What happens to a mouse after it is poisoned? - briefly
After a toxin is absorbed, the mouse’s nervous and cardiovascular systems fail, causing loss of coordination, respiratory arrest, and death within minutes to a few hours depending on the poison’s potency.
What happens to a mouse after it is poisoned? - in detail
When a rodent consumes a toxic compound, absorption begins almost immediately through the gastrointestinal lining. The poison enters the bloodstream, distributing to vital organs such as the liver, kidneys, heart, and brain. The specific cascade of events depends on the class of toxin, but common patterns emerge.
Anticoagulant agents (e.g., warfarin derivatives) inhibit vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X. Within 12–24 hours, the mouse exhibits internal bleeding: hematuria, gastrointestinal hemorrhage, and ecchymoses. Blood loss reduces circulating volume, leading to tachycardia and hypotension. Without treatment, coagulopathy progresses to fatal exsanguination.
Neurotoxic compounds (e.g., bromethalin, tetrodotoxin) disrupt neuronal ion channels. Within minutes, the animal shows tremors, ataxia, and loss of righting reflex. Paralysis spreads from hind limbs to forelimbs, culminating in respiratory muscle failure. Oxygen deprivation causes rapid decline in blood oxygen saturation, resulting in death typically within 30 minutes to a few hours.
Metabolic poisons (e.g., zinc phosphide, metal phosphides) generate phosphine gas upon contact with stomach acid. Phosphine interferes with mitochondrial oxidative phosphorylation, collapsing ATP production. Cellular energy failure triggers multi‑organ dysfunction: hepatic necrosis, renal tubular injury, and myocardial depression. Clinical signs appear as lethargy, dyspnea, and cyanosis. Mortality occurs in 1–3 hours as systemic collapse ensues.
Acridine‑based rodenticides (e.g., diphacinone) act similarly to anticoagulants but with additional hepatic toxicity. Early signs include reduced activity and weight loss; later stages reveal jaundice and elevated transaminases. Coagulopathy emerges after 48 hours, compounding liver failure.
Physiological markers observable in a poisoned mouse include:
- Decreased platelet count and prolonged prothrombin time (anticoagulants).
- Elevated serum alanine aminotransferase and aspartate aminotransferase (hepatic injury).
- Hyperkalemia and metabolic acidosis from renal impairment.
- Reduced arterial oxygen tension and increased lactate (respiratory toxins).
If the animal survives the acute phase, sublethal exposure may cause chronic organ damage, impaired growth, and heightened susceptibility to secondary infections. Antidotal therapy—vitamin K1 for anticoagulants, supportive ventilation for neurotoxins, or activated charcoal for early gastrointestinal decontamination—must be administered promptly to reverse toxicodynamics and improve survival odds.