Western Equine Encephalomyelitis Virus (WEV) is a virus of the alpha virus genus belonging to the Togavirus family. It belongs to the ecological group of arboviruses and antigenic group A. ZEL virus is the causative agent of Western equine encephalomyelitis in humans.
The ZEL virus is transmitted by the bite of an infected mosquito. The virus primarily circulates in rural areas in the Americas, but cases have been reported in other regions of the world.
The disease causes inflammation of the brain and spinal cord, which can lead to serious consequences such as dysfunction of the nervous system and even death. Horses are especially susceptible to the disease, but sometimes the virus can be transmitted to humans.
The disease begins with high fever, headache, nausea and vomiting. Then symptoms characteristic of brain inflammation appear, such as seizures, loss of coordination, mental disorders and paralysis. Symptoms can develop quickly and lead to death within a few days.
There is a vaccine for equine ZEL virus that can help prevent the spread of the disease. However, there is no vaccine available for humans, so it is important to take precautions to avoid mosquito bites. These measures include using repellents, wearing protective clothing and installing mosquito nets on windows and doors.
Overall, Equine Western Encephalomyelitis Virus poses a serious threat to the health of horses and sometimes to humans. Therefore, it is necessary to take precautions and monitor the health of animals and people in areas where the virus is widespread.
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**Western equine encephalomyelitis virus (WEL)** is a virus of a disease that occurs with meningoencephalitic and mengopochitic forms. There are 2 serotypes of the vel virus - 5 and 8. It is transmitted through contact with infected horses through blood or virus-infected semen, an aborted fetus and placenta\. The infection is natural and widespread among both wild and domestic horses. The incidence increases during periods of severe epizootic tension.
The causative agent of the disease was first described by Dullin and Roberts in 1936. In 1978, a group of scientists led by K. Murphy discovered serotype 1 of VEV, which was named serotype 5 according to its antigenic formula Gk56. A few years later, in 2005, Dutch researchers discovered another serovariant of the virus, called serotype 8. It is this finding that scientists attribute to the cause of the syndrome of accidental deaths of horses registered earlier. The results of more recent studies make it possible to define the disease as a type of eastern and western encephalomyelitis. The causative agent of the disease is contagious for at least two years, which is extremely important for agriculture in all areas and veterinary practice, since the virus maintains the tension of the epizootic process. Outside the body of infected horses, the pathogen quickly loses its infectivity and dies after 2–3 hours; it is also destroyed at high temperatures, under the influence of disinfectants and during etherization. Transfer of pathogens in a non-living state is rarely encountered in veterinary practice. Most often, infection occurs through hemato- or gynecological examination.
A change in the incubation period of the disease is noted: 7 days for serotype Gk+56 and 17 days for serotype C340 (C358) according to K. N. Abramov and I. V. Arkhipova (2011), which is facilitated by the individual reactivity of the animal’s body, the possibility of latent (hidden) ) forms of the disease, as well as spontaneous recovery among small calves in contact with sick horses. The disease occurs intracerebrally with damage to the gray and white matter of the brain and spinal cord, and the meninges. Respiratory syndrome is rarely detected, mainly clinical symptoms of lung damage. The severity of the disease varies from a mild form, characterized by anamnestic signs, to furunculous, accompanied by abscesses in the face, back, and limbs; damage to the conjunctiva, oral mucosa, and oral cavity. A distinctive feature is inflammation of the peritoneum and the presence of necrotic lesions on the skin of the intermaxillary area. It is possible to detect significant prothrombin activity and specific agglutination of erythrocytes of infected horses during the period of clinical manifestations of the disease. In different age groups of animals, different features of the course of infection are noted: in newborns - hemorrhagic myelitis, characterized by paresis of the hind limbs, in
Western equine encephalitis virus (WEEV) is a virus of the alphavirus genus of the togavirus family. This disease in a horse can lead to the development of rabies, and in humans it can cause inflammation of the meninges (meningitis) or encephalitis.
The name of the virus comes from the fact that it usually develops in the summer and the horse becomes infected with rabies, possibly through a tick that accidentally acquired the virus in the saliva of infected animals. For humans, the virus can also be acquired through the skin through the bite of an infected cat. EVD is currently recognized as mildly dangerous to humans. The virus enters the animal’s body and then spreads through the blood to all organs and tissues of the body. The incubation period lasts from 2 to 21 days. Symptoms appear suddenly and can be very painful. If the uterus is infected, the probability of death at the initial stage is 50%, but survivors can suffer a milder form of the disease. With encephalitis, almost all animals do not live more than a day. Most cases of infestation in horses occur from pregnant mares infected by tick bites that they catch and bring into their home. This virus is also dangerous for aquatic animals - seals and walruses. Some rodents can act as carriers. There may also be cases of infection from cats that were close to the source of infection. Infection is also possible through contact with animal products. In Canada, people were vaccinated in 1983. The first cases of leprosy in humans in the United States appeared in July 2015, the last cases in December 2022. The risk of infection also increases with contact