Staphylococcus aureus enterotoxin B (SEB) administered intravenously may exert its toxicity by damaging capillary endothelium in the large intestine and, thereby, permit absorption of endotoxin into the circulation. To investigate this possibility, we measured an index of the level of plasma endotoxin. This index was the ability of plasma to cause gelation of limulus amebocyte lysate (GLAL), before and after intravenous administration of SEB (800-1,000 microng/kg of body weight) to 13 rabbits. All samples taken before administration of SEB were negative for GLAL, but GLAL activity was detectable in the plasma of 10 of the rabbits 12 hr after SEB was injected. Only rabbits that developed GLAL activity died; the levels of GLAL in plasma were comparable to those detected by other workers after administration of an intravenous, lethal dose of endotoxin to rabbits.
Activation of the kallikrein-kinin system, as indicated by increased plasma kallikrein and depleted plasma kininogen, prekallikrein, and kallikrein inhibitor, was observed in five patients with Rocky Mountain spotted fever. Four of the patients had petechial rashes characteristic of vasculitis. Three patients had alterations in coagulation consistent with disseminated intravascular coagulation, although no hemorrhagic syndrome was found. Our data, along with the known physiologic actions of kinins, suggest a possible role for the kallikrein-kinin system in the pathophysiology of vasculitis, disseminated intravascular coagulation, circulatory shock, and other complications of infection with Rickettsia rickettsii.
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