Infant botulism represents a distinct entity of botulism. Ingestion of the 
ubiquitously present spores of Clostridium botulinum leads to germination of the 
organism and neurotoxin production in the infant intestine. Symptoms typically 
develop gradually in contrast to classical food botulism in which an acute onset 
of symptoms shortly after the ingestion of preformed toxin in a food is 
characteristic. Microbiologically, the diagnosis is established by 
identification of Clostridium botulinum organism and toxin in stool specimen. 
However, positive results in these tests provide only indirect evidence for the 
clinical relevance of the neurotoxin since asymptomatic carriers have been 
found. The toxin irreversibly blocks the release of acetylcholin from the 
motoric end plate which results in muscle weakness and paralysis. Depending on 
the amount of toxin produced, infant botulism exhibits a broad clinical spectrum 
ranging from oligosymptomatic forms to a fulminant course with acute respiratory 
failure within hours leading to sudden death. Unrecognized mild forms or 
beginning muscle weakness can be a co-factor for other risk factors of sudden 
infant death (SIDS). In studies analyzing infants who died from SIDS, botulism 
bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore 
represents an important differential diagnosis of unexplained and inconclusive 
muscular hypotonia in the first year of life.