Journal List > J Korean Med Assoc > v.47(11) > 1080323

Kim: Botulism

Abstract

Botulism is a life threatening disorder caused by a neurotoxin produced from the anaerobic, spore-forming bacterium Clostridium botulinum. There are seven antigenically distinct types of botulinum neurotoxins (types A through G), and the human botulism is primarily caused by toxin types A, B, and E. Four clinical forms of botulism occur in humans: foodborne botulism, wound botulism, infant botulism, and adult infectious botulism. Botulism is characterized by symmetric, descending, flaccid paralysis of motor and autonomic nerves, usually beginning with the cranial nerves. Dry mouth, blurred vision, and diplopia are usually the earliest neurologic symptoms. Botulism should be suspected in a patient with an acute onset of gastrointestinal, autonomic, and cranial nerve dysfunction. Confirmation of the diagnosis of botulism depends on the detection of the toxin or the organism in the patient. The most reliable method for the detection of the toxin is the mouse inoculation test. The mainstay of treatment for severe botulism is supportive therapy with mechanical ventilation. The administration of antitoxin is the only specific pharmacologic treatment available for botulism. Botulism is a rare but potentially fatal illness, so timely recognition of the clinical symptoms plays an important role in decreasing the mortality rate.

Figures and Tables

Table 1
jkma-47-1056-i001

Shapiro RL, et al. Ann intern Med 1998 ; 129 : 221 - 8

CT*=computed tomography, MRI=magnetic resonance imaging

References

1. van Ermengem E. Classics in infectious disease. A new anaerobic bacillus and its relation to botulism. Rev Infect Dis. 1979. 1:701–719. [Reprint of van Ermengem's original article, first published in 1897] (Cited from Reference 7).
3. Lund BM. Foodborne disease due to Bacillus and Clostridium species. Lancet. 1990. 336:982–986.
crossref
4. Simpson LL. Molecular pharmacology of botulinum toxin and tetanus toxin. Ann Rev Pharmacol Toxicol. 1986. 26:427–453.
crossref
5. Lamana C. The most poisonous poison. Science. 1959. 130:763–772.
crossref
6. Eitzen LT, Caudle MA. Medical Management of Biological Casualties. 1993. Fort Detrick, MD: U.S. Army Medical Research Institute of Infectious Disease;Publication no. 20170-5011.
7. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States:A clinical and epidermiologic review. Ann Intern Med. 1998. 129:221–228.
crossref
9. Woodruff BA, Griffin PM, McCroskey LM, Smart JF, Wainwright RB, Bryant RG, et al. Clinical and laboratory comparison of botulism from toxin types A, B, and E in the United States, 1975-1988. J Infect Dis. 1992. 166:1281–1286.
crossref
10. Hughes JM, Blumenthal JR, Merson MH, Lombard GL, Dowell VR Jr, Gangarosa EJ. Clinical features of types A and B food-borne botulism. Ann Intern Med. 1981. 95:442–445.
crossref
11. Merson MH, Dowell VR Jr. Epidemiologic, clinical and laboratory aspects of wound botulism. N Engl J Med. 1973. 289:1005–1010.
crossref
12. Wilson R, Morris JG Jr, Snyder JD, Feldman RA. Clinical characteristics of infant botulism in the United States: A study of the non-Califonia cases. Pediatr Infect Dis. 1982. 1:148–150.
13. St Louis ME. Evans AS, brachman PS, editors. Botulism. Bacerial Infections of Humans:Epidemiology and Control. 1991. 2nd ed. New York: Plenum Medical;115.
crossref
14. Hatheway CL. Balows A, Hausler WH, Lennette EH, editors. Botulism. Laboratory diagnosis of infectious disease:Principles and Practice. 1988. vol 1. New York: Springer-Verlag;111.
crossref
15. Wictome M, Newton K, Jameson K, Hallis B, Dunnigan P, Shone C, et al. Development of an in vitro bioassay for Clostridium botulinum type B neurotoxin in foods that is more sensitive than the mouse bioassay. Appl Environ Microbiol. 1999. 65:3787–3792.
crossref
16. Fach P, Perelle S, Dilasser F, Grout J, Dargaignaratz C, Broussolle V, et al. Detection by PCR-enzyme-linked immunosorbent assay of Clostridium botulinum in fish and environmental samples from a coatal area in northern France. Appl Environ Microbiol. 2002. 68:5870–5876.
crossref
17. Hatheway CL, Snyder JD, Seals JE, Edell TA, Lewis GE Jr. Antitoxin levels in botulism patients treated with trivalent equine botulism antitoxin to toxin types A, B, and E. J Infect Dis. 1984. 150:407–412.
crossref
18. Tacket CO, Shandera WX, Mann JM, Hargrett NT, Blake PA. Equine antitoxin use and other factors that predict outcome in type A foodborne botulism. Am J Med. 1984. 76:794–798.
crossref
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