Question
Read the clinical history and answer the following questions: A 24 years old man was admitted in medical ward with a history of diarrhea for the past two days. On clinical examination he was severely dehydrated. The macroscopic appearance of the stool resembled ‘rice water’. Answer the following:
- (a) What is the probable diagnosis and name the causative agent 1 mark(s)
- (b) Mention the method of sample collection and transportation of the sample to the 2 mark(s)
- (c) What is the pathogenesis of the above disease. 2 mark(s)
- (d) Describe the laboratory diagnosis. 4 mark(s)
- (e) What is the prophylaxis. 1 mark(s)
Answer
a) Probable diagnosis and causative agent Cholera — acute-onset profuse watery diarrhoea with severe dehydration and characteristic “rice-water” stool (colourless, flecked with mucus, odourless) is pathognomonic. Causative agent: Vibrio cholerae (serogroups O1 — biotypes classical and El Tor — and O139).
b) Sample collection and transportation Stool sample (or rectal swab, in the early stage/before purging is established) collected in a sterile, wide-mouthed container, ideally before antibiotics are started. For transport, the sample is placed in Venkatraman-Ramakrishnan (VR) medium (an alkaline transport medium specifically for V. cholerae) or Cary-Blair medium; prompt transport at ambient temperature (organism is sensitive to acid, so glycerol-saline transport media used for other enteric pathogens are avoided, as glycerol is toxic to V. cholerae).
c) Pathogenesis V. cholerae is non-invasive; it colonizes the small intestinal mucosa via flagellar motility and adhesins, without penetrating the epithelium. The organism elaborates cholera toxin (choleragen), an AB-type exotoxin — the B subunit binds the GM1 ganglioside receptor on enterocytes, facilitating entry of the A subunit, which ADP-ribosylates the Gs protein, causing persistent activation of adenylate cyclase and a sustained rise in intracellular cAMP. This drives massive, unregulated active secretion of chloride (and passive water/sodium/bicarbonate) into the gut lumen, overwhelming the intestine’s absorptive capacity and producing the profuse, isotonic, rice-water diarrhoea characteristic of the disease, leading rapidly to severe dehydration and hypovolaemic shock if untreated.
d) Laboratory diagnosis
- Direct microscopy — hanging-drop preparation showing characteristic “darting/shooting-star” motility; immobilized by specific antiserum (confirms V. cholerae).
- Culture — enrichment in alkaline peptone water (pH 8.6, selectively favours V. cholerae over other gut flora), then plated on TCBS (thiosulfate-citrate-bile salts-sucrose) agar, giving characteristic yellow (sucrose-fermenting) colonies.
- Biochemical confirmation and slide agglutination with specific O1/O139 antisera for serogroup identification (and Ogawa/Inaba/Hikojima subtyping of O1).
- String test — a rapid presumptive test (a loopful of growth in 0.5% sodium deoxycholate forms a mucoid string when the loop is lifted).
e) Prophylaxis Safe drinking water and sanitation, food hygiene, health education; oral cholera vaccines (killed whole-cell, e.g., Dukoral, Shanchol) for high-risk/outbreak settings; prompt case management with oral/IV rehydration to prevent secondary transmission; chlorination of water sources during outbreaks.