Pediatric emergency medicine trisk 3103 3103
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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 1 to 6 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.
