Digestive system infections:. Barriers to infection: 1-The stomach acid of a pH less than or equal to 4. 2- Shedding of mucosal epithelium lining the alimentary system. 3-A variety of local defense mechanisms; mucus formation and gut motility ( Peristalsis ).
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Barriers to infection:
1-The stomach acid of a pH less than or equal to 4.
2-Shedding of mucosal epithelium lining the alimentary
3-A variety of local defense mechanisms; mucus
formation and gut motility( Peristalsis).
4- The normal flora of intestinal tracts.
5-The glycocalyx (mucin-rich layer) of epithelial-cells
(Clostridium difficileproduces anti-mucin toxins)
6-The Bile salts detergent action.
7-The secreted antimicrobial peptides.
(EnterotoxigenicE.coliproduces heat-labile toxin that
suppress these peptides.
8-Mcells of Peyer patches have surveillance function.
The defense barriers are changed in favor of the microbe due to:
A-Obstructionsto the flow of intestinal secretions
B-Surgery may create intestinal “blind loops” that are
isolated from the moving stream of intestinal
Absence of flushing action of intestinal secretions.
Bacterial overgrowth syndrome; malabsorption.
2-Changes in stomach acidity; due to proton-pump
-Decreased pathogenic dose results in colonization of
intestinal mucosa; ExampleSalmonella species.
-Shigella species and E.coliO157:H7 are acid resistance.
3-Alterations to the normal flora; due to broad-spectrum
Pseudomembrane colitis; Clostridium difficile.
4-Invasion of Gut by virulent microbial strains.
1-Invasive Enteritis, and dysentery (bloody diarrhea):
Pathogenic dose: less than 200 CFU.
Reservoir: human colon only (no animal carriers).
Transmission: Fecal-Oral, Person to Person.
- Endotoxin triggers inflammation.
- Shiga toxin type I: Enterotoxic and cytotoxic activities.
It is interfering with 60S ribosomal subunit; necrosis.
-The microbe invades the M cell in the lumen of Gut.
Multiply inside these cells, using actin polymerization to infect neighboring epithelial cells.
Released , engulfed by intestinal macrophages.
Escape from APC, infects other epithelial cells.
Very Shallow ulceration of intestinal mucosa.
Enterocolitis, shigellosis (most severe form is dysentery).
Fever , lower abdominal cramps; diarrhea first watery,
then bloody with mucus.
Invasive infection: shallow ulcerative Enterocolitis.
Gram-negative short bacilli,
Nonmotile, Non-spore formers.
Enterobacteriaceae grow best on XLD.
Facultative anaerobic, non-Lactose fermenters.
Can not produce H2S and identify by API 20E
- Transmission: food (hamburger), milk, Fecal-Oral.
- Incubation period: 3-5 days.
- Reservoir: Cattle; bovine feces, pork.
- Pathogenic dose: 10-100 CFU.
- Toxin: Verotoxin : Exotoxin
- EHEC bind to cells in the large intestinal
- Verotoxin-Epithelial receptor interaction.
- Decrease protein synthesis by interfering with 60 S
- Intracellular localization inside lysozyme.
- Cell death; apoptosis.
- Mucosal necrosis; Hemorrhagic Colitis with
- Shiga like exotoxins; Hemolytic-uremic syndrome.
-Gram negative short bacilli.
- Metallic green sheen on
- Indole positive.
3-Invasive Enteritis and Bloody watery diarrhea:
A- Campylobacter jejuni infection:
Reservoir: intestinal tracts of humans, cattle, sheep, dogs, cats, and Poultry.
-Fecal-Oral (direct cont.), Ingestion of contaminated meat
(poultry), contaminate water, or unpasteurized milk.
with polar flagella.
- Microaerophilic ( 10% CO2, 5% O2, and 85% N2) microbe
with an optima of 42˚C temp.
- Humidity should be > 95%.
- Resistance for Cephalothin.
- Sensitive for Nalidixic acid.
- Catalase and oxidase positive.
Pathogenicdose: as few as 500 CFU.
The microbe invades the small and large intestinal mucosa.
Colonization of intestinal epithelial layer, engulfed by intestinal dendritic cells(DC).
DC release inflammatory mediators, chemotaxis, cellular
Ulcerative, inflammatory lesions in the jejunum, and ileum.
Pus and RBCs in stool; AcuteEnteritis (common cause of
infectious diarrhea worldwide).
- Traveler’s diarrhea and pseudo-appendicitis.
-Human: Large intestinal tracts: Carriage state.
-Animals: most important: Chicken.
1-Fecal-Oral from carrier person.
2-Ingestion of contaminated
(raw chicken, eggs).
Incubationperiod: 6-48 hours.
TheMicrobe invades the ileocecal region lymphoid tissue.
Invasion of Lamina propria; endotoxin activity.
Dendritic cell activation; production of TNF and IL-8.
PMN cells chemotaxis and PG response.
PG stimulate cellular cAMP of epithelial cells.
Release of NaCl from intestinal epithelial cells; dehydration.
PMN cells prevent mesenteric lymph node and RES invasion.
Bloody watery diarrhea.
Clinical: abdominal symptoms and fever.
Laboratory: Stool culture: similar to Salmonellatyphi.
Associated food and Transmission:
-Unpasteurized milk products, undercooked meat & raw
-Fresh soft cheese.
Incubation period: 8 - 48 hrs.
Invasion of intestinal epithelium.
Intracellular survival: Listeriolysin-O.
Watery bloody diarrhea.