Discussion

West Nile virus (WNV) is a RNA Flaviviridae (Arbo) virus. West Nile virus infection in horses has been reported in all states within the US, in the Canadian provinces, northern Mexico, parts of South America, northern Africa, the Middle East, as well as parts of Europe (especially Spain and Italy), Australia and parts of Asia. Current knowledge suggests that there is a low-level and recurrent circulation of West Nile virus (WNV) in some areas in Europe, with sporadic human and/or equines cases (Chevalier et al. 2011). There is evidence that WNV is spreading geographically in Europe possibly due to climatic change and/or change in vector populations/dynamics. There is also a concern that infected mosquitoes may arrive by planes or ships from endemic countries. There are 2 lineages of the virus, 1 and 2, and 1 is responsible for most clinical disease although lineage 2 infection has been reported to cause illness in horses in Greece and Africa. West Nile virus is transmitted to horses by mosquitoes, i.e. Culex spp. Birds serve as the reservoir host and large numbers of bird mortalities may be noted just prior to outbreaks in horses. Horses are incidental hosts that apparently do not produce a level of viraemia capable of transfer of virus to mosquitoes. There are several risk factors for WNV in horses including vaccination status, geographic location (endemic area), age (adults more common) and season of year (fall most common). The initial outbreak of WNV in horses (and humans) in North America occurred in 1999 with 25 equine cases. The greatest yearly number of cases (15,257) was in 2002. The outbreak initially spread from the northeastern US to the southeastern US, followed by a western spread that eventually involved horses in all of the continental states. The percentage of infected horses that demonstrated clinical signs is unknown but was likely <10%. Clinical signs of WNV are variable since disease may occur in any part of the central nervous system resulting in either changes in mentation, signs of cranial nerve deficits (uncommon), fasciculations, ataxia and/or paresis. Ataxia in multiple limbs is the most common clinical sign and fasciculations seemed to be unusually common compared to most other adult equine CNS disorders. Fever is not found in many of the naturally- occurring cases and was not present even in some experimentally infected horses. It is unknown why only a small percentage of infected horses develop clinical signs but potential reasons for this include; the magnitude of viraemia, the permeability of the BBB, and balance between the immune clearance and the inflammatory response. Diagnosis is by knowledge of risk factors of disease, clinical signs which may look similar to several other CNS diseases of the horse, CSF cytology (mostly a mild to moderate lymphocytic pleocytosis) and most importantly finding a positive capture IgM ELISA or by seroconversion. Vaccination does not cause a positive IgM capture ELISA. Post mortem diagnosis is best determined by PCR as immunohistochemistry is known to have only a moderate sensitivity. Treatment of WNV infection in horses is supportive in addition to administration of anti-serum early in the course of the disease. Hyperimmune WNV equine origin plasma is available in the US and recent studies using animal models and naturally-occurring human patients have documented clinical improvement in neurological signs when specific antibodies against WNV was administered. Mortality rate in clinically affected horses has been variable, but generally
<30%. Recumbent horses have a poor prognosis. Clinically diseased horses that have rapid improvement in the first week of illness often appear to have full recovery. Some horses may have clinical improvement but maintain residual CNS deficits. There are at least 3 vaccines that are currently approved for WNV vaccination in horses in the US and all appear to be highly efficacious if administered properly. Lineage 1 WNV vaccines are likely protective again lineage 2 infections.