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Published on: April 7, 2023
Catastrophic presentation of infant botulism may obscure or delay diagnosis
Wendy G Mitchell1, Linda Tseng-Ong
1Pediatric Neurology Division, Childrens Hospital Los Angeles, Keck School of Medicine, Los Angeles, California, USA. wmitchell@chla.usc.edu
Insights
Atypical infant botulism presentations in three infants highlight diagnostic challenges. Early symptoms like poor feeding can mask this serious condition, delaying crucial treatment.
Area of Science:
- Pediatrics
- Infectious Diseases
- Neurology
Background:
- Infant botulism is a serious neuroparalytic illness caused by Clostridium botulinum toxin.
- Typical presentations include constipation, ptosis, and facial weakness, but atypical cases can be challenging to diagnose.
- Early recognition is crucial for timely intervention and improved outcomes.
Observation:
- Three infants presented with severe, atypical symptoms including rapid deterioration, cardiopulmonary arrest, and respiratory arrest.
- Initial symptoms of poor feeding or poor suck were misattributed to other conditions such as sepsis or metabolic disorders.
- None of the infants initially presented with classic signs like constipation, ptosis, or facial weakness.
Findings:
- All three infants were ultimately diagnosed with infant botulism, a condition often missed due to atypical early signs.
- Antibiotic administration prior to diagnosis may have contributed to the rapid deterioration observed in these cases.
- Delayed diagnosis precluded treatment with botulism immunoglobulin in all three infants.
Implications:
- Clinicians should consider infant botulism in infants presenting with unexplained neurological deterioration, even without typical symptoms.
- Recognizing subtle signs of bulbar weakness, such as poor feeding or suck, is critical for early diagnosis.
- Increased awareness of atypical infant botulism presentations can improve diagnostic timeliness and patient management.
Abstract:
Three infants with infant botulism are presented to illustrate how atypical, early, and severe features may obscure or delay diagnosis. Two boys aged 6 weeks and 20 days, respectively, presented with rapid deterioration after brief periods of poor feeding, one with an apparent life-threatening event at home and the other with a full cardiopulmonary arrest. Initial abnormal laboratory findings of coagulopathy suggested sepsis in the first infant. In the second infant, severe acidosis and hypoglycemia suggested an underlying metabolic disorder. A third infant, aged 1 month, was hospitalized originally with an admitting diagnosis of "pharyngitis" resulting from his inability to take adequate feedings. He received intravenous fluids and antibiotics. One week later he suffered a respiratory arrest. Laboratory findings of severe hyponatremia and acidosis at the time of his arrest suggested a metabolic etiology. Even retrospectively, none of these infants had the typical initial complaint of constipation, and none were noted to have ptosis or facial weakness before catastrophic collapse. However, in each case, the parent had initially brought the child to the physician for "poor feeding" or "poor suck," which was not recognized by medical personnel as a result of bulbar weakness. Ultimately, all 3 infants were found to have infant botulism. All 3 had received antibiotics before catastrophic collapse, possibly contributing to the rapidity of the deterioration. Each recovered, although the delay in diagnosis made them ineligible for treatment with botulism immunoglobulin.
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