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Tick-borne encephalitis - Overview
Medical expert of the article
Last reviewed: 05.07.2025
Tick-borne encephalitis (spring-summer encephalitis, taiga encephalitis, Russian encephalitis, Far Eastern encephalitis, tick-borne encephalomyelitis) is a natural focal viral infectious disease with a transmissible mechanism of transmission of the pathogen, characterized by fever and predominant damage to the central nervous system.
ICD-10 codes
A84.0. Far Eastern tick-borne encephalitis (Russian spring-summer encephalitis).
A84.1. Central European tick-borne encephalitis.
Epidemiology of tick-borne encephalitis
Tick-borne encephalitis is a natural focal disease. Strains of the Central European variant are widespread in Europe up to Siberia. Beyond the Ural Mountains, the Ural-Siberian and East Siberian genotypes of the virus predominate, and in the Far East, the Far Eastern variant. The differences in the clinical picture of tick-borne encephalitis in Europe, Siberia, and the Far East are apparently related to the genetic diversity of the pathogen.
The main reservoir and carrier of the virus in nature are ixodid ticks Ixodes persulcatus, Ixodes ricinus with transphase (larva-nymph-imago) and transovarial transmission of the pathogen. Additional reservoirs of the virus are rodents (chipmunk, field mouse), hares, hedgehogs, birds (thrush, goldfinch, redpoll, chaffinch), predators (wolf, bear), large wild animals (elk, deer). Some farm animals are also susceptible to the tick-borne encephalitis virus, among which goats are the most sensitive. Due to the fact that the range of reservoir hosts is quite wide, there is a continuous circulation of the virus in nature.
The tick becomes infected with the virus when bitten by mammals in the viremic phase. The main route of human infection is transmission through tick bites. The risk of human infection is closely related to tick activity. The seasonal peak of this activity depends on the climatic features of the geographic regions, but is maximum in spring and summer (from April to August). People aged 20-60 years are most often affected. Urban residents currently predominate in the structure of those infected. Transmission of the virus is also possible through food (during consumption of raw milk from goats and cows), as well as as a result of crushing a tick when removing it from the human body, and, finally, through aerosols when working conditions in laboratories are violated.
Susceptibility to tick-borne encephalitis is high, regardless of gender and age, especially among people visiting a natural focus for the first time. Subclinical forms of infection predominate among indigenous people (one clinical case per 60 inapparent).
Immunity after tick-borne encephalitis is stable and lifelong. Virus-neutralizing antibodies remain in the blood of those who have recovered from the disease throughout their entire lives.
The patient as a source of infection is not dangerous to others.
[ What causes tick-borne encephalitis?
Tick-borne encephalitis is caused by the tick-borne encephalitis virus, which belongs to the Flaviviridae family. The virus is 45-50 nm in size and consists of a nucleocapsid with a cubic type of symmetry and is covered by a membrane. The nucleocapsid contains RNA and protein C (core). The membrane consists of two glycoproteins (membrane M, envelope E) and lipids.
Tick-borne encephalitis virus is cultivated in chicken embryos and tissue cultures of various origins. With prolonged passaging, the pathogenicity of the virus decreases. Among laboratory animals, white mice, rat sucklings, hamsters and monkeys are most susceptible to infection with the virus, and among domestic animals - sheep, goats, pigs and horses. The virus has varying degrees of resistance to various environmental factors: it dies within 2-3 minutes when boiled, is easily destroyed by pasteurization, treatment with solvents and disinfectants, but is able to remain viable for a long time at low temperatures and in a dried state. The virus persists for quite a long time in food products such as milk or butter, which can sometimes be sources of infection. The virus is resistant to low concentrations of hydrochloric acid, so foodborne infection is possible.
Pathogenesis of tick-borne encephalitis
After introduction, the tick-borne encephalitis virus locally multiplies in skin cells. Degenerative-inflammatory changes develop in the tissues at the site of the bite. In the case of alimentary infection, the virus is fixed in the epithelial cells of the gastrointestinal tract.
The first wave of viremia (transient) is caused by the penetration of the virus into the blood from the sites of primary localization. At the end of the incubation period, the second wave of viremia occurs, coinciding in time with the beginning of the virus reproduction in the internal organs. The final phase is the introduction and replication of the virus in the cells of the central nervous system and the peripheral nervous system.
What are the symptoms of tick-borne encephalitis?
The incubation period for tick-borne encephalitis when infected through a tick bite is 5-25 (on average 7-14) days, and when infected through food, it is 2-3 days.
The course of tick-borne encephalitis can be latent, mild, moderate or severe.
Depending on the nature of the course, a distinction is made between acute, two-wave and chronic (progressive) course.
Tick-borne encephalitis, regardless of its form, begins acutely in the vast majority of cases. Rarely, a prodromal period lasting 1-3 days occurs.
The febrile form of tick-borne encephalitis is registered in 40-50% of cases. In most patients, tick-borne encephalitis begins acutely. The febrile period lasts from several hours to 5-6 days. During the acute period of the disease, the body temperature rises to 38-40 °C and higher. Sometimes two-wave and even three-wave fever is observed.
Where does it hurt?
How is tick-borne encephalitis diagnosed?
The diagnosis of tick-borne encephalitis is based on anamnestic, clinical-epidemiological and laboratory data. In endemic regions, great importance is attached to visiting a forest, park, or summer cottage in the spring-summer period, the fact of tick bite, and also the consumption of unboiled goat or cow milk.
During examination, attention is paid to the presence of hyperemia of the face, neck and upper body, injection of scleral vessels, conjunctivitis and hyperemia of the oropharynx. Patients are lethargic and adynamic. It is necessary to carefully examine the skin, since dots or hyperemic spots of various sizes may remain at the site of tick attachment. All patients need to be examined for neurological status.
What do need to examine?
How to examine?
What tests are needed?
How is tick-borne encephalitis treated?
Strict bed rest is recommended, regardless of the general condition and well-being during the entire febrile period and 7 days after the temperature has returned to normal. No special diet is required (common table). During the febrile period, plenty of fluids are recommended: fruit drinks, juices, hydrocarbonate mineral waters.
Etiotropic treatment of tick-borne encephalitis is prescribed to all patients with tick-borne encephalitis, regardless of whether they were vaccinated against tick-borne encephalitis or anti-encephalitis immunoglobulin was used for prophylactic purposes.
What is the prognosis for tick-borne encephalitis?
In most cases, tick-borne encephalitis ends in recovery. In the convalescent period, in 20-50% of cases, an asthenic state develops of varying duration - from several weeks to several months.
In focal forms, patients in most cases become disabled.