How does rat poison affect mice? - briefly
Rat poison disrupts blood clotting, causing internal bleeding that leads to death within hours to days, depending on the dose and compound. Surviving mice may exhibit weakness, lethargy, and hemorrhagic lesions before succumbing.
How does rat poison affect mice? - in detail
Rodenticide compounds, primarily anticoagulants such as warfarin, bromadiolone, and difenacoum, interfere with the vitamin K cycle in mice. By blocking the enzymatic reduction of vitamin K epoxide, they prevent the γ‑carboxylation of clotting factors II, VII, IX, and X. The resulting coagulopathy manifests as internal bleeding, typically observed within 24–72 hours after ingestion.
Key physiological effects include:
- Hemorrhagic lesions in the lungs, gastrointestinal tract, and brain, identifiable as ecchymoses or hematomas upon necropsy.
- Reduced platelet aggregation secondary to depleted clotting proteins, leading to prolonged bleeding times.
- Anemia from chronic blood loss, reflected in lowered hemoglobin and hematocrit values.
- Hypovolemia and shock in severe cases, accompanied by tachycardia and pale mucous membranes.
The toxic dose varies with the specific agent and formulation. First‑generation anticoagulants require multiple feedings to achieve lethal levels (LD₅₀ ≈ 100 mg kg⁻¹), whereas second‑generation compounds are potent enough to cause death after a single exposure (LD₅₀ ≈ 0.5 mg kg⁻¹). Sub‑lethal exposure can produce delayed mortality, with symptoms appearing up to a week after ingestion.
Metabolic elimination proceeds through hepatic cytochrome P450 enzymes. Species differences affect susceptibility: mice possess higher hepatic clearance rates for certain anticoagulants, which can shorten the duration of toxic effects compared with rats. Nonetheless, accumulation occurs with repeated dosing, leading to progressive coagulopathy.
Therapeutic intervention focuses on rapid restoration of vitamin K activity. Intravenous administration of vitamin K₁ (phytonadione) at 5–10 mg kg⁻¹ can reverse clotting deficits if delivered before irreversible hemorrhage. Supportive care includes fluid therapy, blood transfusion, and hemostatic agents. Anticoagulant poisoning is confirmed by measuring prolonged prothrombin time and reduced plasma levels of clotting factors.
In summary, rodenticide exposure disrupts the vitamin K‑dependent clotting cascade, causing internal bleeding, anemia, and potentially fatal shock. Toxicity severity depends on the compound’s potency, dose, and frequency of ingestion, while timely vitamin K₁ treatment can mitigate lethal outcomes.