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Clinical presentation

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Clinical signs of acute organophosphate toxicity develop within minutes to hours depending on dose, route and toxicity of the compound and include:

• Muscarinic signs (associated with parasympathetic stimulation) such as hypersalivation, lacrimation, urination, increased gastrointestinal motility, defecation, bradycardia, dyspnoea and miosis;

• Nicotinic signs (associated with skeletal muscle stimulation) such as muscle fasciculations and tremors, which may result in a rigid stance and gait, and eventually weakness and paralysis;

• CNS signs including anxiety, restlessness, hyperactivity, obtundation to coma and generalized seizures.

All of the above clinical signs are not necessarily seen in every case and variability depends on toxicant type, dosage, formulation, route of exposure, poisoned species and stage of intoxication. Cats are generally more susceptible to AChE inhibitors than dogs. Death from either organophosphates or carbamates is associated with respiratory dysfunction resulting from respiratory tract secretions, bronchiolar constriction, intercostal and diaphragm muscle paralysis and CNS-mediated respiratory paralysis.

The intermediate and chronic (also named organophosphate-induced delayed neuropathy) syndromes are characterized by generalized neuromuscular weakness. The reader is referred to other textbooks for further information on these syndromes that are not characterized by seizures.

Canine and Feline Epilepsy

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