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|Infected countries/areas in Eurasia|
|Classification and external resources|
|Patient UK||Tick-borne encephalitis|
Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis, or meningoencephalitis. Although TBE is most commonly recognized as a neurological disorder, mild fever can also occur. Long-lasting or permanent neuropsychiatric consequences are observed in 10 to 20% of infected patients.
The number of reported cases has been increasing in most countries.
The tick-borne encephalitis virus is known to infect a range of hosts including ruminants, birds, rodents, carnivores, horses, and humans. The disease can also be spread from animals to humans, with ruminants and dogs providing the principal source of infection for humans.
Signs and symptoms
The virus can infect the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis). In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs.
In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.
TBE is caused by tick-borne encephalitis virus, a member of the genus Flavivirus in the family Flaviviridae. It was first isolated in 1937. Three virus sub-types are described: European or Western tick-borne encephalitis virus, Siberian tick-borne encephalitis virus, and Far-Eastern tick-borne encephalitis virus (formerly known as Russian spring summer encephalitis virus).
The former Soviet Union conducted research on tick-borne diseases, including the TBE viruses.
Prevention and treatment
Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis in the form of a vaccination. Tick-borne encephalitis vaccines are very effective and available in many disease endemic areas and in travel clinics. Trade names are Encepur N and FSME-Immun CC.
The disease is incurable once manifested, so there is no specific drug therapy for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary.
The disease is most common in Central and Eastern Europe, and Northern Asia. About ten to twelve thousand cases are documented a year but the rates vary widely from one region to another. Most of the variation is the result of variation in host population, particularly that of deer. In Austria, an extensive free vaccination program since the 1960s has reduced incidence by roughly 85%. In Sweden, most cases of TBE occur in a band running from Stockholm to the west, especially around lakes and the nearby region of the Baltic sea. This reflects the greater population involved in outdoor activities in these areas. Although in some regions of Russia and Slovenia the prevalence of cases can be as high as 70 cases per 100,000 people per year, in most regions it is far lower, and overall, for Europe the estimated risk is roughly 1 case per 10,000 human-months of woodland activity. Travelers to endemic regions do not experience many cases, with only 5 cases reported among U.S. travelers returning from Eurasia between 2000 and 2011, a rate so low that the U.S. Centers for Disease Control and Prevention recommend vaccination only for those who will be extensively exposed in high risk areas.
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