How do rats die from poisoning? - briefly
Toxicants disrupt essential physiological functions, causing seizures, respiratory failure, and cardiac arrest. The exact mechanism varies with the poison, for example anticoagulants induce internal bleeding while neurotoxins produce paralysis.
How do rats die from poisoning? - in detail
Rats exposed to toxic agents die through a series of physiological disruptions that depend on the poison’s chemical class, dose, and route of entry.
Anticoagulant rodenticides (e.g., brodifacoum, difenacoum) block vitamin K recycling, preventing synthesis of clotting factors II, VII, IX, and X. Blood loss begins within 24–48 hours, progresses to internal hemorrhage, and culminates in hypovolemic shock. Coagulopathy manifests as bruising, bloody feces, and rapid decline in activity.
Warfarin‑type anticoagulants act similarly but require higher, repeated doses; death may take 4–7 days as cumulative depletion of clotting proteins occurs.
Metal phosphides (zinc phosphide, aluminum phosphide) react with stomach acid to release phosphine gas. Phosphine interferes with cellular respiration by inhibiting cytochrome c oxidase, causing mitochondrial failure, metabolic acidosis, and multi‑organ collapse. Clinical signs appear within minutes: labored breathing, frothing at the mouth, and convulsions. Fatality typically follows within 30 minutes to a few hours, depending on the amount ingested.
Bromethalin, a neurotoxic anticoagulant, uncouples oxidative phosphorylation in neuronal mitochondria. Energy depletion leads to cerebral edema, seizures, and paralysis. Mortality usually occurs 24–48 hours after ingestion, preceded by ataxia, tremors, and loss of coordination.
Strychnine and other convulsant poisons block inhibitory glycine receptors in the spinal cord, producing uncontrolled muscle contractions. The animal experiences intense, painful spasms (opisthotonus) and eventually succumbs to respiratory failure as the diaphragm and intercostal muscles become locked. Death follows within minutes to an hour.
Organophosphates (e.g., chlorpyrifos) inhibit acetylcholinesterase, causing accumulation of acetylcholine at synapses. Excessive stimulation of muscarinic and nicotinic receptors leads to salivation, lacrimation, bronchoconstriction, bradycardia, and seizures. Respiratory arrest and cardiac arrhythmias result in death typically within 1–3 hours.
Aconitine, a plant‑derived alkaloid, binds voltage‑gated sodium channels, maintaining them in an open state. Persistent depolarization produces ventricular arrhythmias, hypotension, and rapid collapse. Fatal outcomes appear within 30 minutes to 2 hours.
The route of exposure influences onset time. Ingestion delivers the fastest systemic absorption; inhalation of volatile toxins (e.g., phosphine) accelerates respiratory involvement; dermal contact yields slower, variable absorption, often delaying symptoms by several hours.
Dose–response relationships dictate whether sublethal effects (e.g., reduced foraging, lethargy) precede mortality. Subclinical exposure may impair immune function and reproductive capacity, increasing susceptibility to subsequent lethal doses.
Post‑mortem examination typically reveals organ-specific lesions: hemorrhagic foci in anticoagulant cases, pulmonary edema in phosphine poisoning, neuronal degeneration in bromethalin exposure, and widespread muscle necrosis in convulsant intoxication. Toxicological analysis confirms the agent, guiding appropriate pest‑control strategies and safety protocols.