Question
Toxic shock syndrome
Answer
Toxic shock syndrome (TSS) is a severe, acute, multisystem illness caused by superantigen exotoxins — classically TSST-1 produced by certain strains of Staphylococcus aureus (originally linked to prolonged high-absorbency tampon use), and analogous streptococcal pyrogenic exotoxins produced by Streptococcus pyogenes in invasive streptococcal disease.
Pathogenesis: the toxin acts as a superantigen, bypassing conventional antigen processing by directly cross-linking the MHC class II molecule on antigen-presenting cells to the T-cell receptor’s Vβ chain outside the normal peptide-binding groove — this causes massive, non-specific activation of a large proportion of T cells (up to 20%, versus <0.01% in a conventional response), triggering a “cytokine storm” (IL-1, IL-2, TNF-α, IFN-γ) that produces capillary leak, hypotension, and multiorgan dysfunction.
Clinical features: abrupt high fever, hypotension/shock, a diffuse macular (sunburn-like) erythematous rash with subsequent desquamation (especially palms/soles), and dysfunction of ≥3 organ systems.
Laboratory diagnosis: largely a clinical diagnosis based on case-definition criteria; culture of the toxin-producing organism from the primary focus (vaginal/wound site) supports the diagnosis, though blood cultures are often negative (a toxin-mediated, not bacteraemic, illness).
Management: removal of the causative focus (tampon removal, wound debridement), aggressive fluid resuscitation and haemodynamic support, and antistaphylococcal/antistreptococcal antibiotics (clindamycin, which additionally suppresses toxin synthesis, combined with a beta-lactam).