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Methods of Secretion. Protein Secretion. Type II Secretion (GEP). Sec dependent Signal peptide Chaperone 2 Stage E.g IgA-protease, Pertussis toxin, Serratia haemolysin. General Secretion Pathway (Type II). Type II:Export. Type I Secretion. Sec independent
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Type II Secretion (GEP) • Sec dependent • Signal peptide • Chaperone • 2 Stage • E.g IgA-protease, Pertussis toxin, Serratia haemolysin
Type I Secretion • Sec independent • ABC (ATP Binding Cassette) • COOH recognition peptide • 1 Stage • E.g cytolysins, hydrolases, B. pertussis adenylate cyclase
Type III Secretion • Sec independent • Secretion co-translational • Translocation into host cell • Polar or non-polar secretion • E.g Yersinia spp. Yops, Shigella IpaB, C & D; EPEC EspA, B, C, Tir
Paradigms of Host-Cell Interactions I: Enterobacter • Vibrio cholera • E coli spp. • Shigella spp.
Enteropathic E coli • Serotypes and serogroups: e.g O111:H4,O111:H12 • Virotypes: ETEC EAggEC EPEC EHEC EIEC
ETEC • Similar to V. cholera in symptoms and colonization • Causes “Traveller’s Diarrhea” • Two toxins: heat-labile (LT) and heat-stable(ST)
EAGGEC • Causes persistent diarrhea • Resembles ETEC in colonization except that adherence to small intestinal cells non-uniform. • Produce ST-like toxin and hemolysin-like toxin.
EPEC • Like EAGGEC, adherence also in clumps. • Causes attachment and effacement lesions. • More invasive than ETEC or EAGGEC • Induces inflammatory response.
EHEC • Can cause acute kidney failure (hemolytic-uremic syndrome [HUS]) • Disease similar to that of Shigella dysentary.
EIEC • Symptoms similar to Shigella dysentary. • Actively invades colonic cells with adjacent spread like Shigella, although no toxin produced.