Vibrio choleraeVibrio cholerae

Cholera

Vibrio sp.Gram-negative rodsCCurves or comma shapedurves or comma shapedNon-spore forming Highly motile-single polar flagella Associated with salt waterOxidase positiveFacultative anaerobe

Tolerate alkaline conditions to pH9.0 Tolerate alkaline conditions to pH9.0

RReadily cultivatedeadily cultivated,, SSimple nutritional reqimple nutritional requirementsuirements

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 V. cholerae - Transmission

food

feces

waterwater– freshfresh– saltsalt

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

Virulence factors of V.cholerae O1 and O139

Virulence factor Biological effect

Cholera toxin Hypersecretic of electrolytes and water

Coregulated pilus Adherence to mucosal cells adhesin

Accessory colonization factor adhesinHemagglutination protease Releases bacteria from mucosal

cells

Zona occludens Exotoxin Accessory cholera enterotoxin

Exotoxin

Flagellum Motility

Siderophores Iron sequestration

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 regul

ates 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 vomi

ting– Rice water stools– Severe fluid and electrolyte loss-dehydrat

ion, 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

• Strong immunity after recovery, SIgA

Bacteriological Diagnosis

• Specimens: stool, vomitus.

• Stained smear• Culture: alkaline pepton

e 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 parahemolyticusVibrio parahemolyticus

• One kind of halophilic vibrios; optimal NaOne kind of halophilic vibrios; optimal NaCl concentration contained in culture medCl concentration contained in culture media is 3.5%; hemolysin related to its pathogia is 3.5%; hemolysin related to its pathogenicity, can be detected by human or rabbenicity, can be detected by human or rabbit RBC test (Kanagawa test); cause food pit RBC test (Kanagawa test); cause food poisoning in human beings. oisoning 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