How do mice die from poison? - briefly
Poison disrupts critical physiological processes, causing organ failure and death. Rodenticides typically act by preventing blood clotting, leading to internal hemorrhage, or by impairing neural transmission, resulting in respiratory arrest.
How do mice die from poison? - in detail
When a rodent consumes a toxic compound, death results from a cascade of physiological disruptions that depend on the poison’s chemical class.
Neurotoxic agents (e.g., organophosphates, bromethalin) interfere with nerve transmission. Organophosphates inhibit acetylcholinesterase, causing excessive acetylcholine accumulation. Muscles, including respiratory diaphragm, become locked in contraction, leading to respiratory failure within minutes to hours. Bromethalin blocks mitochondrial ATP production in nerve cells, producing cerebral edema and seizures; death follows from uncontrolled convulsions or respiratory collapse.
Anticoagulant rodenticides (warfarin, brodifacoum) obstruct vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X. Blood loss begins silently; internal hemorrhage progresses over days. Clinical signs appear as lethargy, pale mucous membranes, and bruising; fatal outcome is usually massive internal bleeding, often in the gastrointestinal tract or thoracic cavity.
Metallic poisons (zinc phosphide, arsenic) generate phosphine gas or disrupt cellular enzymes. Zinc phosphide reacts with stomach acid to release phosphine, a potent respiratory toxin that collapses mitochondrial membranes, causing multi‑organ failure. Arsenic binds sulfhydryl groups, halting ATP production and inducing cellular necrosis; death follows from cardiac arrhythmia and renal failure.
Sodium fluoroacetate (1080) enters the citric acid cycle as fluorocitrate, which blocks aconitase. Energy production stalls, leading to hypoglycemia, cardiac dysfunction, and eventual cardiac arrest. Clinical progression includes tremors, hyperventilation, and seizures before collapse.
Acute gastrointestinal irritants (sodium azide, certain detergents) cause rapid mucosal damage, leading to perforation, peritonitis, and septic shock. The animal may die within hours due to systemic infection and circulatory collapse.
Across all categories, the final common pathway is failure of vital systems—respiratory, cardiovascular, or neurological—resulting in loss of consciousness and cessation of heart activity. The speed of death varies from minutes (highly potent neurotoxins) to several days (anticoagulants), reflecting the poison’s mode of action and dose ingested.