Toxins botulinum

BOTULINUM TOXIN TYPE A (Botox powder for injection) 

Blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylchohne. Produces temporary chemical denervation of sweat glands and local reduction in sweating when injected intrader-mally. Botulinum toxin type A is indicated in the treatment 

BOTULINUM TOXIN TYPE B (Myobloc solution, injectable 5000 units/mL) 

Botulinum toxin type B interferes with neurotransmitter release by cleaving synaptic vesicle-associated membrane protein. It is indicated in reduction of severity of abnormal head position and neck pain in adult patients with cervical dystonia. 

The integration of bomlinum toxin into the orbicularis muscle can cause reduced blinking and lead to corneal exposure and ulceration. 

This chapter deals with botulinum toxin type A (BOTOX) in the treatment of strabismus, blepharospasm, and related disorders. Botulinum toxin type A (BOTOX) has been used to treat strabismus, blepharospasm, Meige s syndrome, and spasmodic torticollis. By preventing acetylcholine release at me neuromuscular junction, botulinum toxin A usually causes a temporary paralysis of the locally injected muscles. The variability in duration of paralysis may be related to me rate of developing antibodies to me toxin, upregulation of nicotinic cholinergic postsynaptic receptors, and aberrant regeneration of motor nerve fibers at me neuromuscular junction. Complications related to this toxin include double vision (diplopia) and lid droop (ptosis). 

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Clonal Selection Clostridial Neurotoxins Clostridium Botulinum Toxin Clotting CNTF... 

Botulinum antitoxin Neutralizatien ef the lethal effects of botulinum toxins A, B and E in mice SOOlUmI- eftypeA 5001U mM ef Type B 50IU ml- ef Type E... 

There are reports of the benefits of botulinum toxin in the treatment of cerebral palsy in children. The toxin, produced by Clostridium botulinum, is a powerful and deadly poison, but is also an effective muscle relaxant. It is not licensed for use as such in the UK but is undergoing clinical trials. Current evidence suggests that repeat injections are necessary some 4-6 months after the first. 

Much evidence supports a role for these proteins in exocytosis. For instance, injection of recombinant SNAP into the squid giant axon increases vesicular exocytosis. Also, membrane SNAP-25 and syntaxin are both targets for botulinum toxin while the vesicule protein, synaptobrevin, is a target for tetanus and botulinum toxins both these toxins are well known for disrupting transmitter release. 

MS patients usually have upper motor neuron spasticity. This type of spasticity cannot be treated with muscle relaxants such as carisoprodol. MS patients must be treated with agents specific for upper motor neuron spasticity (Table 26—8).48 MS spasticity is classified as focal or generalized. If the spasticity primarily involves only one muscle group, it is focal and may benefit from botulinum toxin administration.11 Systemic medications are used for generalized spasticity. No clear conclusion can be reached regarding the superiority in efficacy of one antispasticity agent over another medication selection is usually based on adverse effects (see Table 26-8).11,48... 

Focal spasticity Botulinum toxin Prevents release of acetylcholine in the neuromuscular junction Individualized... 

Botulinum toxin Descending muscle weakness/paralysis 18 to 36 hours... 

Toxins (typically high molecular weight proteins), such as botulinum toxin, ricin, or Staphyloccocal enterotoxin (SEB) or T-2 toxin (which actually is a small molecule). 

Bacteria, viruses, and rickettsiae have similar symptom progressions in that exposure is followed by a period of reproductive growth (often nonsympto-matic) in the body. As their numbers increase, they often eventually overcome the immune system. Many produce toxins that interfere with bodily functions. Purified toxins such as botulinum toxin (produced by the Clostridium botulinum bacteria) act in a similar manner to chemical agents since, as complex chemical compounds, they do not reproduce but immediately interfere with bodily functions. However, most toxins are not absorbed through the skin, as... 

Representatives of medium-size analytes detected by affinity biosensors based on spectroscopy of guided modes include food-safety related analytes such as staphylococcal enterotoxin B , botulinum toxin, and E. coli... 

Delayed-action paralytic neurotoxins that block the release of acetylcholine causing a symmetric, descending flaccid paralysis of motor and autonomic nerves. Paralysis always begins with the cranial nerves. Toxins are obtained from an anaerobic bacteria (Clostridium botulinum). Toxin A is a white powder or crystalline solid that is readily soluble in water. It is stable for up to 7 days as an aqueous solution. All toxins are destroyed by heat and decompose when exposed to air for more than 12 h. 

Human toxicity values have not been fully established or have not been published. However, based on available information, this material appears to have approximately half as toxic as Botulinum toxins (C16-A005). 

David L. Swerdlow, and Kevin Tonat. "Botulinum Toxin as a Biological Weapon Medical and Public Health Management." Journal of the American Medical Association 285 (2001) 1059-70. 

Suggested Alternatives for Differential Diagnosis See Botulinum toxin (C16-A005). Mortality Rate (untreated) See Botulinum toxin (C16-A005). 

Suggested Alternatives for Differential Diagnosis Campylobacteriosis, cryptosporidiosis, cyclosporiasis, E. coli infections, Listeria monocytogenes, shigellosis, Vibrio infections, yersiniosis, ingestion of bacterial toxins such as staphylococcal enterotoxins or botulinum toxin. 

Synaptobrevins (VAMPs) Synaptogyrin Synaptophysins PKA but diverge C-terminally. Synapsins Ia/b contain C-terminal phosphorylation sites for CaMKII and CDK 5. Interact with microfilaments, neurofilaments, microtubules, SH3 domains, calmodulin and annexin VI in vitro. Small-membrane proteins that are cleaved by tetanus toxin and by botulinum toxins B, D, F and G. Polytopic membrane protein that is tyrosine-phosphorylated. Function unknown. Polytopic membrane proteins, including synaptoporin, that are tyrosine-phosphorylated and bind to synaptobrevins. May regulate SNARE function... 

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