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Production Animal Clinical Toxicology
CNS Disorders: Organophosphates
Chemicals | Pathogenesis | Clinical Signs | Clinical Pathology | Necropsy | Diagnosis | Treatment
Return to Production Animal Clinical Toxicology Index
Chemicals
Compounds
- carbophenothion
- coumaphos
- diazinon
- dichlorvos
- fenthion
- malathion
- parathion
- trichlorphon
Sources
- used mainly as contact or systemic insecticides
Pathogenesis
- organophosphates are lipid soluble and are readily absorbed by all routes
- generally compounds are rapidly metabolised and excreted so subacute or chronic poisoning due to accumulation does not occur
- metabolism and excretion are complex and are dependent on:
- compound itself
- hepatic microsomes
- age of animal
- health of animal
- organophosphates bind with and phosphorylate cholinesterases
- reversal of the reaction is extremely slow
- the esterase is virtually permanently inhibited
- acetylcholine accumulates at synapses
- depending on site of accumulation clinical signs will mimic muscarinic, nicotinic and CNS actions of acetylcholine, i.e. overstimulation of the parasympathetic and post-ganglionic nerves of the sympathetic nervous system
Clinical Signs
- may occur within minutes to several hours
- initially muscarinic effects are observed
- hypersalivation, lacrimation, sweating
- nasal discharge
- myosis
- brachycardia (occasionally tachycardia)
- dyspnoea, coughing
- vomiting, diarrhoea, abdominal pain
- frequent urination
- nicotinic effects include:
- muscular fasciculation
- tetany, stiff-legged gait
- torticollis in cattle and sheep
- CNS effects
- nervousness and apprehension
- ataxia
- convulsions, coma
- death is usually due to respiratory failure or cardiac arrest and can occur 12-24 hours after onset of signs
- a delayed neurotoxicity may occur, from a slow centripetal degeneration of nerves
- reported in horses
- disturbances in proprioception leading to ataxia
- severe cases, peripheral neuropathy and paralysis
Clinical Pathology
- cholinesterase activity in red cells
Necropsy
Diagnosis
- history
- clinical pathology
Treatment
- atropine to abolish muscarinic effects
- pralidoxime (PAM) to combine with the bound organophosphate to regenerate the enzyme
- sedatives are contra-indicated
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