GIT Infections PDF

DISEASE MORPHOLOGY PATHOGENESIS CLINICAL FEATURES LOCATION BACTERIAL ENTEROCOLITIDES...

DISEASE MORPHOLOGY PATHOGENESIS CLINICAL FEATURES LOCATION BACTERIAL ENTEROCOLITIDES Virulence factors: -​ Flagellar proteins: motility and attachment -​ Cholera toxin (A and B): causes the disease -​ Hemagglutinin: detachment and shedding Affected: small intestine Reservoir: Shellfish and plankton Toxin B subunits binds to GM1 Cholera Minimal histologic alterations Mostly asymptomatic ganglioside → Toxin A subunit is Endemic in India and Africa unfolded in ER → Toxin A subunit Agent: Vibrio cholerae No invasion → remains in the lumen In severe cases: fragment is transported to cytosol Transmission: contaminated water, -​ Rice water stool w/ fishy odor for refolding → interacts with fecal-oral -​ Voluminous cytosolic ARFs → active Gsa subunit → adenylate cyclase is activated → high cAMP → CFTR is opened → blocked Cl and Na absorption → accumulation of Cl ions → secretion of bicarbonate and Na → massive diarrhea Mucosal and intraepithelial infiltrates Cryptitis: Neutrophils sa gilid ng crypts Crypt abscesses: Neutrophils sa lumen ng crypts Virulence factors: Affected site: colon -​ Flagella Crypt architecture is preserved -​ Cytotoxins: cholera toxin-like Acute, self-limiting colitis enterotoxin In C. jejuni infection: -​ Invasion Traveller’s Diarrhea and food Reservoir: Chicken, sheep, pigs, -​ (+) cryptitis poisoning cattle -​ (+) crypt abscess Organism attaches and proliferates Campylobacter enterocolitis → invades the enterocyte via Dysentery Children and travelers In Yersinia infection: endocytosis → exits to the Agent: Campylobacter jejuni -​ Erosion of surface epithelium submucosa via exocytosis → In px with HLA-B27, reactive Transmission: ingestion of by neutrophils detection and phagocytosis by arthritis improperly cooked chicken -​ Infiltration of lamina propria by macrophages → apoptosis of plasma cells with lymphocytes macrophages that engulfed the Erythema nodosum and neutrophils bacteria → release of organism in submucosa → proliferation and Guillain-Barré syndrome (flaccid In EHEC O157:H7 infection: invasion of the next enterocyte. paralysis) -​ Ischemia-like -​ Surface atrophy and erosion In EIEC infection: -​ Normal crypt architecture -​ Abundant intraepithelial neutrophils Shigellosis Mucosa is hemorrhagic and Virulence factors: Affected site: left colon and ileum Reservoir: Humans  ulcerated -​ Resistant to acidic Agent: Shigella spp. environment Watery and Bloody diarrhea Transmission: fecal-oral, (-/+) food pseudomembranes -​ Low infective dose contaminated food and water -​ Virulence plasmids Reiter syndrome (-/+) aphthous-appearing ulcers -​ Shiga toxin (Stx) -​ HLA-B27-positive men (20-40 y/o) Crypts abscess w/ inflammatory Organisms are taken up by M cells -​ Reactive arthritis cells in lamina propria → proliferation → escape into -​ Urethritis lamina propria → inflammatory -​ Conjunctivitis response that damages surface epithelia → ingested by Hemolytic uremic syndrome macrophages → apoptosis of (HUS) macrophages → invasion of epithelial cells via basolateral membrane Virulence factors: -​ Virulence genes -​ Flagellin -​ Bacterial LPS Virulence genes transfers bacterial Affected site: colon and small proteins into M cells and intestine enterocytes → active host Rho Young children and older adults Salmonellosis GTPases → actin rearrangement Self-limited Non-specific and bacterial endocytosis → Transmission: contaminated food, Agent: Salmonella enteritidis bacterial growth in endosomes → Antibiotic is NOT recommended raw meat, poultry, eggs, milk bacterial flagellin activates TLR5 -​ Killing of pathogens → → high inflammatory response → exacerbated symptoms. bacterial LPS activates TLR4 → secretion of molecule by salmonella → release of eicosanoid hepoxilin A3 → intense inflammation in the lumen → potentiated mucosal damage. Affected site: small intestine Peyer patches’ hyperplasia Initial dysentery → short asymptomatic phase → bacteremia Mucosal ulceration (90% of px) Organisms are taken up by M cells → invasion of M cells → Phagocyte accumulation → Salmonella osteomyelitis mononuclear cells engulf the Enlarged draining mesenteric -​ In px w/ sickle cell disease Reservoir: humans only bacteria → systemic reactive Typhoid fever (enteric fever) lymph nodes → harbor of (gallbladder is the chronic reservoir) hyperplasia of phagocytes and organisms Rose spots lymphoid tissues. Agent: Salmonella enterica Transmission: person-to-person, -​ S. typhi in endemic countries Spleen Abdominal tenderness mimics contaminated food/water S. typhi → lymphatic and blood -​ S. paratyphi in travellers -​ Obliterated follicular markings appendicitis vessels → systemic manifestations. -​ Prominent phagocyte Children and adolescents hyperplasia Sustained high fevers in initial Resides in gallbladder → bile febrile phase (~2 weeks) secretion → reinfection Liver -​ Typhoid nodules replace Complication: hepatocytes -​ Encephalopathy and seizure -​ Myocarditis and endocarditis -​ Pneumonia  -​ Cholecystitis and cholelithiasis Affected site: Ileum, appendix, right colon Neutrophil infiltrates and Yersinia binds to B-1 integrins of Mimic acute appendicitis Reservoir: Pigs, cows, puppies, granuloma host cats Yersinia Extraintestinal symptoms: Regional nodal hyperplasia. Iron uptake system mediates iron -​ Pharyngitis Transmission: ingestion of pork, Agent: Y. enetrocolitica, Y. capture and transport. -​ Athralgia raw milk, contaminated water pseudotuberculosis, Y. pestis Mucosa: hemorrhagic and ulcerated -​ Erythema nodosum Iron enhances virulence and Common in Europe Peyer patch hyperplasia stimulates systemic dissemination. Chronic forms of anemia/hemochromatosis -​ Px with high non-heme iron. Virulence factors: -​ Heat-labile toxin (LT) → activates adenylate cyclase → Traveller’s diarrhea high cAMP -​ Heat-stable toxin (ST) → Transmission: contaminated food Watery diarrhea Agent: Enterotoxigenic E. coli binds to guanylate cyclase → and water (ETEC) high cGMP LT and ST → secretion of Cl and H2O, blocked fluid absorption Virulence factors: -​ Attaching and effacing (A/E) lesions -​ Locus of enterocyte Infant’s diarrhea effacement (LEE) Developed and developing Watery diarrheal outbreaks in countries Agent: Enteropathogenic E. coli LEE pre-school and daycare centers (EPEC) -​ Encodes proteins for A/E Children