
shorten the illness, and may prolong excretion of
salmonellaa in the faeces.
There is some evidence that symptomatic
treatment with drugs that reduce diarrhoea has
the same adverse effect.
2. Salmonella Prevention
Prevention : breaking the chain between animal and
human, and between human; clean drinking water;
proper sewage disposal; and education programmes
on hygienic food preparation
Following an episode of salmonellae diarrhoea, people
may continue to carry and excrete organism in their
feaces for several weeks
Although in the absence of the symptom the m.o. will
not be disperse so liberally into the environment,
proper hand washing prior to handling is essential
Person who food handler are not work until 3
specimen of faeces have failed to grow salmonellae
I. Bacterial causes of Diarrhoea
3. Campylobacter - epidemiology
Characteristic are : gram negative; slender, spirally
curved-rod, motile (single polar flagellum)
Campylobacter are important pathogens in
animals and in the past 10 years have become the
most frequent cause of bacterial gastroenteritis in
human, the most common C.jejuni.
As with Salmonella, there is a large animal
reservoir, so that infections are acquired by
consumption of contaminated food, especially
poultry, milk, or water
3. Campylobacter Pathogenesis
Not all infections are symptomatic, some patients
may become asymptomatic excreters
The incubation period is usually 2-5 days (2-11
days), duration 3 days-3 weeks
Diarrhea may be preceded by fever, myalgia, and
abdominal pain. Abdominal pain mimic acute
peritonitis. Vomiting rare.
Diarrhea lasts about 2-3 days but abdominal pain
may persist. Stool may contain fresh blood, pus or
mucus, indicating colorectal inflammation
C. jejuni causes infectious proctitis in homosex. man
3. Campylobacter Lab. Diagnosis
and Treatment
Direct examination of fresh by dark-field or phase
contrast microscopy can be used in the diagnosis
of Campylobacter enteritis.
Selective media with and without blood have been
used to isolate organism from stool
Chemotherapy is not warranted, and
erythromycin is the antibiotic of choice for cases
of diarrhoea disease that are severe enough to
treatment
Invasive infection may require treatment with an
aminoglycoside
3. Campylobacter Prevention
Preventionof Campylobacter infection is
possible when (like prevention salmonella):
1) water supply are purified properly
2) milk for human consumption is
heat-treated
3) there is hygienic handling of raw
meats, and
4) there is control of infection at all
stages of poultry production
4. Vibrio cholerae Introduction
Vibrio are straight or curved rods belong to
the family Vibrionaceae comma-shaped
gram negative, facultative anaerobes, that
are motile by a polar flagellum or flagella.
The most important of Vibrio is V. cholerae,
the etiological agent of cholera
Cholera is still a major cause of
gastrointestinal illness in dweveloping
countries.
4. Vibrio cholerae Epidemiology
V. cholera is free-living inhabitant of fresh water
but causes infection only humans
Asymptomatic human carriers are believed to be a
major reservoir
The disease is spread via contaminated food;
shelfish grown in fresh waters all type of shelfish
product may be the source of infection
Thus cholera continues to flourish in communities
where the provision of clean dringking water and
adequate sewage disposal is absent or unrealible
Cases still occur in develop countries, and drinking
contaminated water is also a means of infection
4. Vibrio cholerae Epidemiology
V. cholerae
can be subdevided into
serotype based on somatic (O)
antigen
Serotype O1 is the most important
and it is further devided into 2
biotype : Classical and El Tor.
The El Tor biotype differs from
classical V. cholerae is several ways.
4. Vibrio cholerae Pathogenesis
Vibrio cholerae O1 :
Cholera caused by V. cholerae O1 is spread
from person to person by ingestion of
contaminated water or uncooked foods,
especially fish
M.o. is very susceptible to gastric secretion.
Ingestion of 109 vibrios in food or water is
required to initiate disease.
If the individual s gastric content have been
neutralized by bicarbonate or other antacid,
106 vibrio may cause disease
4. Vibrio cholerae Pathogenesis
The incubation period for cholera is
approximately 2-3 days and is followed by a
period of vomiting and diarrhea up to 7 days.
10-25 liters of fluid may be lost during
infection
Rapid dehydration is accompanied by loss of
electrolyte such as potassium and
bicarbonate. The loss of electrolytes is due to
a microbial enterotoxin
Protration can occur at any time and is
directly related to the amount of fluid lost
4. Vibrio cholerae Pathogenesis
The major causes of death in cholera are shock,
metabolic acidosis, and renal failure
The relationship between adherence properties
and pathogenesis has not been clearly it is
believe that flagellum is s prerequisite to
attachment to the epithelial surface
The flagellum enables the m.o. to penetrate the
mucous gel covering the intestinal epithelial
surface
Adherence to the epithelial surface may also be
mediated by other types of surface adhesins
4. Vibrio cholerae Pathogenesis
Once attached to the epithelial surface,
the m.o. can multiply and produce
enterotoxin
Enterotoxin is a protein composed of A
and B subunits. The subunits B attach to
receptor dissociation of subunit and
entry of subunit A to plasma membrane
activation of subunit A cause
activation of adenyl cyclase that
change ATP to cAMP.
4. Vibrio cholerae Pathogenesis
IncreasecAMP alters the ion
transport mechanism associated
with the cytoplasmic membrane.
Permeability changes involving
sodium (Na+) and chlorine (CL-)
cause an efflux of water from the
mucosal surface and hence cause
diarrhea
4. Vibrio cholerae Pathogenesis
Vibrio cholerae non-O1 :
Non O1 organism produce a cholera-like
toxin that is believed to beassociate with
gastrointestinal sympom,. Most cases are
sporadic, and not associated with
pandemics, as classic cholera is
The symptoms of non O1 disease are
similar to those of classical cholera but
are less severe
4. Vibrio cholerae Lab. diagnosis
In country where cholera is prevalent ,
diagnosis based on clinical ground. Because
ETEC infection can resemble cholera an its
severity, so fluid and electrolyte replacement
are of important

For diagnosis of sporadic and detection of


carriers , culture is required to distinguish
cholera from other acute diarrhoeas
4. Vibrio cholerae Treatment
Cholera is a self-limiting disease when water and
electrolytes are replaced.
Prompt oral or intravenous rehydration with fluids
and electrolytes is central to the treatment of
cholera.
A replacement fluid consisting of NaCl, sodium
bicarbonate, and potasium chloride can be given IV
for patient in severe shock
Oral rehydration therapy for patient with less severe
disease includes the use of glucose or sucrose in
addition to the salt just mentioned
4. Vibrio cholerae Treatment
The addition of sugars permits fluid balance
in the gut by preventing the loss of sodium
Antibiotic are not necessaary , but
tetracycline may be given as some evidence
indicates that this treatment reduces the
time of secretion of V. cholera thereby
reducing the risk of transmission
Tetracyclin is used for adults while
trimetoprim-sulfamethoxazole and
furazolidone are used for childres and
pregnant women respectively
4. Vibrio cholerae Prevention
As with other diarrhoeal disease, a clean
drinking-water supply adequate sewage
disposal are fundamental to the prevention of
cholera.
Be possible to eliminate the disease because
there is no animal reservoir
A killed, whole-cell vaccine is available and is
given parenterally, but is only effective in
about 50% of vaccinees, with protection
lasting only for 3-6 months
5. Shigellosis Introduction
Shigellosisis also known as bacillary
dysenthry because in its more severe
form it is characterized by an invasive
infection of the mucosa of large intestine,
causing inflammation and resulting in pus
and blood in the diarrhoeal stool
However symptoms range from mild to
severe depending on the species of
shigella involved and on the underlyying
state of health of the host
5. Shigellosis Epidemiology
Thre are 4 species, of which Shigella dysenteriae is the
most serious.
Shigellosis is primarily a paediatric disease. When
associated with severe malnutrition it may precipitate
complication such as the kwashiorkor
Shigella are human pathogens without animal reservoir,
being spread from person-to-person by the fecal-oral
route and less frequently by contaminated food and
water
Shigella able to initiate infection from a small infective
dose thus spread is easily in situation where
sanitation / personal hygiene may be poor (nurseries,
day care centre, and institution for the handycapped)
5. Shigellosis Pathogenesis
Shigella are effective pathogen, cause disease with
doses as low as 10-100 m.o.; whereas with
Salmonellae, Campylobacter, and V. cholera, higher
doses are usually required

Incubation periode 1-4 days, duration 2-3 days.


Vomiting rare. The m.o. attach to and invade the
mucosal epithelium of the distal ileum and colon,
causing inflammation and ulceration. Abdominal cramp
and fever positif

However they rarely invade throught the gut wall to


the bloodstream. Enterotoxin is produced but it role
in pathogenesis is uncertain since toxin-negative
mutants still produce disease
5. Shigellosis Clinical features,
Treatment, and Prevention
Diarrhoea is usually watery at first but later contains
mucus and blood. Lower abdominal cramps may be
severe
The disease is usually self-limiting but dehydration can
occur, especially in the young and elderly.
Complication may be associated with malnutrition.
Treatment : Rehydration may be indicated. Antibiotic
not be given except in severe cases.
Prevention : education in personal hygiene and proper
sewage disposal are important. Cases may continue to
excrete shigellae for a few weeks. Because of no animal
reservoir, the disease is potentially eradicable
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