Effect of staphylococcal enterotoxin B on the electroencephalogram of monkeys.
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.
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000502:physiology*; D004569:Electroencephalography; D004837:Epinephrine / Q000494:pharmacology; D000882:Haplorhini; D002534:Hypoxia, Brain / Q000209:etiology; D012771:Shock, Hemorrhagic / Q000209:etiology; D012772:Shock, Septic / Q000503:physiopathology; D014118:Toxins, Biological / Q000494:pharmacology*
D014118:Toxins, Biological; D004837:Epinephrine