Canine Distemper in a Captive Indochinese Tiger (Panthera tigris corbetti)
American Association of Zoo Veterinarians Conference 1998
Kenneth N. Cameron1, DVM; Mark K. Campbell1, DVM; Philip H. Long2, DVM, PhD, DACVP; Linda Munson3, DVM, PhD, DACVP; A. Alan Chambers4, MD; Jenny L. Kroll1; Brian A. Summers5, BVSc, PhD, MRCVS
1Veterinary Services, Cincinnati Zoo & Botanical Garden, Cincinnati, OH, USA; 2The Procter & Gamble Co., Cincinnati, OH, USA; 3Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, The University of California, Davis, CA, USA; 4Department of Radiology, Section of Neuroradiology, University of Cincinnati Hospital, Cincinnati, OH, USA; 5Department of Pathology, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY, USA; 6Mountain Gorilla Veterinary Center, Kigali, Rwanda


A 10-yr-old captive-born female Indochinese tiger (Panthera tigris corbetti) housed at the Cincinnati Zoo presented with mild neurologic signs. The animal was housed with an adult male in an outdoor yard and had access to an indoor area during inclement weather. Initial signs included mildly uncoordinated ambulation and difficulty jumping down from a platform in the indoor area. Eleven days later, marked ataxia and paraparesis were observed, with forelimbs more severely affected than hind limbs. The animal was restrained in a squeeze cage for phlebotomy. Hematology and serum chemistries were unremarkable. Titers for feline leukemia virus, feline infectious peritonitis virus, feline immunodeficiency virus and toxoplasmosis were negative. Primary muscle origin was ruled out based on SGOT and CPK values being within reference ranges.

Neurologic signs were unchanged on day 16. The animal was immobilized with tiletamine and zolezepam (Telazol™, Fort Dodge Laboratories, Incorporated, Fort Dodge, IA, USA) 500 mg i.m. by dart and maintained on isoflurane (AErrane™, Ohmeda Pharmaceutical Products Division Inc., Liberty Corner, NJ, USA). Physical examination revealed normal muscle mass and tone and normal-to-hyper-reflexia in all limbs. Urinalysis was unremarkable. Plain radiographs of cervical and thoracic spine showed fractures of dorsal spinous processes of caudal cervical and cranial thoracic vertebrae. Trauma was added to the list of differential diagnoses. Recovery from anesthesia was unremarkable. On day 17, the animal was eating well, but had developed mild head tremors which persisted for two days.

By day 27, the paraparesis had worsened. On day 30 the patient was immobilized a second time, following the same protocol, and a cisternal spinal tap was performed. Analysis of cerebrospinal fluid showed a mild pleocytosis, but was otherwise unremarkable. A cervical and thoracic myelogram showed a possible extradural mass at C2-3. Recovery from anesthesia was prolonged and mild head tremors, which lasted for several days, were again observed.

At day 35, the patient was immobilized again and taken to a local human hospital where a magnetic resonance imaging (MRI) workup of cranium and cervical and thoracic spine was performed. A 1.5 Tesla GE signa scanner was used with standard pulse sequences. A brain MRI was within normal limits. A cervical spine exam was done without contrast. This showed an abnormal cervical spinal cord. Patchy mixed signal extended from the C-1 level to the C5-6 level. This signal was predominately high T2 without any sign of cord expansion. Some minimal intervertebral disc bulges were seen at C2-3 and C3-4, which contacted the anterior cervical spinal cord but did not compress the cord. Incidental old spinous process fractures were noted at thoracic levels 3 and 4. MR Angiography was done in the cervical region and showed normal vertebral and carotid arteries. The abnormal signal in the cervical spinal cord was nonspecific. Tumor and post traumatic changes were considered unlikely. An inflammatory, demyelinating, metabolic or possibly toxic process was considered.

Over the next several days neurologic signs worsened further. Based on the progressive neurologic signs and poor prognosis suggested by MRI images, the tiger was anesthetized a final time on day 38 and euthanatized by intravenous barbiturate overdose (Beuthanasia-D Special™, Schering-Plough Animal Health, Union, NJ, USA).

Gross postmortem examination revealed healing fractures of dorsal spinous processes of C7, T1, T3, and T4. No other significant lesions were noted. Histopathologic lesions were most pronounced in the brain stem and cervical spinal cord. Within these areas, there was marked nonsuppurative meningitis, gliosis and small regions with neuronal swelling and necrosis of neuropil. Many neurons and astrocytes in the most severely affected areas had eosinophilic intranuclear inclusion bodies that were confirmed to be canine distemper virus by immunohistochemistry. Descending tracts in the spinal cord white matter had demyelinization and axonal swelling. No significant lesions were noted in other tissues.

The source of infection of this tiger is unknown. However, following this case, two wild raccoons showing neurologic signs were captured on zoo grounds. Histologic lesions consistent with canine distemper were identified.


Speaker Information
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Kenneth N. Cameron, DVM
Veterinary Services
Cincinnati Zoo & Botanical Garden
Cincinnati, OH, USA

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