Snail Bait (Molluscicides)
Slug bait, also known as molluscicides, comprises various chemical substances used to control slugs and snails. The most common active ingredients in commercial slug pellets are metaldehyde, methiocarb, and iron phosphate. Metaldehyde, in particular, poses a significant danger to pets. This organic compound is synthesized from acetaldehyde and acts as a contact and ingestion poison in slugs by disrupting their mucus production and leading to dehydration. In dogs and cats, however, metaldehyde causes severe neurological disorders because it can cross the blood-brain barrier and impair the activity of important neurotransmitters.
The most important facts at a glance
Slug bait poisoning represents a serious and potentially life-threatening emergency for dogs and cats. The main active ingredient, metaldehyde, causes severe neurological symptoms due to its neurotoxic effect, which can rapidly lead to death without adequate treatment. Clinical signs typically develop within a few hours of toxin ingestion and include gastrointestinal complaints, excitement, muscle tremors, seizures, and hyperthermia.
Diagnosis is primarily based on anamnesis and the characteristic clinical picture. Treatment must be initiated immediately and consists of decontamination, symptomatic treatment of neurological symptoms, and supportive measures to stabilize vital functions. Although no specific antidote exists, early and intensive treatment can significantly improve survival chances.
Preventive measures are of great importance to avoid poisoning cases. Pet owners should refrain from using metaldehyde-containing slug pellets and instead resort to pet-safe alternatives such as iron phosphate-based products or apply biological control methods. If slug bait poisoning is suspected, immediate action is required – the earlier treatment begins, the better the chances of a full recovery.
Causes, development and progression
Snail bait poisoning is one of the most common intoxications in pets during the warmer months, when garden owners increasingly use molluscicides. Curious young animals and dogs that tend to ingest foreign substances are particularly at risk. The toxicity of metaldehyde is considerable: The median lethal dose (LD50) in dogs is approximately 100 mg/kg body weight and in cats is 207 mg/kg body weight. In practice, this means that even one tablespoon of snail bait can be enough to cause severe poisoning symptoms in a 5 kg dog. Snail bait usually contains metaldehyde.
This is highly toxic to dogs and cats and can lead to fatal poisoning.
Metaldehyde is partially converted in the gastrointestinal tract into substances that can be excreted via the kidneys. However, a portion is absorbed and is able to cross the normal blood-brain barrier, causing severe neurological symptoms.
The main cause of snail bait poisoning in pets is the direct oral ingestion of snail bait preparations. These are often applied in gardens, parks, or agricultural areas and are attractive to animals due to their smell and taste properties. Some preparations are formulated with attractants that can also appeal to pets.
The mechanism of action of metaldehyde is based on a disruption of the neurotransmitter system in the central nervous system. It specifically inhibits the activity of GABA (gamma-aminobutyric acid), an inhibitory neurotransmitter that normally regulates neuronal excitability. The reduced GABA activity leads to excessive neuronal excitation, which manifests as muscle tremors, seizures, and other neurological symptoms. Additionally, the function of the neurotransmitters norepinephrine and serotonin is also impaired.
Metaldehyde is absorbed relatively quickly via the gastrointestinal tract. A portion is converted into acetaldehyde in the gastrointestinal tract, which can be excreted via the kidneys. However, the absorbed portion crosses the blood-brain barrier and exerts its neurotoxic effect there. The tremor triggered by the poisoning leads to increased muscle activity, which in turn causes hyperthermia (increased body temperature) and metabolic acidosis (acidification of the body) – both factors that further worsen the condition of the poisoned animal.
Mechanism of action
Metaldehyde influences the activity of neurotransmitters. The activity of the neurotransmitters GABA (gamma-aminobutyric acid), norepinephrine, and serotonin is reduced, which is associated with states of excitation.
The associated tremor can lead to a critical increase in body temperature and an exacerbation of metabolism-related metabolic acidosis.
One gram of snail bait contains 60 mg of metaldehyde.
The acute oral LD50 for metaldehyde is 100 mg/kg body weight for dogs and 207 mg/kg for cats.
Signs of intoxication can be expected in a 5 kg dog after ingesting approximately one tablespoon of snail bait.
The median lethal dose is stated as 11.8 g of snail bait / kg body mass.
For dogs – and less commonly for cats – snail bait represents a serious source of poisoning. The product is usually granulated and contains attractants, which makes it particularly appealing to dogs. Toxicity depends on the active ingredient contained. The most important toxic components are:
- Metaldehyde (most common toxic ingredient)
- Less common: Iron(III) phosphate or Methiocarb
The toxicological mechanism of action of metaldehyde, the most common toxic component, is described in detail below, as it is responsible for most poisoning cases in dogs and cats.
Toxicology of Metaldehyde
Metaldehyde is a polymer of acetaldehyde that can break down into free acetaldehyde molecules in the body. Its toxic effect primarily affects the central nervous system (CNS) and the metabolic system, leading to seizures, hyperthermia, and organ failure.
Mechanism of Action of Metaldehyde
Neurotoxic Effect on the CNS
- After oral ingestion, metaldehyde is rapidly absorbed and crosses the blood-brain barrier.
- It affects GABAergic neurotransmission:
- GABA (gamma-aminobutyric acid) is an inhibitory neurotransmitter in the brain.
- Metaldehyde lowers GABA concentration in the CNS, leading to uninhibited neuronal excitability.
- Result: Muscle tremors, ataxia, seizures, hyperreflexia
Acetaldehyde Release
- In the gastrointestinal tract and tissues, metaldehyde is partially converted to acetaldehyde
- Acetaldehyde acts as:
- Cytotoxic
- CNS-activating
- Hepatotoxic and nephrotoxic
- Leads to disturbances in cellular respiration and metabolic stress
Hyperthermia and Metabolic Acidosis
- Persistent muscular activity due to seizures causes massive heat production.
- Additionally, lactic acidosis leads to an acidic pH in the blood, which exacerbates organ damage.
- Hyperthermia can reach temperatures >42°C → thermal cell damage, coagulopathy, multi-organ failure
Further Effects
- Hepatotoxicity: Enzyme elevation (ALT, AST), jaundice possible
- Nephrotoxicity: due to acidosis, dehydration, and myoglobinuria resulting from muscle breakdown
- Gastrointestinal irritation: due to direct contact → vomiting, salivation, diarrhea
Species Differences
Dog: Very Sensitive
- Readily ingests snail bait, often in significant quantities
- Symptoms within 30 minutes to 3 hours
- Lethal dose of metaldehyde: 100–200 mg/kg BW
Cat: Rarely Affected, but Sensitive
- Rarely intentionally ingests snail bait (no interest in attractants)
- Ingestion usually by licking contaminated paws or prey animals
- Symptoms are comparable, but usually occur with smaller amounts
Summary of the Toxic Mechanism
| Target Structure | Toxic Mechanism | Clinical Consequence |
| CNS (primarily GABAergic pathways) | Inhibition of GABA synthesis and release | Seizures, tremors, neurological hyperexcitability |
| Muscles | Persistent irritation due to CNS stimulation | Hyperthermia, muscle breakdown (rhabdomyolysis) |
| Metabolism | Lactic acidosis, electrolyte disturbances | Organ failure, cardiac arrhythmias |
| Liver and Kidneys | Secondary organ damage due to acidosis and hyperthermia | Hepatopathy, acute kidney failure |
Snail bait poisoning – primarily by metaldehyde – represents a veterinary emergency with high lethality in dogs. The mechanism of action is based on central nervous system overstimulation due to GABA inhibition, accompanied by massive muscle activity, hyperthermia, and metabolic acidosis. Cats are less commonly affected but are sensitive even to small amounts. Without immediate symptomatic intensive therapy, the poisoning can be fatal within 24 hours.
Symptoms of intoxication
On average, 3 hours pass between the ingestion of snail bait and the onset of symptoms.
Symptoms include:
- Irritation of the mucous membranes of the gastrointestinal tract
- States of excitation
- Anxiety
- Coordination disorders
- Muscle tremors
- Seizures
- Ataxia
- Hyperthermia (increase in body temperature) due to tremors
- Metabolic acidosis
- Increased respiratory rate
- Death due to respiratory failure
Clinical signs of snail bait poisoning usually appear within 1–3 hours after ingestion, but in severe cases, they can manifest as early as 30 minutes. The course of poisoning is often dramatic and can lead to death within 4–24 hours without rapid veterinary intervention.
Characteristic symptoms of metaldehyde poisoning initially include gastrointestinal complaints such as vomiting, increased salivation, and abdominal pain, which are due to the direct irritant effect of the poison on the mucous membranes of the gastrointestinal tract. Neurological symptoms quickly follow, dominating the clinical picture: restlessness and anxiety, coordination disorders (ataxia), fine to coarse muscle tremors, which can escalate to generalized seizures. Animals often show an increased respiratory rate (tachypnea) and heart rate (tachycardia), as well as significant hyperthermia with body temperatures exceeding 41 °C, caused by increased muscle activity.
In advanced stages, disturbances of consciousness can occur, ranging from stupor to coma. Persistent seizures and hyperthermia lead to metabolic acidosis, which, along with dehydration and electrolyte imbalances, can result in circulatory failure and ultimately death due to respiratory paralysis. It is particularly concerning that relapses can occur even after apparent recovery, as metaldehyde can be stored in the body and released with a delay.
Diagnosis
The diagnosis of slug bait poisoning is primarily based on the anamnesis and clinical presentation. Crucial to this is a thorough history taking, where the pet owner is asked about possible contact with slug pellets or other molluscicides. Information about walks in gardens or parks where slug control agents have recently been applied, as well as the accessibility of such products in their own household, is particularly important.
The clinical examination focuses on assessing the neurological status and vital parameters. Typical findings include elevated body temperature, accelerated respiratory and heart rates, and neurological abnormalities such as muscle tremors, ataxia, and seizures. However, these symptoms are not pathognomonic for metaldehyde poisoning and can also occur with other intoxications or neurological diseases.
Laboratory diagnostic tests primarily serve to rule out differential diagnoses and assess secondary damage. A blood count can indicate dehydration (elevated hematocrit), while blood chemistry provides information on liver and kidney function as well as acid-base balance. Typical changes in metaldehyde poisoning include metabolic acidosis, electrolyte shifts, and possibly elevated liver enzyme levels.
Definitive detection of metaldehyde is possible through toxicological analysis of stomach contents, vomit, or suspicious material, but is rarely performed in practice, as therapy usually needs to be initiated based on clinical symptoms and anamnesis. In unclear cases, a differential diagnosis to other poisonings (e.g., organophosphates, strychnine, ethylene glycol) or to primary neurological diseases (e.g., epilepsy, meningitis) may be necessary.
Therapeutic principles
There is no direct antidote.
Decontamination targets the gastrointestinal tract.
If assessable, decontamination should be performed for metaldehyde ingestion starting from 2 mg/kg body mass, but also as a precautionary measure in unclear circumstances.
Vomiting can be induced if the ingestion of snail bait occurred within the last 30 minutes and, crucially, no seizures have yet occurred.
If large amounts of snail bait are suspected to have been ingested, repeated gastric lavage under general anesthesia is advisable.
Symptomatic therapy primarily involves controlling tremors and seizures, and in this context, monitoring body temperature.
Regarding vital functions, the water, electrolyte, and acid-base balance are particularly important.
Initially, the following are indicated:
- Sedatives
- Anticonvulsants
- Anesthetics
- Intravenous fluid replacement
- Correction of metabolic acidosis
Further therapy depends on other symptoms such as vomiting.
The treatment of snail bait poisoning requires a rapid and comprehensive therapeutic approach. Since no specific antidote for metaldehyde exists, therapy focuses on three main aspects: decontamination, symptomatic treatment, and supportive measures.
Decontamination aims to prevent further absorption of the poison. If ingestion occurred less than 30 minutes ago and the animal is not yet showing seizures, vomiting can be induced under veterinary supervision, typically by administering apomorphine in dogs or xylazine in cats. For larger suspected amounts of poison or if ingestion occurred longer ago, gastric lavage under general anesthesia may be considered. Subsequent administration of activated charcoal (1–4 g/kg body weight) can reduce the absorption of poison not yet absorbed, with multiple doses potentially being beneficial due to the enterohepatic recirculation of metaldehyde.
Symptomatic therapy primarily targets the neurological manifestations. To control muscle tremors and seizures, anticonvulsants such as diazepam (0.5–2 mg/kg IV), phenobarbital (2–6 mg/kg IV), or propofol (1–6 mg/kg IV for induction, then 0.1-0.4 mg/kg/min as a continuous drip infusion) are used. In cases of therapy-resistant seizures, deep sedation or even controlled general anesthesia with intubation and mechanical ventilation may be necessary.
Supportive measures include intravenous fluid therapy to correct dehydration, electrolyte imbalances, and metabolic acidosis. Sodium bicarbonate may be indicated for severe acidosis. Active cooling with wet towels or fans is essential for hyperthermia, and body temperature should be closely monitored. Additionally, depending on the clinical picture, antiemetics for vomiting, gastroprotectants to protect the gastric mucosa, and, if necessary, antibiotics for suspected aspiration pneumonia may be used.
Prognosis & follow-up care
In an evaluation of 772 reported cases where dogs had ingested snail bait, 21.7% showed no symptoms, 61.7% of the dogs recovered, and 16.6% of the dogs died or were euthanized.
The prognosis should therefore be considered cautious.
The prognosis for snail bait poisoning is cautious and depends on various factors. Crucial factors are the amount of poison ingested, the time elapsed between ingestion and the start of treatment, and the response to initial therapy. Evaluations of clinical cases show that approximately 60–65% of affected dogs fully recover, while the mortality rate is 15–20%. The remaining animals may suffer long-term neurological deficits or organ damage.
Animals that respond to therapy within the first 12–24 hours and whose seizures are controllable generally have a more favorable prognosis. Conversely, the occurrence of persistent status epilepticus, severe metabolic acidosis, kidney failure, or disseminated intravascular coagulation (DIC) is associated with a poorer prognosis.
Aftercare plays an important role in complete recovery. After stabilization, animals should be monitored in-hospital for at least 24–48 hours, as relapses can occur. Regular monitoring of body temperature, heart and respiratory rates, and neurological parameters is important. Laboratory tests to monitor kidney and liver function, as well as acid-base balance, should be repeated at appropriate intervals.
After discharge, a calm environment is important for the animal to avoid further stress stimuli. Food and water intake should be gradually normalized. For animals showing persistent neurological symptoms, long-term anticonvulsant therapy may be necessary, which is then gradually reduced. Follow-up examinations after 1–2 weeks and, if necessary, after one month serve to assess complete recovery and rule out long-term consequences.
Research outlook
Research in the field of molluscicide poisoning in pets currently focuses on several promising areas. On the one hand, new biomarkers are being investigated that should enable earlier and more specific diagnosis. Studies on metabolic signatures in the blood of poisoned animals could lead to faster and more precise diagnostic tests in the future, which also allow for better differentiation from other intoxications.
Another research focus is on the development of more effective treatment protocols. Newer anticonvulsants like levetiracetam show promising results in initial studies for controlling seizures caused by metaldehyde and could supplement or partially replace conventional therapies. Innovative detoxification procedures such as specific lipid emulsion therapies are also being investigated for their effectiveness in lipophilic toxins like metaldehyde.
In parallel, scientists are working on developing safer slug control agents. In addition to the already available iron phosphate-based products, new formulations are being researched that are toxic to slugs but harmless to mammals. Biological control methods, such as the use of nematodic parasites or natural predators, are also gaining importance as environmentally friendly and pet-compatible alternatives.
Last but not least, research is dedicated to improving prevention strategies. Epidemiological studies analyze risk factors and seasonal patterns of poisoning cases to enable more targeted awareness campaigns. Innovative product designs with improved warning labels, child-resistant packaging, and formulations unattractive to pets could further reduce the risk of poisoning in the future.
Frequently asked questions (FAQs)
- How quickly do symptoms of snail bait poisoning appear?
The first symptoms typically appear within 1–3 hours after ingestion of the poison. In severe cases, initial signs such as salivation or restlessness can occur as early as 30 minutes. - Which snail baits are safe for my pets?
Iron phosphate-based snail baits are considered significantly safer for pets than products containing metaldehyde or methiocarb. Nevertheless, these should also be kept out of reach of animals, as excessive ingestion can cause gastrointestinal upset. - What should I do if I suspect my pet has ingested snail bait?
Contact your veterinarian or a veterinary emergency clinic immediately. Do not attempt to induce vomiting yourself, as this can be dangerous if neurological symptoms are already present. If possible, take the snail bait packaging with you to the veterinary practice. - Can my pet fully recover from snail bait poisoning?
With early and adequate treatment, full recovery is possible in approximately 60–65% of cases. The prognosis depends on the amount of poison ingested, the time until treatment, and the individual response to therapy. - How long does my pet need to stay at the veterinary hospital after slug bait poisoning?
In-hospital monitoring usually lasts 24–48 hours, but can vary depending on the severity of the poisoning and the occurrence of complications. Close monitoring is important, as relapses can occur. - Are there long-term consequences after recovering from poisoning?
Most animals recover without lasting damage. However, in some cases, persistent neurological deficits, liver, or kidney damage may occur, requiring long-term treatment. - How can I protect my pet from snail bait poisoning?
Avoid slug pellets containing metaldehyde or methiocarb in areas accessible to your pets. Store garden products safely and keep your animals away from freshly treated areas. Consider alternative slug control methods such as coffee grounds, beer traps, or the use of natural predators. - Are certain animal species or breeds more susceptible to slug bait poisoning?
Dogs are generally more frequently affected than cats due to their exploratory behavior. Young, curious animals and breeds with a strong hunting or play drive are particularly at risk. Smaller breeds can be more severely affected by even smaller absolute amounts of poison. - How effective are biological alternatives for slug control?
Biological methods such as the use of nematodes, setting up beer traps, or promoting natural predators can be effective with consistent application, but usually require more time and patience than chemical agents. Their effectiveness can vary depending on weather conditions and slug species. - Can slug bait poisoning also endanger humans?
Yes, metaldehyde is also toxic to humans, especially children. Symptoms of poisoning are similar to those in animals. Therefore, slug pellets should always be stored out of reach of children, and protective gloves should be worn during application.
Literature
- Bates, N., Rawson-Harris, P. and Edwards, N., 2015. Common questions in veterinary toxicology. Journal of Small Animal Practice, 56(5), pages 298–306.
- Bates, N. S., Sutton, N. M. and Campbell, A., 2012. Suspected metaldehyde slug bait poisoning in dogs: a retrospective analysis of cases reported to the Veterinary Poisons Information Service. Veterinary Record, 171(13), page 324.
- Berny, P., Caloni, F., Croubels, S. et al., 2010. Animal poisoning in Europe. Part 2: Companion animals. The Veterinary Journal, 183(3), pages 255–259.
- Dolder, L. K., 2003. Metaldehyde toxicosis. Veterinary Medicine, 98(3), pages 213–215.
- Gupta, R. C., 2018. Veterinary Toxicology: Basic and Clinical Principles. 3rd edition. Cambridge, MA: Academic Press.
- Löwe, G. and Löwe, O., 2021. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 208 pages.
- Vetpharm – Toxicological Database of the University of Zurich. Plant data sheet on metaldehyde. Available online at: https://www.vetpharm.uzh.ch/CLINITOX/TOXDB/KLT_010.HTM?Submit=done [Accessed on July 6, 2025].
- Yas-Natan, E., Segev, G. and Aroch, I., 2007. Clinical and neurological manifestations of metaldehyde toxicosis in dogs. Journal of Small Animal Practice, 48(8), pages 438–443.