Toxic shock syndrome — ABIM Board MCQ
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Correct answer: A — Superantigen-mediated T-cell activation
This is menstrual staphylococcal toxic shock syndrome, classically associated with tampon use, fever, diffuse erythroderma, hypotension, multiorgan dysfunction, negative blood cultures, and delayed desquamation. Toxic shock syndrome toxin-1 acts as a superantigen by cross-linking MHC class II molecules on antigen-presenting cells with T-cell receptors outside the conventional antigen-binding site. The resulting polyclonal T-cell activation and massive cytokine release cause shock and organ injury. IgE-mediated anaphylaxis can cause erythema, vomiting, and hypotension but not this febrile illness with delayed desquamation. C1 inhibitor deficiency causes bradykinin-mediated angioedema. Erythrocyte invasion suggests malaria or babesiosis, and immune complex deposition does not explain the characteristic systemic syndrome.
Reference: Atchade E, et al. Toxic Shock Syndrome: A Literature Review, Pathophysiology section. Antibiotics (Basel). 2024;13(1):96. https://ndc.services.cdc.gov/case-definitions/toxic-shock-syndrome-1990/