Eastern equine encephalitis

Eastern equine encephalitis virus
Colourised TEM micrograph of a mosquito salivary gland: The virus particles (virions) are coloured red. (83,900x magnification)
Virus classification
(unranked):	Virus
Realm:	Riboviria
Kingdom:	Orthornavirae
Phylum:	Kitrinoviricota
Class:	Alsuviricetes
Order:	Martellivirales
Family:	Togaviridae
Genus:	Alphavirus
Species:	Eastern equine encephalitis virus

The causative agent, later identified as a togavirus, was first isolated from infected horse brains in 1933. In 1938, the first confirmed human cases were identified when 30 children died of encephalitis in the Northeastern United States. These cases coincided with outbreaks in horses in the same regions. The fatality rate in humans is 33%, and currently no cure is known for human infections. This virus has four variations in the types in lineage. The most common to the human disease is group 1, which is considered to be endemic in North America and the Caribbean, while the other three lineages, groups IIA, IIB, and III, are typically found in Central and South America, causing equine illness.[1]

These two clades may actually be distinct viruses.[5] The North American strains appear to be monotypic with a mutation rate of 2.7 × 10⁻⁴ substitutions/site/year (s/s/y). It appears to have diverged from the other strains 922 to 4,856 years ago. The other strains are divided into two main clades and a third smaller one. The two main clades diverged between 577 and 2,927 years ago. The mutation rate in the genome has been estimated to be 1.2 × 10⁻⁴ s/s/y.

EEEV is capable of infecting a wide range of animals, including mammals, birds, reptiles, and amphibians. The virus is maintained in nature through a bird—mosquito cycle. Two mosquito species are primarily involved in this portion of the cycle; they are Culiseta melanura and Culiseta morsitans. These mosquitoes feed on the blood of birds. The frequency of the virus found in nature increases throughout the summer as more birds and more mosquitoes become infected.

Transmission of EEEV to mammals (including humans) occurs via other mosquito species, which feed on the blood of both birds and mammals. These other mosquitoes are referred to as "bridge vectors" because they carry the virus from the avian hosts to other types of hosts, particularly mammals. The bridge vectors include Aedes taeniorhynchus[6], Aedes vexans, Coquillettidia perturbans, Ochlerotatus canadensis, and Ochlerotatus sollicitans. Ochlerotatus canadensis also frequently bites turtles.

Humans, horses, and most other infected mammals do not circulate enough viruses in their blood to infect additional mosquitoes. Some cases of EEE have been contracted through laboratory exposures or from exposure of the eyes, lungs, or skin wounds to brain or spinal cord matter from infected animals.

A disease-incidence map for human cases of EEE, 1964–2010

Several states in the Northeast U.S. have had increased virus activity since 2004. Between 2004 and 2006, at least ten human cases of EEE were reported in Massachusetts. In 2006, about 500,000 acres (2,000 km²) in southeastern Massachusetts were treated with mosquito adulticides to reduce the risk of humans contracting EEE. Several human cases were reported in New Hampshire, as well.[9][10]

On 19 July 2012, the virus was identified in a mosquito of the species Coquillettidia perturbans in Nickerson State Park on Cape Cod, Massachusetts. On 28 July 2012, the virus was found in mosquitos in Pittsfield, Massachusetts.[11]

As of September 2019, a notable uptick in cases erupted in New England and Michigan, prompting some health departments to declare an outbreak.[12][13][14][15][16][17][18] As of 31 October 2019, five people died in Michigan,[19][20] three people died in Connecticut,[21] one person died in Rhode Island,[18] one person died in Alabama,[22] one person died in Indiana,[23] and three people died in Massachusetts.[24][25][26] The virus was also found in goats,[27] in turkeys,[28] in deer,[28] and in horses.[29][20][30][18][28]

As of September 9, 2020, there were 5 confirmed human cases between Massachusetts and Wisconsin.[31] As of October 9, 2020, one person died in Michigan,[32] and one person died in Wisconsin.[33]

In October 2007, a citizen of Livingston, West Lothian, Scotland became the first European victim of this disease. The man had visited New Hampshire during the summer of 2007, on a fishing vacation, and was diagnosed as having EEE on 13 September 2007. He fell ill with the disease on 31 August 2007, just one day after flying home, and later fell into a coma.[34] He later awoke from the coma with severe brain injuries.[35]

After inoculation by the vector, the virus travels via lymphatics to lymph nodes, and replicates in macrophages and neutrophils, resulting in lymphopenia, leukopenia, and fever. Subsequent replication occurs in other organs, leading to viremia. Symptoms in horses occur 1–3 weeks after infection, and begin with a fever that may reach as high as 106 °F (41 °C). The fever usually lasts for 24–48 hours.

Nervous signs appear during the fever that include sensitivity to sound, periods of excitement, and restlessness. Brain lesions appear, causing drowsiness, drooping ears, circling, aimless wandering, head pressing, inability to swallow, and abnormal gait. Paralysis follows, causing the horse to have difficulty raising its head. The horse usually suffers complete paralysis and death 2–4 days after symptoms appear. Mortality rates among horses with the eastern strain range from 70 to 90%.