Effect of Staphylococcal Enterotoxin B on the Electroencephalogram of Monkeys

Abstract

A highly purified preparation of staphylococcal enterotoxin B was administered intravenously, 1 mg/kg, to rhesus monkeys. Electroencephalograms (EEG) were recorded from electrodes attached to the skin or implanted on the dura. The dose of toxin employed consistently produced a sequence of vascular collapse followed by death; in control studies. animals were bled periodically to produce a similar pattern of shock. Regardless of the time to death following administration of the enterotoxin, there were essentially no changes from base line EEG patterns until shortly before death. With the development of preterminal severe shock, there was a marked decrease in EEG wave frequency and an initial increase in amplitude. The latter diminished progressively to produce an isoelectric tracing immediately prior to death. This could be reversed for a brief period by epinephrine. An identical sequence of EEG changes was observed during the terminal period of hemorrhagic shock. It is postulated that cerebral anoxia, caused by inadequate blood flow, is the primary cause of the altered EEG patterns that accompany enterotoxin toxicity. In this respect, staphylococcal enterotoxin B produces changes apparently similar to bacterial endotoxin but distinctly different from the EEG effects reported after botulinum toxin, anthrax toxin, or rattlesnake and cobra venom.

Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

“…Previous studies have indicated that other organ systems may also be involved in the toxic responses to SEA (7,13,16,17,24,25,35). The kidney has been suggested as the principal site for lysosome-mediated catabolism of intravenously (i.v.)…”

“…The potential association of SEA with GI neuronal structures was suggested by the presence of SEB within neurons of brain tissue taken from monkeys after i.v. challenge (13). An assessment of the roles of these tissues and cells in the response to orally administered SEA in addition to the role of the GI tract must be considered.…”

Pathogenesis of Lethal Shock After Intravenous Staphylococcal Enterotoxin B in Monkeys

“…Pressures were recorded with either a mercury manometer or a strain gauge pressure transducer amplification system (Sanborn Co., Waltham, Mass.). Animals were challenged iv with the same purified preparation of SEB (12) used in other studies performed in this laboratory (4,5,7,10,11). Control animals were studied in a similar manner but received diluent without toxin.…”

“…Staphylococcal enterotoxin type B (SEB), an exotoxin long incriminated as a causative substance of certain outbreaks of food poisoning, has been reported to cause lethal shock when injected intravenously into monkeys (5,7,11). Although the relationships between specific toxins and the clinical findings during a generalized staphylococcal infection have not been determined, the possibility exists that SEB, even though produced only in minute quantities, might play a role in the pathogenesis of arterial hypotension during staphylococcal sepsis.…”

“…53149. which follow a lethal intravenous challenge of purified SEB. These included the clinical syndrome which terminated in shock (5,7,11), multiple changes in clinical chemistries (4), a hypotension-associated fall in renal function (10), and terminal depression of electroencephalographic patterns (7). Other workers have reported on the pyrogenic and emetic effects (2,3,14).…”