GASTROINTESTINAL

TRACT INFECTIONS

Ike Irmawati P.A

Introduction

Gastroenteritis gastrointestinal
symptons : nausea, vomiting, diarrhea &
abdominal discomfort

Diarrhea
abnormal fecal discharge : frequent &/or
fluid stool
Resulting from disease small intestine
fluid & electrolyte loss

Dysentry
An inflammatory disorder of GIT
Associated with : blood & pus in feces
Symptoms : pain in anus, fever, abdominal
cramps
Resulting from disease large intestine
Enterocolitis inflammation involving the
mucosa small & large intestine

Pathogenesis

21/1
2/08

Infections
ingested in sufficient number
Elude host defenses of upper GIT & reach
the intestine

Diarrhea the most common outcome of

GIT infection

anamnesis

Patients recent food

Travel history

Macroscopic & microscopic of the feces

blood, pus/ mucous

Escherichia coli

Escherichia coli

Normal gut flora

May also inhabit female genital tract

Possess virulence factors intestinal

tract or at other site (eg. Urinary tract)

Escherichia coli

Spectrum of disease:
Bacterimia
Urinary tract infection: caused 80% case; hemolisin
(+), virulensi factor pili P UPEC (uropathogenic
E.coli)
Neonatal meningitis: E. coli K1 MNEC
(meningitis/ sepsis-associated E.coli)
Nosocomial infection
Gastroenteritis (Diarrea) by E. coli

6 classes (virotypes) of E. coli that

cause diarrheal diseases :
1.enterotoxigenic

E. coli (ETEC)
2.enteroinvasive E. coli (EIEC)
3.enterohemorrhagic E. coli (EHEC)
4.enteropathogenic E. coli (EPEC)
5.enteroaggregative E. coli (EAEC)
6.diffuse-aggregative E. coli (DAEC)

Mechanism of virulence

Patogenesis

ETEC
Virulence
fimbrial adhesins e.g. CFA I, CFA II, K88,
K99
non invasive
produce LT and/or ST enterotoxin
watery diarrhea in infants and travelers; no
inflammation, no fever
Transmitted by contaminated food and
water

ETEC

Adult self-limited 1-3 day

LT Eksotoxin (subunit A & B) activation of

adenilat cyclase cAMP hypersecretion of
water & Cl- , as well as inhibiting the reabsorption
Na+ hipermotilitas & diarrhea Be antigenic
and similar to V. cholerae enterotoxin

ST Toxin : activation of guanylate cyclase

cGMP water secretion

Bacteria has colonization factor in the small

intestine epithelium gen faktor kolonisasi terkait
plasmid

Patogenesis ETEC

EPEC

non fimbrial adhesin (intimin) & Tir

(translocated intimin receptor), Bfp
(bundle-forming pili) and
EPEC adherence factor (EAF) enables
localized adherence of bacteria to
mucosal intestinal cells changes in cell
surface (loss of microvilli)

does not produce LT or ST; some reports

of shiga-like toxin

EPEC

usually infants diarrhea & child in

developing country; watery diarrhea
self-limited/ chronic diarrhea

some inflammation, no fever; symptoms

probably result mainly from invasion
rather than toxigenesis

EHEC

= VTEC = STEC
adhesins not characterized, probably fimbriae
moderately invasive
produce shiga toxin Verotoxin
pediatric diarrhea,
Inflammation & bleeding mucosa of large
intestine (hemorrhagic colitis)
may be complicated by hemolytic uremia
syndrome (toxin mediated damage to kidneys)
characterized by: hemolytic anemia & low platelet
count

EHEC

after attachment at mucosa of colon

produce toxin effects on the intestinal
epithelium diare
Caused hemorrhagic colitis and hemolytic
uremic syndrome (HUS) verotoxin
receptors found in renal epithelium
Acute renal failure
Isolate E. coli O157:H7 & O26 (Jepang,
2001), sorbitol (-)
Transmitted by ingestion of undercooked
beef or raw milk

EHEC

EIEC

nonfimbrial adhesins
possibly outer membrane protein
invasive (penetrate and multiply within
epithelial cells)
dysentery-like diarrhea (mucous, blood)
necrosis, ulceration & inflammation of the
large bowel
high fever, malaise, headache, abdominal
pain

EIEC

Usually seen in young children living in

areas of poor sanitation

Test Laktosa (-), test Sereny (+),

leukocytes in feses

Patogenesis EIEC
E. coli invade by endocytosis inside
epithelial cell they lyse endocytic
vakuola multiply & spread to
adjacent cells tissue destruction,
inflammation , necrosis & ulceration
blood & mucus in stools

Patogenesis EIEC

EAEC

Probably involves binding by pilli

non invasive
produce ST-like toxin (EAST) and a
hemolysin-like toxins
persistent watery diarrhea in young
children without inflammation or fever

EAEC

The bacteria can attach in cultur cell &

forming aggregates (stacked brick)
plasmid-associated fimbriae
associated with a global aggregative
regulator gene ( AggR) responsible for
cellular adherence

Stool specimen : no bloody & no white

blood cell

DAEC

Produce alpha hemolysin & cytotoxic

necrotizing factor 1
Diarrhea : children

diagnose

Culture : Endo agar metalic colony

Inflammatory gastroenteritis

Enterotoxigenic (ETEC) E. coligram negative rod

Enteropathogenic (EPEC) E. coli

also called enteroadherent E. coligram negative rod

Enteroaggregative (EAEC) E. coligram negative rod

Ingestion of comtaminated
water or food.

Ingestion of comtaminated
water or food.

Ingestion of comtaminated
water or food.

ETEC has multiple

pathogenic mechanisms
which include at least
Traveler's Diarrhea; watery,
2 distinct toxins; a heat-labile
self-limited diarrhea,
toxin (LT) and a heat stable
vomiting, cramps, nausea,
toxin (ST). LT is similar to
low-grade fever, 1-3 days
cholera toxin. The ST acts
duration.
by stimulation of guanylate
cyclase with resultant cyclic
GMP accumulation in
mucosal cells.

EPEC produces no
demonstrable extracellular
toxin. Bfp mediates loose
attachment to microvillus
cells which leads to
Infant diarrhea with fever,
increases in Ca levels and nausea, vomiting, nonbloody
then rearrangements in
diarrhea
actin, Intimin protein needed
for intimate contact will
human cells and final stages
of cell destruction.

Aggregative pattern due to

certain thin pili (GVVPQ
fimbriae)

Developing countries,
persistant watery diarrhea
with vomiting and
dehydration in infants. Can
lead to bloody stools

Invasive gastroenteritis

Escherichia coli
Ingestion of
Enteroinvasive E. coli
contaminated food
(EIEC)- gram negative
and water.
rod

Escherichia coli
Enterohemorrhagic E.
coli (EHEC) includes
serotype O157:H7gram negative rod

Ingestion of
contaminated food
(undercooked
hamburgers), and
water

Plasmid mediated
invasion of epithelial
cells

fever, cramping,
watery diarrhea,
followed by scant
bloody stools

Verotoxin-blocks
protein synthesis

bloody diarrhea and in

severe cases can lead
to hemolytic uremic
syndrome (HUS)

Therapy

Supportive therapy : oral rehydration

HUS by EHEC : transfusion & hemodialysis
Antimicrobial therapy may shorten the
duration of illness, but many of these
infection resolve without such therapy
Antimicrobial therapy for non-lifethreatening infection contraindicated
develop resistance
Food sanitation and environment

Salmonella

 Morphology:

Rod, Gram (-), motile, facultative

anaerobic
No fermentation lactose & sucrose
produce H2S
Freezing temperature resistant

The genus Salmonella has three kinds of

major antigens :
1.somatic (O) heat stabile & alcohol
resistant LPS
2.surface ( K) Vi antigen virulence factor
capsular polysaccharide
3.flagellar (H) heat-labile protein
Salmonella enterica serovars (e.g.,
Enteritidis, Typhi) peritrich flagella

the Salmonella strains isolated from humans

and other warm-blooded animals.

Hospes:
Human S. typhi; S. paratyphi A, B, C
S. cholera-suis
Pig
Cow S. dublin
Sheep S. abortus suis

Infective doses S. typhi: 106 - 109

In humans, Salmonella are the cause of

three diseases called salmonellosis:

1.

enteric fever (typhoid), prolonged fever

& multisystem involvement ( blood, lymp
nodes, liver & spleen
caused by: S. serotype Typhi, Paratyphi
A,B or C

Cont.
2. Gastroenteritis & diarrhea
production infection limited to the
mucosa & sub mucosa of the
gastrointestinal tract
caused by: S. serotype Typhimurium &
S. serotype Enteritidis
acute gastroenteritis, resulting from a
foodborne infection/intoxication

3. Bacterimia & extraintestinal infections

occur by spread from GIT
Etiology: S. choleraesuis
S. dublin

Salmonella enterica serovar Typhi.

Also called Salmonella Typhi

the causative agent of typhoid fever.

The symptoms of typhoid fever include
nausea, vomiting, fever and death.
S. Typhi can only infect humans

Salmonella enterica serovar Typhimurium (S. Typhimurium)

the most common cause of food

poisoning
In humans S. Typhimurium does not cause
as severe disease as S. Typhi,
The disease is characterized by diarrhea,
abdominal cramps, vomiting and nausea,
and generally lasts up to 7 days.

Salmonella enterica serovar Enteritidis

S. Enteritidis causes a disease almost

identical to the very closely related S.
Typhimurium.

S. enteritidis

Bakteri menempel pd
epitel ilium terminal
Bakteri berpenetrasi dlm sel &
bermigrasi ke lamina propia pd
ileocecal berkembangbiak pd
folikel limfoid hiperplasia dan
hipertrofi reticuloendothelial

DIARE

cAMP meningkat
sekresi cairan
meningkat

PMN Infeksi terbatas

pada traktus
gastrointestinal
Respon inflamasi
pelepasan Prostaglandin

Salmonellosis

1 billion Salmonella per gram of feces

Mortality rate < 1 %

Higher in infants and elderly

Recovery in a few days

Some may shed bacteria in feces for 6 months

Salmonellosis

Incubation time 12 36 hours

Bacteria invade the intestinal mucosa and

multiply

May pass thru mucosa into lymphatic or

circulatory system and become systemic

Fever, abdominal pain, cramps and

diarrhea

Patogenesis Salmonellosis

Mucosa invasion by Salmonella

Routes Of Transmission And Other Sources Of Salmonellosis

1.The most common route of infection is through oral

ingestion.

2.Infection can occur through an open cut, sore or wound

into the bloodstream.

3.Infection can occur through splashing of contaminated

material into the eyes.

4.Infection can occur through inhalation of sprayed

contaminated solutions/aerosols.

5.Animals and animal products are the most common

sources of infection.

Cont.

6.Improperly cooked meats, especially poultry and chopped

beef/pork/turkey.

7.Recontamination of cooked meats through contact with

raw meats/fluids.

8.Contamination of foods by salmonella contaminated hands

of servers/preparers.

9.Contact with, ingestion or inhalation of soil contaminated

with animal feces.

10.Raw milk (especially among farm families) and

contaminated pasteurized milk.

11.Fish meal, bone meal and meat meal; fertilizers and

animal feeds.

Enterocolitis

manifestation: vomiting, stomach ache,

diarrea & fever
Onset: 6- 48 hour
Duration: 2 day 1 week, self-limited
lab: feses (+) Salmonella

Enterocolitis

Laboratory

Bacterial isolation e.g. Gaal culture, SS

agar, MacConkey agar, ADP, Endo agar

Serologi e.g. Test Widal enterik fever

Terapi

Enteric fever & Bacteremia antibiotic:

Khloramfenikol, ampisilin, trimetoprimsulfomethoxazol, sefalosporin

Enterocolitis:
Diarrea fluid & electrolyte replacement
Antibiotic do not reduce the sympton & may
prolong excretion of salmonella in the feces

Carrier: kholisistektomi & antibiotik

prevention

Food sanitation & clean drinking water

Vacination

Salmonella typhi,
Salmonella paratyphi A,
B, and C, Salmonella
cholerasuis

ingestion of fecally
contaminated food or
water

Salmonella enteriditis
(contains 7 subgroups
and 1500 serotypes)gram negative rod

Fecal-oral transmission
via contaminated water,
food
(poultry, eggs, or dairy
products), or directly in
young children

able to survive in
neutrophils

typhoid fever, paratyphoid

or enteric fevers=
anorexia, lethargy,
malaise, general aches,
pains, dull continuous
headache usually
confined to the frontal
regions, nonproductive
cough, nosebleed (10% of
patients), vague
abdominal pain and
discomfort, constipation
(20% of patients have
mild diarrhea), abdominal
distension due to gas in
the intestines, bloody
feces

nausea, vomiting,
diarrhea

Dr Ekta, Microbiology

21/1
2/08