Can a cat ingest mouse poison? Risks and recommendations

Understanding Mouse Poison

What is Mouse Poison?

Types of Rodenticides

Rodenticides are chemical agents designed to control rodent populations, and they fall into several distinct categories based on active ingredients and mode of action. First‑generation anticoagulants, such as warfarin, diphacinone, and chlorophacinone, interfere with vitamin K recycling, causing delayed internal bleeding. Second‑generation anticoagulants—including brodifacoum, bromadiolone, difethialone, and difenacoum—exhibit higher potency and longer half‑lives, leading to cumulative toxicity after a single exposure. Non‑anticoagulant compounds comprise three main groups: metal phosphides (zinc phosphide, aluminum phosphide) release phosphine gas that damages cellular respiration; neurotoxic agents (bromethalin, chlorophacinone) disrupt nerve function; and metabolic poisons (cholecalciferol, sodium fluoroacetate) cause hypercalcemia or inhibit the citric‑acid cycle. Each class presents a specific risk profile for accidental ingestion by non‑target species.

Cats that encounter bait, carcasses, or contaminated environments may absorb any of these agents through oral consumption or grooming. Anticoagulant exposure typically manifests as pale mucous membranes, prolonged bleeding from minor wounds, and bruising. Metal phosphide ingestion produces rapid respiratory distress, frothing at the mouth, and abdominal pain. Neurotoxic rodenticides cause tremors, ataxia, and seizures, while metabolic poisons lead to vomiting, polyuria, and cardiac arrhythmias. Toxicity severity depends on the rodenticide type, dose, and the cat’s size and health status.

Preventive measures include storing bait in sealed containers, removing dead rodents promptly, and selecting low‑risk formulations (e.g., first‑generation anticoagulants at minimal effective concentrations) when control is necessary. Veterinary consultation is essential if exposure is suspected; prompt decontamination and antidotal therapy—vitamin K1 for anticoagulants, calcium gluconate for metal phosphides, and supportive care for other classes—improve outcomes.

How Rodenticides Work

Rodenticides are chemicals formulated to cause lethal physiological disruption in rodents. They fall into two principal categories: anticoagulant agents and non‑anticoagulant agents, each employing a distinct biochemical pathway.

Anticoagulant rodenticides interfere with the vitamin K cycle. By inhibiting vitamin K epoxide reductase, they prevent the regeneration of active vitamin K, which is required for γ‑carboxylation of clotting factors II, VII, IX, and X. The resulting deficiency impairs blood coagulation, leading to uncontrolled hemorrhage. Typical steps include:

Ingestion of the bait.
Absorption of the compound through the gastrointestinal tract.
Binding to vitamin K epoxide reductase in the liver.
Progressive depletion of functional clotting factors.
Onset of internal bleeding after several days.

Non‑anticoagulant rodenticides act through alternative mechanisms:

Bromethalin uncouples oxidative phosphorylation in mitochondria, causing cellular energy failure and cerebral edema.
Cholecalciferol (vitamin D₃) induces hypercalcemia by stimulating intestinal calcium absorption and bone resorption, leading to renal failure and cardiac arrhythmia.
Zinc phosphide reacts with stomach acid to generate phosphine gas, a potent respiratory toxin that disrupts cellular respiration.

Pharmacokinetic properties determine the potential for secondary poisoning. Rodenticides are often lipophilic, allowing accumulation in adipose tissue. They exhibit slow metabolism and prolonged elimination half‑lives, resulting in detectable residues in the carcass for weeks after the primary lethal event. Tissue distribution includes liver, kidney, and muscle, providing a source of toxin for predators that consume the whole prey.

When a cat consumes a rodent that has ingested any of these agents, the same biochemical disruptions apply. Anticoagulant exposure can produce delayed internal bleeding, while non‑anticoagulant exposure may cause rapid neurologic collapse, electrolyte imbalance, or respiratory failure, depending on the specific compound. The severity correlates with the amount of contaminated tissue ingested and the cat’s metabolic capacity to detoxify the agent.

Risks of Cat Ingestion

Why Cats are at Risk

Hunting Behavior

Cats possess a strong predatory drive that compels them to stalk, chase, and capture small vertebrates such as rodents. This drive operates through visual acuity, acute hearing, and rapid reflexes, enabling cats to seize prey with minimal hesitation.

When a mouse has been exposed to anticoagulant or neurotoxic rodenticides, the cat’s hunting sequence often brings it into direct contact with the poisoned animal. Consumption of the entire carcass, or even ingestion of a few contaminated tissues, introduces lethal compounds into the feline’s bloodstream.

Anticoagulant poisons interfere with vitamin K recycling, leading to progressive bleeding, bruising, and internal hemorrhage. Neurotoxic agents disrupt neurotransmission, causing tremors, seizures, or respiratory failure. Clinical signs may appear within hours or days, depending on the toxin’s potency and the amount ingested.

Recommendations for owners:

Store all rodent bait in locked containers inaccessible to pets.
Use tamper‑proof bait stations placed out of reach of cats.
Replace poison‑based control with mechanical traps or professional pest‑management services.
Inspect any caught rodent before allowing a cat to interact with it; discard immediately if poison is suspected.
Monitor cats for unexplained lethargy, bleeding, or neurological symptoms; seek veterinary assistance without delay.

Curiosity and Exploration

Cats investigate surroundings through tactile and olfactory cues, often sampling unfamiliar objects with their mouths. This instinctive exploration makes them prone to encounter rodent bait placed in homes, garages, or gardens. When a cat discovers a poisoned mouse or a bait station, ingestion can occur directly (eating the contaminated prey) or indirectly (licking or chewing the bait material).

Rodent poison typically contains anticoagulant compounds or neurotoxins. Anticoagulants interfere with blood clotting, leading to internal bleeding that may manifest as lethargy, pale gums, or bruising. Neurotoxic agents disrupt nervous system function, producing tremors, seizures, or respiratory distress. Onset of symptoms varies from several hours to a few days, depending on the toxin type and dose.

Preventive actions reduce exposure risk:

Store all rodent control products in locked cabinets unreachable by pets.
Place bait stations outside the cat’s roaming area, preferably in sealed containers.
Remove dead rodents promptly; dispose of them in sealed bags.
Supervise outdoor excursions, especially in environments where bait is known to be used.
Conduct regular visual checks of the cat’s environment for stray bait or poisoned carcasses.
If ingestion is suspected, contact a veterinarian immediately; early administration of vitamin K1 or specific antidotes improves prognosis.

Veterinary guidance emphasizes prompt diagnosis and treatment. Monitoring for subtle signs—such as reduced appetite, altered gait, or unexplained bleeding—allows timely intervention and minimizes long‑term health consequences.

Symptoms of Poisoning

Common Signs to Look For

Cats that have swallowed rodent bait may display a predictable set of clinical signs. Early detection relies on recognizing these symptoms promptly.

Typical manifestations include:

Excessive drooling or foaming at the mouth
Repeated vomiting, sometimes with blood
Diarrhea, which may be watery or contain blood
Noticeable weakness or lethargy, often progressing to collapse
Unsteady gait, tremors, or loss of coordination
Rapid, shallow breathing or difficulty inhaling
Convulsions or seizures, which can occur suddenly
Elevated heart rate or irregular rhythm
Pale or bluish gums indicating poor oxygenation

Symptoms often appear within minutes to a few hours after ingestion, but some toxins may delay onset for up to 24 hours. The intensity of signs correlates with the amount and type of poison consumed. Immediate veterinary assessment is warranted when any of these indicators are observed, as early intervention improves the likelihood of a favorable outcome.

Severity Based on Poison Type

The seriousness of a cat’s exposure to rodenticide varies according to the active ingredient. Toxicity classification reflects the speed of onset, the organ systems affected, and the likelihood of irreversible damage.

Second‑generation anticoagulants (e.g., brodifacoum, difethialone). Moderate to severe. Cause progressive blood‑clotting failure; symptoms appear 24–48 hours after ingestion and may lead to internal hemorrhage if untreated.
First‑generation anticoagulants (e.g., warfarin, diphacinone). Mild to moderate. Similar mechanism but lower potency; clinical signs develop later and are less likely to be fatal with prompt care.
Bromethalin. High severity. Disrupts neuronal mitochondria; neurological signs (tremors, seizures, paralysis) emerge within 12–24 hours and can progress to coma.
Cholecalciferol (vitamin D3). High severity. Induces hypercalcemia, renal failure, and cardiac arrhythmias; symptoms may be delayed up to 72 hours, increasing risk of permanent organ damage.
Zinc phosphide. Very high severity. Releases phosphine gas in the stomach, causing rapid respiratory failure, hepatic necrosis, and death within hours.
Metaldehyde. Moderate severity. Causes excessive salivation, tremors, and seizures; onset typically 30 minutes to 2 hours after ingestion.

Severity assessment must consider dose, body weight, and individual health status. Early veterinary intervention—inducing emesis, administering activated charcoal, and providing antidotes such as vitamin K1 for anticoagulants—significantly improves outcomes. Delay in treatment reduces the probability of recovery, especially for high‑severity agents like bromethalin, cholecalciferol, and zinc phosphide.

Long-Term Health Consequences

Organ Damage

Ingestion of mouse poison introduces anticoagulant compounds that interfere with vitamin K recycling, producing widespread hemorrhagic injury. The resulting blood loss compromises organ perfusion and triggers direct toxic effects on several vital systems.

Liver: impaired clotting factor synthesis, hepatic necrosis, elevated transaminases.
Kidneys: micro‑hemorrhages in glomeruli, reduced filtration, azotemia.
Heart: myocardial bleeding, arrhythmias, reduced contractility.
Central nervous system: intracranial hemorrhage, seizures, altered consciousness.
Gastrointestinal tract: ulceration, melena, perforation risk.

Clinical presentation often includes pale mucous membranes, prolonged bleeding from minor wounds, hematuria, vomiting blood, lethargy, and neurological signs such as ataxia or seizures. Laboratory evaluation typically reveals prolonged prothrombin time, low platelet count, increased liver enzymes, and elevated blood urea nitrogen.

Immediate veterinary intervention is essential. Recommended actions:

Contact a veterinarian without delay; provide details of suspected exposure.
If advised, induce vomiting within 30 minutes of ingestion using a safe emetic.
Administer activated charcoal to limit further absorption.
Initiate vitamin K1 therapy to restore clotting factor function; dosing continues for several weeks.
Provide supportive care: fluid therapy for renal protection, blood transfusions for severe anemia, and analgesics for pain management.

Prompt treatment minimizes organ damage, improves survival odds, and reduces long‑term complications.

Neurological Issues

Mouse bait commonly contains anticoagulants, bromethalin, or organophosphates, each capable of affecting the feline nervous system. Anticoagulants cause progressive anemia, leading to cerebral hypoxia that manifests as disorientation, seizures, or coma. Bromethalin interferes with mitochondrial function, producing cerebral edema and resulting in tremors, ataxia, and loss of coordination. Organophosphate compounds inhibit acetylcholinesterase, causing excessive cholinergic activity that presents as muscle twitching, drooling, and, in severe cases, respiratory failure accompanied by paralysis.

Neurological signs typically appear within hours to days after ingestion, depending on the toxin’s potency and the dose consumed. Early indicators include:

Unsteady gait or stumbling
Head tilt or circling behavior
Convulsive activity or tremors
Dilated pupils and altered responsiveness
Excessive salivation or difficulty swallowing

Prompt veterinary intervention is essential. Recommended actions:

Contact a veterinarian immediately; provide details about the suspected toxin and amount.
Induce emesis only under professional guidance; some poisons become more harmful if vomited.
Administer activated charcoal if advised, to bind residual toxin in the gastrointestinal tract.
Initiate antidotal therapy: vitamin K1 for anticoagulants, specific anticholinesterase agents for organophosphates, and supportive care for bromethalin exposure.
Monitor vital signs, neurological status, and blood parameters continuously until stabilization.

Prevention reduces the risk of neurotoxicity. Secure bait in locations inaccessible to cats, use pet‑safe formulations, and store all rodent control products out of reach. Regularly inspect the environment for discarded bait to eliminate accidental exposure.

Immediate Actions and Veterinary Care

What to Do if You Suspect Poisoning

Do Not Induce Vomiting

Cats that have potentially swallowed anticoagulant rodenticide should not be forced to vomit. The act of inducing emesis can cause aspiration of the toxic material into the lungs, leading to severe pneumonia or airway obstruction. Additionally, many rodenticides are formulated as bitter or oily liquids that irritate the esophagus when expelled, increasing the risk of tissue damage.

Veterinary guidance recommends immediate professional evaluation rather than home‑based vomiting induction. Clinicians can assess the amount ingested, determine the specific toxin, and administer appropriate antidotes such as vitamin K1, along with supportive care.

Do not attempt to make the cat vomit at home.
Contact a veterinarian or an emergency animal poison control center promptly.
Provide details about the product (brand, active ingredient, amount) and the time of exposure.
Follow the professional’s instructions for possible activated charcoal administration, antidote therapy, or monitoring.
Keep the cat calm, limit movement, and prevent access to additional toxins while awaiting care.

Contact Your Veterinarian

If you suspect your cat has consumed rodenticide, immediate communication with a veterinary professional is essential. Delay increases the likelihood of severe toxicity, which can progress rapidly.

When you call, provide the following details:

Exact time of exposure or discovery of symptoms.
Type and brand of poison, if identifiable from packaging or the bait.
Quantity the cat may have ingested, even an estimate.
Cat’s age, weight, and any pre‑existing medical conditions.
Current symptoms: vomiting, drooling, lethargy, seizures, or bleeding.

The veterinarian will assess risk based on this information and may advise:

Inducing vomiting or administering activated charcoal, if the ingestion occurred within a short window and the cat is stable enough for the procedure.
Initiating specific antidotal therapy, such as vitamin K1, which counteracts anticoagulant toxins.
Conducting blood work to evaluate clotting factors and organ function.
Monitoring the cat in a clinic for a defined period, typically 24‑48 hours, to detect delayed effects.

Do not attempt home treatment without professional guidance. Follow all instructions precisely, including dosage, timing, and any required follow‑up appointments. Keep a record of all communications and treatments for future reference.

If the veterinarian recommends bringing the cat to the clinic, transport the animal safely, minimizing stress and preventing further exposure to the poison. Prompt, accurate reporting and adherence to veterinary advice markedly improve the chance of a full recovery.

Veterinary Treatment Options

Diagnosis

When a cat is suspected of having consumed rodenticide, the clinician must confirm exposure promptly to initiate appropriate therapy. Initial assessment includes a thorough history focusing on recent hunting behavior, access to bait stations, and observed clinical signs. Physical examination should note mucous membrane color, respiratory rate, heart rhythm, and any neurological abnormalities such as tremors, seizures, or ataxia.

Key diagnostic indicators:

Coagulopathy: prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) suggest anticoagulant poisoning.
Anemia: reduced hematocrit and hemoglobin may result from hemorrhage.
Renal involvement: elevated blood urea nitrogen (BUN) and creatinine indicate possible nephrotoxic effects of metal phosphides.
Electrolyte disturbances: hyperkalemia can accompany tissue breakdown.

Laboratory confirmation relies on specific assays:

Rodenticide screening: high‑performance liquid chromatography (HPLC) or mass spectrometry detects anticoagulant residues in blood or urine.
Serum vitamin K1 measurement: low levels support anticoagulant toxicity.
Toxin‑specific ELISA kits: available for common anticoagulants and metal phosphide compounds.

Imaging is rarely required but may be useful if internal bleeding is suspected; abdominal ultrasound can reveal hemoperitoneum or organ hemorrhage.

Differential diagnosis should include trauma, clotting disorders, hepatic disease, and other toxicants (e.g., NSAIDs, anticoagulant‑containing plants). Excluding these conditions prevents misdirected treatment.

A definitive diagnosis combines clinical signs, coagulation profile, and toxin detection. Early confirmation allows rapid administration of vitamin K1 therapy for anticoagulant exposure or specific antidotes such as sodium thiosulfate for metal phosphide poisoning, improving survival prospects.

Antidotes and Supportive Care

When a cat is suspected of having consumed rodenticide, immediate veterinary intervention is essential. The primary therapeutic goal is to neutralize the toxin and sustain vital functions until the poison is cleared.

Antidotal therapy

Vitamin K1 (phytonadione) administered orally or intravenously; dosage and duration depend on the specific anticoagulant involved.
Activated charcoal given orally to bind residual toxin; effective only if administered within the first hour after ingestion.
Lipid emulsion therapy for lipophilic anticoagulants such as bromadiolone; infusion rate follows established protocols for toxin sequestration.
Antivenom products are not applicable; however, specific antidotes for metaldehyde or bromethalin are unavailable, making supportive measures critical.

Supportive care

Intravenous crystalloid fluids to maintain perfusion and promote renal excretion of the poison.
Continuous monitoring of prothrombin time (PT) and activated partial thromboplastin time (aPTT) to assess coagulation status.
Blood product transfusion (fresh frozen plasma or packed red cells) when severe bleeding or anemia is documented.
Oxygen supplementation and analgesia to address respiratory distress and pain.
Hospitalization for observation, typically 48–72 hours, with repeat coagulation testing to guide ongoing Vitamin K1 therapy.

Prompt administration of Vitamin K1, combined with diligent monitoring and fluid therapy, markedly improves survival prospects for cats exposed to anticoagulant rodenticides. In cases involving non‑anticoagulant formulations, aggressive supportive care remains the only viable strategy.

Monitoring and Follow-Up

After a cat potentially consumes rodent bait, immediate observation is essential. Watch for signs such as vomiting, drooling, loss of appetite, lethargy, trembling, or abnormal bleeding. Record the time of exposure, the amount of bait observed, and any symptoms that develop.

If symptoms appear, contact a veterinarian without delay. Provide the veterinarian with details of the product (active ingredient, concentration) and the cat’s weight. Prompt administration of an appropriate antidote, such as vitamin K1 for anticoagulant toxins, can significantly improve outcomes.

If no symptoms are evident, continue monitoring for at least 24 hours. Conduct regular checks every 2–4 hours during the first 12 hours, then every 6 hours until the 24‑hour mark. Note any delayed reactions, especially gastrointestinal upset or subtle changes in behavior.

Follow‑up actions include:

Scheduling a veterinary check‑up within 24–48 hours, even if the cat appears normal.
Requesting blood work to assess clotting parameters and organ function.
Discussing preventive measures, such as securing bait in inaccessible locations or using pet‑safe alternatives.

Maintain a written log of observations, veterinary instructions, and treatment outcomes. This documentation supports ongoing care and helps veterinarians adjust therapy if the cat’s condition changes.

Finally, reassess the household’s pest‑control strategy after the incident. Replace hazardous products with non‑toxic options, and educate all household members about the risks to pets. Continuous vigilance reduces future exposure and safeguards feline health.

Prevention Strategies

Safe Rodent Control Methods

Traps and Baits

Rodent control devices commonly employed in homes include snap traps, electronic traps, and bait stations. Snap and electronic traps contain exposed killing mechanisms that a curious cat may investigate, especially if the trap is placed within reach of furniture or floor space. Bait stations conceal poisonous pellets or liquids inside plastic compartments; the compartments are designed to prevent accidental access by non‑target animals, yet a determined cat can pry open low‑profile units or knock them over.

The toxic agents most frequently used in mouse poison—anticoagulants such as bromadiolone, difenacoum, and brodifacoum—interfere with blood clotting. Ingesting even a small amount can cause internal bleeding, weakness, and, without prompt veterinary care, death. Secondary exposure occurs when a cat consumes a poisoned mouse, introducing the same anticoagulant into the cat’s system. Symptoms may include pale gums, bruising, coughing up blood, and prolonged bleeding from minor wounds.

Recommendations for minimizing feline risk:

Install bait stations on elevated surfaces unreachable by cats, preferably behind appliances or in utility closets.
Choose tamper‑resistant models that lock securely and cannot be opened without a tool.
Use snap or electronic traps only in areas sealed off from cat traffic, such as basements or crawl spaces.
Consider non‑chemical alternatives, such as live‑catch traps with immediate release, to avoid poisons altogether.
Regularly inspect trap locations for signs of cat interference and replace damaged units promptly.
Keep all poison products and used traps in locked containers inaccessible to pets.

Adhering to these practices reduces the likelihood that a cat will encounter or ingest rodent poison, thereby protecting the animal’s health while maintaining effective pest control.

Professional Pest Control

Professional pest‑control operators must recognize that rodenticide products pose a direct hazard to household cats when placed in accessible areas. Anticoagulant baits, for example, contain active ingredients that can be ingested by a cat either by consuming the bait itself or by hunting a poisoned rodent. Even a single exposure may trigger internal bleeding, kidney failure, or death, depending on the toxin’s potency and the animal’s size.

Typical clinical signs appear within hours to days and include lethargy, pale gums, vomiting, nosebleeds, and bruising. Early detection relies on vigilant observation of behavior changes and prompt veterinary evaluation. Blood tests for clotting factors confirm exposure, while activated charcoal can limit absorption if administered shortly after ingestion.

Preventive strategies for pest‑control professionals include:

Deploying bait stations that meet regulatory standards for tamper‑resistance and animal safety.
Locating stations behind appliances, under cabinets, or in wall voids inaccessible to pets.
Selecting low‑toxicity formulations (e.g., non‑anticoagulant rodenticides) when pets are present.
Providing clients with clear instructions on securing bait stations and monitoring for stray rodents.
Conducting regular site inspections to verify proper placement and integrity of stations.

If a cat is suspected of contacting rodenticide, immediate steps are:

Contact a veterinarian and describe the product, dosage, and time of exposure.
Transport the animal to a veterinary clinic without delay.
Administer prescribed antidotes such as vitamin K1 under professional supervision.
Follow up with repeat clotting‑factor assessments as directed.

Effective pest management balances rodent eradication with pet safety. By adhering to industry guidelines, using secure baiting systems, and educating homeowners, professionals can minimize the risk of accidental feline poisoning while maintaining control over rodent populations.

Protecting Your Cat

Keeping Poisons Out of Reach

Cats are naturally curious and may investigate small containers or food items that contain rodent control substances. When such products are left within a cat’s reach, accidental ingestion can occur, leading to severe toxicity, organ failure, or death. Preventing exposure hinges on strict control of the environment.

Effective measures include:

Store all bait, pellets, and liquid poisons in locked cabinets or high shelves inaccessible to pets.
Use child‑proof, tamper‑resistant containers that require tools to open.
Place bait stations outdoors, away from doors, windows, and pet pathways; secure them with sturdy covers.
Keep feeding areas for cats separate from areas where rodent control is applied.
Inspect the home regularly for stray bait or spilled residues; clean any spills immediately with appropriate protective gear.
Educate household members and visitors about the hazards and the necessity of keeping poison supplies out of sight.

Implementing these practices eliminates the most common route of accidental ingestion and reduces the likelihood of life‑threatening incidents.

Supervising Outdoor Cats

Free‑roaming felines frequently encounter anticoagulant rodenticides, which can cause internal bleeding, organ failure, and death. The probability of exposure rises when cats hunt in areas where bait or poisoned carcasses are present.

Supervision reduces this risk by limiting contact with contaminated prey and enabling immediate intervention if ingestion occurs. Controlled outdoor access, such as enclosed patios or catios, prevents cats from roaming into zones where rodent control products are applied.

Keep bait stations out of reach: place traps and poison containers inside locked sheds or behind barriers inaccessible to cats.
Remove dead rodents promptly: dispose of carcasses in sealed bags to eliminate secondary poisoning sources.
Use non‑toxic deterrents: replace chemical baits with humane traps or electronic repellents in the cat’s environment.
Provide regular feeding: scheduled meals decrease hunting drive, lowering the chance of a cat seeking poisoned prey.
Employ a bell or tracker: a collar with a bell alerts wildlife to the cat’s presence, while a GPS tracker allows owners to locate the animal quickly if it disappears.

If a cat shows signs of rodent poison ingestion—such as lethargy, pale gums, nosebleeds, or bruising—seek veterinary care immediately. Early administration of vitamin K1 therapy improves survival rates. Continuous observation and rapid response are essential components of responsible outdoor cat management.

Educating Yourself and Others

Understanding the hazards of rodenticide exposure is essential for any cat caretaker. Accurate knowledge reduces the likelihood of accidental ingestion and improves response if exposure occurs.

To acquire reliable information, follow these steps:

Consult veterinary professionals for species‑specific guidance.
Review product safety data sheets and label warnings.
Access peer‑reviewed veterinary journals or reputable animal health websites.
Participate in continuing‑education webinars offered by veterinary associations.

When sharing the information, adopt a clear, concise approach:

Summarize the most critical facts: toxic ingredients, symptoms of poisoning, emergency actions.
Provide written handouts or digital resources that list local veterinary clinics and poison control contacts.
Use real‑world examples to illustrate how quickly a cat can encounter bait in indoor and outdoor environments.
Encourage questions and verify that listeners understand the recommended preventive measures.

Consistent education—both personal and communal—creates a protective network that minimizes the risk of a cat consuming mouse poison and ensures swift, effective intervention if exposure happens.