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What causes tick-borne viral encephalitis?
Last reviewed: 23.04.2024
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Causes of tick-borne viral encephalitis
The causative agent of tick-borne viral encephalitis belongs to the genus Flaviviruses. The virion has a spherical shape, a diameter of 40-50 nm, contains RNA, reproduces well in many tissue cultures. From laboratory animals white mice, hamsters, monkeys, cotton rats are most sensitive to the virus. Susceptible to tick-borne encephalitis virus and many domestic animals.
Pathogenesis of tick-borne viral encephalitis
From the sites of primary localization (skin, subcutaneous tissue, GIT), the virus lymphogenous and hematogenous pathways penetrates into the total blood flow (viremia), and then into the central nervous system. The gray substance of the brain and spinal cord is affected. The process involves hard and soft meninges. In connection with viremia, intoxication and lesion of visceral organs (adrenal glands, spleen, as well as cardiovascular system, etc.) occur.
The greatest morphological changes are found in the central nervous system. Soft and hard meninges are sharply edematous and full-blooded. On the cut, the substance of the brain and spinal cord is flabby, edematous, with pinpoint hemorrhages. In histological study, scattered perivascular infiltrates, degenerative-dystrophic changes in nerve cells up to complete necrosis, proliferation of neuroglia with the formation of small gliotic nodules are determined. Particularly pronounced changes are found in the anterior horns of the spinal cord, brainstem, visual hillock, hypothalamic region, in the cerebellum. Morphological changes correspond to the picture of diffuse meningoencephalitis. At the final stages of the disease at the site of the dead parts of the nervous tissue glial scars with complete loss of functions are formed. Inflammatory changes are also present in other organs.