Clinical Signs



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.



Diagnosis



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.



Treatment



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.

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