A 60-year-old diabetic with leg wound infection has an anaerobic culture growing Clostridium perfringens. The pathogenesis of myonecrosis (gas gangrene) is primarily driven by which toxin, and what is its enzymatic mechanism?
- A Theta toxin (perfringolysin O); pore-forming activity on RBC membranes causing haemolysis
- B Epsilon toxin; pore-forming toxin on intestinal epithelium leading to permeability change
- C Alpha toxin; lecithinase (phospholipase C) that hydrolyses phosphatidylcholine in cell membranes causing lysis and widespread tissue destruction ✓
- D Iota toxin; ADP-ribosylation of actin disrupting cytoskeleton of muscle cells
Explanation
The alpha toxin (CPA) of C. perfringens Type A is the major virulence factor responsible for gas gangrene. It is a phospholipase C (lecithinase) that cleaves phosphatidylcholine and sphingomyelin in host cell membranes, releasing diacylglycerol. This causes lysis of red blood cells, platelets, endothelial cells, and muscle cells, producing massive myonecrosis with gas (from fermentation). Alpha toxin is detected by the Nagler reaction on egg-yolk agar — an opalescence around colonies inhibited by C. perfringens antitoxin. Theta toxin (perfringolysin O) has a supplementary haemolytic role. Epsilon toxin is produced by Type B/D strains affecting the intestine. Iota toxin is from Type E.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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