| Tick-borne meningoencephalitis | |
|---|---|
| Classification and external resources | |
| ICD-10 | A84 |
| ICD-9 | 063 |
| DiseasesDB | 29274 |
| MeSH | D004675 |
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 sequelae are observed in 10-20% of infected patients.
The number of reported cases has been increasing in most countries.[1]
The virus is known to infect a range of hosts including ruminants, birds, rodents, carnivores, horses and humans. The disease can also be zoonotic, with ruminants and dogs providing the principal source of infection for humans.[2]
Contents |
The virus can infect the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis).[3] 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.[2]
In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.[2]
It is transmitted by the bite of several species of infected ticks, including Ixodes scapularis, Ixodes ricinus and Ixodes persulcatus,[4] or (rarely) through the non-pasteurized milk of infected cows.
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).
Russia and Europe report about 5,000-7,000 human cases annually.[1] [5]
The former Soviet Union conducted research on tick borne diseases, including the TBE viruses.
The TBE virus may be present in a seronegative strain or subtype. In such cases a marker for TBE infection is elevated IFN-g in CSF.
Viral antigen can usually be found in brain tissue. Serological testing can also be performed with an ELISA.[2]
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, but infection can be reliably prevented by vaccination.
Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis (vaccine, TBE immunoglobulin). TBE vaccine is very effective and available in some disease endemic areas.[6]
|
||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||