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, 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

Possess virulence factors intestinal
tract or at other site (eg. Urinary tract)

Escherichia coli

Manifestasi klinis:
Septisemia: asal infeksi adalah infeksi
saluran kemih atau penjalaran kuman
dari usus
Infeksi saluran kemih: penyebab 80%
kasus; kuman hemolisin (+), tahan
serum, faktor virulensi pili P
Meningitis pada neonatus: E. coli K1
Gastroenteritis (Diare) karena E. coli


1.
2.
3.
4.
5.
6.

6 classes (virotypes) of E. coli that cause

diarrheal diseases :
enterotoxigenic E. coli (ETEC)
enteroinvasive E. coli (EIEC)
enterohemorrhagic E. coli (EHEC)
enteropathogenic E. coli (EPEC)
enteroaggregative E. coli (EAEC)
diffuse-aggregative E. coli (DAEC)

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Mekanisme virulensi E. coli

Diarrheagenic E. coli: virulence determinants and characteristics of disease

ETEC
fimbrial adhesins e.g. CFA I, CFAII, K88. K99
non invasive
produce LT and/or ST toxin
watery diarrhea in infants and travelers; no inflammation, no fever
EIEC
nonfimbrial adhesins, possibly outer membrane protein
invasive (penetrate and multiply within epithelial cells)
does not produce shiga toxin
dysentery-like diarrhea (mucous, blood), severe inflammation, fever
EPEC
non fimbrial adhesin (intimin)
EPEC adherence factor (EAF) enables localized adherence of bacteria to intestinal
cells
moderately invasive (not as invasive as Shigella or EIEC)
does not produce LT or ST; some reports of shiga-like toxin
usually infantile diarrhea; watery diarrhea, some inflammation, no fever; symptoms
probably result mainly from invasion rather than toxigenesis
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EAEC
adhesins not characterized
non invasive
produce ST-like toxin (EAST) and a hemolysin
persistent diarrhea in young children without inflammation or
fever
EHEC
adhesins not characterized, probably fimbriae
moderately invasive
does not produce LT or ST but does produce shiga toxin
pediatric diarrhea, copious bloody discharge (hemorrhagic
colitis), intense inflammatory response, may be complicated
by hemolytic uremia

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Patogenesis

ETEC

penyebab diare pada bayi, traveler's diarrhea

Pd dewasa sembuh sendiri 1-3 hari

Eksotoksin LT (subunit A dan B) maktifkan

adenilat siklase cAMP hipersekresi air dan
Cl- serta menghambat reabsorpsi Na+
hipermotilitas & diare
Bersifat antigenik &
serupa dengan enterotoksin V. cholerae.

Toksin ST: aktifitas guanilat siklase cGMP

sekresi air

kuman mempunyai faktor kolonisasi pd epitel usus

halus gen faktor kolonisasi terkait plasmid

Patogenesis ETEC

EPEC

Penyebab diare (cair) pada bayi dan anak

di negara berkembang self-limited atau
kronis

Faktor virulensi : Bfp (bundle-forming pili),

intimin & Tir (translocated intimin
receptor) attachment pd sel epitel usus
halus perusakan microvillus

EHEC

Menghasilkan Verotoksin (= toksin Shiga)

Setelah attachment dg mukosa usus besar
produksi toksin efek pd epithelium
usus diare
Penyebab kolitis hemoragik dan hemolytic
uremic syndrome (HUS) reseptor
verotoksin terdapat di renal epithelium
gagal ginjal akut
Isolat tersering E. coli O157:H7 dan O26
(Jepang, 2001), sorbitol (-)
Sumber penularan daging giling, susu

EHEC

EIEC

Diare pd daerah dg tingkat hygiene , pd

anak malnutrisi
Penyebab diare serupa dengan
shigellosis, epitel mukosa kolon rusak
Diare berdarah akut disertai : malaise,
nyeri kepala, demam & nyeri abdomen
Laktosa (-), tes Sereny (+), leukosit pd
feses

Patogenesis EIEC

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
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EAEC
Kuman

mampu menempel pada

biakan sel dan membentuk agregat
(stacked brick) plasmid-associated
fimbriae
Penyebab diare akut / kronis pada
anak, diare tanpa darah & tidak
menginvasi mukosa
Memproduksi toksin LT
hemolisin

DAEC

Menghasilkan alpha hemolysin & cytotoxic

necrotizing factor 1
Diare pada anak

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Inflammatory gastroenteritis

Enterotoxigenic (ETEC) E.
coli- gram negative rod

Ingestion of comtaminated
water or food.

Enteropathogenic (EPEC) E.
coli also called
Ingestion of comtaminated
enteroadherent E. coli- gram water or food.
negative rod

Enteroaggregative (EAEC)
E. coli- gram negative rod

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

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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)

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Terapi & Pencegahan

Koreksi gangguan keseimbangan cairan

dan elektrolit
Antibiotik tidak dianjurkan
Sanitasi makanan dan lingkungan

Salmonella

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In humans, Salmonella are the cause of

two diseases called salmonellosis:
enteric fever (typhoid), resulting from
bacterial invasion of the bloodstream, and
acute gastroenteritis, resulting from a
foodborne infection/intoxication.

the Salmonella strains isolated from humans

and other warm-blooded animals.
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1.
2.
3.

the genus Salmonella has three kinds of

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

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Hospes:
Manusia S. typhi; S. paratyphi A, B, C
Babi S. cholera-suis
Sapi S. dublin
Domba S. abortus suis

Dosis infektif S. typhi: 106 - 109

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Morfologi:

Batang, Gram (-), gerak (+),

anaerob fakultatif
Tidak meragi laktosa dan sukrosa
Menghasilkan H2S
Tahan suhu pembekuan

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

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

Contamination
Meats, poultry, eggs, pet reptiles (turtles)

Undercooked or Raw Eggs

Patogenesis Salmonellosis

Invasi sel mukosa oleh Salmonella

Enterokolitis (gastroenteritis)

Gejala: muntah, sakit perut, diare dan

demam
Onset: 6- 48 jam
Durasi: 2 hari 1 minggu, sembuh
spontan
Pemeriksaan lab: feses (+) Salmonella

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
Prostaglandin terlepas

Enterocolitis

Pemeriksaan Laboratorium

Isolasi bakteri e.g. Gaal Kultuur

Serologi e.g. Tes Widal, hanya berguna
untuk demam enterik

Terapi

Demam enterik dan Bakteremia

antibiotik:
Khloramfenikol, ampisilin, trimetoprimsulfomethoxazol, sefalosporin

Enterokolitis:
Diare berat penggantian cairan & elektrolit
Antibiotik akan memperpanjang gejala klinis
dan lamanya ekskresi kuman

Carrier: kholisistektomi & antibiotik

Pencegahan

Sanitasi makanan
Vaksinasi

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

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Dr Ekta, Microbiology

21/1
2/08