Robert Schechter MD*
California Department of Health Services, Berkeley, California, USA

In infant botulism. the intestine is colonized temporarily with a clostridium producing botulinum neurotoxin, which enters the circulation repeatedly to intoxicate peripheral motor nerve endings. With rare exception, Clostridium botulinum only colonizes the infant, whether human, rodent or horse. Infant botulism is the most frequently recognized form of human botulism in the United States (US), with over 1500 cases diagnosed since 1976, and an incidence less than 1 per 10.000 newborns. The toxin type of illness varies by region, with a majority of cases in the Western US and Argentina due to type A C. botulium and a majority in the Eastern US due to type B C. botulium. A few infant botulism cases recognized in the US and Hungary have been caused by C. baratii producing type F neurotoxin, and in Eurasia by C. butyricum producing type E neurotoxin.

Risk factors for infant botulism include consumption of honey and decreased intestinal motility. Onset is characterized by decreased frequency of bowel movements, poor feeding and other cranial nerve weaknesses followed by extremity weakness and hypotonia. The pace of illness and maximal severirty are quite variable, with severity ranging from mild feeding weakness to complete, prolonged paralysis. Laboratory diagnosis in the US is most often in stool by culture along with detection of neurotoxin by mouse bioassay. Until recently, care has been limited to respiratory and nutritional support and treatment of complications such as secondary infection. In a randomized clinical trial for infant botulism in California completed in 1997, the use of human Botulism Immune Globulin reduced the duration of illness. The prognosis of a baby hospitalized with infant botulism generally is survival with complete recovery after a lengthy paralysis, though there is evidence of infants dying from fulminant disease prior to hospitalization.