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Pemoline
Extreme agitation, hyperactivity, and vomiting that began within 24 hours after ingestion of approximately 750 mg of pemoline, a CNS stimulant used in humans for treating attention deficit-hyperactivity disorder in adolescents, was reported in a 3 year old German Shorthaired Pointer [139]. The dog was tachycardic, hyper-responsive, pyrectic, disoriented, and had mydriasis. These signs were consistent with excessive stimulation of the CNS and sympathomimetic effects resulting from pemoline toxicosis. Plasma pemoline concentration was markedly elevated (32 hours after ingestion the plasma concentration was 368 mg/ml, compared with a therapeutic concentration of 1.7 to 7.0 mg/ml reported for children). Several sedatives were administered intravenously to alleviate clinical signs and to allow administration of activated charcoal and fluids. Clinical signs resolved approximately 72 hours after ingestion of pemoline.

Pyrethrin and Pyrethroid Insecticides
These compounds are used as parasiticides and formulated for use in dogs and cats as shampoos and dips. Pyrethrins are natural insecticides while pyrethroids (e.g., permethrin and fenvalerate) are synthetic compounds and classified as type I (no alpha cyano-3-phenoxybenzyl group) or type II (with alpha cyano-3-phenoxybenzyl group) [2,140]. These insecticides are thought to interfere with sodium channels (type I pyrethroids and pyrethrins), enhance sodium ion conductance, and block post-synaptic GABA-A receptor-chloride ionophore complexes (type II pyrethroids). Cats may be more susceptible to pyrethrin/pyrethroid poisoning than dogs [11]. Signs of toxicosis may occur within hours of exposure (but may be delayed) and include tremors, salivation, ataxia, vomiting, depression, hyperexcitability, hyperactivity, seizures, dyspnea, and death [2]. Treatment is symptomatic and supportive, including dermal decontamination, emesis induction within 1 hour (e.g., apomorphine at 0.03 mg/kg IV or 0.04 mg/kg IM), activated charcoal (2 g/kg, qid), magnesium sulfate or sodium sulfate (0.5 g/kg PO as a 10% solution in water), anticonvulsants, oxygenation (if necessary), and fluid therapy. The syndrome is generally reversible, with most animals recovering within 72 hours [33].

Strychnine Poisoning
Strychnine is a rodenticide poison used for "control" of squirrels, gophers, rabbits and other wild carnivora [63]. Dogs, and infrequently cats, become poisoned when they eat strychnine baits, especially in rural areas, although dogs also may be poisoned maliciously in rural and urban areas [63,141-144]. In one report on 261 cases of strychnine poisoning in dogs in Canada [145], strychnine poisoning occurred more often in younger dogs, with 61% of the cases being in animals less than 2 years old. Large breeds of dogs and male dogs were affected more often. In this study, the German Shepherd was the most common breed of dog affected.
Strychnine acts at the brainstem and spinal cord level by stereochemically and competitively blocking the motor inhibitory neurotransmitter, glycine. Some supraspinal signs may also be associated with strychnine inhibition of gamma-aminobutyric acid (GABA). Clinical signs of poisoning are induced by uncontrolled impulses reaching skeletal muscles and are characterized by retraction of the corners of the mouth, drawing together of the ears, stiffness of muscles of the neck, chest and abdomen, stiffness of gait and assumption of a "sawhorse" stance followed by tonic extension of the limbs, opisthotonus, vocalization, and difficult respiration. Affected animals are hypersensitive to auditory, visual (e.g., bright light), and tactile stimuli [11]. Consciousness is not lost during initial "seizural" attacks. After several minutes, the attack(s) may subside only to be followed by further episodes. Eventually, the respiratory muscles may be unable to function. Apnea can lead to cerebral anoxia, loss of consciousness and death. The entire course may last from 30 minutes to 1 to 2 hours, if the animal is untreated. Atypical signs, including absence of seizures or tetanic spasms, and time course (e.g., 10 hours) have been reported in dogs [216].
A presumptive diagnosis is based on a history of ingestion and characteristic clinical signs. In one report, chemical analysis of tissues and ingesta containing strychnine indicated that the highest concentrations were in stomach contents, followed by the liver, and the kidney [145]. Vomitus and urine can also be screened. The dimethoxy derivative of strychnine, brucine (2,3-dimethoxystrychnidin-10-one), may be detected in serum [216]. Prognosis is guarded, depending on the amount of poison ingested and/or promptness of treatment. The main objectives of treatment are to keep the muscles relaxed and to prevent asphyxia. The drug of choice in dogs has been pentobarbital, at 30 mg/kg, IV (or via intraperitoneal or intrathoracic routes if the animal is difficult to manage or is having seizures). Thiobarbiturates, such as thiopental sodium or thiamylal sodium, given IV to effect, are recommended for cats. Muscle relaxants recommended include glyceryl guaiacolate ether given in an intravenous dose of 110 mg/kg in either a 5 or 33 1/3% solution [146]. This drug controls "seizures" for up to 60 minutes. It can be safely repeated as needed. Methocarbamol (Robaxin®) also can be used, at a dose of 150 mg/kg IV, and repeated as needed. Supportive treatment includes prompt gastric or enterogastric lavage using 1 to 2% tannic acid or 1:2000 potassium permanganate and enemas, followed by administration of activated charcoal. Forced diuresis with 5% mannitol in isotonic saline and acidification of urine with 150 mg/kg body weight of ammonium chloride PO, will enhance urinary elimination of strychnine.
If the animal survives 24 hours, prognosis for complete recovery is very good. The clinical signs and necropsy findings closely resemble plastic explosive type 4 (PE4 containing cyclonite) toxicity [147]. Roquefortine (a diketopiperazine alkaloidal tremorgenic mycotoxin) and strychnine poisoning may be difficult to differentiate clinically [148].