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**Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
**Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
*Pathogenesis:
*Pathogenesis:
**Endospores introduced via damaaged tissues e.g. penetrating wounds
**Endospores introduced via damaged tissues e.g. penetrating wounds
**Anaerobic conditions in the damaged tissue creates an anaerobic environment, allowing germination of spores
**Damaged tissue creates an anaerobic environment, allowing germination of spores
**Tetanospasmin made by bacteria replicating in damaged tissue
**Tetanospasmin made by bacteria replicating in damaged tissue
**Absorbed toxin affects neuromuscular junction distant from site of toxin production
**Absorbed toxin affects neuromuscular junction distant from site of toxin production
**Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
**Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
**Toxins transported to terminals of inhibitory neurons where they block transmission of signals
**Toxins transported across synapse to terminals of inhibitory neurons where they block transmission of signals
**Spastic paralysis results
**Spastic paralysis by constant tensing of muscles results
**Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
**Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
*Clinical signs:
*Clinical signs:
===''Clostridium botulinum''===
===''Clostridium botulinum''===
*
*Ubiquitous organism
*The toxin also causes [[Muscles - degenerative#Botulism|botulism]]
*Oval, subterminal endospores; spores survive boiling for hours
*Toxin produced in decaying organic matter absorbed from GIT into the blood and affects neuromuscular junction
*Causes [[Muscles - degenerative#Botulism|botulism]], a potentially fatal intoxication
*Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
*Intoxication on ingestion and absorbtion of toxin from GIT into the blood
*Occasionally germination of spores in wounds or GIT
*Neurotoxin carried to peripheral nervous system
*Toxin binds gangliosides irreversibly at the neuromuscular junction
*Blocks release of acetylcholine
*Flaccid paralysis and death
*Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
*Toxoid vaccine
*Implicated in [[Intestines - physical disturbances#Equine dysautonomia, or grass sickness|equine grass sickness]]
*Implicated in [[Intestines - physical disturbances#Equine dysautonomia, or grass sickness|equine grass sickness]]