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Background: Metaldehyde is a toxic pesticide used mainly as a molluscicide, responsible for intoxication and deaths in both humans and animals. Accidental exposure to metaldehyde in dogs is considered rare, but severe. Data concerning clinical and veterinary forensic toxicology are largely incomplete, especially regarding case reports in dogs. The present work reports a complete and detailed description of a case from the history, clinical evolution, pathological exams and toxicological diagnosis in an accidental case of metaldehyde poisoning in dog., Case Presentation: An eleven-month-old, 3.0 kg, male German Spitz was presented for emergency care with acute vomiting and seizures 3 hours after suspected accidental ingestion of commercial molluscicide containing 3% metaldehyde (Lesmax®). The animal was in lateral recumbency and showed stuporous mentation, salivation, tonic-clonic status epilepticus, systemic tremors, bilateral miosis, absent palpebral, corneal, oculovestibular and gag reflexes, severely depressed spinal reflexes, dyspnea and tachycardia. Despite treatment, the patient progressed to comatose mentation and died. Necropsy examination revealed discrete lesions in the liver and central nervous system, while stomach examination revealed content of feed, activated charcoal and blue-green granules, compatible to the commercial formula of metaldehyde. Histology examination revealed extensive hemorrhage and severe centrolobular necrosis of the liver and tumefaction of Kupfer cells. Brain samples showed discrete hemorrhage and hyperemia. In order to confirm the diagnosis, samples from feces, stomach content, spleen, liver, heart, kidneys and brain were submitted gas chromatography analysis. Results confirmed the presence of metaldehyde in all samples. We describe clinicopathological abnormalities of a fatal case of metaldehyde poisoning in a dog, as well as postmortem diagnosis using gas chromatography., Conclusion: Metaldehyde poisoning is rarely reported, since the diagnosis is often difficult and the notifications scarce. To our knowledge, this is the first report describing clinical signs, pathological findings and chromatographic diagnosis. This report aims to contribute to the understanding of the pathogenesis of metaldehyde intoxication, to further explore veterinary forensic toxicology diagnosis.

A retrospective analysis of telephone enquiries to the Veterinary Poisons Information Service found 772 cases with follow-up concerning suspected metaldehyde slug bait ingestion in dogs between 1985 and 2010. Half the enquiries occurred in the summer months. The amount and strength of the slug bait ingested was rarely known. In 56, cases the quantity consumed was estimated and was on average 229.6 grams of bait. Clinical signs developed in 77.3 per cent of dogs; common signs were convulsions, hypersalivation, twitching, hyperaesthesia, tremor, vomiting, hyperthermia and ataxia. Only 4.6 per cent of dogs developed hepatic changes, and only one developed renal impairment. The average time to onset of signs was 2.9 hours post-ingestion, with 50.3 per cent of dogs developing effects within one hour. Increased muscle activity (twitching, convulsions) lasted on average 15.2 hours. Recovery time was reported in 61 cases and occurred on average at 39.3 hours. Common treatments were gut decontamination, anticonvulsants, anaesthetics and intravenous fluids. Of the dogs that were treated with sedatives, 45.8 per cent required more than one sedative or anaesthetic agent. Methocarbamol was rarely used, probably due to unavailability. The outcome was reported in 762 dogs; 21.7 per cent remained asymptomatic, 61.7 per cent recovered and 16 per cent of dogs died or were euthanased. Where known (only six cases), the fatal dose of bait ranged from 4.2 to 26.7 g/kg (average 11.8 g/kg).

The aim of the present study was to investigate if prolonged status epilepticus (SE), secondary to a chemoconvulsant, can induce spontaneous recurrent seizures in dogs. Clinical records at two UK referral hospitals were searched for dogs that presented in SE secondary to intoxication. Dogs were only included in the study if there was clear historical evidence of intoxication and a prolonged SE. Clinical and follow-up information was retrieved and verified by using a combination of clinical records from the two hospitals and the referring veterinarian and by contacting the owners using a telephone questionnaire. Twenty dogs met the inclusion criteria: 17 presented for metaldehyde toxicity, one for moxidectin toxicity, one for theobromine toxicity and one for mycotoxin toxicity. Of these 20 dogs, three dogs had an SE duration between 0.5 and one hour, four dogs between one and 12 hours, 10 dogs between 12 and 24 hours and three dogs greater then 24 hours. Median follow-up time for the 20 dogs was 757 days (range 66 to 1663 days). No dog had any further seizures after its SE. The present study supports the view that dogs with a prolonged SE following intoxication with the aforementioned toxins might not need long-term treatment with antiepileptic drugs after the SE has been controlled.

Objectives: To describe the clinical signs, clinicopathological abnormalities and outcome of metaldehyde intoxication in dogs., Methods: Medical records of dogs presenting between 1989 and 2005 with a diagnosis of metaldehyde toxicity were reviewed retrospectively. Data obtained from the medical record included signalment, history, clinical signs, laboratory tests results, hospitalisation period length, treatments and outcome., Results: Eighteen dogs fulfilled the inclusion criteria. The most prevalent clinical signs were seizures, hyperthermia, tachycardia and muscle tremors. Serum biochemistry abnormalities included increased serum muscle enzymes activities, acidaemia (six dogs) and decreased blood bicarbonate (eight dogs). Treatment was symptomatic and supportive. Hyperbilirubinaemia was observed in two dogs. Diazepam was the most commonly used anticonvulsant followed by phenobarbitone and pentobarbital. General inhalant anaesthesia was required in nine of 18 dogs with seizures unresponsive to anticonvulsants. The survival was 83 per cent (15 of 18 dogs)., Clinical Significance: This clinical study recorded, for the first time in the veterinary literature, several clinicopathological abnormalities from severely intoxicated dogs. Metabolic acidosis was common, while acute or delayed hepatotoxicity was an uncommon complication.

In 1975, the California Department of Food and Agriculture required registered manufacturers of snail and slug baits to present data showing the unattractiveness of these products to dogs, in order to reduce the number deaths in dogs due to poisoning by eating these baits. A cooperative project involving the University of California, the California Department of Food and Agriculture, and the snail and slug bait manufacturers was designed to assist the manufacturers in assessing the palatability of their products by dogs and to develop criteria for the regulatory agencies to use to ensure that the products they were registering were unattractive to dogs. The studies showed that most recently formulated baits were relatively unpalatable for dogs. A 2-panel consumption testing procedure was developed and is being used by the California Department of Food and Agriculture and the Environmental Protection Agency as criteria for registration. Current reports indicate a dramatic decrease in snail and slug bait poisonings in California after these criteria were established as requirements for registration of snail and slug baits.

Snail and slug baits were the most common cause of poisoning in dogs and cats in a survey of 34 veterinary practices. During a 7-month period, 280 dogs and 12 cats were poisoned by metaldehyde (57%) or methiocarb (43%) containing baits with case fatality rates of 8.1% and 9.1% in dogs and 16.7% and 50% in cats, respectively. The ages of poisoned dogs ranged from 2 months to 17 years and cats from 3 months to 5 years. There was no decrease in frequency of poisoning or case fatality rate demonstrated with increasing body size in dogs. Poisoning was most frequent in the month of October. Baits were eaten off the ground or obtained from storage areas, often despite a variety of preventive measures. It is suggested that these products should be reformulated to make them less attractive to domestic pets.