Regional incidence

Only a few published reports in the veterinary literature discuss the epidemiologic aspects of strychnine poisoning cases in animals. Most of these reports describe a regional incidence of strychnine poisoning in dogs. In one report, among the rodenticides, strychnine was listed as the most common agent involved (415 incidents), and the highest number of cases (37%; n=154) was reported from the Midwest region.⁴

Figure 2. Regional distribution of strychnine poisoning cases in the United States. Source: AnTox Database, Urbana, Ill: ASPCA Animal Poison Control Center, 1992-2008.

Figure 3. Seasonal distribution of strychnine poisoning cases in the United States. Source: AnTox Database, Urbana, Ill: ASPCA Animal Poison Control Center, 1992-2008.

CLINICAL SIGNS

According to ASPCA APCC data, 93 dogs had clinical signs of strychnine poisoning, and the most commonly reported sign was seizures (56%, n=52) (ASPCA APCC Database: Unpublished data, 1992-2008). Other signs included tremors (26%, n=24), rigidity or stiffness (20%, n=19), panting (14%, n=13), hyperthermia (12%, n=11), vomiting (11%, n=10), ataxia (10%, n= 9), and hyperesthesia (9%, n=8). Of the 93 dogs that exhibited clinical signs, nine (10%) died or were euthanized. Most dogs in the current report had a combination of central nervous system signs (seizures, tremors, ataxia, and hyperesthesia).

Strychnine is a competitive and reversible inhibitor of the inhibitory neurotransmitter glycine at postsynaptic neuronal sites in the spinal cord and medulla.^1,2,10 The resulting unchecked reflex stimulation of motor neurons affects all the striated muscles, resulting in generalized rigidity and tonic-clonic seizures.

The onset of strychnine poisoning is rapid. Signs normally appear within 10 minutes to two hours after oral administration.⁷ Early signs may consist of apprehension, nervousness, tenseness, and muscle stiffness.^1,2 Severe tetanic seizures may appear spontaneously or may be initiated by external stimuli such as touch, sound, or a sudden bright light. Usually, extreme and often overpowering extensor rigidity causes the animal to assume a sawhorse stance. The tetanic convulsion may last from a few seconds to about a minute. Intermittent periods of relaxation are observed during convulsions and become less frequent as the clinical course progresses. During convulsions, the animal exhibits opisthotonos, the forelimbs are extended, the pupils are dilated, the eyeballs protrude, and the mucous membrane color is cyanotic. The frequency of the tonic-clonic seizures increases, and death eventually occurs from respiratory failure or exhaustion during seizures. The entire syndrome, if untreated, may last less than one or two hours.

Postmortem examination reveals no characteristic lesions. Patients that have prolonged convulsions before death may exhibit agonal hemorrhages of the heart and lungs and cyanotic congestion due to anoxia. Death usually results from respiratory arrest and exhaustion from prolonged seizures.^1,2

TOXICOKINETICS

Strychnine is ionized in an acidic pH; thus, it is mainly absorbed in the small intestine.¹ It is metabolized in the liver by microsomal enzymes. In vitro studies indicate that cytochrome P-450 monooxygenase is the predominant metabolic enzyme involved and that strychnine-N-oxide is the major metabolite.² Strychnine does not appear to concentrate in nervous tissues. Its highest concentration is found in the blood, liver, or kidneys.¹ Strychnine and its metabolites are mainly excreted in urine.^1,2 About 10% to 20% of the parent compound appears unchanged in the urine within 24 hours.² Depending on the quantity ingested and the treatment measures taken, most of the toxic dose is eliminated within 24 to 48 hours after exposure. The approximate lethal dose in dogs and cats is 0.75 mg/kg and 2 mg/kg, respectively.¹

DIAGNOSIS

Strychnine poisoning can be tentatively diagnosed based on a history of exposure, typical clinical signs (rapid onset of muscular rigidity, tonic seizures, sawhorse stance, rapid rigor mortis), and a lack of postmortem lesions. Poisoned animals may have undigested red or green strychnine-laced seeds or grain such as peanuts, wheat, milo, or barley in their stomach. Analytical detection of strychnine alkaloid in the vomitus, stomach content, liver, kidneys, or urine should be considered diagnostic.^1,2,8,11

In living animals, the best chance of finding strychnine alkaloid is in stomach content (in vomitus or through stomach washings)⁹ or in urine if samples are collected within the first several hours of exposure. Urine samples may not contain detectable amounts of strychnine if they are collected one or two days after exposure. Samples (stomach content, liver, or kidney) should be sealed in a plastic bag, frozen, and submitted to a veterinary diagnostic laboratory for strychnine analysis.

Strychnine poisoning can be confused with—and should be ruled out from—several other types of poisonings such as metaldehyde, chlorinated hydrocarbon pesticides, zinc phosphide, fluoroacetate, nicotine, 4-aminopyridine, organophosphate pesticides, carbamate pesticides, permethrin (in cats), and tremorgenic mycotoxins such as penitrem A and roquefortine by obtaining a thorough history and requesting additional toxicological analyses.^1,2,5

TREATMENT

Treatment of strychnine poisoning is considered an emergency and should be instituted quickly. The objectives of treatment are 1) decontamination in asymptomatic animals, 2) controlling seizures and preventing asphyxiation in symptomatic animals, and 3) supportive care.