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86 PRACTICAL TOXICOLOGY PEER REVIEWED Aspiration has been reported and is a worrisome complication; when heavy sedation is necessary to control tremors, the risk of aspiration increases. 4,5 DIAGNOSTICS Baseline laboratory tests should include a complete blood cell count (CBC), blood chemistry, electrolytes, and urinalysis. Elevations in liver and kidney values as well as creatine kinase have been noted. 2 Penitrem A has been isolated from the liver and kidney in an intoxicated dog, but the role it plays in the liver and kidneys is not known. 2 Other potential causes of elevations in liver and kidney values include significant muscle activity and adverse effects of drugs used to control clinical signs. 2 Patients may develop dehydration and electrolyte changes secondary to vomiting and diarrhea. Additionally, disseminated intravascular coagulopathy may occur secondary to severe hyperthermia. DIAGNOSIS In many cases, a presumptive diagnosis of tremorgenic mycotoxin toxicity is made based on clinical signs and a history including access to compost piles, moldy food, or roaming behavior. A more definitive diagnosis may be made through testing suspected foodstuffs, stomach ingesta, or vomitus for the presence of penitrem A or another metabolite, roquefortine C, which is often found in tandem with penitrem A. 6 On necropsy, penitrem A has been isolated from the liver, kidney, and brain. 2 Since patients may present with an unknown exposure history, considering other diagnostic differentials is important. These differentials may include pyrethroids, metaldehyde, bromethalin, strychnine, organophosphates/ carbamates, paintballs, methylxanthines (caffeine, theophylline, theobromine), ivermectin, macadamia nuts, cocaine, amphetamines, ethylene glycol, and some heavy metals. 7 Nontoxic diagnostic differentials may include steroid-responsive tremor syndrome (idiopathic tremor syndrome), cerebellar disease, idiopathic episodic tremors, metabolic disorders (eg, hypoglycemia), hypocalcemia, and hepatic encephalopathy. Infectious diseases such as distemper and rabies should also be included under nontoxic differentials. 7 MECHANISM OF ACTION As with many toxins, the exact mechanism of action of penitrem A is not known. However, it is known that its primary site of action is the central nervous system. Most likely, penitrem A has dual roles affecting both inhibitory and excitatory neurotransmission. 8 Penitrem A appears to be rapidly absorbed, with onset of clinical signs starting as soon as 15 minutes after exposure up to several hours later. The dose of penitrem A may affect how quickly clinical signs occur. In one study, mice administered larger doses of penitrem A had faster onset of clinical signs. 8 In most patients, signs resolve within 24 to 48 hours; however, there are rare reports of signs lasting longer. In one patient, mild signs persisted for 7 months, and another patient had signs still present 3 years later. 2 TREATMENT There are two important goals when treating toxicosis: 1. Prevent absorption of the toxin (decontamination). 2. Treat the clinical effects of the intoxication. Induction of emesis, gastric lavage, and administration of activated charcoal have all been BOX 1. Clinical Signs Associated With Tremorgenic Mycotoxin Intoxication • Muscle tremors • Ataxia • Seizures • Vomiting • Diarrhea • Hyperesthesia • Nystagmus • Hyperthermia