Vibrio cholerae O1 El Tor biotype produces cholera toxin (CT) which activates Gs-adenylyl cyclase. However, the specific virulence mechanism enabling V. cholerae to colonize the intestine and avoid peristaltic clearance requires an additional surface structure. This is:
- A Toxin-coregulated pilus (TCP), a type IV pilus that is the intestinal colonization factor and also serves as the receptor for CTXφ phage (which carries the CT gene) ✓
- B O-antigen LPS, which mediates adhesion to mucus
- C Haemagglutinin protease, which degrades intestinal mucin for penetration
- D Neuraminidase, which exposes GM1 ganglioside receptor for cholera toxin
Explanation
The toxin-coregulated pilus (TCP), encoded by the tcp gene cluster on the Vibrio pathogenicity island, is indispensable for intestinal colonization. TCP bundles facilitate microcolony formation in the intestinal mucus layer and are co-regulated with cholera toxin by the ToxR/ToxT regulatory cascade. Crucially, TCP also serves as the receptor for the filamentous bacteriophage CTXφ, which carries the ctx genes (ctxA and ctxB). This phage integration event is how environmental V. cholerae acquired toxin-producing capability.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.