Duration of Fecal Excretion of Clostridium Botulinum and Botulinum Neurotoxin in Patients Recovering from Infant Botulism

Dabritz, Haydee A.; Payne, Jessica R; Khouri, Jessica M.

doi:10.1016/j.jpeds.2023.113396

Cited by 2 publications

(1 citation statement)

References 32 publications

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“…We earlier reported a botulism case of 3-month old infant and showed that, despite prompt clinical recovery, C. botulinum (Group I) type A persisted and produced BoNT in the infant gut for 27.7 weeks [58]. In contrast, in most infant botulism cases caused by C. botulinum type A, the median excretion of C. botulinum and the toxin was reported to be 5.9 weeks [59]. To further understand the exceptionally long colonization of the infant gut by C. botulinum in this particular case, we performed an extensive genomic analysis of C. botulinum isolates collected from the infant feces over time and identified possible pheno-genotypic adaptation traits of C. botulinum to the gut environment [60].…”

Section: Introductionmentioning

confidence: 99%

Case report: Aberrant fecal microbiota composition of an infant diagnosed with prolonged intestinal botulism

Douillard,

Derman,

Jian

et al. 2024

Gut Pathog

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Background Intestinal botulism is primarily reported in small babies as a condition known as infant botulism. The condition results from the ingestion of environmental or foodborne spores of botulinum neurotoxin (BoNT) producing Clostridia, usually Clostridium botulinum, and subsequent spore germination into active botulinum neurotoxinogenic cultures in the gut. It is generally considered that small babies are susceptible to C. botulinum colonization because of their immature gut microbiota. Yet, it is poorly understood which host factors contribute to the clinical outcome of intestinal botulism. We previously reported a case of infant botulism where the infant recovered clinically in six weeks but continued to secrete C. botulinum cells and/or BoNT in the feces for seven months. Case presentation To further understand the microbial ecology behind this exceptionally long-lasting botulinum neurotoxinogenic colonization, we characterized the infant fecal microbiota using 16S rRNA gene amplicon sequencing over the course of disease and recovery. C. botulinum could be detected in the infant fecal samples at low levels through the acute phase of the disease and three months after recovery. Overall, we observed a temporal delay in the maturation of the infant fecal microbiota associated with a persistently high-level bifidobacterial population and a low level of Lachnospiraceae, Bacteroidaceae and Ruminococcaceae compared to healthy infants over time. Conclusion This study brings novel insights into the infant fecal composition associated with intestinal botulism and provides a basis for a more systematic analysis of the gut microbiota of infants diagnosed with botulism. A better understanding of the gut microbial ecology associated with infant botulism may support the development of prophylactic strategies against this life-threatening disease in small babies.

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Section: Introductionmentioning

confidence: 99%

Case report: Aberrant fecal microbiota composition of an infant diagnosed with prolonged intestinal botulism

Douillard,

Derman,

Jian

et al. 2024

Gut Pathog

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Infant Botulism: In Search of Clostridium botulinum Spores

Harris,

Dabritz

2024

Curr Microbiol

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Infant botulism is now the most common form of human botulism in Canada and the United States. Infant botulism is a severe neuroparalytic disease caused by ingestion of the spore-forming neurotoxic clostridia, including Clostridium botulinum that colonize the large intestine and subsequently produce botulinum neurotoxin in situ. It has been over a century since the first surveys documenting the ubiquitous prevalence of C. botulinum in soils around the world. Since then, honey has been identified as the only well-known risk factor for infant botulism despite a multitude of international environmental surveys isolating C. botulinum spores from ground soil, aquatic sediments, and commonly available infant foods. Associations of infant botulism cases with confirmed sources of C. botulinum exposure have primarily implicated outdoor soil and indoor dust, as well as commonly ingested foods including honey, dry cereals, and even powdered infant formula. Yet the origin of infection remains unknown for most infant botulism cases. This review summarizes the various surveys from around the world for C. botulinum in environmental soils and sediments, honey, and other infant foods, as well as laboratory-confirmed associations with documented infant botulism cases. Additional factors are also discussed, including the composition of infant gut microbiota and the practice of breastfeeding. We make several recommendations to better identify sources of exposure to C. botulinum spores that could lead to effective preventive measures and help reduce the incidence of this rare but life-threatening disease.

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Duration of Fecal Excretion of Clostridium Botulinum and Botulinum Neurotoxin in Patients Recovering from Infant Botulism

Cited by 2 publications

References 32 publications

Case report: Aberrant fecal microbiota composition of an infant diagnosed with prolonged intestinal botulism

Case report: Aberrant fecal microbiota composition of an infant diagnosed with prolonged intestinal botulism

Infant Botulism: In Search of Clostridium botulinum Spores

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