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Infant botulism results from ingestion of Clostridium botulinum spores, their colonization of the large intestine, and toxin production in vivo.
Infant botulism occurs most often in infants < 6 mo. The youngest reported patient was 2 wk, and the oldest was 12 mo. Unlike food-borne botulism, infant botulism is not caused by ingestion of a preformed toxin. Most cases are idiopathic, although some have been traced to ingestion of honey, which may contain C. botulinum spores; thus, infants < 12 mo should not be fed honey. Most cases involve type A or B toxin.
Constipation is present initially in 90% of cases and is followed by neuromuscular paralysis, beginning with the cranial nerves and proceeding to peripheral and respiratory musculature. Cranial nerve deficits typically include ptosis, extraocular muscle palsies, weak cry, poor suck, decreased gag reflex, pooling of oral secretions, poor muscle tone (floppy baby syndrome), and an expressionless face. Severity varies from mild lethargy and slowed feeding to severe hypotonia and respiratory insufficiency.
Infants are hospitalized, and supportive care (eg, ventilatory support) is given as needed. Because the organism and toxin are excreted in the stool for weeks to months after symptom onset, appropriate contact precautions must be followed.
Specific treatment is with human botulism immune globulin, which is available from the Infant Botulism Treatment and Prevention Program (IBTPP— 231-7600; see also the IBTPP web site). The antitoxin is derived from pooled human donors who have high titers of antibodies to A and/or B toxin. Treatment is started as soon as the diagnosis is suspected; waiting for confirmatory test results is dangerous. The dose is 75 mg/kg IV once, given slowly. The horse serum heptavalent antitoxin used in adults is not recommended for infants.
Antibiotics are not given because they may lyse C. botulinum in the gut and increase toxin availability.
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