How does poison affect rats and dogs? - briefly
Poison induces rapid organ failure, seizures, and cardiovascular collapse, frequently leading to death; rodents and canines differ in susceptibility because of distinct metabolic pathways and dose thresholds.
How does poison affect rats and dogs? - in detail
Poison exposure triggers a cascade of physiological disturbances in both rodents and canines, though the severity and progression depend on the toxin’s chemical class, dose, and route of entry.
In rats, common rodenticides such as anticoagulants (e.g., warfarin, brodifacoum) inhibit vitamin K–dependent clotting factors. Within hours, internal bleeding begins, first evident as hematuria or melena, followed by lethargy, weakness, and rapid decline in body weight. Neurotoxic agents (e.g., organophosphates) block acetylcholinesterase, causing excessive cholinergic stimulation: salivation, lacrimation, tremors, seizures, and potentially fatal respiratory paralysis. Metabolic poisons like sodium fluoroacetate disrupt the citric‑acid cycle, leading to hypoglycemia, cardiac arrhythmias, and multi‑organ failure within a day.
Dogs respond similarly to anticoagulant ingestion, but clinical signs often appear later because canines metabolize some compounds more efficiently. Early manifestations include bruising, petechiae, and prolonged clotting times. Advanced bleeding may involve hemoperitoneum, pulmonary hemorrhage, or intracranial hemorrhage, producing ataxia and coma. Organophosphate poisoning in canines produces a cholinergic crisis: drooling, vomiting, bronchospasm, and muscle fasciculations, which can progress to status epilepticus without prompt anticholinergic therapy. Metabolic toxins induce rapid onset of vomiting, diarrhea, cardiac dysrhythmias, and central nervous system depression.
Key factors influencing outcomes:
- Dose‑response relationship: Higher concentrations accelerate symptom onset and increase mortality.
- Absorption route: Ingestion leads to gastrointestinal absorption; dermal exposure may delay systemic effects but still cause toxicity.
- Species‑specific metabolism: Rats possess higher hepatic enzyme activity for certain anticoagulants, making them more susceptible at lower doses compared with dogs.
- Antidote availability: Vitamin K1 reverses anticoagulant effects; atropine and oximes counteract organophosphate toxicity; supportive care (fluid therapy, seizure control) improves survival for metabolic poisons.
Prompt identification of toxin type, dosage estimation, and immediate administration of appropriate antidotes are critical for mitigating lethal outcomes in both animals.