Botulinum Toxin is categorized as a neurotoxin. Having a fatal dose of merely one to two micrograms it is considered one of the most lethal neurological agents known. The toxin is a microbial product synthesized by an anaerobic, gram-positive, spore-forming bacteria Clostridium botulinum whose natural habitat is soil (Qiagen). There are seven antigenically distinguishable exotoxins differentiated by the use of the prefix BoNT followed by the letters A-G. Although each has a slightly different protein structure, the mechanism of action is fundamentally the same.
There are four main categories in which humans acquire the neurotoxin, three of which can be deadly if not diagnosed and treated promptly. The three organic routes of acquisition include …show more content…
It is a zinc-dependent protease that cleaves soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (SNARE) proteins, most notably Syntaxin, SNAP 25 and Synaptobrevin. The seven different serotypes of botulinum toxin have affinities for different SNARE proteins. These SNARE proteins are vital for the synaptic vesicles filled with Acetylcholine to dock to the terminal of the neuromuscular junction when an impulse is received. The vesicles then fuse and release the Acetylcholine into the synaptic cleft. Acetylcholine binds to ligand-gated ion channels, opening them and initiating muscle contraction. By cleaving the SNARE proteins, the entire process is disrupted and paralysis of the myosin filaments …show more content…
This can take anywhere from 12-20 weeks. Axonal sprouting and endplate elongation occurs, but is believed to be a transient phenomenon not responsible for the termination of the Botulinum Toxin effect (Dressler). Antitoxins are available for injection shortly after symptoms occur that can aid in prevention of further effect but will not reverse paralysis that has already
There are four main categories in which humans acquire the neurotoxin, three of which can be deadly if not diagnosed and treated promptly. The three organic routes of acquisition include …show more content…
It is a zinc-dependent protease that cleaves soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (SNARE) proteins, most notably Syntaxin, SNAP 25 and Synaptobrevin. The seven different serotypes of botulinum toxin have affinities for different SNARE proteins. These SNARE proteins are vital for the synaptic vesicles filled with Acetylcholine to dock to the terminal of the neuromuscular junction when an impulse is received. The vesicles then fuse and release the Acetylcholine into the synaptic cleft. Acetylcholine binds to ligand-gated ion channels, opening them and initiating muscle contraction. By cleaving the SNARE proteins, the entire process is disrupted and paralysis of the myosin filaments …show more content…
This can take anywhere from 12-20 weeks. Axonal sprouting and endplate elongation occurs, but is believed to be a transient phenomenon not responsible for the termination of the Botulinum Toxin effect (Dressler). Antitoxins are available for injection shortly after symptoms occur that can aid in prevention of further effect but will not reverse paralysis that has already