The bacteria replicate in the anaerobic environment formed within the wound and release the exotoxin tetanospasmin. Tetanospasmin then diffuses into the blood vessels where it spreads throughout the body. Tetanospasmin has an affinity for neural where it acts to inhibit release. This causes unopposed muscular contraction and tetanic spasm. Predispositions are horses that have suffered from a deep wound, especially puncture wounds, castration, tail docking and tooth abstraction. Clinically tetanus is seen as spasm and of the muscles. This pattern of muscular contraction causes a stiff gait, trismus (lock-jaw), facial spasms, stiff and elevated carriage of the neck and tail, opisthotonos (saw-horse stance), pricked ears, flared nostrils, prolapse of the 3 rd eyelid, sweating, increased blood pressure, respiratory rate, temperature and heart rate, dysphagia, seizure and death due to . Diagnosis for tetanus can be made by the clinical signs and symptoms, and through serology and culture. Treatment is the administration of tetanus , which provides short-term, passive immunity. If the antitoxin is administered before there are signs of systemic infection there is a good prognosis and the individual is not likely to develop clinical signs of disease. If antitoxin is not administered until tetany has developed, the prognosis is guarded to poor. Animals showing clinical signs of disease require extensive supportive care including catheterization, feeding tubes and the maintenance or artificial airways. Tetanus can be prevented by annual vaccination. It is especially important to vaccinate horses against tetanus as the species is especially vulnerable to the effects of tetanus exotoxin. Prognosis is poor. Mortality rate is 50-75%. Those who can survive the 1 st week tend to make a full recovery with no lasting effects.
Botulism
Botulism is the most powerful known biological agent. The exotoxin produced by the anaerobic Clostridium botulinum bacteria is a powerful neurotoxin that attacks the - junction. This toxin binds to the axon terminal of the presynaptic cell and inhibits the release of from the motor neuron causing paralysis of the target muscle. Once the toxin is bound it cannot be removed, making the paralysis permanent. The only method of restoring function to the neuromuscular junction is for the axon terminal to be removed and regenerated. Axon regeneration is a slow process and in many cases it does not occur.
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