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Organophosphate compounds include some of the most toxic chemicals used in agriculture. Included in the organophosphate group are disulfoton, phorate, dimethoate, ciodrin, dichlorvos, dioxathion, ruelene, carbophenothion, supona, TEPP, EPN, HETP, parathion, malathion, ronnel, coumaphos, diazinon, trichlorfon, paraoxon, potasan, dimefox, mipafox, schradan, sevin, chlorpyrifos and dimeton. These insecticides are esters, amides, or simple derivatives of phosphoric and thiophosphoric acids. Some of the less toxic compounds are used as systemic insecticides in animals against internal and external parasites. These include chlorthion, thichlorphon, diazinon, fenchlorphos, and dichlorvos. The organophosphate insecticides can be grouped according to their toxic action on insects. Malathion, paraoxon, parathion, and potasan have an action similar to chlorinated hydrocarbons and act as contact poisons, while others such as dimefox, mipafox, and schradan are selective systemic insecticides which are absorbed into the plant sap and remain active for long periods of time. Selective systemic organophosphate insecticides are toxic to plant pests but not to their predators.
Transmission and Development
Organophosphate toxicity is due to the ability of these compounds to inhibit acetylcholinesterase at cholinergic junctions of the nervous system. These junctions include postganglionic parasympathetic neuroeffector junctions (sites of muscarinic activity), autonomic ganglia and the neuromuscular junctions (sites of nicotinic activity) and certain synapses in the central nervous system. Acetylcholine is the neurohumoral mediator at these junctions. Since acetylcholinesterase is the enzyme that degrades acetylcholine following stimulation of a nerve, its inhibition allows acetylcholine to accumulate and result in initial excessive stimulation followed by depression.
Some compounds have a direct effect on the inhibition of acetylcholinesterase while others such as parathion are converted in the liver to metabolites which inhibit acetylcholinesterase. In addition to the anti-acetylcholinesterase activity of these compounds, HETP has carcinogenic activity and mipafox causes demyelination in peripheral nerves, causing lesions which resemble those due to thiamine deficiency. Many of these compounds are excreted in milk and are able to cross placental membranes causing toxicity in offspring.
Organophosphate compounds vary greatly in their toxic capabilities and have the advantage over other types of insecticides in that they produce little or no tissue residues. All have a cumulative effect with chronic exposure causing progressive inhibition of cholinesterase. Liquid organophosphates are absorbed readily by all routes, although malathion, which is the least toxic of these chemicals, is only slightly absorbed through the skin.
Acute signs can result within 1-12 hours following inhalation or cutaneous absorption and more rapidly following ingestion. The clinical signs of organophosphate poisoning occur as a result of excess acetylcholine at nerve endings, which mimics hyperactivity of the parasympathetic nervous system. Signs relative to the alimentary tract include excess salivation, lacrimation, abdominal pain, vomiting, intestinal hypermotility, and diarrhea. The muscarinic effects of acetylcholine cause bronchoconstriction and an increase in bronchial secretions. The nicotinic effects of acetylcholine consist of involuntary irregular, violent muscle contractions and weakness of voluntary muscles. Death occurs as a result of respiratory failure.
Clinically affected animals may lose weight due to the inability to feed and drink because of muscular weakness. Clinical signs in birds include goose stepping, ataxia, wing spasms, wing droop, dyspnea (difficulty in breathing), tenesmus (spasm of anal sphincter), diarrhea, salivation, lacrimation, ptosis (drooping) of the eyelids, and wing-beat convulsions. Non-fatal cases usually recover within 48 hours. Susceptibility to organophosphate toxicity varies greatly among individuals of any species and can be increased by frequent repeated mild exposure which results in greater susceptibility due to exhaustion of the body's store of cholinesterase.
No definite postmortem changes are seen and when present, are usually secondary to the symptoms and include pulmonary edema, asphyxia, gastroenteritis, and rarely kidney and liver degeneration.
As postmortem findings are usually not revealing, diagnosis is usually made by laboratory analysis. The most reliable diagnostic test is the determination of the acetylcholinesterase level in red blood cells, but it must be performed on fresh samples. Acetylcholinesterase levels can be determined on red blood cells, whole blood or plasma. The analysis which is usually used is the detection of organophosphate degradation products in the stomach contents and liver and kidney tissue. Analysis of brain tissue for decreased acetylcholinesterase levels is also good if done within a few days following death.
If organophosphate toxicity is diagnosed, treatment with atropine and 2-PAM (2-pyridine aldoxime methiodide) can alleviate some of the symptoms. Decontamination of the skin, stomach and eyes of the animal may be necessary, along with symptomatic treatment and respiratory support.
Precautions should be taken to prevent drift or drainage of organophosphates to adjoining fields, pastures, ponds, streams or other premises outside the treated area.
Occasional organophosphate poisonings are seen in Michigan wildlife following exposure to recently treated areas. Diazinon intoxication in Canada geese, mallard ducks and wild turkeys is the most common organophosphate poisoning seen. Parathion poisoning in ring-billed gulls and disulfoton intoxication in a mallard, sevin poisoning in bees, and chlorpyrifos poisoning in a mallard have occurred as the use of organophosphates has increased. These deaths are usually sporadic and infrequent in occurrence.
As with any pesticides, precautions need to be taken to prevent human exposure and subsequent poisoning.
For questions about wildlife diseases, please contact the Michigan DNR Wildlife Disease Laboratory.
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