Abstract
Toxic Shock Syndrome Toxin I (TSST-I), a reliable marker for TSS staph, has not yet been proven to be the sole responsible toxin. We and others find that TSS staph, but not other S. aureus, inoculated in subcutaneous chambers in rabbits → shock and death with renal, hepatic, muscular and hematologic changes of TSS. TSST-I is produced in chamber by 4 hr, reaching peak of 7.4 μg/ml (∼120 μg total) at 47 hrs. TSST-I is disseminated to blood with peak of 3.4 ng/ml and excreted in urine over 48 hrs. To determine if TSST-I alone is responsible for changes seen in the infection model, we injected purified TSST-I into chamber and produced a syndrome indistinguishable from live infection and clinical TSS. Hypotension, renal impairment, hypocalcemia and death occurs by 25 hrs at dose of 300 μg and a chronic, ultimately fatal illness lasting 8 days with profound renal failure, hypocalcemia and multiorgan dysfunction occurs at a 150 μg TSST-I depot. At the higher dose, TSST-I peak conc, in chamber is 17 μg/ml, plasma levels peak at 9 ng/ml and cumulative urine excretion is 18 to 30 μg. Lower dose → peak chamber conc. of 10 μg/ml and peak plasma levels of 2 ng/ml. These plasma values equal those found in human TSS. Passive administration of TSST antibody blocks TSS in this model while anti-endotoxin (J5) does not. TSST-I is therefore the toxin responsible for the major physiologic changes of TSS and does not require host-derived endotoxin for its action. Anti-toxin therapy has promise in therapy of established human TSS.
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Melish, M., Frogner, K., Hirata, S. et al. 1141 PATHOGENESIS OF TOXIC SHOCK SYNDROME (TSS). Pediatr Res 19, 301 (1985). https://doi.org/10.1203/00006450-198504000-01171
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DOI: https://doi.org/10.1203/00006450-198504000-01171