How does mouse poison affect mice? - briefly
Mouse poison induces internal hemorrhaging and disrupts blood clotting, causing organ failure and death within a few hours. Affected rodents exhibit paralysis, seizures, and severe weakness before succumbing.
How does mouse poison affect mice? - in detail
Rodenticides are chemical agents designed to disrupt essential biological processes in rodents, leading to morbidity and mortality. The most common classes—anticoagulants, neurotoxins, and metabolic poisons—interfere with blood clotting, nervous system function, or cellular energy production, respectively.
Anticoagulant compounds, such as warfarin‑based substances, inhibit vitamin K epoxide reductase, preventing the regeneration of active vitamin K. This blockage halts synthesis of clotting factors II, VII, IX, and X, causing progressive internal bleeding. Clinical signs appear within 24–48 hours and include weakness, pale mucous membranes, and hemorrhage from the gastrointestinal tract, lungs, or internal organs. Lethal outcomes typically occur after 3–5 days, depending on dose and individual susceptibility.
Neurotoxic rodenticides, exemplified by bromethalin and zinc phosphide, disrupt neuronal ion gradients or generate toxic phosphine gas after gastric acid activation. Bromethalin uncouples mitochondrial oxidative phosphorylation, leading to cerebral edema and paralysis. Zinc phosphide reacts with stomach acid to release phosphine, a potent respiratory toxin that impairs cellular respiration. Observable effects comprise tremors, ataxia, seizures, and rapid respiratory distress, often culminating in death within hours.
Metabolic poisons, such as cholecalciferol (vitamin D₃) formulations, cause hypercalcemia by elevating intestinal calcium absorption. Excess calcium deposits in soft tissues, producing renal failure, cardiac arrhythmias, and calcification of blood vessels. Symptoms develop over several days and may include polyuria, lethargy, and cardiac murmur before fatal organ damage ensues.
Sublethal exposure can produce chronic health issues: anemia from incomplete clotting, neurological deficits from partial neurotoxin binding, and organ dysfunction from persistent metabolic imbalance. Survivors may exhibit reduced reproductive capacity, altered foraging behavior, and heightened susceptibility to secondary infections.
Dose‑response relationships vary among compounds. Median lethal dose (LD₅₀) values range from 0.1 mg/kg for potent neurotoxins to 10 mg/kg for first‑generation anticoagulants. Second‑generation anticoagulants display lower LD₅₀ values (0.005–0.05 mg/kg) and prolonged action due to higher affinity for the target enzyme.
Resistance mechanisms include genetic mutations in the vitamin K epoxide reductase gene, reducing anticoagulant binding, and enhanced metabolic detoxification pathways. Documented resistant populations require alternative active ingredients or integrated pest management strategies.
Overall, mouse poison exerts its effect by targeting specific physiological pathways, producing a cascade of clinical signs that progress from subtle impairment to irreversible organ failure and death. Detailed understanding of each class’s mode of action informs appropriate selection, dosage, and risk mitigation.