Metaldehyde is a commonly used slug bait in the domestic garden situation. It has also been used as a portable solid fuel (meta fuel) for certain kinds of camp stoves, has been registered as an anaesthetic, and is a common toxin associated with accidental and malicious poisonings of pet animals.
Metaldehyde (or metacetaldehyde) is produced by the polymerization of acetaldehyde by a solution of ethanol, in the presence of acid. Most commercial formulations of slug bait contain approximately 3% metaldehyde and are presented as liquid, pelleted, flake or granule preparations. Most of these preparations incorporate a green or blue dye.
NB: Slug and snail baits may contain metaldehyde, methiocarb or Iron EDTA. It is imperative that the veterinarian ask which product/ingredient the animal has ingested as the treatment is different for each poison.
Toxicity in all species has been reported but dogs, cats and poultry have more exposure to metaldehyde due to environmental circumstances, and the fact that these particular animals find the pellets extremely attractive.
Unfortunately the ingredients of the slug pellets (soyabean meal, apples, rice, sorghum and oats) increase their palatability.
Alamask, an animal repellant for use in slug bait formulations has been approved since 1981. Bitrex is another deterrent added to slug and snail baits. However repellants are not a total deterrent.
The lethal dose of metaldehyde varies greatly between and within a given species. This variation is thought to relate to the rate of degradation of the metaldehyde polymer and hence the quantity of toxic fragments. Gastric acid (hydrochloric acid) speeds up the decomposition of metaldehyde, as does storage of metaldehyde compounds in soldered tin plate containers. Ducks are thought to be more susceptible than chickens because metaldehyde moves down their digestive tracts faster.
Oral lethal dose of metaldehyde for various species (mg/kg bodyweight)
| Dog | 60-1000 |
| Cat | 207 |
| Chickens | 2000 |
| Ducks | 500 |
| Rabbits | 290-1250 |
| Goat | 780 |
| Donkey | 360 |
| Horse | 60-360 |
| Cattle | 200 |
| Sheep | 300 |
| Human | 100 |
| Rat | 227 |
Fish Toxicity 9hr LD50 (ppm).
| Rainbow trout | 62 |
| Bluegill | 10 |
Most commercially available slug bait poisons contain approximately 3% metaldehyde.
The exact mechanism of toxicity is unknown. Metaldehyde is rapidly hydrolysed to acetaldehyde by gastric acid (dog and cat). Fragments of the polymer and acetaldehyde are readily absorbed from the gut and render hepatic enzymes incapable of detoxification. The resulting intoxication produces gastrointestinal irritation and brain damage causing loss of consciousness with depression of the medullary respiratory centre and vasomotor control centres.
Metaldehyde has been reported to decrease the concentration of serotonin (5 hydroxytryptamine) and gamma amino butyric acid (GABA) in the brain. Loss of GABA allows signs of excitation. As the levels of GABA decreased so did the survival rates.
The clinical signs of poisoning which are similar in the various mammalian species usually occur from within minutes to three hours following ingestion of the chemical. Initially these include; depression, vomiting, increased respiration, tachycardia, profuse salivation and watery diarrhoea. As intoxication progresses there may be muscle tremors, incoordination leading to continuous convulsions or CNS depression and narcosis. Seizures are not provoked by external stimuli in dogs, but may be in cats. Cyanosis, acidosis, loss of consciousness and hypothermia usually follow the convulsions.
Hypersalivation, hyperaesthesia, nystagmus, tremors and convulsions are characteristic signs in the dog. There is also incoordination, increased respiratory rate, pulse rate and loss of consciousness. Death is due to respiratory failure.
These species appear to be susceptible to metaldehyde poisoning. Clinical signs specific for them include fractious behaviour, colic, profuse sweating and hypothermia. Hyperaesthesia of sudden onset has been reported in two horses that had access to spilled metaldehyde pellets. Other clinical signs reported in horses include: mild leg tremors, diarrhoea, hyperpnoea, tachycardia, clonic spasms, incoordination, head extension and convulsive spasms.
Nystagmus is a characteristic sign in the metaldehyde intoxicated cat. Clonic convulsions may be stimulated by external stimuli. Depression, dyspnoea, convulsions and tachycardia have been reported.
This species demonstrates predominantly nervous signs, particularly headpressing, epileptiform convulsions and nystagmus. Tremors of all limbs, ataxia and cyanosis have been reported.
Cattle tend to show severe ascending convulsions. The convulsions may become severe enough to cause affected animals to fall directly forwards. Hypersalivation, diarrhoea and inability to rise are also recorded. Other clinical signs may include: tremors, cyanosis, loss of blink “reflex” and blindness.
Ducks manifest incoordination, dyspnoea, polypnoea, tremors and torticollis. Turkey poults either die suddenly in brief terminal convulsions, or die following a prolonged comatose state.
The prognosis for the animal may be related to the depth of narcosis. If the agent produces narcosis beyond a medium depth, the animal will probably die due to respiratory failure. However if the narcosis is less deep, there will be a slow recovery over 24 36 hours, unless there is latent liver and kidney damage leading to delayed death after 1 3 days. Unusual sequelae associated with recovery from metaldehyde poisoning in the dog include chronic diarrhoea, memory loss and temporary blindness. It was postulated that haemorrhage, producing pressure upon the optic nerve was a cause of this blindness. Poor blood clotting is not a reported common symptom of metaldehyde poisoning, but this feature has been reported in dogs and was a necropsy finding following intoxication in cattle. Other complications of methiocarb and metaldehyde intoxication include; aspiration of vomitus, persistent diarrhoea, intussusception and gastric dilation. The incidence of complications is higher following poisoning with methiocarb than with metaldehyde.
Postmortem examinations may reveal congestion, hyperaemia and interstitial haemorrhages in the liver, kidney and lungs. Haemorrhages in the gastrointestinal mucosa, endocardium and lymph nodes have also been reported and pulmonary oedema with froth in the trachea and bronchi is commonly seen. In cattle blood may fail to clot.
Metaldehyde bait may be visible in the stomach and the stomach contents may emit a characteristic formaldehyde like (acetaldehyde) odour.
Microscopic lesions are nonspecific, but include hepatic swelling and degeneration, and neuronal degeneration in the brain.
Suitable specimens include whole blood, serum, liver and stomach contents/vomitus (100g).
Demonstration of the presence of aldehydes in the stomach contents or vomitus is based on a reaction between secondary aliphatic amines, sodium nitroprusside and aldehydes. A quantitative analysis of the aldehydes is not a useful indicator of the severity of poisoning as the rate of liberation of aldehydes from metaldehyde, and the absorption of toxic fragments of the polymer by the animal, will vary. This is complicated by not knowing which fragments of the metaldehyde polymer are toxic. Detection of aldehydes on analysis must be considered alongside the clinical and pathological findings, as significant acetaldehyde levels may be present in decomposing carcasses.
There is no specific antidote to metaldehyde. The treatment instituted is symptomatic, designed to remove the poison, control the convulsions and spasms and support the body systems involved in the intoxication.
If the animal is convulsing, diazepam should be given iv to effect (usually 0.5-5mg/kg). This usually only lasts about 20 minutes, and animals quickly become tolerant to repeated doses. Phenobarbitone iv to effect (usually 3-6mg/kg in dogs and cats, up to 20mg/kg in foals) is usually necessary following diazepam. If an iv preparation of phenobarbitone is not available, pentobarbitone can be used (15-25mg/kg). If all else fails, thiopentone will work, but only at anaesthetic doses.
The use of a variety of drugs has been reported in different species: sedative doses of diazepam, methocarbamol, acepromazine or pentobarbitone in dogs; diazepam, acepromazine or thiobarbituates in cats; and acepromazine plus xylazine in horses.
Good success in recovery has been reported by using large doses of acepromazine (up to 1.0 mg/kg), repeated until the animals are slightly hyperaesthetic, but still conscious and in control of vital reflexes.In rare instances, this may cause twitching resembling convulsions and is not recommended. If the muscle relaxant methocarbamol can be obtained, it can be useful (Robaxin inj. 0.55-2.2 ml/kg or Robaxin tabs. 132 mg/kg initial, maintenance 55-132 mg/kg day).
General anaesthesia, usually with pentobarbitone, should only be used to control severe convulsions. The animal should be anaesthetised as lightly as possible. It is extremely important to maintain an open airway and provide artificial ventilation and oxygen if required. Any anaesthesia should be allowed to periodically wear off, so that the the animal can be reevaluated.
Stomach contents should be removed by emesis using xylazine (cats) or apomorphine (dogs) if the animal is fully conscious and not showing any convulsive tendencies or respiratory depression. Otherwise gastric lavage under anaesthesia and activated charcoal or liquid paraffin and a laxative may be required to remove the material.
Fluids and sodium bicarbonate should be administered to promote urine flow and combat acidosis as necessary. Glucose or calcium gluconate may be indicated for possible liver damage.
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Clarke, M.L., Harvey, D.G. and Humphreys, D.J. (1981). Veterinary Toxicology. 2nd Edtn. Bailliere Tindall, London. 159.
Cruickshank, A.K. (1982). Metaldehyde and paraquat poisoning. Vet Rec. 102: 149 150.
Egyed, M.N. and Brisk, Y.L. (1966). Metaldehyde poisoning in Farm animals. Vet Rec. 78: 753 754.
Foley, A.J. (1981). Metaldehyde: Pet poisonings. N Z vet J. 29: 185.
Hayes, T.J. (1970). Poisoning by slug bait. N Z vet J. 18: 18.
Sadler, R. (1999). Slug and snail bait poisonings – soon to be a problem of the past. Vetscript XII (4): 10 11.
Snelson, J.T. (1986). Metaldehyde. A monograph of information on its use as a molluscicide and the level, fate and effect of residues. Pesticide Section. Department of Primary Industry, Canberra, Australia. Document P.B.283.
Studdert, V.P. (1985). Epidemiological features of snail and slug bait poisoning in dogs and cats. Aust Vet J. 62: 269 271.
Sutherland, C. (1983). Metaldehyde poisoning in horses. Vet Rec. 112(3): 64 65.
Surveillance (1974)1(2):13 Metaldehyde poisoning
Surveillance (1975) 2(4): 9 Slug baits and metaldehyde poisoning.
Surveillance (1978) 5(4):16 Metaldehyde poisoning of turkeys
Surveillance (1981) 8(3): 7 Slug pellet poisoning gets attention