Clostridium difficile colitis is mediated by two exotoxins. The specific mechanism by which Toxin B (TcdB) causes mucosal cell death is:
- A ADP-ribosylation of actin monomers
- B Metalloprotease cleavage of SNAP-25 blocking neurotransmitter release
- C Adenylate cyclase activation increasing cAMP and causing chloride secretion
- D Glucosylation of Rho GTPases (Rac1, Cdc42, RhoA) inactivating the actin cytoskeleton ✓
Explanation
C. difficile Toxin B (TcdB) is a glucosyltransferase that modifies Rho family GTPases (Rho, Rac, Cdc42) by adding glucose to their threonine-37 residue, locking them in the inactive GDP-bound state; this disrupts actin cytoskeleton dynamics, causing cell rounding and death (cytopathic effect). Toxin A (TcdA) has a similar mechanism. ADP-ribosylation of actin monomers is the mechanism of Clostridium botulinum C2 toxin and Clostridium perfringens iota toxin. SNAP-25 cleavage is the mechanism of botulinum neurotoxin. Adenylate cyclase activation describes cholera toxin.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.