Strychnine is a pesticide that typically causes toxicosis in companion and production animals by accidental ingestion or malicious poisoning.
Strychnine is an indole alkaloid obtained from the seeds of the tree Strychnos nux-vomica, native to India and southeast Asia. Strychnine-containing baits are banned in some countries or have strict restrictions for use. Grain-laced or pelleted commercial baits (usually < 0.5%) are often dyed red or green. In the past, strychnine has been used as a pesticide to control rats, moles, gophers, and coyotes. Strychnine is highly toxic to most domestic animals with an oral LD50 of 0.5–1 mg/kg in dogs, cattle, horses, and pigs and 2 mg/kg in cats.
Malicious or accidental strychnine toxicosis occurs mainly in small animals, especially dogs and occasionally cats, and rarely in production animals. Most toxicosis occurs when nontarget species consume commercial baits. Young and large-breed sexually intact male dogs may be more likely to be affected.
Strychnine is ionized in the acidic pH of the stomach and then rapidly and completely absorbed in the small intestine. It may also be absorbed dermally and through mucous membranes. Once absorbed into the body, the highest concentrations of strychnine are found in the blood, liver, and kidneys. Strychnine is metabolized in the liver by microsomal enzymes and excreted in the urine. Depending on the quantity ingested and treatment measures taken, most of the toxic dose is eliminated within 24–48 hours.
Strychnine competitively and reversibly inhibits the inhibitory neurotransmitter glycine at postsynaptic neuronal sites in the spinal cord and medulla. This results in unchecked reflex stimulation of motor neurons affecting all the striated muscles. Because the extensor muscles are relatively more powerful than the flexor muscles, they predominate to produce generalized rigidity and tonic-clonic seizures. Death results from anoxia and exhaustion.
Clinical Signs of Strychnine Poisoning in Animals
The onset of toxicosis from strychnine toxicosis is rapid, with clinical signs appearing within 10–120 minutes. Presence of food in the stomach can delay onset.
Early clinical signs include nervousness, tenseness, and stiffness. Extensor rigidity causes the animal to assume a sawhorse stance with splayed, stiff legs. Vomiting is possible but uncommon. Severe tetanic seizures may appear spontaneously or may be initiated by stimuli (touch, sound, or a sudden bright light). Respiration may stop momentarily. Intermittent periods of relaxation occur during seizures but become less frequent as the clinical course progresses.
The mucous membranes become cyanotic and the pupils dilated. Rhabdomyolysis and secondary renal failure may occur due to prolonged muscle activity. Hyperthermia and seizures often occur in dogs. Frequency of the seizures increases, and death eventually occurs secondary to respiratory paralysis and hypoxia. If untreated, the entire course may last only 1–2 hours. (See video of strychnine toxicosis, dog.)
Differential diagnoses may include other causes of tremors and seizures:
metaldehyde
tremorgenic mycotoxins
sodium fluoroacetate (1080)
4-aminopyridine
caffeine
plant ingestion (Taxus spp, Dicentra spp, Cicuta spp, certain mushrooms)
medications for humans (tricyclic antidepressants, 5-fluorouracil, metronidazole, isoniazid)
Primary neurological disease, hypoglycemia, and severe metabolic diseases can also produce clinical signs that resemble strychnine toxicosis.
Diagnosis of Strychnine Poisoning in Animals
Diagnosis of strychnine poisoning in animals is based on the following:
Analysis of stomach contents for strychnine alkaloid
Chemistry panel and venous blood gas to evaluate organ function and monitor for metabolic acidosis (pH < 7.35)
Urinalysis for evidence of myoglobinuria
Treatment of Strychnine Poisoning in Animals
Strychnine toxicosis is an emergency, and treatment should be instituted quickly. Treatment should be aimed at decontamination, control of tremors and seizures, prevention of hypoxia, and supportive care.
Limit stimulation. Sedate patient in a quiet, dimly lit room with cotton earplugs placed to prevent auditory stimulation.
Administer IV fluid therapy at twice the maintenance dose to maintain hydration and perfusion and aid in elimination.
Acidify urine with ammonium chloride (100 mg/kg, PO, every 12 hours) to encourage excretion in urine, but only if venous blood gas is normal.
Control hyperthermia with active cooling until body temperature is < 39.7°C (103.5°F).
Decontamination in Strychnine Poisoning
Induce emesis if ingestion is recent and no clinical signs are present.
If unable to induce emesis, perform gastric lavage with sedation and protection of the airway with a cuffed endotracheal tube.
Administer activated charcoal (1–2 g/kg, PO, as aqueous slurry) with a cathartic in patients that are clinically normal and have a low risk of aspiration or via gastric tube if gastric lavage performed.
Seizure and Tremor Control in Strychnine Poisoning
Diazepam (0.5–2 mg/kg, IV, to effect, or 0.5 mg/kg, per rectum)
Phenobarbital (4 mg/kg, IV, every 20–30 minutes to effect, up to a maximum 24-hour dose of 20 mg/kg)
Levetiracetam (30–60 mg/kg, slow IV over 5–15 minutes; repeat every 8 hours as needed)
Anticonvulsant Drugs and Muscle Relaxants in Strychnine Poisoning
Muscle relaxants such as methocarbamol (55–220 mg/kg, IV, to effect). Total doses may need to exceed the maximal recommended cumulative dose of 330 mg/kg/day. The patient will need to be monitored closely for respiratory depression if using high doses of anticonvulsants and methocarbamol.
Additional Therapies for Severely Affected Patients in Strychnine Poisoning
Mannitol (0.25–2 g/kg, IV, over 20–30 minutes; discontinue IV fluids during administration) if increased cranial pressure is suspected secondary to repeat seizure activity.
IV lipid emulsion therapy (1.5–4 mL/kg of 20% sterile lipid solution, IV bolus, followed by 0.25–0.5 mL/kg/min, IV CRI for 30–60 minutes); repeat bolus dose after 4–6 hours once serum is no longer lipemic.
Intubation and mechanical ventilation may be needed in severely affected patients.
Duration of treatment may be 1 to 3 days.
The prognosis is guarded until seizures are controlled but fair once seizures are controlled.
Key Points
Companion animals are often poisoned by malicious or accidental exposure to strychnine.
Onset of clinical signs in strychnine toxicosis is rapid (< 2 hours), and immediate intervention is needed for decontamination and treatment.
Primary treatment goals are controlling seizures, treating muscle rigidity, limiting stimulation, preventing hypoxemia, and maintaining cerebral perfusion.
For More Information
Talcott PA. Strychnine. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. Elsevier; 2013:827-832.
Khan SA, McLean K. Toxicology brief: epidemiology and management of strychnine toxicosis. DVM360.
Sykes, C. Strychnine. In: Hovda LR, Brutlag AG, Poppenga RH, Epstein SE, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. 3rd ed. Wiley-Blackwell; 2024:819-824.
Also see pet owner content regarding strychnine poisoning.
