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- Author or Editor: Michael B. Porter x
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Abstract
Objective—To evaluate CSF in horses with confirmed West Nile virus encephalomyelitis.
Design—Retrospective study.
Animals—30 horses.
Procedure—Results of CSF analyses from horses with acute neurologic signs attributed to West Nile virus infection that was confirmed by immunoglobulin M antibody capture ELISA were reviewed and analyzed.
Results—Among 30 CSF samples, findings in 8 (27%) were within reference ranges and in 22 (73%) were abnormal. Among the 22 abnormal samples, mononuclear pleocytosis was found in 16 (73%) and high protein concentration with nucleated cell count within reference range was found in 6 (27%) samples. A predominance of lymphocytes was found in 11 of 16 samples with mononuclear pleocytosis, and a predominance of large mononuclear cells was found in 5 of 16 samples. Sensitivities of analyses of CSF obtained from the lumbosacral and atlanto-occipital regions of the spinal cord were 89 and 50%, respectively.
Conclusions and Clinical Relevance—Results suggest that in horses with acute onset of neurologic signs caused by West Nile virus encephalomyelitis, findings in the CSF are likely to be abnormal, mononuclear pleocytosis with lymphocytic predominance may be most commonly observed, and CSF collected from the lumbosacral region may be abnormal more commonly than CSF collected from the atlanto-occipital region. (J Am Vet Med Assoc 2002;221:1303–1305)
Abstract
Objective—To determine signalment, clinical findings, results of diagnostic testing, outcome, and postmortem findings in horses with West Nile virus (WNV) encephalomyelitis.
Design—Retrospective study.
Animals—46 horses with WNV encephalomyelitis.
Procedure—Clinical data were extracted from medical records of affected horses.
Results—On the basis of clinical signs and results of serologic testing, WNV encephalomyelitis was diagnosed in 46 of 56 horses with CNS signs. Significantly more males than females were affected. Increased rectal temperature, weakness or ataxia, and muscle fasciculations were the most common clinical signs. Paresis was more common than ataxia, although both could be asymmetrical and multifocal. Supportive treatment included anti-inflammatory medications, fluids, antimicrobials, and slinging of recumbent horses. Results of the IgM capture ELISA and the plaque reduction neutralization test provided a diagnosis in 43 horses, and only results of the plaque reduction neutralization test were positive in 3 horses. Mortality rate was 30%, and 71% of recumbent horses were euthanatized. One horse that had received 2 vaccinations for WNV developed the disease and was euthanatized. Follow-up communications with 19 owners revealed that most horses had residual deficits at 1 month after release from the hospital; abnormalities were resolved in all but 2 horses by 12 months after release.
Conclusions and Clinical Relevance—Our findings were similar to those of previous WNV outbreaks in horses but provided additional clinical details from monitored hospitalized horses. Diagnostic testing is essential to diagnosis, treatment is supportive, and recovery rate of discharged ambulatory horses is < 100%. (J Am Vet Med Assoc 2003;222:1241–1247)
