Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

Abstract

The pathogenesis of shock in the rhesus monkey given intravenous staphylococcal enterotoxin B (SEB) is not understood. Several cardiovascular changes produced by a highly purified preparation of SEB were studied after administration of doses ranging from 50 to 1,000 ;ug/kg. Irreversible

Superantigen-induced cytokine release from whole-blood cell culture as a functional measure of drug efficacy after oral dosing in nonhuman primates

“…In particular, in vivo studies with SE using mouse models require potentiating agents to enhance the toxic effects of SE (Stiles et al, 1993;Blank et al, 1997) because mice are less sensitive to SE due to lower affinity of SE to mouse MHC class II molecules (Mollick et al, 1991). Rhesus macaques have been used as a lethal model for inhaled SEB, as pathogenic features of SEB intoxicated monkeys resemble those of humans (Hodoval et al, 1968). Therefore, NHP may provide a consistent model for the development of therapeutics for SEinduced shock in humans.…”

Effects of staphylococcal enterotoxin B on complex operant behavior in monkeys.

“…The majority of toxicological investigations deal with physinlogical effects from which behavioral changes are inferred (2). It is, however, of qualitative interest to determine the degree of impairment oxposure to toxic compounds may have on an organism's ability to function within eitablished baseline standards.…”

Staphylococcal Enterotoxin A Acts through Nitric Oxide Synthase Mechanisms in Human Peripheral Blood Mononuclear Cells To Stimulate Synthesis of Pyrogenic Cytokines

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The staphylococcal enterotoxins (SE) are secreted by a variance of Staphylococcus aureus and cause most common staphylococcal food poisoning and staphylococcus-associated toxic shock syndrome in humans and primates (1,9,15,17,19). The SE are classified into different toxin serotypes, such as SEA, SEB, SEC1, SEC2, and SEE (30).

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“…The SE are 26-to 30-kDa proteins that bind with major histocompatibility class II molecules on antigen-presenting cells and stimulate T cells bearing V␤s on their receptor variable region (1,5,7). Intravenous administration of SEA is shown to produce fever, lethargy, shock, and death in cats, rabbits, and monkeys (3,9,17,23,26). In addition, our recent results demonstrate that the febrile responses are associated with increased levels of circulating interleukin-2 (IL-2), interferon (IFN), and tumor necrosis factor (TNF) in rabbits.…”