Abstract
Botulism and tetanus are two severe neurological diseases in man and animals. While botulism is characterized by a descendant flaccid paralysis, tetanus consists in spastic paralysis. In the severe forms of both diseases, death occurs by respiratory distress. Botulism and tetanus are caused by neurotoxins, botulinum neurotoxin (BoNT), and tetanus toxin (TeNT), respectively, which are produced by anaerobic sporulating bacteria, Clostridium botulinum and Clostridium tetani, respectively. In contrast to C. tetani, which forms a homogeneous bacterial species, BoNT-producing Clostridia are divided into several bacterial species and groups. These Clostridia are widely distributed in the environment, including food notably for C. botulinum, where they can survive during long periods in the sporulating forms. BoNTs and TeNT share a common structural organization consisting in a light (L) chain (about 50 kDa) linked by a disulfide bridge to the heavy (H) chain (about 100 kDa). Only a unique TeNT is known, while BoNTs encompass seven toxinotypes (A to G, BoNT/A, B, and E mainly involved in human botulism, and BoNT/C and D mainly responsible for animal botulism), which are subdivided into several subtypes according to amino acid sequence variations. H chain, which contains a C-terminal receptor-binding domain and an N-terminal translocation domain, delivers the L chain into target neurons. BoNTs target the motoneuron endings or neuromuscular junctions, and TeNT is transported to central inhibitory interneurons through a retrograde axonal pathway along motoneurons. Both BoNT and TeNT block the release of neurotransmitter by an L chain-mediated proteolytic cleavage of SNARE proteins (synaptobrevin, SNAP25, or syntaxin) which are involved in the neuroexocytosis process. Blockage of acetylcholine release at the neuromuscular junctions by BoNTs induces a flaccid paralysis, whereas TeNT-dependent inhibition of glycine or GABA exocytosis in inhibitory interneurons results in spastic paralysis. Botulism is mainly acquired by ingestion of preformed BoNT in food, but it may also occur subsequently to intestinal or wound colonization by C. botulinum. Tetanus essentially results from a wound contamination by C. tetani. BoNT/A is the most potent toxin with a long activity duration in neurons, and it is also a therapeutic agent widely used to treat hypercholinergic diseases including localized muscle spasticity, dystonia, autonomic dysfunctions (hyperhidrosis, hypersalivation), and also pain such as migraine headaches.
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Popoff, M.R., Mazuet, C., Poulain, B. (2013). Botulism and Tetanus. In: Rosenberg, E., DeLong, E.F., Lory, S., Stackebrandt, E., Thompson, F. (eds) The Prokaryotes. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30144-5_97
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