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Clostridium difficile colitis associated with infant botulism: near-fatal case analogous to Hirschsprung's
R Schechter1, B Peterson, J McGee
1Division of Communicable Disease Control, California Department of Health Services, Berkeley 94704, USA. rschecht@dhs.ca.gov
Insights
Infant botulism and Hirschsprung's disease can cause severe Clostridium difficile-associated diarrhea (CDAD) in children. Colonic stasis plays a role in CDAD susceptibility and severity.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
Background:
- Clostridium difficile-associated diarrhea (CDAD) is a significant concern in pediatric populations.
- Infant botulism, caused by Clostridium botulinum, is a rare condition in infants.
Observation:
- This study reports five cases of CDAD in children with infant botulism.
- Two severe cases of colitis with colonic stasis (one from infant botulism, one from Hirschsprung's disease) are compared.
- Clinical manifestations included hypovolemia, hypotension, ascites, pulmonary effusion, and thrombosis.
Findings:
- Laboratory findings revealed leukocytosis, hypoalbuminemia, hyponatremia, and coagulopathy.
- Clostridium difficile toxin was detected in ascites in the infant botulism case.
- Recurrent CDAD occurred despite negative stool cytotoxin tests after treatment.
Implications:
- Colonic stasis, whether acquired (infant botulism) or congenital (Hirschsprung's disease), may predispose children to CDAD.
- Understanding the role of colonic stasis is crucial for managing severe CDAD in pediatric patients.
- This research highlights a potential link between botulism and C. difficile infections in children.
Abstract:
We present the first five reported cases of Clostridium difficile-associated diarrhea (CDAD) in children with infant botulism caused by Clostridium botulinum. We compare two fulminant cases of colitis in children with colonic stasis, the first caused by infant botulism and the second caused by Hirschsprung's disease. In both children, colitis was accompanied by hypovolemia, hypotension, profuse ascites, pulmonary effusion, restrictive pulmonary disease, and femoral-caval thrombosis. Laboratory findings included pronounced leukocytosis, hypoalbuminemia, hyponatremia, coagulopathy, and, when examined in the child with infant botulism, detection of C. difficile toxin in ascites. CDAD recurred in both children, even though difficile cytotoxin was undetectable in stool after prolonged initial therapy. Four children who had both infant botulism and milder CDAD also are described. Colonic stasis, whether acquired, as in infant botulism, or congenital, as in Hirschsprung's disease, may contribute to the susceptibility to and the severity of CDAD.