What happens to a rat after poisoning? - briefly
The poison interferes with metabolic pathways, causing convulsions, respiratory failure, and cardiac arrest. Death follows within minutes to several hours, depending on the toxin’s potency and dose.
What happens to a rat after poisoning? - in detail
A toxicant introduced to a rat initiates a cascade of physiological disturbances that progress from initial exposure to eventual death, depending on the poison’s class, dose, and the animal’s health.
The first minutes after ingestion often involve irritation of the oral cavity and gastrointestinal tract. Nausea, retching, and salivation may occur, especially with corrosive agents such as zinc phosphide or metal phosphides, which release phosphine gas in the stomach. Rapid absorption of the toxin into the bloodstream follows, leading to systemic distribution.
Anticoagulant rodenticides (e.g., warfarin, brodifacoum) interfere with vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X. Clinical signs emerge after 24–48 hours and include:
- Petechial hemorrhages on mucous membranes
- Hematuria and melena
- Spontaneous bruising and internal bleeding
- Weakness and lethargy due to blood loss
Bromethalin, a neurotoxic agent, uncouples oxidative phosphorylation in mitochondria. Within 2–4 hours, rats display:
- Tremors and ataxia
- Hyperexcitability progressing to paralysis
- Respiratory distress as neuromuscular control fails
Metal phosphides generate phosphine, a potent cellular poison that inhibits cytochrome c oxidase. Early manifestations (30 minutes–2 hours) consist of:
- Severe respiratory distress, cough, and frothy secretions
- Cardiovascular collapse, hypotension, and arrhythmias
- Multi‑organ failure, particularly hepatic and renal necrosis
Cholecalciferol (vitamin D3) overdose causes hypercalcemia. Signs appear after 12–24 hours:
- Polyuria and polydipsia
- Calcification of soft tissues, especially kidneys and blood vessels
- Renal insufficiency, leading to azotemia and eventual death
The terminal phase varies by toxin. Anticoagulants typically result in fatal hemorrhage when clotting factors fall below critical thresholds. Neurotoxins cause respiratory arrest due to loss of diaphragmatic drive. Phosphine poisoning leads to irreversible mitochondrial dysfunction, culminating in systemic organ failure. In all cases, death follows a combination of the specific toxic mechanism and secondary complications such as shock, acidosis, and electrolyte imbalance.
Post‑mortem examination reveals characteristic lesions that aid identification of the agent:
- Diffuse hemorrhages in anticoagulant cases
- Cerebral edema and neuronal degeneration for bromethalin
- Pulmonary congestion and hepatic necrosis with phosphides
- Soft‑tissue calcifications in vitamin D toxicity
Understanding these patterns enables accurate diagnosis, informs humane euthanasia protocols, and guides selection of appropriate antidotes or supportive care when intervention is possible.