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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

  • nonspecific

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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Last Modified: Tuesday 08 July, 2008
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