West Nile virus is a vector-borne flavivirus that was historically endemic to Africa, West Asia, and the Middle East. West Nile virus was first recognized to cause disease within the United States in equids, birds, and humans in New York in 1999. After the introduction of WNV to the United States in 1999, the virus spread westward.1 By 2002, the virus had spread to 43 states, including Colorado; clinical disease attributable to WNV infection was diagnosed in > 15,000 equids.2
West Nile virus infection in endemic areas was thought to cause subclinical or mild infection in equids; however, cases of WNV in the United States have been associated with severe clinical disease and a case fatality rate of 25% to 30%.1,3,4 Clinical signs in equids infected with WNV include muscle fasciculation, ataxia or paralysis, hyperexcitability, convulsions or twitching, recumbency with some equids unable to rise, incoordination, and obtunded mentation.5 The incidence of laboratory-confirmed WNV infection among equids with clinical signs consistent with WNV has not been described.
The IgM capture ELISA is the standard diagnostic test used for detection of WNV in equids with clinical signs of disease. Sensitivity and specificity of the IgM ELISA presently being used are not known. The presence of IgM antibodies specifically directed against WNV in a serum sample indicates that the equid was naturally exposed to the wild form of the virus but does not confirm that WNV is the cause of current disease.4,5 Vaccination with a WNV vaccine has not been found to result in a positive IgM ELISA result but has been found to induce an antibody response as detected by the plaque reduction neutralization test response experimentally.5 The IgM antibodies can persist in equine serum for as long as but not > 6 to 8 weeks.
A killed WNV vaccine, which was designed to prevent viremia, became available for equids in August 2001.2 This WNV vaccine prevents viremia in experimentally infected equids and reduces the severity of disease in equids with positive ELISA results.2,6 The effect of vaccination on the ability to detect WNV infection via ELISA is not known. The number of equids vaccinated against WNV in Colorado in 2003 is not known. Prior to the summer of 2002, vaccination was likely limited because of the uncertainty of when or whether WNV would be detected in Colorado. The incidence and severity of disease caused by WNV in the equine population that was seen in Colorado in 2002 was unexpected, and a large number of horses were not fully vaccinated against the virus when the virus was first detected in the state.2 Unlike 2002, in 2003, owners had ample access to the vaccine as well as the opportunity to vaccinate their animals prior to the onset of the vector season, and an effort was made to educate owners regarding the need to vaccinate their animals.a
Several factors affect the occurrence of WNV in an equine population, including the level of viral challenge, host susceptibility, and measures taken to limit exposure of susceptible hosts to infected mosquitoes in a given geographic region.7 The lack of full vaccination of many equids in Colorado and the high level of natural exposure potentially resulted in a large number of cases of WNV infection in equids in Colorado in 2002.2 Other environmental and geographic factors may affect the incidence of WNV infection in equids likely by affecting the vector population. The prevalence of disease among animals kept at high elevations appears to be low.8 Ambient temperature, precipitation, and mosquito abatement also likely play a role in viral challenge and subsequent attack rate of WNV infection in equids.7,8
The purpose of the study reported here was to evaluate factors associated with positive IgM capture ELISA results in equids with clinical signs compatible with WNV infection. Prevalence of WNV infection in equids was also described.
West Nile virus
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