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J Infect Dis. 2014 Dec 1;210(11):1711-22. doi: 10.1093/infdis/jiu331. Epub 2014 Jun 12.

Molecular epidemiology of infant botulism in California and elsewhere, 1976-2010.

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Infant Botulism Treatment and Prevention Program, Division of Communicable Disease Control, Center for Infectious Diseases, California Department of Public Health, Richmond.
Bioscience Division.
Computing, Computational and Statistical Sciences Division, Los Alamos National Laboratory, New Mexico.



Infant botulism (IB), first identified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, and produce botulinum neurotoxin (BoNT) in the immature intestine. From 1976 to 2010 we created an archive of 1090 BoNT-producing isolates consisting of 1012 IB patient (10 outpatient, 985 hospitalized, 17 sudden death), 25 food, 18 dust/soils, and 35 other strains.


The mouse neutralization assay determined isolate toxin type (56% BoNT/A, 32% BoNT/B). Amplified fragment-length polymorphism (AFLP) analysis of the isolates was combined with epidemiologic information.


The AFLP dendrogram, the largest to date, contained 154 clades; 52% of isolates clustered in just 2 clades, 1 BoNT/A (n=418) and 1 BoNT/B (n=145). These clades constituted an endemic C. botulinum population that produced the entire clinical spectrum of IB. Isolates from the patient's home environment (dust/soil, honey) usually located to the same AFLP clade as the patient's isolate, thereby identifying the likely source of infective spores. C. botulinum A(B) strains were identified in California for the first time.


Combining molecular methods and epidemiological data created an effective tool that yielded novel insights into the genetic diversity of C. botulinum and the clinical spectrum, occurrence, and distribution of IB in California.


Clostridium baratii; Clostridium botulinum; Clostridium butyricum; botulinum toxin; clinical spectrum; honey; infant botulism; molecular epidemiology; sudden infant death

[Indexed for MEDLINE]

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