A 55-year-old diabetic man develops necrotizing fasciitis of the left lower limb after a minor abrasion. Blood cultures grow Streptococcus pyogenes (Group A Streptococcus). He develops high fever, shock, and multi-organ failure — consistent with streptococcal toxic shock syndrome (STSS). The virulence factor primarily mediating the toxic shock is:
- A Streptolysin O causing direct cardiac toxicity
- B Hyaluronidase enabling deep tissue invasion and systemic bacteremia
- C M protein causing complement-mediated intravascular coagulation
- D Streptococcal pyrogenic exotoxins (SPE A, C) acting as superantigens ✓
Explanation
Streptococcal pyrogenic exotoxins (SPE A and SPE C, also called erythrogenic toxins) are the primary mediators of STSS. These function as superantigens — they bypass normal antigen presentation by simultaneously crosslinking MHC class II on APCs with Vβ-specific regions of T cell receptors, causing polyclonal T cell activation and massive cytokine release (TNF-α, IL-1β, IL-6, IFN-γ), leading to shock and organ failure. SPE A is associated with the most severe STSS. Streptolysin O has cardiac effects but is not the primary toxin in STSS; M protein resists phagocytosis but does not cause superantigen-driven shock.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.