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IN 1978, Todd et al.1 described a multisystem clinical syndrome (toxic shock syndrome) characterized by the sudden onset of fever, rash, vomiting and diarrhea, hypotension, conjunctival injection, and strawberry tongue, followed by desquamation during recovery. The syndrome has been associated with colonization or infection by a toxin-producing Staphylococcus aureus. A toxin with a molecular weight of 22,049, toxic shock syndrome toxin-1, formerly termed staphylococcal enterotoxin F or pyrogenic exotoxin C, has been identified as the staphylococcal product responsible for the disorder.2 3 4 5 All three toxins are chemically and immunologically identical. Recently, staphylococcal enterotoxin B has been associated with nonmenstrual toxic . . .
Cone et al. (1987) studied this question.