Rodenticide Poisoning in Companion Animals

Scott Fritz DVM, PhD, DABVT

Fall is fast approaching. While we look forward to cooler temperatures, football, and family time, it’s also a season when certain home and property tasks may pose poisoning risks to companion animals.

As you winterize campers, barns, or homes, deploying rodenticides is common—but the choice of compound matters. In this article, I review the major classes of over‑the‑counter (OTC) rodenticides, how they differ, and the challenges of detecting them in non-target animals. There are four main groups of OTC rodenticides, each with a distinct mechanism of action and a different clinical signature.

It’s important to remember anticoagulants are not necessarily the most commonly encountered pet poisoning today, and the differences among anticoagulants, bromethalin, cholecalciferol, and phosphides are significant in terms of onset, clinical signs, diagnosis, and therapy.

Anticoagulant Rodenticides
These are perhaps the best known and remain widely available. From a pet owner standpoint, they are relatively safer than other rodenticides when an accidental ingestion occurs, and dogs are more sensitive than cats.

These compounds inhibit the activation of vitamin K, which is essential for synthesizing clotting factors II, VII, IX, and X. Because each clotting factor has a different half‑life, the development of coagulopathy is delayed—typically 3–5 days after ingestion of a sufficient dose. Clinical signs stem from hemorrhage and are variable depending on site(s) of bleeding. Many animals bleed into the lungs leading to epistaxis or hemoptysis, often accompanied by lethargy, exercise intolerance, dyspnea, or pale mucous membranes. Other signs may include melena, hematuria, lameness, paralysis, abdominal distension, or skin bruising.

Confirmatory testing is available via KVDL’s Anticoagulant Panel (TOX-1016). Samples include serum, plasma, liver, or bait material. Identifying the specific anticoagulant can guide the duration of therapy. Vitamin K₁ is the antidote, but coagulation may not normalize until up to 12 hours after dosing, so close monitoring is needed. In severe cases, blood transfusions may be required.

Bromethalin
Bromethalin is a non‑anticoagulant rodenticide and is increasingly seen in pet poisonings. Cats are more sensitive to bromethalin than dogs.

Bromethalin and the metabolite desmethylbromethalin uncouple oxidative phosphorylation in mitochondria, especially in the brain. Loss of ATP impairs the sodium/potassium pumps, leading to ionic imbalance and intracellular water shifts, producing cerebral edema. The clinical presentation is dose-dependent: At high doses, clinical signs typically begin 2–24 hours post-ingestion and may include severe tremors, hyperexcitability, and seizures. At lower doses (more common), signs may be delayed sometimes several days and manifest as hind-limb ataxia or paresis similar to tick paralysis or botulism. There is no antidote for bromethalin toxicosis. Supportive care and aggressive decontamination are key. To confirm, request the KVDL Bromethalin (TOX-1059) test.

Cholecalciferol (Vitamin D₃)
This class is effectively a rodenticide formulation of hypervitaminosis D. Clinical signs are delayed typically 36–48 hours post-exposure, initially nonspecific signs like anorexia, weakness, depression are seen followed by vomiting, polyuria/polydipsia, and dehydration. Acute renal failure develops within 2–3 days of exposure.

Hypercalcemia and hyperphosphatemia are hallmarks. These levels are often high enough to cause soft‑tissue mineralization. Treatment is prolonged and expensive, often involving combinations of calcitonin, bisphosphonates, corticosteroids, and loop diuretics.

Prognosis is guarded to poor especially when hypercalcemia, hyperphosphatemia, or tissue mineralization is present. Antemortem diagnostics should include serum calcium and phosphorus levels (Calcium and Phosphorus Profile (CP-213)); postmortem diagnosis relies on histopathology and the presence of calcification.

Phosphides (Zinc & Aluminum Phosphide)
These are some of the most acutely dangerous rodenticides, though not as commonly discussed in companion animal toxin reviews. Zinc phosphide is more commonly used; aluminum phosphide is less frequent but similar in mechanism.

In an acidic environment like the stomach, the phosphide is hydrolyzed to phosphine gas, a potent systemic toxin. Clinical signs are rapid—often within one hour of ingestion—starting with severe gastrointestinal distress with vomiting, and hemorrhage which progresses to systemic signs including cellular hypoxia, shock, convulsions, and often rapid death. The zinc moiety itself is an emetic, which can be protective in some cases, but once phosphine gas forms, it is highly toxic.

Phosphine gas also poses a hazard to veterinary staff: animals should be handled outdoors or in very well-ventilated areas. Phosphine has a fishy or garlic-like odor, detectable in humans at ~2 ppm which is double the EPA 1 ppm limit for brief exposure. Protecting staff against exposure is important.

There is no specific antidote. Treatment is supportive: decontamination and antacid therapy may help. Diagnostics are limited; phosphine does not persist in tissues, making detection in postmortem samples very difficult.

Key Take‑Home Points and Practical Notes
Clinicians and pet owners must appreciate the wide diversity among “rat poisons.” A history of “rat poison ingestion” is a starting point—but this cannot substitute for identifying the specific active compound.

Some commercial brands sell multiple types of rodenticides (e.g. anticoagulant plus bromethalin) under the same label. Therefore, relying on bait color, dye, or branding alone is risky—though postmortem stomach content examination may still be informative even if it doesn’t tell you which compound is present.

Whenever possible, reference the package label to confirm the active ingredient(s). When submitting to the diagnostic lab, include the suspected compound if known, the specific sample type, and the relevant KVDL test codes to streamline processing.

Because of metabolic transformations, especially bromethalin → desmethylbromethalin, and phosphide → phosphine gas, some toxins are very challenging to detect postmortem, reinforcing the importance of rapid collection, proper sample handling, and early diagnosis. Treatment and prognosis differ markedly among classes—so accurate classification is critical to guide therapy.

Dr. Fritz is a Clinical Assistant Professor and Toxicologist in the Kansas Veterinary Diagnostic Laboratory at Kansas State University.