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In the United States, equine encephalitides for which vaccines are available include eastern equine encephalomyelitis (EEE), western equine encephalomyelitis (WEE), Venezuelan equine encephalomyelitis (VEE) and West Nile Virus encephalomyelitis. The distribution of EEE has historically been restricted to the eastern, southeastern and some southern states (but disease incidence is also reported in the upper Midwestern states of Ohio, Michigan and Wisconsin). Outbreaks of WEE have been recorded in the western and mid-western states. Variants of WEE have caused sporadic cases in the northeast and southeast, most notably Florida. VEE occurs in South and Central America but has not been diagnosed in the United States for more than 40 years. The availability of licensed vaccine products combined with an inability to completely eliminate risk of exposure justifies immunization against EEE and WEE as core prophylaxis for all horses residing in or traveling to North America and any other geographic areas where EEE and/or WEE is endemic. 

Transmission of EEE/WEE/VEE is by mosquitoes, and infrequently by other bloodsucking insects, to horses from wild birds or rodents, which serve as natural reservoirs for these viruses. Human beings are also susceptible to these diseases when the virus is transmitted to them by infected mosquitoes; however, horse-to-horse or horse-to-human transmission by mosquitoes is highly unlikely, because the level and duration of viremia is insufficient to infect mosquitoes that might feed on a horse affected withEEE or WEE. On the other hand, the viremia that occurs in horses infected with VEE virus subtypes 1AB and 1C is much higher. Direct horse-to-horse or horse-to-human transmission of VEE is possible. Of these 3 encephalomyelitides, WEE has the lowest mortality (approx. 50%). Eastern equine encephalomyelitis is the most virulent for horses, with mortality approaching 90%. Epidemiological evidence indicates that young horses are particularly susceptible to disease caused by EEE virus. Venezuelan equine encephalomyelitis caused by subtypes 1AB and 1C can give rise to mortality rates ranging from 20 to 80%; however, some horses develop subclinical infection that results in lasting immunity.

The risk of exposure and geographic distribution of EEE and WEE vary from year-to-year with changes in distribution of insect vectors and reservoirs important in the natural ecology of the virus. EEE activity in mosquitoes and birds, and resultant disease in humans and equids, continues to cause concern along the East Coast and demonstrates northward encroachment. WEE has caused minimal disease in horses in the last two decades; however, the virus continues to be detected in mosquitoes and birds throughout the Western states. In addition, variants that cause clinical disease in equids have been detected in the eastern U.S.

VEE is a reportable foreign animal disease. Epidemics of VEE occur when the virus undergoes genetic change and develops greater virulence for humans and equid species. Viral variants, ;which belong to subtypes 1AB and 1C, are able to multiply to high levels in the horse which serves as a amplifying host of the virus in these outbreaks. Strains of subtype 1E have also been shown to cause morbidity and mortality in horses but on a much lesser scale.1,2 Areas of Southern Texas, California, Louisiana, Mississippi, Alabama and the West Coast of Florida are likely at the most risk for natural VEE encroachment from Central and South America.  Vaccination against VEE is controversial because:

1) Vaccination against a foreign animal disease may confound testing in the event of an outbreak. However, vaccination against EEE/WEE will also result in cross-reaction to VEE virus in certain serologic tests.

2) Experimental and field data have demonstrated that previous infection with either EEE or WEE may provide cross protection against VEE. It is therefore possible that EEE/WEE bivalent vaccination may provide partial cross-protection, although it is likely to be less than that following infection.

3) A conditionally available modified live (MLV) VEE vaccine has been released during previous outbreaks and provides superior protection against the disease and high titered viremias. Should an outbreak occur, it is likely that this highly attenuated MLV would be released for restricted use subject to certain conditions being met.

In summary, horses that receive annual EEE/WEE vaccines may be partially protected against VEE infection. In the event of an outbreak, the availability of and vaccination with the highly effective MLV product would induce rapid, complete immunity while allowing for accurate surveillance before VEE specific vaccination.  The use of killed VEE vaccine should be performed only in high-risk areas of the US, at the discretion of the attending veterinarian, or when necessary, with input from state agriculture officials. The use of the inactivated VEE vaccine is less effective than the MLV VEE vaccine, and will reduce immune responses to the MLV VEE vaccine.


EEE/WEE vaccines currently available are formalin inactivated adjuvanted whole virus products. Early testing of bivalent (EEE/WEE) vaccines was performed by intracranial challenge with either EEE and WEE; the formalin inactivated preparations were shown to be highly efficacious in protecting against clinical disease.

Currently, the only available VEE vaccines are killed products; a MLV would likely be conditionally released in the face of an outbreak.


Vaccination Schedules EEE/WEE:

Adult horses previously vaccinated against EEE/WEE: Annual revaccination must be completed prior to vector season in the spring. In animals of high risk or with limited immunity, more frequent vaccination or appropriately timed vaccination is recommended in order to induce protective immunity during periods of likely exposure. In areas where mosquitoes are active year-round, many veterinarians elect to vaccinate horses at 4- to 6- month intervals to ensure uniform protection throughout the year, although this practice is not specifically recommended by manufacturers of vaccines.

Adult horses, previously unvaccinated against EEE/WEE or of unknown vaccinal history: Administer a primary series of 2 doses with a 4 to 6 week interval between doses. Revaccinate prior to the onset of the next vector season and annually thereafter.

Pregnant mares, previously vaccinated against EEE/WEE: Vaccinate 4 to 6 weeks before foaling.

Pregnant mares, unvaccinated or having unknown vaccinal history: Immediately begin a 2-dose primary series with a 4-week interval between doses. Booster at 4 to 6 weeks before foaling or prior to the onset of the next vector season—whichever occurs first.

Foals of mares vaccinated against EEE/WEE in the pre-partum period: Administer a primary 3-dose series beginning at 4 to 6 months of age. A 4 to 6 week interval between the first and second doses is recommended. The third dose should be administered at 10 to 12 months of age prior to the onset of the next mosquito season.

In the southeastern U.S., due to earlier seasonal disease risk, vaccination may be started at 2 to 3 months of age. When initiating vaccinations in younger foals, a series of 4 primary doses should be administered, with a 4-week interval between the first and second doses and between the second and third doses. The fourth dose should be administered at 10 to 12 months of age prior to the onset of the next mosquito season.

Foals of unvaccinated mares or having unknown vaccinal history: Administer a primary series of 3 doses with a 4-week interval between the first and second doses and an 8-week interval between the second and third doses. If the primary series is initiated during the mosquito vector season, an interval of 3 to 4 weeks between the second and third doses is preferable to the above described interval of 8 weeks.

NOTE: Foals in the Southeastern USA – The primary vaccination series should be initiated at 3 months of age due to early seasonal vector presence.  

Horses having been naturally infected and recovered: Recovered horses likely develop lifelong immunity. Consider revaccination only if the immune status of the animal changes the risk of susceptibility to infection. Examples of these conditions would include the long-term use of corticosteroids and equine pituitary pars intermedia dysfunction (PPID).