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The Mechanism of Action of Tetanus and Botulinum Neurotoxins

1996; Springer Science+Business Media; Linguagem: Inglês

10.1007/978-3-642-61105-6_32

0171-9750

Cesare Montecucco, Giampietro Schiavo, Ornella Rossetto,

Hereditary Neurological Disorders

Tetanus and botulinum neurotoxins were identified about a century ago as the cause of the neuroparalytic syndromes of tetanus and botulism (Faber, 1890; Tizzoni & Cattani, 1890; van Ermengem, 1897). Bacteria of the genus Clostridium produce one tetanus neurotoxin (TeNT) and seven different serotypes of botulinum neurotoxins (BoNT/A, /B, /C, /D, /E, /F, and /G). These bacteria show a widespread distribution in the environment, mainly as spores, which can germinate under appropriate anaerobic conditions. Tetanus follows the contamination of necrotic wounds with spores of Clostridium tetani, limited bacterial proliferation and toxin production. Botulism derives from ingestion of uncooked anaerobic food, where spores of Clostridium botulinum, or related species, have germinated with the production of the toxin (foodborne botulism). More rarely, spores germinate in anaerobic areas of the newborn intestine giving rise to infant botulism (Simpson, 1989; Montecucco, 1995). Since tetanus is caused solely by intoxication with TeNT, it was possible to prepare a anti-tetanus vaccine simply by treating TeNT with paraformaldheyde, a chemical modification that inactivates the toxin, but preserves its immunogenic properties (Ramon & Descombey, 1925).