Introduction: The patient is a 6 month old male with no significant past medical history who presented with poor feeding. He was seen by his PCP one week prior to presentation for URI symptoms and prescribed amoxicillin for otitis media. After several days, he had improved, but mom noted that he was breastfeeding less with a weak latch and suck. He then became increasingly tired and limp and stopped feeding. He was taken to an outside hospital and admitted for IV rehydration and continued on ampicillin. The following day, he was noted to be excessively sleepy with a weak cry, suck and gag, ptosis and head lag. He had not passed a stool in four days. Concern for infantile botulism was raised, and he was transferred to a pediatric ICU. In review of his risk factors, he lived with his mother, father, identical twin sibling and two older siblings all of whom were asymptomatic. There was no family history of neuromuscular disorders. The twins were born at 37 weeks gestation with no complications. Both had been developing appropriately with full head control, rolling and ability to sit independently for brief periods. In the week prior to presentation, the patient's twin had a similar upper respiratory infection, but had not received antibiotics. The twin had no signs of weakness. The infants had never spent any significant time apart and slept in the same crib. They were both exclusively breastfed, but both were introduced to cereal one week prior to presentation. The family lived in southeastern Pennsylvania, an area with a high concentration of infantile botulism cases. There was no proximity to farms or current construction sites, and no family members had consistent soil exposure. On arrival to the ICU, the patient was noted to be alert but hypotonic with limited head control, ptosis, weak gag, absent reflexes and limited movement of limbs. He was admitted for close monitoring of neurologic and respiratory function. Given his classic presentation and residence in an endemic area, infantile botulism was strongly suspected. Botulism immune globulin (Baby BIg) was obtained and administered the day after admission. The patient did not require any respiratory support. He was unable to feed orally, and was started on enteral transpyloric tube feeds. No evidence of otitis media was noted in the hospital, so antibiotics were not continued, as there was concern for potentiation of toxin effect. Slight improvement was noted in his weakness within two days of receiving BIg. Stool collection subsequently tested positive for C botulinum toxin type B. The patient continued to show slow improvement and was discharged home on enteral tube feeds after 13 days in the hospital. The infant in this case study demonstrated a typical presentation and recovery from infantile botulism. His exact mechanism of exposure was unclear, but he fit the classic risk factors of residence in an endemic area and exclusive breastfeeding with a recent introduction of solid foods and likely had incidental spore contact. His identical twin did not have any signs of illness despite sharing the same risk factors, genetic predisposition and exposures. This included sleeping in the same crib, which has previously been described as a risk factor by Istre in 1986. One difference between the brothers was antibiotic exposure. Multiple studies have demonstrated that aminoglycosides can potentiate neuromuscular weakness in infants with botulism (Santos 1981). Other studies have hypothesized that any alteration to infant gut flora may allow for increased effect of ingested spores (Long 1985, 2001). Studies have shown increased botulism colonization in mice given antibiotics (Burr 1982). Given the twins' recent introduction to solid foods, their gut flora was likely changing. It is possible that antibiotic exposure in our patient led to increased colonization with ingested spores, higher toxin levels, and therefore the clinical manifestations of infantile botulism.
© 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins