An approximately 4-month-old, free-ranging male raccoon (Procyon lotor) was presented to the Atlantic Veterinary College Teaching Hospital with an acute onset of seizures, dyspnea, and abnormal mentation. The good Samaritan who brought the raccoon to the hospital reported that an adult female raccoon with 3 or 4 young had been living in her barn on Prince Edward Island for the summer. They appeared in good health until the day of presentation, when she found a raccoon under a fallen board in her barn in lateral recumbency, semicomatose, and in respiratory distress.
On physical examination, the raccoon was recumbent and dyspneic, with a rectal temperature of 34.7°C. The raccoon was unresponsive to painful stimuli applied to its limbs. The mucous membranes were pale, and the fur around the mouth was covered in saliva. The raccoon had occasional twitching of all 4 limbs. During examination, the raccoon experienced a generalized tonic-clonic seizure, which lasted several minutes.
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Differential diagnoses for acute onset seizures and abnormal mentation in raccoons should include rabies encephalitis, canine distemper encephalitis, head trauma, aberrant parasitic migration, congenital intracranial disorder, and intoxication. The terrestrial strains of rabies virus are not endemic on Prince Edward Island, but cases of rabies involving the bat strain of the rabies virus have been reported in wild foxes from the Island (1). Therefore, due to the potential risk of exposure of hospital personnel to zoonotic disease, the financial expenditure involved, and the guarded to poor prognosis, the raccoon was euthanized with an IV overdose of pentobarbital. The body was submitted for a postmortem examination.
Gross postmortem examination revealed that the animal was in excellent body condition with normal muscle mass and abundant subcutaneous and internal adipose tissue stores. Pulmonary congestion and edema were the only gross abnormalities observed. Microscopically, a large number of the renal cortical tubules contained irregularly shaped sheaves of crystalline foreign material that were birefringent with polarized light and stained positively with Pizzolato’s stain (2), compatible with calcium oxalate crystals. Many of the affected tubules had degeneration or attenuation of the tubular epithelial cells, and the lumina of some tubules were distended by proteinaceous fluid. In the brain, the perivascular space of a few blood vessels was swollen by a moderate accumulation of fluid. The lumen of one of the affected blood vessels contained crystals similar to those observed in the renal tubules. There were no gross or microscopic abnormal findings in the heart, liver, pancreas, spleen, lungs, or adrenal glands. No additional bacteriologic or virologic testing was performed. A nonsuppurative encephalitis consistent with rabies or distemper viral infections was not identified.
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A diagnosis of ethylene glycol toxicosis (antifreeze poisoning) was made on the basis of the characteristic histologic findings. Ethylene glycol toxicity is rarely reported in free ranging wildlife (3,4), despite its relatively routine diagnosis in wildlife species (Canadian Cooperative Wildlife Health Centre, personal communication). The central nervous system (CNS) signs of depression, ataxia, seizures, and coma are primarily due to glycoaldehyde, a metabolite of ethylene glycol, and the metabolic acidosis induced by glycolic acid, another ethylene glycol metabolite (5). To a lesser extent, calcium oxalate deposition in the brain, causing hemorrhage, perivascular infiltration, and neuronal degeneration, may also contribute to CNS dysfunction (5).
With a physical examination only, it can be difficult for a clinician to discriminate between the possible etiologies of neurological disease in raccoons, but certain physical findings can suggest one differential diagnosis be considered more likely than others. Rabies should always be considered in wild animals exhibiting CNS signs and abnormal behavior. Rabid free-ranging animals may display aggression, or an uncharacteristic lack of avoidance of humans. Rabid raccoons may also attack porcupines, and present with porcupine quills embedded in the face and muzzle. Raccoons infected with canine distemper virus may show evidence of mucopurulent oculonasal discharge in addition to CNS signs. In addition to CNS signs, animals with ethylene glycol toxicosis often present with oliguric or anuric renal failure; however, acute renal failure in free-ranging animals is often difficult to appreciate on physical examination alone. Traumatic injuries may simply indicate that a healthy animal experienced a mishap. Animals with neurological disease, however, can be predisposed to traumatic injuries. Clinical signs of trauma, therefore, may or may not rule out the possibility of other neurological problems.
Terrestrial strains of the rabies virus have not been endemic in the Maritime provinces since the early 1970s. Since September 2000, however, 61 cases of rabies involving the raccoon strain of the virus have been diagnosed in 52 raccoons and 9 skunks in the vicinity of the town of St. Stephen in southwestern New Brunswick (J. Goltz, personal communication). This recent introduction of raccoon rabies to the Maritimes is a significant human health issue, which will necessitate disease surveillance in raccoon populations. The postmortem examination of raccoons exhibiting neurological signs will allow not only those infected with rabies to be identified, but also other disease conditions occurring in their populations to be diagnosed and documented. This report highlights the merits of including ethylene glycol toxicity on the list of differential diagnoses for abnormal mentation and seizures in free-ranging raccoons. CVJ
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