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VIII.19 - Botulism

from Part VIII - Major Human Diseases Past and Present

Published online by Cambridge University Press:  28 March 2008

Kenneth F. Kiple
Affiliation:
Bowling Green State University, Ohio
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Summary

To date, seven immunologically distinct forms of botulinum toxins, labeled A through G, have been identified. Botulism in humans has generally been associated with A, B, E, or F toxins, whereas the C and D toxins have been identified in botulism outbreaks among various animal species, as shown in Table VIII.19.1.

Clinical Manifestation and Pathology

The onset of disease usually occurs within 12 to 36 hours of ingestion of food contaminated with botulinum toxin. Botulism typically presents with an array of distressing signs of motor nerve dysfunction, including double or blurred vision and difficulty with speech and swallowing. The unabated disease progresses to generalized paralysis and death from respiratory muscle involvement.

Diagnosis is confirmed by detecting botulinum toxin in the blood, feces, or wound site of the patient. Depending on the dose of toxin, untreated botulism carries a high fatality rate. Early treatment with antitoxin accompanied by respiratory assistance and other supportive intensive care may be life-saving.

The pathophysiology involves inhibition of release of the neurotransmitter substance acetylcholine at the neuromuscular junction, thus preventing the initiation of the electrical impulse needed for muscle contraction. Electromyography shows a characteristic decrease in amplitude of the evoked muscle action potential in response to an electrical stimulus.

Infant botulism, a condition confined to babies between 2 weeks and 9 months of age, typically presents with listlessness and generalized weakness (“floppy baby”) and has been shown to cause some cases of sudden infant death syndrome (SIDS). It has been associated with ingestion of various processed infant foods–honey in particular–that contain botulinum spores.

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Publisher: Cambridge University Press
Print publication year: 1993

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References

Arnon, Stephen S., Karla, Damus, and Chin, James. 1981. Infant botulism: Epidemiology and relation to sudden infant death syndrome. Epidemiologic Reviews 3.CrossRefGoogle ScholarPubMed
Barker, William H., et al. 1977. Type B botulism outbreak caused by a commercial food product. Journal of the American Medical Association 237.Google ScholarPubMed
Merson, Michael H., and Dowell, V. R.. 1973. Epidemiologic, clinical and laboratory aspects of wound botulism. New England Journal of Medicine 289: 1005–10.CrossRefGoogle ScholarPubMed
Meyer, K. F. 1956. The status of botulism as a world health problem. Bulletin of the World Health Organization 15.Google ScholarPubMed
Smith, Louis. 1977. Botulism: The organism, its toxins, the disease. Springfield, Ill..Google Scholar
,U.S. Public Health Service. Centers for Disease Control. 1979. Botulism and the United States, 1899–1977: Handbook for epidemiologists, clinicians and laboratory workers. Atlanta.

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  • Botulism
  • Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
  • Book: The Cambridge World History of Human Disease
  • Online publication: 28 March 2008
  • Chapter DOI: https://doi.org/10.1017/CHOL9780521332866.081
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  • Botulism
  • Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
  • Book: The Cambridge World History of Human Disease
  • Online publication: 28 March 2008
  • Chapter DOI: https://doi.org/10.1017/CHOL9780521332866.081
Available formats
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  • Botulism
  • Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
  • Book: The Cambridge World History of Human Disease
  • Online publication: 28 March 2008
  • Chapter DOI: https://doi.org/10.1017/CHOL9780521332866.081
Available formats
×