Strychnine is an indole alkaloid obtained from the seeds of
the Indian tree Strychnos
nux-vomica. Strychnine-containing baits are currently labelled for
below-ground use and are intended for the control of pocket gophers. Their use as
indoor pesticides has been eliminated since 1989. 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. Its oral LD50 in dogs,
cattle, horses, and pigs is 0.5–1 mg/kg, and in cats is 2 mg/kg. Strychnine is
considered a restricted-use pesticide. Its sale is forbidden in a number of states.
Grain-laced or pelleted commercial baits (usually <0.5%) are often dyed red or
green. Malicious or accidental strychnine poisoning, although not very common in
the USA, occurs mainly in small animals, especially dogs and occasionally cats, and
rarely in livestock. Most poisonings occur when nontarget species consume commercial
baits. Young and large-breed, intact male dogs are more likely to be involved. Most
poisonings are reported from the western USA.
Strychnine is ionized in an acidic pH and then rapidly and
completely absorbed in the small intestine. It is metabolized in the liver by
microsomal enzymes. The highest concentrations of strychnine are found in the
blood, liver, and kidneys. Strychnine and its metabolites are excreted in the
urine. Depending on the quantity ingested and treatment measures taken, most of
the toxic dose is eliminated within 24–48 hr.
Strychnine inhibits competitively and reversibly 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
The onset of strychnine poisoning is fast. After oral
exposure, clinical signs may appear within 30–60 min. Presence of food in the
stomach can delay onset. Early signs, which may often be overlooked, consist of
apprehension, nervousness, tenseness, and stiffness. Vomiting is possible but
uncommon. Severe tetanic seizures may appear spontaneously or may be initiated
by stimuli such as touch, sound, or a sudden bright light. An extreme and
overpowering extensor rigidity causes the animal to assume a “sawhorse” stance.
Hyperthermia (104°–106°F [40°–41°C]) due to stiffness and seizures is often
present in dogs. The tetanic convulsions may last from a few seconds to ~1 min.
Respiration may stop momentarily. Intermittent periods of relaxation are seen
during convulsions but become less frequent as the clinical course progresses.
The mucous membranes become cyanotic and the pupils dilated. Frequency of the
seizures increases, and death eventually occurs from exhaustion or asphyxiation
during seizures. If untreated, the entire syndrome may last only 1–2 hr. There
are no characteristic necropsy lesions. Sometimes, because of prolonged
convulsions before death, agonal hemorrhages of heart and lungs and cyanotic
congestion from anoxia may be seen. Animals dying from strychnine poisoning have
rapid rigor mortis.
Tentative diagnosis of strychnine poisoning is usually
based on history of exposure and clinical signs. Recovery of strychnine alkaloid
from the stomach contents, vomitus, liver, kidneys, or urine should be
considered diagnostic. Sometimes, urine may not have a detectable amount of
strychnine present if analyzed 1–2 days after exposure; therefore, multiple
samples should be collected and analyzed. Occasionally, poisoned animals may
show presence of undigested grain-laced red or green strychnine bait in the
Strychnine poisoning can be confused with poisonings by
several other seizurigenic substances such as metaldehyde; tremorgenic
mycotoxins (penitrem a); organochlorine, organophosphate, or carbamate
insecticides; fluoroacetate (1080); zinc phosphide; nicotine; 4-aminopyridine;
caffeine; or human medications (tricyclic antidepressants, 5-fluorouracil,
metronidazole, isoniazid). Acute, massive hepatic necrosis (hepatic
encephalopathy) can also produce clinical signs that resemble those of
Strychnine poisoning is an emergency, and treatment should
be instituted quickly. Treatment should be aimed at decontamination, control of
seizures, prevention of asphyxiation, and supportive care. Seizures should be
controlled, and symptomatic animals stabilized before decontamination is
Decontamination consists of removal of gastric contents by
inducing emesis or gastric lavage, and binding of remaining bait in the GI tract
with activated charcoal. Because of the rapid onset of clinical signs, emesis
may be of limited value in most cases. If exposure is recent and no clinical
signs are present, emesis should be induced with 3% hydrogen peroxide (small
animals and pigs) at 1–2 mL/kg, PO, maximum 3 tbsp, repeated once after 30 min
if vomiting has not occurred; apomorphine (dogs only) at 0.03 mg/kg, IV, or 0.04
mg/kg, IM; or xylazine (dogs or cats) at 0.5–1 mg/kg, IV or IM. If emesis cannot
be induced, gastric lavage should be performed with tepid water. Animals already
seizuring should be anesthetized first (with pentobarbital), and an endotracheal
tube passed before gastric lavage. After emesis or gastric lavage, activated
charcoal should be administered at 2–3 g/kg in small animals and 0.5–1 g/kg in
large animals with a cathartic such as magnesium sulfate at 250 mg/kg, PO, or
sorbitol at 1–3 mL/kg, PO.
Seizures should be controlled in small animals with
pentobarbital, IV to effect, repeated as necessary. Muscle relaxants such as
methocarbamol at 100–200 mg/kg, IV, also work well; they should be repeated as
needed with a maximal dose of 330 mg/kg/day. In large animals, chloral hydrate
or xylazine can be used to control seizures. Other medications such as glyceryl
guaiacolate (5%, 110 mg/kg), diazepam, and xylazine have been used in dogs to
control seizures with variable success. Propofol (3–6 mg/kg, IV, or 0.1–0.6
mg/kg/min as a constant-rate IV infusion) can also be tried to control seizures
in dogs or cats. Isoflurane inhalation anesthesia can be used in small animals
if preceding measures to control seizures do not work.
Severely affected dogs should be intubated, and artificial
respiration provided. Acidification of urine with ammonium chloride (100 mg/kg,
bid, PO) may be useful for ion trapping and urinary excretion of the alkaloid.
IV fluids should be administered to force diuresis and maintain normal kidney
function. Hyperthermia treatment (fans, cool bath) should be given if necessary.
Acid-base balance should be monitored and corrected as needed. Most clinical
cases may require 1-–3 days of treatment.
Last full review/revision November 2013 by Safdar A. Khan, DVM, MS, PhD, DABVT