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Staphylococcal food poisoning is probably the most common cause of such cases in the United States The heat-stable toxins typically produce acute abdominal pain, nausea, vomiting, and diarrhea within to hours of eating the contaminated meal The illness is usually self-limiting, although occasionally, patients develop severe symptoms and dehydration Other bacterial toxin-induced diarrheal food poisonings include those secondary to B cereus, Clostridium perfringens, and Vibrio species The onset of clinical illness and usual food sources of these and staphylococcal disease are outlined in Table 102.14 All these illnesses are generally self-limiting, and treatment is supportive, with careful attention to fluid and electrolyte status in severe cases (e.g., the rare occurrence of cholera in the United States) Clostridium botulinum toxin causes foodborne botulism when the toxin is ingested A distinct clinical scenario, infant botulism, shares many pathophysiologic and clinical features with foodborne botulism, but is the result of unique vulnerability in young infants, which allows C botulinum spores to proliferate and release toxin after ingestion (see Chapter 73 Septic-Appearing Infant ) The etiology of the foodborne disease differs in that preformed toxin is ingested at the time of consuming contaminated food, typically improperly homecanned, low-acidity vegetables (e.g., potatoes, onions, beans) or poorly refrigerated pot pies or meats The incubation period is usually 12 to 36 hours, with initial GI symptoms soon followed by weakness, malaise, and then cranial nerve symptoms, particularly diplopia, dysphagia, and dysarthria The neurologic examination is notable for normal mental status and symmetric ocular findings, such as ptosis, lateral rectus weakness, and pupillary abnormalities Diagnosis should be suspected clinically and patients should be treated empirically with heptavalent botulism antitoxin while awaiting results of serum and/or stool analyses for botulism toxin Scombroid Poisoning Scombroid poisoning occurs shortly after ingestion of spoiled fish from the Scombroidea family (e.g., tuna, bonita, skipjack), as well as ingestion of nonScombroidea fish (e.g., bluefish, mahi mahi) The ingested toxin(s) has not been completely characterized, but large quantities of histamine-like compounds are found in these fish when tissue histidine decomposes The clinical picture of scombroid poisoning consists of sudden-onset headache, facial flushing, a peppery taste in the mouth, dizziness, nausea, and vomiting An urticarial eruption with pruritus may develop In its extreme, patients may develop tachycardia, bronchospasm, respiratory distress, and hypotension
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