Eleven-month-old, female intact bobcat (Lynx rufus)In summer, 2006, the kitten was found orphaned at approximately 2 months of age and taken to a wildlife rehabilitation facility. In September the animal developed slowly progressive neurological disease including a head tremor, nystagmus, ataxia and loss of hind limb function. The animal was considered unsuitable for reintroduction, humanely euthanized and submitted to the Colorado State University veterinary diagnostic lab by the Colorado Division of Wildlife.
The animal was in moderate body condition with minimal autolysis.Â The brain had been removed immediately following euthanasia; both fresh and fixed brain was submitted with the carcass.Â No abnormalities were observed on gross post mortem examination.
Present on each slide are sections of spinal cord taken from the cervical and mid-thoracic region.Â Blood vessels in both grey and white matter are cuffed by lymphocytes, plasma cells and rare macrophages that often extend into adjacent neuropil.Â In rare sections perivascular hemorrhage is present.Â Glial nodules are present in both the grey and white matter.Â Most commonly in areas of gliosis, individual neuronal cell bodies are degenerate or necrotic characterized by hypereosinophilia, loss of Nissl substance, nuclear pyknosis and variable neuronophagia.Â Occasionally perikaryonic vacuolization and rarefaction of the neuropil is present.Â Astrocytes numbers are moderately increased and often surround degenerate neurons (satellitosis).Â Within the white matter there is a variable amount of axonal degeneration, spongy change and occasional digestion chambers.Â The severity of lesion varies between submitted sections.Â
Spinal cord; lymphoplasmacytic myelitis, chronic, moderate with neuronal necrosis, astrocytosis, perivascular cuffing and glial nodules
1.Â Rabies (FA, brain): Negative
2.Â Canine distemper virus (PCR, brain): Negative
3.Â Toxoplasma gondii (PCR, brain): Negative
4.Â Canine parvovirus/feline panleukopenia virus (PCR, brain): Positive
5.Â West Nile virus (IHC, brain and spinal cord): Positive
6.Â West Nile virus (PCR, brain): Negative
West Nile virus
West Nile virus emerged as a significant pathogen of birds, humans and horses in the northeastern United States in 1999.Â The arthropod-borne Flavivirus subsequently expanded north and westward resulting in widespread morbidity, and variable mortality, in susceptible species.Â Reports of WNV infection in non-avian wildlife are largely opportunistic and to our knowledge infection has not been previously reported in a bobcat.
Histologic lesions observed in this case are consistent with those previously reported in other mammals including horses,1 fox squirrels,2 white-tailed deer4 and a dog5.Â The discordance between the WNV PCR and IHC results in this case may reflect the protracted nature of the disease and available tissue for testing.Â In the brain only very rare neurons stained weakly with IHC while neuronal cell bodies and occasional leukocytes in the spinal cord had abundant antigen; however only fresh brain, and no spinal cord, was available for PCR.Â The paucity of staining in the brain may represent remnant antigen while no RNA was present for amplification.
Classical gross and histological evidence of CPV or FPV infection in brain or gastrointestinal tract were absent in this case.Â The PCR product was sequenced and determined to be canine parvovirus 2b; the significance of this finding is unknown.Â Parvoviral infections have been reported in numerous wild carnivoirs8 and it has been suggested that CPV 2a and 2b are more common in large, wild cats compared to domestic felids.7 Recently, parvovirus infection has been reported in association with non-suppurative meningoencephalitis in dogs and cats and proposed as a new parvoviral disease pattern;6 similar lesions were observed in the brain of this bobcat.Â Canine parvovirus is also widely distributed throughout the environment and the positive PCR result may be the result of contamination of the tissue sample during brain removal.Â
Spinal cord, cervical and thoracic segments
(per contributor): Myelitis, lymphoplasmacytic,
multifocal, mild, with moderate axonal degeneration,
bobcat (Lynx rufus).
Following its initial identification
in the United States in 1999, West Nile Virus has
subsequently spread throughout most of the United States
and the southern parts of Canada.Â The virus is genetically
divided into two lineages.3 Lineage 1, occasionally
highly virulent (clade 1a), is seen in North America and
other areas of the world.3 Lineage 2, usually nonpathogenic
or only mildly virulent, is present primarily
within enzootic areas of Africa.3
The virus is maintained in the environment within the wild bird population through a bird-mosquito-bird cycle. Culex spp are the primary vectors of transmission, although the virus has been identified in ticks.Â Additionally, transmission has been documented through direct contact and viafomites.3
Histologic lesions often can be very mild even in severe disease and include nonsuppurative encephalomyelitis, gliosis, and glial nodule formation with occasional neuronal degeneration and necrosis.3 The primary target cell is the neuron with additional damage to microglial cells.9 Apoptotic cell death appears to be the mechanism of neuronal injury.9 Conference participants slides were quite variable in the presence and severity of perivascular cuffing and hemorrhage.
Primarily an infection of birds, WNV has also been documented in horses, humans, ruminants, cervids, canids, felids, squirrels, rodents, and swine.2,3,4
1.Â Cantile C, Del Piero F, Di Guardo G, Arispici M: Pathologic and immunohistochemical findings in naturally occurring West Nile virus infection in horses.Â Vet Pathol 38:414-421, 2001
2.Â Kiupel M, Simmons HA, Fitzgerald SD, Wise A, Sikarskie JG, Cooley TM, Hollamby SR, Maes R: West Nile virus infection in Eastern fox squirrels (Sciurus niger).Â Vet Pathol 40:703-707, 2003
3.Â Maxie MG, Youssef S: Nervous system.Â In: Jubb, Kennedy, and Palmers Pathology of Domestic Animals.Â ed.Â Maxie MG, 5th ed., vol.Â 1, pp.Â 421-422.Â Saunders Elsevier, Endinburgh, 2007
4.Â Miller DL, Radi ZA, Baldwin C, Ingram D: Fatal West Nile virus infection in a white-tailed deer (Odocoileus virginianus).Â J Wildl Dis 41: 246-249, 2005
5.Â Read RW, Rodriguez DB, Summers BA: West Nile virus encephalitis in a dog.Â Vet Pathol 42:219-222, 2005
6.Â Schwab S, Herden C, Seeliger F, Papaioannou N, Psalla D, Polizopulou Z, Baumgartner W: Non-suppurative Meningoencephalitis of Unknown Origin in Cats and Dogs: an Immunohistochemical Study.Â J Comp Pathol 136:96-110, 2007
7.Â Steinel A, Munson L, van Vuuren M, Truyen U: Genetic characterization of feline parvovirus sequences from various carnivores.Â J Gen Virol 81:345-350, 2000
8.Â Steinel A, Parrish CR, Bloom ME, Truyen U: Parvovirus infections in wild carnivores.Â J Wildl Dis 37:594-607, 2001
9.Â Zachary JF: Nervous system.Â In: Pathologic Basis of Veterinary Disease, eds.Â McGavin MD, Zachary JF, 4th ed., pp.Â 882-883.Â Elsevier, St.Â Louis, MO, 2007