Bovis ISSN 2398-2993

Organophosphate insecticide poisoning

Synonym(s): OP toxicity

Contributor(s): Nicola Bates , Alan Murphy

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Introduction

  • Cause: exposure, usually dermal or oral, to organophosphate insecticide.
  • Signs: hypersalivation, ataxia, respiratory distress, muscle fasciculation, weakness, bradycardia and convulsions. 
  • Diagnosis: based on clinical signs, history of exposure and laboratory findings.
  • Treatment: supportive care with atropine administration.
  • Prognosis: good in animals with mild signs; poor in animals with severe neurological signs. 

Pathogenesis

Etiology

  • Organophosphate insecticide poisoning in cattle may occur in various circumstances.
    • Spills of pesticide near food stores or feeding areas.
    • Contamination of feed or water sources.
    • Animals breaking into storage areas and accessing pesticide products.
    • Using pour on ectoparasiticide products at incorrect concentration/dilution.
    • Overzealous use of spray products leading to inhalation and conjunctival contamination in poor environmental conditions (eg windy).
    • Use of agricultural products on animals in error.
    • Exposure from airplane dusting of insecticides.
    • Inappropriate disposal of empty pesticide containers or use of old insecticide containers as feed utensils.
    • Grazing in recently sprayed land or on land contaminated with spray drift.
    • Use of old products where the original organophosphate insecticide has decomposed to a more toxic compound.

Predisposing factors

General

  • The following may be at increased risk of poisoning:
    • Tired or stressed animals. 
    • Water-deprived animals.
    • Chilled animals.

Specific

  • Organophosphate insecticides have two main toxic effects: 
    1. Cholinesterase inhibition.
    2. Delayed neurotoxicity.

Cholinesterase inhibition

  • Organophosphate insecticides bind to and inhibit acetylcholinesterase resulting in accumulation of acetylcholine.
  • This results in central effects (as organophosphate compounds cross the blood brain barrier), nicotinic and muscarinic effects:
    • Muscarinic effects usually occur first with bronchial constriction and increased mucous secretion. In the gut there is increased peristalsis and salivation. These signs are commonly referred to by the acronyms: 
      • SLUDGE: salivation, lacrimation, urination, defecation/dyspnea, gastrointestinal upset and emesis (in animals that can vomit).
      • DUMBELS: diaphoresis/diarrhea, urination, miosis, bradycardia, bronchospasm/bronchorrhea, emesis/excess lacrimation and salivation.
    • Nicotinic effects involve skeletal muscle responses with twitching, tremor, seizures, weakness and paralysis. 
  • Spontaneous reversal of enzyme inhibition by organophosphate insecticides can occur depending on the compound involved. 
    • This occurs after hydrolysis of the phosphorylated cholinesterase. 
  • Some compounds, however, undergo ‘aging’ where the phosphorylated enzyme is very stable (and irreversibly inhibited). 
    • Recovery of cholinesterase activity occurs through synthesis of new enzyme. 
  • There are two antidotes to organophosphate insecticide poisoning:
    1. Atropine acts as a non-competitive antagonist by blocking the effect of the muscarinic receptors on target organs. 
    2. Oximes such as pralidoxime, accelerate the hydrolysis of the phosphorylated enzyme to reverse inhibition but have no effect on an ‘aged’ phosphorylated enzyme. 

Delayed neurotoxicity

  • Organophosphorus-induced intermediate syndrome (IMS):
    • Poorly described in animals, although it has been reported in humans, cats and dogs. 
    • It does not appear to have been reported in cattle; it was only recognized in humans in the 1980s. 
    • There is severe acetylcholinesterase inhibition but muscle fasciculations and hypersecretion associated with muscarinic receptor effects are absent.
  • Organophosphorus-induced delayed neurotoxicity (OPIDN):
    • This form of organophosphate poisoning is characterized by distal degeneration of axons of both the peripheral and central nervous systems and involves phosphorylation and then aging of neuropathy target esterase (NTE) in peripheral nerves.

Timecourse

  • Acute poisoning:
    • Variable, depending on the circumstances: 
      • It can be 15-30 minutes or 6-12 hours, sometimes 1-4 days after dermal exposure or days or weeks after low level chronic exposure.
    • In many incidents reported in cattle deaths began within hours of exposure.  
  • Organophosphorus-induced intermediate syndrome (IMS):
    • 2-4 days after apparent recovery from poisoning.
  • Organophosphorus-induced delayed neurotoxicity (OPIDN):
    • At least 8 days, usually 1-2 weeks but sometimes up to 4 weeks after exposure.

Epidemiology

  • Organophosphate insecticides are very widely used as pesticides.
  • In veterinary medicine they are used as ectoparasiticides and anthelmintics. 

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMed Resource.
  • Oliveira-Filho J C, Carmo P M S, Pierezan F, Tochetto C et al (2010) Intoxicação por organofosforado em bovinos no Rio Grande do Sul. [Poisoning by organophosphate in cattle in southern Brazil]. Pesquisa Veterinária Brasileira 30 (10), 803-806.
  • Castro, M B, Moscardini A R C, Reis J L Jr, Novaes E P F & Borges J R J (2007) Intoxicação aguda por diazinon em bovinos [Diazinon acute toxicosis in cattle]. Ciência Rural 37 (5), 1498-1501.
  • Sharpe R T, Livesey C T, Davies I H, Jones J R & Jones A (2006) Diazinon toxicity in sheep and cattle arising from the misuse of unlicensed and out-of-date products. Veterinary Record 159 (1), 16-19.
  • Khan O (2001) Organophosphate poisoning in a group of replacement heifers and dry cows. Canadian Veterinary Journal 42 (7), 561-3.
  • Braselton W E, Johnson J L, Carlson M P & Schneider N R (2000) Gas chromatography/mass spectrometry identification and quantification of isazophos in a famphur pour-on and in bovine tissues after a toxic exposure. Journal of Veterinary Diagnostic Investigation 12 (1), 15-20.
  • Frank R, Braun H E, Wilkie I & Ewing R (1991) A review of insecticide poisonings among domestic livestock in southern Ontario, Canada, 1982-1989. Canadian Veterinary Journal 32 (4), 219-26. 
  • Sanford SE (1991) Multiple organophosphate poisoning in a beef herd. Canadian Veterinary Journal 32, 626-627.
  • Meerdink G L (1989) Organophosphorus and carbamate insecticide poisoning in large animals. Veterinary Clinics of North America: Food Animal Practice 5 (2), 375-89.
  • Abdelsalam E B (1987) Organophosphorus compounds. 1. Toxicity in domestic animals. Veterinary Research Communications 11, 211-219.
  • Perdrizet J A, Cummings J F & de Lahunta A (1985) Presumptive organophosphate-induced delayed neurotoxicity in a paralyzed bull. Cornell Veterinarian 75,  401-409.

Other sources of information

  • Casarett & Doull's Toxicology: The Basic Science of Poisons. 8th Edition (2013).
  • Gupta R C (2007) Organophosphates and carbamates. In: Veterinary Toxicology, RC Gupta (ed). Amsterdam, Elsevier.
  • Oehme F W (1992) Agricultural and veterinary toxicology of acetylcholinesterases. In: Ballantyne B, Marrs T C (eds). Clinical and Experimental Toxicology of Organophosphates and Carbamates. Oxford, Butterworth Heinemann, pp 261-271.
  • Osweiler G, Carson T L, Buck W B, Van Gelder G A (1985) Clinical and Diagnostic Veterinary Toxicology, 2nd edition. Dubuque, Iowa, Kendall/Hunt Publishing Company, pp 298-317.
  • Radeleff R D (1970) Veterinary Toxicology, 2nd edition. Philadelphia, Lea & Febiger.
  • PPDB: Pesticides Properties DataBase: https://sitem.herts.ac.uk/aeru/ppdb/en/atoz.htm.

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