Botulinum neurotoxins tissues

Miyake M, Ohishi I (1987) Response of tissue-cultured cynomolgus monkey kidney cells to botulinum C2 toxin. In Microbial Pathogenesis. 3 279-86 Montecucco C, Schiavo G (1994) Mechanism of action of tetanus and botulinum neurotoxins. In Molecular Microbiology. 13 1-8 Muller H, von Eichel-Streiber C, Flabermann E (1992) Morphological changes of cultured endothelial cells after microinjection of toxins that act on the cytoskele-ton. In Infect Immun. 60 3007-10... 

So far eight different botulinum toxins (A, B, Cl, C2, D, E, F, G) have been described which are produced by various strains of Clostridium botulinum (1). Whereas seven of the botulinum toxins are neurotoxins and block the release at the cholinergic synapses, botulinum C2 toxin is not neurotoxic and acts on various non-neuronal tissues (1-3). It has been shown that component I of the binary botulinum C2 toxin possesses ADP-ribosyltransferase activity (4) on the eukaryotic substrate non-muscle actin (5). Here we describe another ADP-ribosyltransferase which is produced by certain strains of Clostridium botulinum type C. In order to distinguish the novel ADP-ribosyltransferase from botulinum neurotoxin Cl and botulinum C2 toxin we termed this enzyme C3. 

The mechanism whereby the bacteria produce the disease with its attendant symptoms is often due to the cells ability to produce specific poisons, toxins or aggressins (Chapter 14). Many of these are tissue-destroying enzymes which can damage the cellular structure ofthe body or destroy red blood cells. Others (neurotoxins) are highly specific poisons ofthe central nervous system, for example the toxin produced by Clostridium botulinum is, weight for weight, one ofthe most poisonous substances known. 

A-B Toxins are bacterial toxins composed of two peptide chains one (B) that binds to the invaded cell surface, and the other (A) containing the toxin which is then taken-up into the cell. Some examples of exotoxins secreted by the bacteria into the surrounding medium and highly toxic to certain tissues are pathogens causing botuiism (Clostridium botulinum), tetanus (Clostridium tetani) and diptheria (Corynebacterium diphtheria. An example of an A-B endotoxin is Vibrio cholerae. Botulinum toxin and tetanus toxin have their main toxic actions on neuronal tissues, so are described at NEUROTOXINS. 

These are generally extracellularly liberated proteins, some of which are among the most potent tissue poisons known. Classic examples include botulinum, tetanus, diptheria and Shigella neurotoxins less potent are the haemolysins and leucocidins, produced by various streptococcal and staphylococcal species, which destroy red and white blood corpuscles, respectively. It is suggested that plaque bacteria may produce similar exotoxins although no substances specifically responsible for periodontal disease have been identified. 

Plants are not the only organisms that produce such environmentally transmittable toxins. A number of different bacterial species produce exotoxins, which are chemicals that, once secreted, act at a site removed from the bacterial growth. Exotoxins are usually proteins that interact with host cells, producing a wide variety of responses, and most exotoxins act at tissue sites remote from the bacteria that produce them. Many of these exotoxins cause disease, and some well-known and historically devastating diseases, such as botulism, diphtheria, and tetanus, are caused not by the bacteria themselves but rather by the exotoxins that they secrete. A perfect example of this phenomenon are the neurotoxins produced by the bacteria Clostridium botulinum. 

NEUROTOXIN. A toxin that acts specifically on nervous tissues. Examples include aconitine, botulinum toxin (BTX), and the venom of black widow spiders. 

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