The two most frequently encountered causes of equine encephalitis or equine encephalomyelitis in North America are Eastern equine encephalomyelitis (EEE) and West Nile encephalitis (WNE) viruses. Both are mosquito-borne and neurotropic. The respective viruses are not restricted to equids in terms of their host range; each can be transmitted to humans and certain other mammalian and avian species. Both diseases are a source of concern for the equine industry not only from the potentially life-threatening consequences of either infection, but also from the economic losses involved.
Eastern equine encephalomyelitis poses an annual threat to equids in the Gulf and Atlantic coastal states and the Great Lakes region, extending in certain years as far north as Eastern Canada. It is occasionally recorded in some inland states such as Arkansas, Oklahoma, Tennessee, Kentucky, and Iowa. Evidence of EEE activity is most often reported in Florida, in which it has been confirmed as early as January, as recorded in 2018. Over the past 15 years, the yearly incidence of EEE cases in equids has ranged from 60 (2011) to 712 (2003), with an annual average of 206 cases. In 2017, 86 cases of the disease were reported in 13 states. In temperate regions, transmission of EEE virus is seasonal, occurring in the summer and the fall. In sub-tropical regions such as Florida, there is a year-round risk of EEE, with virus transmission peaking in the summer months.
Equids and humans are tangential or dead-end hosts of EEE virus and neither plays a role in the virus’ natural life-cycle. Infections in horses, mules, and donkeys are frequently life-threatening; case fatality rates can be as high as 90%.
West Nile encephalitis is also a cause of significant concern to veterinary practitioners and members of the equine industry. Within four years following initial introduction of the causal virus in New York State in 1999, the virus had spread to 48 states and several provinces in Canada. Since 1999, the yearly incidence of WNE cases in equids has ranged from 60 (2000) to 15,257 (2002). The annual average number of cases over the past 10 years was 272. In 2017, 307 equine cases were reported in 39 states.
Similar to EEE, WNE virus transmission is seasonal, occurring in the summer and extending well into the fall. Neither equids nor humans serve as amplifying hosts for WNE virus insofar as viremias are insufficient in magnitude and duration to infect mosquitoes. Unlike EEE, only about 10% of WNE virus-exposed horses will develop clinical infections. Reported case-fatality rates in affected horses can reach 30-40 percent, less than half that encountered in cases of EEE.
The American Association of Equine Practitioners (AAEP), in accordance with criteria defined by the American Veterinary Medical Association with respect to “core vaccines”–namely those that protect against diseases that are endemic, of potential public health significance, and represent a risk of causing severe disease—strongly recommends that horses be immunized against EEE and WNE.
Available inactivated whole-virus vaccines against EEE (including Western equine encephalomyelitis) have been shown to be safe and effective in protecting against this disease. Two inactivated whole-virus vaccines, a live canary pox vector vaccine and an inactivated flavivirus chimera vaccine are available against WNE. All have been confirmed safe and effective in preventing the disease.
Despite the AAEP recommendations to horse owners to vaccinate their horses against EEE and WNE, regrettably many fail to do so. The vast majority of equine cases of EEE and WNE either have no history of vaccination against the particular virus or else the vaccination history is incomplete. There is need for an ongoing concerted effort, utilizing all avenues of communication including social media, to alert horse owners of the dangers of these two vector-borne diseases and of the importance of vaccination as an effective means of prevention and averting the losses that continue to occur every year in unprotected horses.
CONTACT: Peter J. Timoney, MVB, MS, PhD, FRCVS—email@example.com—859/218-1094—University of Kentucky Maxwell H. Gluck Equine Research Center, Lexington