Organophosphorus and carbamate insecticide poisoning in large animals

Organophosphorus and carbamate insecticides are used commonly in agriculture to control pests of crops and animals. These compounds are toxic and livestock poisoning has occurred from mistaken addition of unused insecticide to feeds and animal access to improperly disposed of materials or "empty" containers. The morbidity rate approximates a third of animals exposed and about half of those affected die. Organophosphorus and carbamate insecticides generate their toxic effects by bonding to and inhibiting ChE enzymes (most importantly, AChE), which are responsible for breaking down the neurotransmitter ACh. The accumulation of ACh results in uninhibited impulse transmission at the cholinergic endings, including autonomic preganglionic junctions, certain neurons in the central nervous system, and motor nerves to the skeletal muscles. This eventually leads to fatigue of end organs; death usually is a result of respiratory failure. The "delayed neuropathy syndrome" is caused by some OP insecticides, but the pathophysiology of this syndrome does not involve the inhibition of ChE and accumulation of neurotransmitter. Over 100 anticholinesterase insecticides are in use. Variations in toxicity exist among these compounds, but larger diversities exist in the likelihood of poisoning because of differences in formulations, solvents, and conditions of use. Young animals usually are more sensitive than adults. Some of these agents are among the most toxic of manmade chemicals. These insecticides generally do not accumulate in tissues. The "chronic" effects depend on accrued physiological changes from frequent exposure to nonlethal doses. Clinical signs occur within minutes to a few hours and include the muscarinic signs of salivation, excessive lacrimation, frequent urination, and diarrhea. Concurrent nicotinic effects include muscular tremors followed by weakness and paralysis. Topical exposure results in similar poisoning but the onset of clinical signs may be delayed. Certain pour-on insecticides may cause a delayed (more than a week) syndrome in some breeds. Diagnosis of OP or carbamate insecticide poisoning is made by (1) interpretation of clinical signs and history that are consistent with this poisoning, (2) detection of the chemical compound in stomach or rumen contents and tissues, and (3) demonstration of the adverse biological effect, ChE inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)