Abstract
Infant botulism results when Clostridium botulinum spores germinate, colonize the gut, and there produce botulinal toxin, which after absorption causes flaccid muscle paralysis. The observed variation in the severityof the diseasewas linked to the infant's milk source, in that all sudden death cases indistinguishablefrom typical crib death occurred in infants who had been formula-fed, whereas the more gradual onset, hospitalized cases occurred in infants who were predominantly breast-fed. Secretory IgA antibody against C. botulinum vegetative cell antigens was found in human milk from mothers of both healthy infants and patients, a finding that further confirms the functioning of the “mucosal immune system” in humans. The hypothesis that some crib deaths might also result from other intestinally produced bacterial toxins was investigated by injecting infant rhesus monkeys with microgram amounts of purified Clostridium difficile toxins A and B; quiet death pathologically consistent with human crib death occurred within 4 hr to 10 hr. This and other evidence suggest that infant botulism may be the prototype of a putative class of heretofore unrecognized diseases, the “toxigenic intestinal infections of infancy.” Collectively, these illnesses may account for a modest proportion of crib death, against which human milk may provide relative protection.