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Vibrio cholerae. Cholera. Vibrio sp. Gram-negative rods C urves or comma shaped Non-spore forming Highly motile-single polar flagella Associated with salt water Oxidase positive Facultative anaerobe Tolerate alkaline conditions to pH9.0
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Vibrio sp. Gram-negative rods Curves or comma shaped Non-spore forming Highly motile-single polar flagella Associated with salt water Oxidase positive Facultative anaerobe Tolerate alkaline conditions to pH9.0 Readily cultivated,Simple nutritional requirements
Vibrio • Vibrio cholerae -gastroenteritis • Vibrio parahaemolyticus -gastroenteritis, wound infection, bacteremia • Vibrio vulnificus -wound infection, bacteremia
Vibrio cholerae • Antigenic structure • Common heat-labile flagellar H antigen • O lipopolysaccharide confers serologic specificity • More than 150 O antigen serogroups • Only O-1 and 0139 serogroups cause Asiatic cholera • Three serotypes; Ogawa, Inaba, Hikojima • Two biovars; classic and El Tor
2 biotypes of serogroup O-1 Classical biotype El Tor biotype. • Serogroup 139
V. cholerae -Transmission feces • water • fresh • salt • food
Vibrio cholerae • Epidemiology • Epidemic cholera-spread by contaminated water under conditions of poor sanitation • Endemic-consumption of raw seafood • Copepods
Vibrio cholerae • Pathogenesis • Ingest 108-1010 organisms • Non invasive infection of small intestine • Organisms secrete enterotoxin • Watery diarrhea
Cholera toxin • Enterotoxin-cholera toxin-CtxAB • Encoded by a prophage • Molecular mass of 84,000 daltons • A subunit-ADP-ribosylating toxin • B subunit-bind GM1-gangliosides on enterocytes • A subunit ADP ribosylates Gs-alpha which regulates activation of adenlyate cyclase • Result is persistent increase in cAMP levels • Hyper secretion of Na, Cl, K, bicarbonate and H20
Vibrio cholerae-Clinical manifestations • Asymptomatic colonization to fatal diarrhea • Onset 2-3 days after ingestion • Abrupt onset of watery diarrhea and vomiting • Rice water stools • Severe fluid and electrolyte loss-dehydration, metabolic acidosis, hypovolemic shock, renal failure • Death 60% if untreated, 1% if treated for fluid loss
Pathogenicity of V. cholera • Dehydration and death • Massive secretion of ions/water into gut lumen
Immunity • Strongimmunity after recovery, SIgA
Bacteriological Diagnosis • Specimens: stool, vomitus. • Stained smear • Culture: alkaline peptone water of agar plate, and TCBS agar plate. • Quick immunological methods: immunofluorescent “ball” test; PCR.
Vibrio-Prevention and Control • Improved sanitation • Fluid and electrolyte replacement • Antibiotic prophylaxis • Improved food handling
Vibrio parahemolyticus • One kind of halophilic vibrios; optimal NaCl concentration contained in culture media is 3.5%; hemolysin related to its pathogenicity, can be detected by human or rabbit RBC test (Kanagawa test); cause food poisoning in human beings. • raw sea-food
Vibrio parahaemolyticus • Clinical manifestations • Self-limiting diarrhea to mild cholera-like illness • 24 hours after ingestion-explosive water diarrhea • Headache, abdominal cramps, nausea, vomiting, low grade fever for 72 hours or more • Uneventful recovery • Wound infections in people exposed to seawater-containing vibrios