Epidemiology

Eastern equine encephalitis virus (EEEV) was first isolated in 1933 from the brain of a horse that died of encephalitis.[4] The virus has subsequently been isolated from humans, wild birds, small mammals, and mosquitoes across much of eastern and midwestern North America.[5]​

In North America, a human outbreak was first noted in 1938 in Massachusetts, resulting in 34 hospitalisations and nearly as many deaths.[6] Twenty years later, an outbreak in New Jersey resulted in 32 cases of encephalitis, including 22 deaths.[6] During that outbreak, it was estimated that 11 children or 40 adults had asymptomatic or mild infection for every encephalitis case.[7]

Since then, sporadic human cases have been noted in these and other eastern states of North America, with an average of 11 cases of eastern equine encephalitis (EEE) reported per year in the US.[8]​​

  • The number of reported cases varies from year to year. A spike in cases was reported in 2019 (38 cases), but the reasons for this increase are unknown.

  • States with the highest incidence per 100,000 population between 2003 and 2024 were Alabama, Arkansas, Florida, Georgia, Michigan, North Carolina, and South Carolina.

  • In 2024, 19 cases were reported, all with neuroinvasive disease, and 5 deaths. No cases have been reported in 2025 as yet (as of 1 July 2025).

  • CDC: data and maps for eastern equine encephalitis Opens in new window

The average annual incidence is reported to be 0.04 cases per million children and 0.03 cases per million adults.[9] Infection is more common in males, and people aged <15 years or >50 years.[1][10]

Outbreaks have increased in North America over the years, reflecting a broader trend in the resurgence of arboviral diseases. This rise may be attributed to several factors including:[10]

  • Climate change, which influences vector migration and mating patterns

  • Increased development near wetlands

  • Higher rates of travel

  • Growing popularity of outdoor recreational activities

Outbreaks have previously been reported in the Caribbean, but in the last decade outbreaks have resurfaced throughout Latin America including Panama, Peru, and Argentina.[11]​ Better surveillance, enhanced tracking systems, and effective epidemic monitoring are warranted in these countries.

Imported cases have been reported in non-endemic countries. For example, in 2009, a case was reported in the UK in a returning traveller from the US.[12]

In North America, transmission of the virus occurs mainly in and around wooded wetlands in the Atlantic and Gulf Coast states and the Great Lakes region, which is where the enzootic transmission cycle between passerine birds (the natural reservoir for EEEV) and the ornithophilic mosquito Culiseta melanura (the enzootic vector for EEEV) is maintained. During epizootics, the virus is amplified in a broader range of avian hosts by ‘bridge’ vectors such as the mosquito species Coquillettidia perturbans, Aedes vexans, Aedes sollicitans, Aedes albopictus, and Culex erraticus.[13][14][15]​​ These species are more likely than the enzootic vector, C melanura, to bite mammals and cause equine and human disease. Most human infections occur between late spring and early autumn when the mosquito population is at its highest, with more than 80% of reported human cases occurring from July to September.[1]​​[16]​ Nonetheless, freshwater swamp and bog environments provide a source habitat for the virus, even in seasons of low transmission.[10]

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