Seizures are not typically recognized as sequelae of infant botulism. However, there is significant risk given the possible secondary complications. In this case, a 3-month-old girl diagnosed with infant botulism was found to be in nonconvulsive status epilepticus on video EEG, something that would have gone undetected otherwise with potentially severe consequences.

A 3-month-old girl presented with lethargy, lacrimation, difficulty swallowing, poor intake, and constipation. History identified ongoing construction near the family's home. She was admitted to the ICU, intubated, sedated, and paralyzed. Neurologic exam was notable for fixed mydriatic pupils, weakness, and hypotonia. Due to concerns for infant botulism, she was treated with BabyBIG.

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Infant botulism is caused by ingestion of C. botulinum spores which release a toxin blocking presynaptic acetylcholine release. Clinical manifestations are broad, including flaccid paralysis and respiratory failure. Infants are at risk for seizures throughout their illness from hypoxic encephalopathy, hyponatremia, and secondary infection. Given blockade at the neuromuscular junction, seizures in infant botulism may not manifest with clinical signs, ending up underrecognized and underreported. Clinicians should have a low threshold for obtaining EEG to rule out subclinical seizures. Additional research to better characterize prevalence and prognosis of subclinical seizures in infant botulism is warranted.