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). 4- The normal flora of intestinal tracts. 5-The glycocalyx (mucin-rich layer) of epithelial-cells surface. (Clostridium difficile produces anti-mucin toxins)
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 ). - PowerPoint PPT Presentation
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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).
4- The normal flora of intestinal tracts. 5-The glycocalyx (mucin-rich layer) of epithelial-cells surface. (Clostridium difficile produces anti-mucin toxins)
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6-The Bile salts detergent action.
7-The secreted antimicrobial peptides. (Enterotoxigenic E.coli produces heat-labile toxin that suppress these peptides.
8-M cells of Peyer patches have surveillance function.
9-Secretory IgA.
Establishment of infectious diseases in the digestive system:
The defense barriers are changed in favor of the microbe due to:1-Anatomic alterations: A-Obstructions to the flow of intestinal secretions (gallbladder stones). B-Surgery may create intestinal “blind loops” that are isolated from the moving stream of intestinal contents. Absence of flushing action of intestinal secretions. Bacterial overgrowth syndrome; malabsorption.
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2-Changes in stomach acidity; due to proton-pump inhibitors: -Decreased pathogenic dose results in colonization of intestinal mucosa; Example Salmonella species. -Shigella species and E.coli O157:H7 are acid resistance.
3-Alterations to the normal flora; due to broad-spectrum antibiotics. Pseudomembrane colitis; Clostridium difficile.
4-Invasion of Gut by virulent microbial strains.
Intestinal invasive diseases , inflammation and damage:
1-Invasive Enteritis, and dysentery (bloody diarrhea): A-Shigella dysenteriae infection:- Pathogenic dose: less than 200 CFU.- Reservoir: human colon only (no animal carriers).- Transmission: Fecal-Oral, Person to Person.
Pathogenesis: - 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.
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- 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.
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- Enterocolitis, shigellosis (most severe form is dysentery).- Fever , lower abdominal cramps; diarrhea first watery, then bloody with mucus. - Invasive infection: shallow ulcerative Enterocolitis.- Hemolytic-Uremic syndrome.B-Entamoeba histolytica (dysentery).Microbiology:- 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
2-Invasive Enteritis and Hemorrhagic Colitis: Enterohemorrhagic E. coli:
with an optima of 42˚C temp. - Humidity should be > 95%.
- Resistance for Cephalothin. - Sensitive for Nalidixic acid. - Catalase and oxidase positive.
Pathogenesis of Campylobacter jejuni:
Pathogenic dose: 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 infiltration.- Ulcerative, inflammatory lesions in the jejunum, and
ileum.- Ulcerative Colitis. - Pus and RBCs in stool; Acute Enteritis (common cause of infectious diarrhea worldwide). - Traveler’s diarrhea and pseudo-appendicitis.
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Infective Ulcerative Colitis and dysentery:n
B-Salmonella enteriditis and Salmonella typhimurium: Reservoir :
-Human: Large intestinal tracts: Carriage state.-Animals: most important: Chicken .
Transmission :1-Fecal-Oral from carrier person .
2-Ingestion of contaminated chicken products
( raw chicken, eggs.) Incubation period: 6-48 hours.
Pathogenesis:The Microbe 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 .
Diagnosis :Clinical: abdominal symptoms and fever .
Laboratory: Stool culture: similar to Salmonella typhi .
C- Listeria monocytogenes :
Associated food and Transmission:-Unpasteurized milk products, undercooked meat & raw