Infant Botulism


Infant botulism was first diagnosed in California in 1976,12 and it is no coincidence that in 1975, the CDC had advocated examination of stool samples for botulism in suspect cases. Before 1976, there were few recognized cases of infant botulism, but since then, babies have made up the largest percentage of botulism victims.18 By 1 January 1994, there had been 1,270 cases of infant botulism in hospitals nationwide, and only seven of those were not types A, B, or both.15

Striking children between four and twenty-six weeks of age,10 infant botulism is caused when a child consumes C. botulinum spores, which then colonize his or her intestinal tract and reproduce, creating toxin. The main food linked to infant botulism is honey, a carrier of botulinum spores,25 which has been linked to 20 - 35% of known cases.10

Symptoms of infant botulism include constipation for at least three days; lethargy; poor feeding; increasing weakness; expressionless face; feeble cry; ptosis; impaired gag, suck and swallow reflexes; poor head control; hypotonia; and possible eventual respiratory failure.8 These symptoms led many doctors to diagnose other illnesses as the cause. Infant botulism is similar in appearance to dehydration, an electrolyte imbalance, diphtheric polyneuropathy, neonatal myasthenia gravis, poliomyelitis, hypothyroidism, tick paralysis, Werdning-Hoffman spinal muscular atrophy, Leigh disease (subacute necrotizing encephalomyelopathy), congenital myopathy, Guillain-Barré Syndrome, and exposure to toxins such as heavy metals and organophosphates.5 Fortunately there are ways to distinguish botulism from some of the more common incorrect diagnoses. Sepsis and meningitis can be ruled out with blood tests and a spinal tap, myasthenia gravis with edrophonium testing and the persistence of pupillary light and deep tendon reflexes, Guillain-Barré Syndrome by elevated cerebrospinal fluid protein and electromyographic patterns of denervation and proonged nerve conduction velocity, and poliomyelitis by leukocytes in the cerebrospinal fluid.9

Treatment of infants with botulism is a bit more difficult because not only does the antitoxin fail to make a difference,5 but it may, in fact, cause undesirable side effects. Instead, fluids and nutritional supplements are administered to the baby intravenously, and the child may require intubation for either airway protection or increased air flow. No matter how severe the case of botulism, the infant almost always recovers completely, although this may necessitate a long hospital stay.18 The current mortality rate of infant botulism patients in the USA is less than 3%.5

CASE STUDIES


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