1080 poisoning in Dogs (Canis) | Vetlexicon
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1080 poisoning

ISSN 2398-2942


Synonym(s): Sodium monofluoroacetate toxicosis, SMFA poisoning

Introduction

  • Highly toxic pesticide, under strict control in the US and UK. Widely used in New Zealand and Australia by licensed authorities to control pest animals. Dogs are highly susceptible.

Presenting signs

  • Anxiety, frenzy, wild running, progression to tonic-clonic seizures.
  • Vomiting, urination and defecation.
  • Dyspnea.
  • Frothing at the mouth and nose.

Acute presentation

  • Frenzied or seizuring dog.
  • Dogs often cycle between frenzy and seizures.

Geographic incidence

  • 1080 poisoning of dogs is relatively common in some regions of New Zealand, where 1080 is spread from helicopters by the Department of Conservation for control of introduced Brushtail possums.
  • 1080 poisoning is relatively rare in the US where the use of the poison is highly regulated.
  • Recently, malicious poisoning of dogs using 1080 was reported in the USA.

Age predisposition

  • All ages affected.

Breed/Species predisposition

  • In New Zealand, most common in sheep-herding breeds since these dogs are in rural areas and allowed to run free as part of their work.

Public health considerations

  • Humans are at no risk from poisoned dogs, however the occurrence of 1080 poisoning in dogs reflects the presence of poisoned baits in the environment, which may represent a hazard to children.

Cost considerations

  • Treatment, although not highly expensive, is unlikely to be successful.

Pathogenesis

Etiology

  • Sodium fluoroacetate, also known as Compound 1080 is an odorless, colorless, tasteless poison used for control of rodents, rabbits and, in New Zealand, Brushtail possums.

Predisposing factors

General
  • Infestations of rodents, rabbits, possums, or other pest animals in the local area.
  • Dogs allowed to run free without supervision, or out of direct observation.
  • Dead target species pose the greatest risk to dogs, which may be poisoned by eating carcasses (secondary poisoning).

Pathophysiology

  • Fluoroacetate and its poisonous metabolite fluorocitrate are frequently present in vermin that have died of fluoroacetate poisoning.
  • Fluoroacetate is rapidly absorbed from the gastrointestinal tract. It combines with acetyl CoA to form fluoroacetyl CoA, which then combines with oxaloacetic acid to form fluorocitrate.
  • Fluorocitrate inhibits acontiase in the citric acid cycle, blocking the Kreb's (TCA) cycle. Cellular energy production and respiration are blocked. Citric and lactic acids accumulate causing an increased anion gap metabolic acidosis. Plasma ionized calcium complexes with citrate, leading to hypocalcemia. The heart and central nervous system are most severely affected by these changes.

Timecourse

  • Clinical signs are generally delayed at least 30 min, and up to 2 h, after ingestion, while fluoroacetate is absorbed and converted to toxic levels of fluorocitrate.

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 VetMedResource.
  • Goh C S, Hodgson D R, Fearnside S M, Heller J & Malikides N (2005) Sodium monofluoroacetate (Compound 1080) poisoning in dogs. Aust Vet J 83 (8), 474-479 PubMed.

Other sources of information

  • Parton K H (2003) Sodium Fluoroacetate in Clinical Veterinary Toxicology. Ed: Plumlee K H. Mosby.
  • Osweiler G (1996) Toxicology. Williams & Wilkins.

Organisation(s)