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What causes tick-borne viral encephalitis?
Last reviewed: 06.07.2025
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Causes of tick-borne viral encephalitis
The causative agent of tick-borne viral encephalitis belongs to the genus of flaviviruses. The virion is spherical, 40-50 nm in diameter, contains RNA, and reproduces well in many tissue cultures. Of the laboratory animals, white mice, hamsters, monkeys, and cotton rats are most sensitive to the virus. Many domestic animals are also susceptible to the tick-borne encephalitis virus.
[ Pathogenesis of tick-borne viral encephalitis
From the primary localization sites (skin, subcutaneous tissue, gastrointestinal tract), the virus penetrates into the general bloodstream via lymphogenous and hematogenous routes (viremia), and then into the central nervous system. The gray matter of the brain and spinal cord is affected. The process involves the hard and soft meninges. Intoxication and damage to visceral organs (adrenal glands, spleen, as well as the cardiovascular system, etc.) occur due to viremia.
The greatest morphological changes are found in the central nervous system. The soft and hard meninges are sharply edematous and congested. On section, the substance of the brain and spinal cord is flabby, edematous, with pinpoint hemorrhages. Histological examination reveals scattered perivascular infiltrates, degenerative-dystrophic changes in nerve cells up to their complete necrosis, proliferation of neuroglia with the formation of small glial nodules. Particularly pronounced changes are found in the anterior horns of the spinal cord, brainstem, thalamus, hypothalamic region, and cerebellum. Morphological changes correspond to the picture of diffuse meningoencephalitis. In the final stages of the disease, glial scars with complete loss of function are formed at the site of dead areas of nervous tissue. Inflammatory changes are also present in other organs.