# Vibrio > Vibrio for FMGE Microbiology: comma-shaped oxidase-positive V. cholerae, TCBS and alkaline peptone water, cholera toxin mechanism and ORS-based care. - Canonical URL: https://prepelephant.com/topics/fmge/microbiology/vibrio-fmge - Exam / course: FMGE · Subject: Microbiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Vibrio", PrepElephant, https://prepelephant.com/topics/fmge/microbiology/vibrio-fmge ## Direct answer Vibrio cholerae is the comma-shaped, polar-flagellated, oxidase-positive gram-negative bacillus that grows best in alkaline media — alkaline peptone water at pH 8.6 for enrichment and thiosulphate citrate bile salts sucrose agar for plating, where it ferments sucrose into yellow colonies — and produces rice-water stool through one elegant toxin: cholera toxin enters enterocytes and ADP-ribosylates the Gs protein, keeping adenylate cyclase switched on so that cyclic AMP drives chloride out through CFTR with water following. Serogroups O1 (classical and El Tor biotypes; Ogawa, Inaba and Hikojima serotypes) and O139 cause epidemic cholera; non-O1, non-O139 strains cause sporadic mild diarrhoea. ## What you must remember - Laboratory card: darting motility on hanging drop, oxidase positive (the family Enterobacteriaceae is negative), growth at pH 8.6–9.0, yellow sucrose-fermenting colonies on TCBS, and a positive string test with 0.5 per cent sodium deoxycholate. - Cholera toxin structure: one A subunit (the enzymatic ADP-ribosyltransferase) and five B subunits binding the GM1 ganglioside receptor — the same architecture as the heat-labile E. coli toxin, encoded by CTX phi phage. - El Tor biotypes cause milder disease with more asymptomatic carriers and have largely replaced classical biotypes globally, including in Indian outbreaks. - Stool picture: no pus, no blood, flecks of mucus in watery "rice-water" stool, and a field diagnostic of rapid fluid loss with sunken eyes, reduced skin turgor and absent urine output in severe cases. - Rehydration arithmetic governs survival: WHO plan A for no dehydration, plan B (75 millilitres per kilogram over four hours) for some, plan C (100 millilitres per kilogram, half in the first 30 minutes) with rapid intravenous Ringer's lactate when severe. - Antibiotics are adjuncts — azithromycin as a single dose or tetracycline for sensitive strains shorten the illness by about a day and cut shedding; they never substitute for fluids. - V. parahaemolyticus, from seafood, is a common cause of food-borne diarrhoea in coastal Japan and India (Kanagawa haemolysis phenomenon); V. vulnificus causes septicaemia and bullous lesions in liver disease after oysters or seawater exposure. - Outbreak control rests on water, sanitation and notification — chlorination of water sources and hand hygiene — not on chemoprophylaxis of contacts. ## Handling a suspected cholera case from door to report A man from a flood-relief camp passes painless voluminous watery stool with mucus flecks and vomits; the tense abdomen and absent radial pulse say severe dehydration. Resuscitation starts before any test: intravenous Ringer's lactate, 100 millilitres per kilogram, half within the first half-hour, reassessed continuously. The specimen goes into alkaline peptone water via Cary–Blair; a hanging drop examined immediately shows the darting motility that stops dead on adding a drop of antisera — immobilisation is both a bedside and a rapid laboratory clue. After enrichment, TCBS gives yellow colonies; oxidase positivity and the string test complete confirmation. The patient recovers with fluids alone, receives a single dose of azithromycin to shorten shedding, and is counselled about hand hygiene; the public-health team chlorinates the camp's water point and reports the case — in India a notifiable, outbreak-prone disease under Integrated Disease Surveillance Programme criteria. ## Where students slip The oxidase point is under-used: candidates forget that this one positive test lifts vibrios out of the entire oxidase-negative Enterobacteriaceae crowd, which is exactly how the exam frames "which organism differs". Second, the toxin mechanism gets half-remembered — it is permanent activation of Gs (up), not Gi, raising cyclic AMP and opening CFTR chloride channels; sodium and water follow into the lumen. Third, the medium-and-pH trivia invert: alkaline peptone water enriches, TCBS selects and differentiates by sucrose, and pH 8.6 is the number the stem tests. Finally, the therapy question baits "start antibiotics": the mark goes to aggressive rehydration, with azithromycin or tetracycline as the adjunct that shortens shedding. ## Frequently asked questions ### Why does cholera toxin cause secretory diarrhoea? Its A subunit ADP-ribosylates and permanently activates the Gs regulatory protein, keeping adenylate cyclase active; sustained cyclic AMP opens CFTR chloride channels, and water and electrolytes pour into the lumen. ### Which media isolate Vibrio cholerae from stool? Alkaline peptone water at pH 8.6 for enrichment, then TCBS agar where V. cholerae ferments sucrose to yellow colonies; the hanging drop shows characteristic darting motility. ### What distinguishes El Tor from classical biotypes? El Tor causes milder illness with more carriers and survives longer in the environment; bench markers include a positive Voges–Proskauer test and polymyxin resistance, and it has largely displaced classical strains. ### What is the priority in treating severe cholera? Rapid rehydration — intravenous Ringer's lactate at 100 millilitres per kilogram with half given in 30 minutes for severe dehydration — with oral rehydration solution continuing recovery; antibiotics only shorten shedding. ### Which vibrio causes seafood-associated watery diarrhoea with Kanagawa haemolysis? Vibrio parahaemolyticus from seafood, associated with the Kanagawa haemolysin; V. vulnificus is the separate seafood organism causing septicaemia in chronic liver disease.