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BIOL 444
Christine Dupont

BIOL444 – Microorganisms & Diseases Fall 2012 Set 07 – Infectious Diseases of the Intestinal Tract - Developing countries: Normally viral infection (e.g. rotavirus), death due to severe diarrheal ~50% for kids - Developed countries (e.g. Canada & US): Normally due to bacterial infections - Major syndromes: o Diarrhea (e.g. cholera): Fluid-feces discharges, large amounts of fluid & electrolyte loss  Cholera: Temporary colonization, non-invasive, releases enterotoxin – cholera toxin that acts on the small intestine to induce diarrhea o Dysentery (e.g. shigellosis): Inflammation of GI tract, blood & pus are found in feces, not as much fluid loss compare to diarrhea [More serious]  Shigellosis: Invasive colonization, shiga toxin, destroys mucosal cells of the large intestine - Transmission: Fecal-oral, or via fingers, vectors, fomites etc. usually foodborne/waterborne - Control: Sanitary & hygienic measures (disinfection of drinking water) - Cholera: a disease of poor sanitation o Vibrio cholerae: Gram-negative curved rod, polar flagellum, alkali-tolerant, facultative anaerobe  Natural host are humans, but other vibrios (e.g. v. parahaemolyticus) can cause shellfish poisoning (marine organisms picked up by filter feeders such as clamps or oysters)  viable but non-culturable state, stays alive for a really long time  Serogroup “O1” is associated with epidemic cholera  The O-polysaccharide of the Lipopolysaccharide (LPS) is antigen specific  Another phage encodes particular pilli of the V. cholerae coat protein, and the PAI derived phage CTX (found in pathogenic strains) attaches to the pilli o Symptoms: Abrupt onset of massive diarrhea “rice-water” stools, can lose up to 20L of fluid/day, 50- 60% mortality if untreated, but if survived from severe dehydration, disease is often self-limiting o Pathogenesis:  Large # of V. cholerae required (thousands are needed to detect presence in intestine, V. cholerae doesn’t transit well through low pH stomach)  Adheres & multiplies on epithelium of the small intestine (non-invasive)  Cholera toxin: Heat-labile exotoxin encoded by lysogenic phage (similar to a-b toxin), binds irreversibly to GM1 on mucosal cell surface & cholera toxin acts on mucosal cells  ADP-ribosylation of G pSotein o Normal: Adenylate cyclase – G (inactive)  AC – G – GTP (active)  AC – G S S S (inactive) as G1removes GTP to form GDP & P o Cholera toxin: Ribosylation of G Srevents G fr1m acting on the activated AC – G – GTP, so GTP cannot be removed & AC – G – GTP remains activated S S  Lots of cAMP are produced o Normal: CFTR (Cystic Fibrosis Trans-membrane Conductance Regulator) controls ion flux across mucosa-lumen interface - +  Cl is pumped out via CFTR, Na & H O 2ollows via osmosis  Nearly all Na , 2 O & glucose is reabsorbed via Na /glucose sympoter o Cholera toxin: cAMP increases Cl outflow +  Na & H O2follows via electrolyte balance & osmosis  diarrhea  No time for Na & H O2to be re-absorbed o Treatment: + -  Oral rehydration solution (ORS): Containing glucose, water, electrolytes (Na & Cl)  Antibiotics may or may not be useful (bacteria died, but toxin still retained) - Dysentery: Blood and mucus in feces (serious and invasive) o Generic enteric bacterium (e.g. V. cholerae O1, E. coli O157:H7, E. coli K12)  Serotyping (OHK system): Specific antibody that are made to surface molecules  O (Somatic) antigen: Surface-associated LPS outer polysaccharides  H antigen: Flagella associated proteins BIOL444 – Microorganisms & Diseases Fall 2012  K (Vi) antigen: Capsular associated, not produced by all organisms  Type III secretion system: Gram –ves (2x bacterial membrane & 1x host plasma membrane)  E. coli injects through the transport system molecule
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