Strychnine is a highly toxic alkaloid, contained in the seeds of Strychnos nuxvomica, which grows in India, Southwest Asia and Northern Australia. It is no longer used as a vertebrate pesticide
Strychnine has been widely available as an avicide, a pesticide and for the control of vertebrate vermin (rodents, rabbits and dingos). It is these compounds which are most commonly mixed with ground meat, cottage cheese or food scraps which are responsible for the majority of malicious poisonings of pet animals. Traces of strychnine have also been reported in doped racehorses and greyhounds.
Strychnine was used extensively in NZ as a rabbit bait until about 1950. The advantage of strychnine as a poison was that the dead rabbits were found close to the poison line and it was easy to recover their skins. It is a very cruel poison as the animal is subjected to painful convulsions while still conscious.
Strychnine rabbit baits were dyed pink and may remain stable in the environment for a long time. A recent poisoning of two working dogs indicates that old stored supplies of strychnine are still highly toxic.
The crude form of strychnine is a white crystalline substance which is odourless, very bitter and almost insoluble in water, although there is some solubility in alcohol, chloroform or glycerol. Strychnine is precipitated by alkalies, carbonates, bicarbonates, benzoates, dichromates, bromides, iodides, tannic acid, picric acid, salicylates, borax and proteins. The sulphate salt is the most commonly used strychnine salt and is more water soluble than the free base.
Historically strychnine has been used as a medicinal stimulant in tonics and for the treatment of atonic constipation. Certain properties commonly ascribed to strychnine, i.e. stimulation of the gastrointestinal tract and increasing voluntary muscle tone are not evident at therapeutic doses, and are only manifested at toxic levels. There appears to be no rational use for strychnine in modern veterinary medicine, although strychnine is still used as a ruminatinic (nux vomica) and as a stimulant.
Brucine is a structurally close relative of strychnine also found in the strychnos seeds. Brucine has similar physiological effects to strychnine, but is much less potent. The morphine alkaloids thebaine, morphine and codeine are also structurally similar to strychnine, but these compounds tend to show depressant activity rather than the excitatory properties of strychnine.
Dogs, cats and pigs are the most susceptible species to strychnine toxicity; an oral dose of 0.7 mg/kg can be lethal to dogs. Ruminants are more resistant than other species to the oral administration of strychnine, because it is partially destroyed in the rumen. Parenterally administered strychnine is two to ten times more toxic than oral strychnine, and toxic doses of nux vomica about 100 times the corresponding oral lethal dose of strychnine. The lethal dose for most domestic species ranges from 0.2 3.00 mg/kg. Any levels detected in animal specimens are significant.
Toxic doses of strychnine for domestic animals
| LD50 (mg/kg) | Toxic Dose(mg) | |
|---|---|---|
| Dog | 0.75 | |
| Cat | 2.0 | |
| Poultry | 5.0 | |
| Pig | 0.5-1.0 | 10-50 |
| Horse | 0.5 | 200-300 |
| Cattle | 0.5 | 200-400 |
Between 1957 and 1960, 124 cases of strychnine poisoning were reported in New Zealand. This has been significantly reduced, with 20 confirmed cases reported between 1974 and 1983. Most of these were multiple poisonings and the majority were malicious with the pink strychnine powder usually having been inserted into pockets cut into cooked sausage or other meat.
Strychnine is rapidly absorbed following oral and parenteral administration, then distributed around the body by both plasma and erythrocytes, to be readily taken up by all body tissues.
Once absorbed the metabolism of strychnine occurs without delay, principally by hepatic microsomal enzymes, although approximately 10 20% of the poison is excreted unchanged in the urine. A proportion of the absorbed strychnine is secreted back into the acid environment of the stomach and a non fatal dose of strychnine is rapidly eliminated from the body. The half life is estimated to be about 10 hours.
Strychnine produces excitation of all portions of the central nervous system (CNS) by selectively blocking glycine receptors. These are glycine gated chloride channels which provide tonic postsynaptic inhibition in the spinal cord and medulla. Loss of this inhibition enhances the ongoing neuronal activity so that reflex movement and muscle twitching becomes exaggerated and uncontrolled. All of the striated muscles are involved, but the more powerful extensor muscles predominate, resulting in the characteristic extensor rigidity. Strychnine does not accumulate within the nervous or muscular tissue, cause direct pathological changes to these tissues or have a direct effect on the gastrointestinal or cardiovascular systems.
Strychnine is a rapidly absorbed convulsant poison. Signs of intoxication usually appear within 10-30 minutes following ingestion, although latent periods of up to two hours have been reported. A similar clinical appearance has been noted in poisoned dogs, cats, pigs and horses.
The clinical signs exhibited vary; depending upon the quantity of poison consumed and the time elapsed since exposure. Vomiting may occur due to the strychnine's bitter taste and irritant properties, however, food in the stomach may prevent emesis and enhance toxicity. The earliest signs include nervousness, muscle twitching, and a progressive muscle rigidity. The animal initially adopts a "sawhorse" stance until it finds it impossible to stand, and then lies rigidly on its side with the legs stiff and outstretched, neck and back arched, ears erect and lips pulled back from the teeth in a characteristic grimace.
Rigor mortis in animals dying from strychnine poisoning is rapid in onset and of short duration. This is due to an exhaustion of the muscle reserve of muscle glycogen and ATP, during the prolonged and violent contractions.
Post mortem examination reveals changes indicative of a violent and hypoxic state. There are no gross or microscopic lesions characteristic of strychnine poisoning which can be consistently detected. Dark venous blood, cyanosis, petechial or ecchymotic haemorrhages and traumatic lesions may be evident. Ecchymotic haemorrhages are commonly found in organs poorly supported by connective tissues such as the thymus and pancreas. Intramuscular haemorrhages may also be present, and the lungs and cerebral meninges are often filled with blood. Microscopically, ganglionic cells throughout the peripheral and central nervous system are severely damaged.
The food or bait containing strychnine can often be found in the stomach of the untreated animal, particularly as the baits are relatively insoluble in water.
The definitive diagnosis of strychnine poisoning, is made by chemical analysis of samples from the kidney, liver, central nervous system, stomach contents and urine. Strychnine levels can still be detected in cadaver tissues for several months following death. Stomach contents and urine are routinely used for antemortem diagnosis in clinical cases, although serum analysis has also been reported. The stomach contents are the best samples for analysis if collected early in the course of the poisoning. If more than two hours has elapsed, then the analysis of stomach contents is not reliable, as most of the poison has either passed to the lower segments of the gut or been absorbed. Urine samples are not reliable specimens in cases of acute death, as the animals die so rapidly that the amount of strychnine excreted into the urine, is usually insignificant.
Various stimuli, such as touch, sound or sudden bright light may initiate violent tetanic seizures. Initially these spasms are intermittent, with complete relaxation between seizures. As the intoxication progresses, the convulsions become more frequent and sustained. During these convulsions the breathing becomes paralysed resulting in cyanosis, anoxia, pupil dilatation and eventually death from asphyxiation. The animal does not usually lose consciousness until the terminal stages of anoxia.
Conditions with similar clinical signs to strychnine poisoning are:
If treatment can be initiated promptly many animals can be saved because of the rapid metabolism of strychnine. The primary objectives of therapy are to remove the source and prevent further absorption, to maintain muscular relaxation and prevent asphyxiation until the strychnine can be eliminated from the body.
If the animal is presented early following exposure and shows no toxic signs, then an emetic should be used to remove the ingested substance.Xylazine is a good emetic, because it also has muscle relaxant properties.
If convulsions are present or imminent, apomorphine should not be used as the muscular activity involved in emesis may precipitate more convulsions. Drugs that reduce the efferent motor activity in the brain or spinal cord and provide restraint of the animal are indicated. Traditionally intravenous pentobarbitone has been advocated. The intraperitoneal or intrathoracic routes may be used if the dog is extremely hyper reflexic or in convulsions. Cats should be anaesthetised with an intravenous thiobarbituate, as they tend to sleep too long with pentobarbitone. Large domestic species can be anaesthetised with pentobarbitone mixture or they can be just heavily sedated with pentobarbitone. Other successful therapeutic regimes for strychnine toxicosis have included the use of diazepam. Prolonged relaxation can be achieved with halothane anaesthesia, iv methocarbamol (150 mg/kg, repeated doses at 90 mg/kg iv as required) or iv glyceryl guaiacolate (110 mg/kg). Halothane has the advantage of providing the facilities for immediate artificial ventilation and oxygen administration. The advantage of combination therapy is primarily the reduction of high doses of barbiturates.
Once the animal is anaesthetized and stabilized, gastric lavage using dilute potassium permanganate solution to oxidize the strychnine or a 1 2% solution of tannic acid or sodium bicarbonate may be utilized to precipitate the poison. The final infusion should be a slurry of activated charcoal in tap water or normal saline. The charcoal binds and prevents further absorption of the strychnine and should be removed from the system after 30 minutes by giving a high enema or a cathartic to the animal. Gastric lavage significantly improves the animal's chances, but is really only effective if performed less than two hours after the ingestion of the toxin.
The elimination of strychnine may be enhanced by maintaining an adequate urine flow or creating a diuresis, either with 5% dextrose in isotonic saline or with 5% mannitol, administered by a slow drip. Acidification of the urine with oral ammonium chloride (130-150 mg/kg) increases the urinary excretion of the absorbed strychnine. Do not use if the animal is acidotic from exertion. By using diuresis and urinary "ion trapping", the strychnine levels can drop below the toxic level in 12 24 hours.
Administration of calcium borogluconate intravenously has been reported to be beneficial in strychnine toxicosis in preventing respiratory paralysis and neuromuscular blockage.
When the animal wakens from the anaesthetic, it should be carefully observed. If the convulsive tendencies remain, then additional light sedation is indicated with periodic reassessment of the animal's condition. It is important not to create a case of anaesthetic overdose. Warmth and a quiet environment, without any external stimuli are essential for recovery.
Convulsive tendencies may remain for several days particularly if the gastrointestinal tract was inadequately emptied at the onset. Therapy to maintain muscle relaxation and sedation must be continued. Delayed or prolonged recovery may also indicate that the animal has incurred liver and kidney damage and appropriate therapy to support these organs should be undertaken.
With prompt and thorough therapy, a high proportion of strychnine poisonings can be expected to recover.
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Surveillance (1974) 1(3): 22 Strychnine poisoning in dogs
Surveillance (1976) 3(3): 21 Strychnine poisoning (malicious)
Surveillance (1976) 3(4): 20 Strychnine poisoning (malicious)
Surveillance (1977) 4(5): 23 Strychnine poisoning in dogs
Surveillance (1978) 5(1): 19 Strychnine poisoning
Surveillance (1979) 6(4): 25 Strychnine poisoning in a dog and cat
Surveillance (1983) 10(4): 15 Malicious poisoning.
Surveillance (1999) 26(3): 19 Strychnine poisoning in two working dogs