The signs and symptoms of staphylococcal intoxication occur when foods containing enterotoxin are ingested in reasonably small amounts. However, death can occur if large amounts are ingested. The illness is particularly acute (1-7 hr) after the ingestion of toxin-contaminated foods (35), with recovery generally occurring in 1-2 days. The early signs are nausea and possibly abdominal cramping, with resulting primary observable symptoms of vomiting and diarrhea. Secondary symptoms may include retching, dehydration, sweating, weakness, and salivation. In severe cases, the victims may also exhibit headache, sweating, marked prostration, muscular cramping, and a subsequent drop in blood pressure. Fever may occur, or the body temperature may be subnormal. Blood and mucus may be observed in stools and vomit (36).
The complete effect of the staphylococcal enterotoxins on human beings has not been elucidated, since opportunities to study this type of illness in humans are very limited. The amount of toxin has not been precisely determined, although is estimated to be between 100 ng and 35 |g based on challenge studies and the evaluation of foods implicated in food poisoning outbreaks (36-38).
The true nature of the gastrointestinal syndrome is not completely understood. The vomiting reaction is initiated in the intestinal tract, although the specific binding of the enterotoxin to a site in the gastrointestinal system has not been demonstrated (1). It has been shown, however, that these toxins pass through the intestinal tract rapidly and are removed from the circulation by the kidneys in a reasonably short period of time (1). The enterotoxins could be considered neurotoxins based on their mode of action on the subcortical-vomiting center of the brain (39). This effect has been confirmed in monkeys rendered unresponsive to the enterotoxin emetic effects by detachment of the nerves to the brain proximal to the vomiting center (40). Other investigators have further demonstrated that orally administered enterotoxin (Type B) initiated a local neutral reflex in the gut of monkeys triggering the vomiting center, leading to vomiting and hypermobility (41). Additionally, there was no evidence of significant absorption of toxin or stimulation by a central-acting humoral mechanism. The activity of cysteinyl leukotrienes, patent medications of inflammation noted following exposure to these toxins, may be responsible for the enteritis and pseudomembranous enterocolitis in the intestinal tract of animals and humans, respectively (1).
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