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Methiocarb toxicity
Synonym(s): Carbamate, methiocarb, thiocarbamates
Introduction
- Methiocarb is a carbamate pesticide used as an insecticide, acaricide, molluscicide and bird repellent.
- LD50 of methiocarb is 25 mg/kg in the dog.
- Mechanism of poisoning similar to organophosphate poisoning.
- Signs: hypersalivation, vomiting, tremor and convulsions.
- Diagnosis: history, clinical signs.
- Treatment: atropine to effect. Control nervous signs with diazepam (valium). Do not administer barbiturates or other cardiorespiratory depressants.
- Prognosis: excellent if treated early.
Presenting signs
General- Deliberate poisoning is common, with microgranules concealed in meat-based baits.
- Abdominal pain, hypersalivation, vomiting and diarrhea.
- Lacrimation.
- Dyspnea +/- coughing.
- Fine muscle tremors, ataxia.
- Clonic seizures.
Acute presentation
- Hypersalivation.
- Urination and diarrhea.
- Sudden collapse.
- Respiratory distress.
- Death.
Geographic incidence
- Accidental poisoning more common in rural areas.
- Methiocarb molluscicides were banned in the UK and EU in 2015.
Pathogenesis
Etiology
- Exposure to methiocarb, a carbamate pesticide Carbamate poisoning.
Pathophysiology
- Carbamates are cholinesterase inhibitors → accumulation of acetylcholine → muscarinic and nicotinic effects of acetylcholine.
- Death, when it occurs, is due to respiratory failure.
- Rapid absorption by all routes, with rapid distribution.
- Increase in all body secretions, including hypersalivation, lacrimation and an increase in pulmonary secretions.
- Vomiting and diarrhea.
- Abdominal pain due to increased peristaltic activity.
- Incontinence due to relaxation of the sphincters.
- Miosis, sometimes very prominent.
- Bronchial constriction.
- Predominantly neuromuscular.
- Muscle fasciculations beginning at the head and neck, and progressing caudally.
- Muscle stiffness.
- Weakness progressing to paresis and paralysis.
- Clonic spasms.
- Depression.
- Convulsive episodes.
- Coma.
Timecourse
- Signs of poisoning occur soon after ingestion or exposure to the poison.
- The inhibition of cholinesterase by carbamates is reversible and does not last as long as with organophosphate insecticides Organophosphorus insecticide poisoning.
- Death due to respiratory failure may occur within a few hours to several days (according to the compound involved).
- Occasionally → rapidly fatal asphyxia.
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.
- Tinson E, Boller E & Davis M (2017) A suspected case of intermediate syndrome in a dog with carbamate toxicosis. Aust Vet J 95, (6), 201-206 PubMed.
- Corfield G S, Connor L M, Swindells K L et al (2008) Intussusception following methiocarb toxicity in three dogs. J Vet Emerg Crit Care 18 (1), 68-74 VetMedResource.
- Studdert VP (1985) Epidemiological features of snail and slug bait poisoning in dogs and cats. Aust Vet J 62, (8), 269-71 PubMed.
- Udall ND (1973) The toxicity of the molluscicides metaldehyde and methiocarb to dogs. Vet Rec 93 (15), p420-2 PubMed.
Other sources of information
- Talcott PA (2024) Organophosphorus and Carbamate Anticholinesterase Pesticides. Blackwell’s Five-Minute Veterinary Consult Clinical Companion. Small Animal Toxicology. 3rd edn. Wiley USA, pp 633-638.
- Dalefield R (2017) Veterinary Toxicology for Australia and New Zealand pp 89-93.
- Peterson ME and Talcott PA (2006) Small Animal Toxicology 941-955.
- Plumlee KH (2004) Clinical Veterinary Toxicology pp 178-180.
- Lorgue G, Lechenet J & Reviere A (1966) Clinical Veterinary Toxicology. pp 66-68.
Organisation(s)
- ASPCA Animal Poison Control Center. Website: www.aspca.org.
- Veterinary Poisons Information Service (VPIS). Website: www.vpisglobal.com.