Epidemiology

EEEV was first isolated in 1933 from the brain of a horse that died of encephalitis.[5] The virus has subsequently been isolated from humans, wild birds, small mammals, and mosquitoes across much of eastern and midwestern North America. Isolates have also been obtained from the Caribbean and Central and South America, but these variants were observed many years ago and were rarely, if ever, implicated in human disease. Furthermore, they were noted to be antigenically distinct from North American EEEV isolates.[6]

In North America, a human EEEV outbreak was first noted in 1938 in Massachusetts, resulting in 34 hospitalisations and nearly as many deaths.[7] Twenty years later, an outbreak of EEEV in New Jersey resulted in 32 cases of encephalitis, including 22 deaths.[7] During that outbreak, it was estimated that 11 children or 40 adults had asymptomatic or mild infection for every encephalitis case.[8] Since then, sporadic human cases have been noted in these and other eastern states of North America, with an average of 7 human eastern equine encephalitis (EEE) cases reported per year in the US.[9] Between 2010 and 2018, a total of 69 human cases were reported to the US national arboviral surveillance system, ArboNET. An additional 38 cases of EEEV are reported in provisional data from 2019, 19 of which were fatal.[9] In 2019, in the state of Massachusetts, the first human infections with EEEV have been reported since 2013; between January to August, four cases of EEEV were confirmed, including one fatality, prompting warnings from medical officials about particularly intense levels of EEEV activity.[10] The average annual incidence is reported to be 0.04 cases per million children and 0.03 cases per million adults.[11] US states with the highest incidence rates include Florida, Massachusetts, New York, North Carolina, and Michigan.[9] 

In North America, EEEV transmission 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.[12][13][14] 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.[15]

South American EEEV (now known as Madariaga virus [MADV]) is genetically distinct and more heterogeneous than its North American counterpart.[3] Prior to 2010, only three human cases had been reported. In 2010, an outbreak of MADV and Venezuelan equine encephalitis virus (an alphavirus that is endemic in Central and South America) occurred in the eastern province of Darién, Panama.[16] There were 14 confirmed human cases of MADV infection, 8 of whom were hospitalised. All of the hospitalised patients were children, and most suffered seizures and other neurological complications. Subsequently, a serosurvey in the region demonstrated that 16% of the population had evidence of prior MADV infection.[17] Seroprevalence was not age-dependent, indicating that the disease had emerged in recent years. A key risk factor was exposure to farm or pasture land.[17] MADV has been isolated from various Culex (Melanoconion) species, and it is thought that these are its main vector.[18] Evidence of MADV infection has been found in a wide range of vertebrates, including birds, bats, turtles, and rodents.[19] In Panama, the highest rates of infection were seen in the Bolivar rice rat and short-tailed cane rat, pointing to these species as possible enzootic hosts.[17]

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