A 55-year-old diabetic man develops a painful indurated area on his perineum that rapidly progresses to crepitant necrosis over 24 hours with systemic sepsis. Gram stain shows mixed gram-positive cocci and gram-negative rods. What is the virulence mechanism of the streptococcal component (Group A Streptococcus) that most critically drives this necrotising fasciitis phenotype?

• A Exfoliative toxins A and B causing epidermal cleavage
• B Streptolysins O and S causing membrane lysis combined with Streptococcal pyrogenic exotoxin A (SPEA) superantigen activity ✓
• C Streptokinase dissolving fibrin barriers allowing rapid tissue spread
• D M protein resisting phagocytosis allowing establishment of infection

Explanation

In type 2 necrotising fasciitis (monomicrobial, GAS), the most critical virulence factors are streptolysins (SLO and SLS) which lyse RBCs, leucocytes and platelets causing local tissue destruction, and the superantigen toxins especially Streptococcal pyrogenic exotoxin A (SPEA, formerly erythrogenic toxin A) which triggers massive cytokine release leading to streptococcal toxic shock syndrome (STSS). Streptokinase facilitates spread but is not the primary driver of necrotising phenotype. Exfoliative toxins are Staphylococcal virulence factors causing scalded skin syndrome.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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