This work was performed in the Large Animal Clinic of Faculty of Veterinary Science, Szent Istvan University, Hungary. This work was presented at Congress of the British Equine Veterinary Association, 2009, Birmingham, 55th Annual Convention American Association of Equine Practitioners, 2009, Las Vegas.
Equine Encephalomyelitis Outbreak Caused by a Genetic Lineage 2 West Nile Virus in Hungary
Article first published online: 1 APR 2011
Copyright © 2011 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 25, Issue 3, pages 586–591, May/June 2011
How to Cite
Kutasi, O., Bakonyi, T., Lecollinet, S., Biksi, I., Ferenczi, E., Bahuon, C., Sardi, S., Zientara, S. and Szenci, O. (2011), Equine Encephalomyelitis Outbreak Caused by a Genetic Lineage 2 West Nile Virus in Hungary. Journal of Veterinary Internal Medicine, 25: 586–591. doi: 10.1111/j.1939-1676.2011.0715.x
- Issue published online: 3 MAY 2011
- Article first published online: 1 APR 2011
- Submitted June 22, 2010; Revised December 23, 2010; Accepted February 15, 2011.
- Nervous system;
- West Nile virus
Background: The spread of lineage 2 West Nile virus (WNV) from sub-Saharan regions to Europe and the unpredictable change in pathogenicity indicate a potential public and veterinary health threat and requires scientific awareness.
Objectives: To describe the results of clinical and virological investigations of the 1st outbreak of a genetic lineage 2 WNV encephalomyelitis in horses.
Animals: Seventeen horses with neurologic signs.
Methods: Information regarding signalment, clinical signs, and outcome was obtained for each animal. Serology was performed in 15 cases, clinicopathological examination in 7 cases, and cerebrospinal fluid was collected from 2 horses. Histopathology was carried out in 4 horses, 2 of which were assessed for the presence of WNV in their nervous system.
Results: WNV neutralizing antibody titers were between 10 and 270 (median, 90) and the results of other serological assays were in agreement with those of the plaque reduction neutralization test. Common signs included ataxia, weakness, asymmetric gait, muscle tremors, hypersensitivity, cranial nerve deficits, and recumbency. Twelve animals survived. Amplicons derived from the infection-positive specimens allowed molecular characterization of the viral strain.
Conclusions and Clinical Importance: From our results, we conclude that this outbreak was caused by a lineage 2 WNV strain, even though such strains often are considered nonpathogenic. Neurological signs and survival rates were similar to those reported for lineage 1 virus infections. The disease occurrence was not geographically limited as had been the typical case during European outbreaks; this report describes a substantial northwestern spread of the pathogen.