A 25-year-old man is brought to the emergency department due to high-grade fever, chills, myalgias, and skin rash, which started on the day of admission. He also had nausea and 3 episodes of profuse watery diarrhea and is now feeling lightheaded. Two days ago, he underwent corrective surgery for a deviated nasal septum but otherwise has no other past medical history. The patient has not traveled recently and has not been around sick contacts. He does not use illicit drugs. His temperature is 39.4 C (103 F), blood pressure is 85/50 mm Hg, and pulse is 116/min. Oxygen saturation is 98% on room air. He is lethargic but has no focal weakness or nuchal rigidity. Examination shows clear lung fields and tachycardia with normal first and second heart sounds. The abdomen is soft and nontender. There is nasal packing in both nostrils. Skin examination shows a diffuse, red, macular rash that also involves the palms and soles.
Staphylococcus aureus strains producing toxic shock syndrome toxin (TSST) are responsible for most cases of TSS. TSST acts as a superantigen that activates large numbers of helper T cells (compared to a regular antigen, which activates few helper T cells). Superantigens interact with major histocompatibility complex molecules on antigen-presenting cells (eg, macrophages) and with the variable region of the T lymphocyte receptor to cause a nonspecific, widespread activation of T lymphocytes. Activation of T cells is responsible for the release of interleukin (IL)-2 from the T cells and IL-1 and tumor necrosis factor from macrophages. These ILs cause capillary leakage, circulatory collapse, hypotension, shock, fever, skin findings, and multiorgan failure.