ABSTRACT
Clostridium botulinum is a spore-forming, anaerobic gram-positive bacillus found in soils, aquatic sediments, and decaying animal carcasses (Sathyamoorthy and DasGupta, 1985; Hatheway, 1989). Toxigenic strains of C. botulinum elaborate seven antigenically distinct protein neurotoxins (types A, B, C1, D, E, F, and G). These botulinum neurotoxins (BoNTs) act primarily on the neuromuscular junction, causing paralysis of skeletal muscle by impairing the release of the neurotransmitter, acetylcholine (ACh). The clinical symptoms of botulism refl ect toxin-induced blockade of ACh release from neuromuscular and neuroeffector junctions (Ambache, 1951; Simpson, 1981).
