Question
Toxic shock syndrome.
Answer
Toxic shock syndrome (TSS) is a severe, acute, multisystem illness caused by superantigen exotoxins — most classically TSST-1 produced by certain strains of Staphylococcus aureus (originally described with prolonged high-absorbency tampon use), and analogous streptococcal pyrogenic exotoxins (SPE) produced by Streptococcus pyogenes (streptococcal TSS, often associated with invasive soft-tissue infection).
Pathogenesis: TSST-1 acts as a superantigen — instead of being processed and presented conventionally, it directly cross-links the MHC class II molecule on antigen-presenting cells to the T-cell receptor’s Vβ chain outside the normal antigen-binding groove, causing massive, non-specific activation of up to 20% of T cells (compared to <0.01% in a conventional response). This triggers an overwhelming release of pro-inflammatory cytokines (IL-1, IL-2, TNF-α, IFN-γ) — a “cytokine storm” — producing capillary leak, hypotension, shock, and multiorgan dysfunction.
Clinical features: abrupt high fever, hypotension/shock, a diffuse macular (sunburn-like) erythematous rash with subsequent desquamation (especially palms/soles), and involvement of ≥3 organ systems (GI, renal, hepatic, haematological, CNS, muscular).
Laboratory diagnosis: primarily clinical (based on case-definition criteria); isolation of toxin-producing S. aureus/S. pyogenes from the primary site (vagina/wound) supports the diagnosis, though blood cultures are often negative in staphylococcal TSS (toxin-mediated disease, not bacteraemic); toxin detection can be done in reference laboratories.
Management: removal of the focus (e.g., tampon, infected wound debridement), aggressive fluid resuscitation and haemodynamic support, and antistaphylococcal/antistreptococcal antibiotics (e.g., clindamycin, which additionally suppresses toxin synthesis, combined with a beta-lactam).