Tumor necrosis factor-alpha expression in white-tailed deer (Odocoileus virginianus) infected with Epizootic haemorrhagic disease virus.

Epizootic haemorrhagic disease (EHD) is the most important infectious disease of white­tailed deer (WTD), however little is known about the role of inflammatory mediators in the pathogenesis. We characterized the expression of tumor necrosis factor­alpha (TNF-α) ex vivo in tissues of WTD experimentally or naturally infected with EHD virus serotype 2 and in WTD peripheral blood mononuclear cells (PBMC) infected with EHD virus serotype 2 in vitro. Circulating levels of TNF-α were evaluated in serum from experimentally infected deer via cytotoxicity assay. The expression of TNF-α in tissues was evaluated via immunohistochemistry (IHC) in both experimentally and naturally infected deer. Semi­quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to assess the level of TNF-α mRNA in tissues from experimentally infected deer and WTD's PBMC. Circulating levels of TNF-α were not increased in infected animals and TNF-α was not detected in tissues of infected deer. Increased transcription of TNF-α was detected neither in infected WTD nor in the PBMC. Tumor necrosis factor-alpha may not play a significant role in the pathogenesis of EHD virus infection in WTD.

Attempts to identify the source of avian vacuolar myelinopathy for waterbirds.

Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots (Fulica americana), mallard ducks and ducklings (Anas platyrhynchos), quail (Coturnix japonica), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels (Falco sparverius), and American crows (Corvus brachyrhynchos). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla, or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.

Choroid plexus cyst in a dog.

A 6-year-old male Doberman Pinscher had a 2-month history of dysequilibrium. Lesion localization was determined to be the cerebellomedullary pontine angle. In computed tomographic images, a well-defined, circular, hypoattenuating mass was visible at the cerebellomedullary pontine angle. The lesion, which was isoattenuating to cerebrospinal fluid, was 4 x 8 mm in diameter. Peripheral ring enhancement was evident after contrast medium administration. A choroid plexus cyst was diagnosed histopathologically.

Morbidity and mortality factors in key deer (Odocoileus virginianus clavium).

The population health of endangered Key deer (Odocoileus virginianus clavium) was monitored from 10 February 1986 to 28 September 2000 by necropsy of animals that were killed by vehicles, euthanized because of terminal injuries or disease conditions, or found dead. The predominant mortality factor during the period was collision with motor vehicles; however, several infectious diseases were diagnosed, including infections with Arcanobacterium pyogenes, Haemonchus contortus, Salmonella spp., and Mycobacterium avium subsp. paratuberculosis. During the period monitored, the only infectious disease that was thought to have affected population dynamics was haemonchosis. Nevertheless, several of the observed diseases have potential to impact viability of the Key deer population under appropriate environmental conditions.

Paratuberculosis in key deer (Odocoileus virginianus clavium).

Paratuberculosis was diagnosed in an endangered Key deer (Odocoileus virginianus clavium) in November 1996. Between 10 April 1997 and 28 September 2000, the Key deer population was monitored for infection with Mycobacterium avium subsp. paratuberculosis by necropsy of available carcasses (n = 170), fecal cultures, and serology. One additional clinically affected Key deer was discovered in July 1998, and M. avium subsp. paratuberculosis was cultured from the feces of one live, asymptomatic deer. The results of this study provided sufficient evidence to consider the Key deer herd infected with M. avium subsp. paratuberculosis at very low prevalence.