A patient develops Clostridium difficile infection after prolonged ampicillin use. The pathogenic mechanism by which C. difficile exerts its primary cellular effect involves:

• A Toxin A and B glucosylating Rho GTPases, disrupting actin cytoskeleton of colonocytes ✓
• B Superantigen-mediated T-cell activation causing cytokine storm
• C Exotoxin cleaving SNARE proteins at the neuronal junction
• D Binary toxin ADP-ribosylating actin monomers in enterocytes

Explanation

C. difficile toxin A (enterotoxin) and toxin B (cytotoxin) are large glucosyltransferases that glucosylate Rho family GTPases (Rho, Rac, Cdc42) in colonocytes, preventing GTP binding and inactivating them. This causes actin depolymerisation, tight junction disruption, and colonocyte apoptosis, producing pseudomembranous colitis. Option C describes botulinum/tetanus toxins; option D partially describes the binary toxin CDTa component but is not the primary mechanism; option B is superantigen mechanism (S. aureus TSST).

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.