Pathophysiology

The resurgence of GAS invasive infections appears to be the result of the production of more virulent exotoxins from the M-type isolates of GAS. Streptococcal pyogenic exotoxins (SPEs) are produced by 90 percent of GAS isolates.16 Three distinct exotoxins (SPEs A, B, C) have been identified. SPE A, also known as the scarlet fever toxin, is the most powerful and most frequently found SPE in STSS. It has a molecular structure similar to that of enterotoxin B of NMTSS. The SPEs A and B display features similar to those of TSS-mediated exotoxins, including pyrogenicity, superactivation of T cells, and synthesis of TNF, IL-1, and IL-6. 16 These powerful cytokines can induce severe acidosis, shock, and multisystem organ failure, as in TSS. The effects of the "superantigens" SPE A and SPE B are hypothesized to be similar to yet more profound than those of TSST-1, with greater induction of TNF, IL-1, IL-6, and other cytokines, thereby causing more severe signs and symptoms.16 The patients suspected of being most at risk for developing STSS are those without immunity to M-type 1 SPE A- or B-producing strains of GAS. The SPE C has been found in fewer GAS isolates, and its role in STSS is not clear.

The portal of entry of streptococci cannot be proven in about 50 percent of cases and can only be presumed in many others. 12 Most commonly, infection begins at a site of minor local trauma, usually without disruption of the skin. Cases have developed from burns, lacerations, abrasions, hematomas, minor nonpenetrating muscle injuries, surgical procedures, and recent infections with varicella or influenza. 12

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