Вирус восточного энцефалита лошадей: характеристики, распространение и профилактика.

Species of virus
Eastern equine encephalitis virus (EEEV) is closely related to Venezuelan equine encephalitis virus and western equine encephalitis virus.

The incubation period for Eastern equine encephalitis virus (EEEV) disease ranges from 4 to 10 days. The illness can progress either systematically or encephalitically, depending on the person's age. Encephalitic disease involves swelling of the brain and can be asymptomatic, while the systemic illness occurs very abruptly. Those with the systemic illness usually recover within 1–2 weeks. While the encephalitis is more common among infants, in adults and children, it usually manifests after experiencing the systemic illness. 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 WD=Q13852319. 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'''', 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.

The disease can be prevented in horses with the use of vaccinations, which are usually given with vaccinations for other diseases, most commonly western equine encephalitis virus, Venezuelan equine encephalitis virus, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans, no vaccine for EEE is available; prevention involves reducing the risk of exposure. Using insect repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention. such as intravenous fluids, tracheal intubation, and antipyretics. About 4% of humans known to be infected develop symptoms, with a total of about six cases per year in the US.

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 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. 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. as of September 2019, a notable uptick in cases erupted in New England and Michigan, prompting some health departments to declare an outbreak. as of 2019, five people died in Michigan, one person died in Rhode Island, one person died in Indiana, and three people died in Massachusetts. The virus was also found in goats, in turkeys, in deer, As of October 9, 2020, one person died in Michigan, and one person died in Wisconsin.

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. He later awoke from the coma with severe brain injuries.

EEEV was one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological weapons program in 1969, a few years before signing (1972) and then ratifying (1975) the Biological Weapons Convention.

From its natural reservoir in birds, EEEV is known to infect reptiles and amphibians as well as both humans and other mammals, including horses.

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%.