To the Editors: A 3-month-old boy with respiratory failure was admitted to the pediatric intensive care unit of a Northern California medical center in February 2011. The illness began 3 days earlier with progressively worsening lethargy, cough and stridor, decreased oral intake and decreased urine output. A review of systems was notable for decreased bowel movements in the past week and the presence of copious clear secretions from the infant’s nose and oropharynx. The infant was born at term with no complications, was exclusively breastfed other than a dropperful of chicken broth given when the child was ill in the days before admission and had received no vaccines. A nasal aspirate polymerase chain reaction was positive for respiratory syncytial virus. Over the next 4 days, ventilatory settings were weaned as oxygenation normalized. The child was extubated twice, but each time developed hypercapnia requiring reintubation. Seven days after admission, the infant remained intubated and ventilated with poor respiratory effort. Neurologic examination revealed a nearly complete bilateral ptosis; facial diplegia with tears produced under stimulation and no facial grimace. Infant botulism was suspected. Stool was sent for Clostridium botulinum toxin, and botulism immune globulin was administered empirically. Two days later, stool tests revealed C. botulinum toxin type A and the diagnosis of infant botulism was confirmed. During the next 3 weeks, the child received nasogastric feeds and ventilatory support and slowly regained bulbar strength. He was extubated 9 days after botulism immune globulin administration and was discharged to home 1 month after admission with a mixed breastfeeding/tubefeeding regimen. He required supplemental oxygen by nasal cannula until 2 days before discharge. On discharge, the child was still noted to have decreased tone, a weak cry and mildly uncoordinated feeding mechanics. Infant botulism results from ingestion of spores of Clostridium species, which germinate and colonize the infant intestine, producing botulinum toxin. This toxin is absorbed and causes a descending, symmetric paralysis. Constipation is almost always the first sign of illness and is often overlooked (as in the case above).1 Diagnosis is confirmed by identification of C. botulinum organisms in the feces of an infant with a presentation consistent with the disease. Supportive care forms the cornerstone of therapy, though specific treatment has been available in the form of intravenous human botulism immune globulin since 1992, through the California Department of Public Health. Botulism immune globulin should be initiated as early as possible in the course of illness and should not be delayed for laboratory confirmation. Acute coinfection with respiratory syncytial virus and Clostridium spp. has not previously been described. This case serves to demonstrate the necessity to maintain an open differential diagnosis even when presented with laboratory confirmation of an apparent causative etiology. Kevin K. Quinn, MD James D. Cherry, MD, MSc Division of Pediatric Infectious Diseases UCLA David Geffen School of Medicine Neeta R. Shah, MD Laura J. Christie, MD Department of Pediatrics Kaiser Permanente Northern California Oakland, CA
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Jan 1, 2022
Alexander Gipsman + 2
Open Access