Infant botulism causes acute bulbar dysfunction, weakness, and respiratory failure in infants infected with the neurotoxin-producing Clostridium botulinum spores. Common clinical presenting symptoms include constipation, weak cry, poor feeding, ptosis, inactivity, and respiratory distress. Physical findings consist of hypotonia, weakness, diminished or absent gag reflex, ptosis, mydriasis, weak suck, and weak cry. The diagnosis is made by a high clinical suspicion and detection of the botulinum toxin and isolation of the spores from stool samples.

Clinical management is primarily supportive. Historically, an equine antitoxin was used for therapy that neutralized toxin molecules not yet bound to nerve endings. However, side effects occurred in 20% of patients, including hypersensitivity reactions, anaphylaxis, and serum sickness. This was commonly used in adult patients but was never recommended for infant botulism because of the side effects seen in the adult population. The equine antitoxin is no longer considered beneficial, especially in the face of a self-limited disease.