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Tick-borne encephalitis
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. 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.[1] TBE is posing a concerning health challenge to Europe, as the number of reported human cases of TBE in all endemic regions of Europe have increased by almost 400% within the last three decades.[2]

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.[3]

TBE, like Lyme disease, is one of the many tick-borne diseases.

Signs and symptoms

The disease typically follows a biphasic pattern in 72–87% of patients and the median incubation period is 8 days (range, 4–28 days) after tick bite. Non-specific symptoms of mild fever, malaise, headache, nausea, vomiting and myalgias may be present as first manifestation of the disease and spontaneously resolve within 1 week. After another week the patient may develop neurological symptoms.[4] The virus can result in long neurological symptoms, infecting the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis).[5] In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs.

In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death.[3]

In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.[3]


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 also exist: European or Western tick-borne encephalitis virus (transmitted by Ixodes ricinus), Siberian tick-borne encephalitis virus (transmitted by I. persulcatus), and Far-Eastern tick-borne encephalitis virus, formerly known as Russian spring summer encephalitis virus (transmitted by I. persulcatus).[6][7]

Russia and Europe report about 5,000–7,000 human cases annually.[1][8]

The former Soviet Union conducted research on tick-borne diseases, including the TBE viruses.

It is transmitted by the bite of several species of infected woodland ticks, including Ixodes scapularis, I. ricinus and I. persulcatus,[9] or (rarely) through the non-pasteurized milk of infected cows.[10]


Detection of specific IgM and IgG antibodies in patients sera combined with typical clinical signs, is the principal method for diagnosis. In more complicated situations, e.g. after vaccination, testing for presence of antibodies in cerebrospinal fluid may be necessary [11].

PCR (Polymerase Chain Reaction) method is rarely used, since TBE virus RNA is most often not present in patient sera or cerebrospinal fluid at the time of clinical symptoms.


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.[12] Trade names are Encepur N[13] and FSME-Immun CC.[14]


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.[15] 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%.[16] 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.[17][18] 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. Overall, for Europe, the estimated risk is roughly 1 case per 10,000 human-months of woodland activity.[16][19] 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.[20]

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