Non Invasive
Enteritis II
Barriers to GIT infection:
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Stomach acidity (low PH).
Mucus layer and gut motility (peristalsis)→ prevent
adhesion.
The glycocalyx (mucin rich layer) covers the epithelial
cells surface→ entrap invading bacteria.
Shedding of mucosal epithelium lining the GIT.
Bile secretion prevent the growth of non-enteric
bacteria and enveloped viruses.
M cells (microfold) of Peyer’s patches which have a
surveillance function (sampling).
Normal flora of intestinal tract.
Secretory IgA.
Bacterial enteritis:
• Non invasive → multiplication within the lumen and
toxin production → watery diarrhea.
Causative agents:
o V. cholerae.
o Enterobacteriaceae: Enterotoxigenic E. coli,
Enteropathogenic E. coli.
• Local invasion → invade and destruct the mucosa
and the epithelia → bloody diarrhea. E.g. Shigella
and Enterohemorrhagic E.coli, Campylobacter
jejuni, Salmonella enteriditis …….
• Systemic invasion → Cuasative bacteria can be
isolated from the blood; Salmonella Typhi,
Brucella.
Vibrio cholerae
Vibrionaceae: gram negative rods, curved, motile by single
polar flagellum. Alkaliphiles (pH 6.8-10).
Vibrionaceae family:
o Vibrio cholerae → cholera (watery diarrhea).
o Vibrio parahaemolyticus.
o Vibrio vulnificus.
V. cholerae has ≈ 140 serotypes based on its LPS (O
antigen). Serotype O1 is the most common followed by
serotype O139.
V. cholerae serotype O1 has 2 biotypes:
• Classical.
• El Tor.
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Epidemiology:
o Vibrio cholerae O1 biotype classical → 6 pandemics
in Asia for centuries.
o Vibrio cholerae O1 biotype El Tor was isolated from
pilgrims at El Tor station in 1905.It had caused the
seventh pandemic in1961.
o Infections with the new serotype Vibrio cholera O139
(Bengal) appeared in Bangladesh in 1990 and spread
to India and other countries.
o Cholera cause ≈ 3 millions cases and 10000 deaths
yearly.
Pathogenesis and Microbial Virulence:
Transmission:
Source: human cases or carrier.
Human disease only without animal reservoir.
o Waterborne: drinking un-boiled or untreated water.
o Foodborne; Contaminated sea food or shellfish.
o Fecal-oral route: human carriage (colon) is reported in
some cases.
Pathogenesis:
o Pathogenic dose: 108-109 CFU/ml (lower in hypochlorohydria).
o When vibrios reach ampulla of Vater in the duodenum;
surviving organisms are bathed in bicarbonate-buffered
pancreatic juice (pH can be as high as 9).
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o Vibrios reach the epithelia of the small intestine by
flagella & mucinase enzyme that hydrolyses the mucus.
o Adhere to the epithelia of the intestinal tract by type 1
common pili (colonization factor antigen Cfa).
o Vibrios stick to each other and establish colonization
(micro-colonies) by toxin-co-regulated pili (TCP).
o Produce cholera toxin. Cholera toxin (Ctx) binds to the
receptor on epithelial cells → stimulate G protein →
activate the adenylate cyclase → increase cAMP
production → inhibit sodium absorption and increase
chloride secretion by enterocytes → ↑NaCl in the
lumen→ passive secretion of water → severe watery
diarrhea + mucus (the action of the mucinase) → Rice
Water Diarrhea.
Flagella, mucinase, Cfa, TCP
Clinical presentation:
• Incubation period: 2 hours – 5 days (inoculum size)
• Sever watery diarrhea (rice water without faecal
matter) and vomiting of clear fluid. No fever
Dehydration and electrolytes imbalance (patients may
lose 10-20 liters of fluid/ day) dry mouth and skin;
decreased skin turgor.
• Deep rapid breathing due to acidosis:
• Rapid pulse.
• Coma (Na, Cl loss).
• Death: 70% if not treated 0.5% with treatment.
Rice water diarrhea
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Laboratory diagnosis:
Clinical specimens: stool.
Microscopy (diagnostic in endemic area):
• Wet mount: highly motile bacilli which stop moving
when we add specific antisera.
• Gram stain: Vibrios are gram-negative curved bacilli,
motile with a single polar flagellum.
Antigen detection: detect the O1 or O139 antigens or the
cholera toxin.
Cultural and isolation (diagnostic in non endemic area i.e.
gold standard) :
• Media:
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Blood agar: usually beta hemolytic (El Tor).
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MacConkey's agar: non-lactose fermenting colonies.
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Alkaline peptone water: Selective media; pH 8.5-9
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TCBS: Thiosulfate-citrate-bile salts-sucrose agar;
Selective and differential → change the color from
green to yellow.
• Biochemical reactions: catalase, oxidase and indole
positive and can reduce nitrate to nitrite (cholera red
reaction positive).
Diagnosis
Serotyping and biotyping: Epidemiological purposes.
PCR: detect nucleic acid in the sample.
Treatment:
- Fluid and electrolyte replacement in early stage (life
saving).
- Antibiotics: Tetracycline or co-trimoxazole.
Oxidase Test
Indole Test
Prevention:
- Prevent transmission: food and water hygiene &
acidification of food.
- Vaccines: killed vaccine with recombinant binding
subunit of the cholera toxin.
Non Cholera Vibrios
Vibrio parahaemolyticus:
• Halophilic microbes.
• Transmission: consumption of undercooked or raw
seafood; shellfish, and crustaceans.
• Gastroenteritis: fever, abdominal pain, watery
diarrhea some times with blood due to invasive
enteritis.
Vibrio vulnificus:
 Halophilic vibrio.
 Transmission: undercooked shellfish or exposure of
wound to salt water.
 Invasive enteritis; associated with high mortality
rate (septicemia and death).
 Wound infection.
Flesh eating bacteria (V. vulnificus)
Escherichia coli:
E. coli groups associated diarrhea:
 Watery diarrhea:
Enteroaggregative E. coli
 Watery toxin mediated diarrhea:
o Enterotoxigenic E. coli.
o Enteropathogenic E. coli.
 Bloody diarrhea due to invasive enteritis:
o Enterohemorrhagic E. coli.
o Enteroinvasive E. coli.
Enterotoxigenic E. coli:
the causative agent of traveler’s diarrhea.
Produce two enterotoxins:
- Heat labile (LT): activate G protein and adenylate
cyclase; ↑cAMP. (same effect of cholera toxin).
- Heat stable (ST): activate guanylate cyclase.
→ watery diarrhea.
Enteropathogenic E. coli:
Cause watery diarrhea in infants.
Adhere to the epithelial cells by Cfa pilus & insert
exotoxin Tir (translocation intimin receptor) → brush
border damage; malabsorption and watery diarrhea.
Ctx: cholera toxin. ST: heat stable toxin. LT: labile toxin.
Cfa: colonization factor antigen.