Tick-Borne Encephalitis



Tick-borne encephalitis virus (TBEV, genus Flavivirus) causes tick-borne encephalitis (TBE), locally known as Russian spring-summer encephalitis (RSSE), Frühsommer-Meningoenzephalitis (FSME), Ryssjukan or Kumlingesjukan. Viruses of the genus Flavivirus form different antigenic complexes. The main complexes of medical importance are TBE (e.g. TBEV, Louping Ill virus, Powassan virus), dengue (dengue virus 1 to 4) and Japanese encephalitis (e.g. West Nile virus and others).

TBEV can be subtyped into at least three subtypes:

  •  European  subtype: mainly transmitted by Ixodes ricinus
  •  Siberian subtype: mainly transmitted by Ixodes persulcatus
  •  Far-Eastern subtype: mainly transmitted by Ixodes persulcatus

The subtypes can be distinguished by molecular means of their genome. They comprise different virulence patterns in humans and possibly also in animals.

Closely related viruses are Louping Ill virus which causes encephalitis which on clinical ground cannot be distinguished from tick-borne encephalitis. Furthermore, Omsk Hemorrhagic Fever virus is closely related to TBEV. In India Kyasanur Forest virus is closely related to TBE virus. In Northern America and Far-eastern Asia tick-borne Powassan virus may cause a severe form of encephalitis in humans.

The family Flaviviridae contains a number of viruses that are known to be transmitted by arthropods to warm-blooded animals during blood feeding. Replication of the virus in the arthropod vector is observed, which may lead to a more effective transmission to the host, as a constant and high virus titre can be reached in the arthropod. These viruses are commonly called ARBO viruses (arthropod-borne) in contrast to those, which are known to be transmitted only mechanically by arthropod vectors.


Seropositivity for TBEV has been found in nature in many different wild and also domesticated animals. In endemic areas in Switzerland a higher seroprevalence has been reported in dogs than in humans. The small numbers of clinical canine cases in Switzerland as well as in Austria, Germany and Sweden prove that the risk for a TBE virus-infected dog to develop clinical manifest TBE is rather small. Experimental infections with TBEV could not prove the evidence of pathogenicity or susceptibility in animals, esp. dogs. In these studies seroconversion occurred without clear correlation of clinical findings. In a serological survey performed in dogs from Sweden in 1992, 18 of 225 dogs (8%) were seropositive. 16 of the 18 dogs showed neurological signs, as ataxia, atonic paresis and sensitivity to sound (Bjöersdorff, 2002). In contrast to these findings, experimental infection of dogs in Japan did not provide evidence for a correlated clinic. Likewise, from the seropositive dogs investigated in Denmark in 2005 and 2006, non was associated with a clinical picture suggestive for TBE.

Further information

  • Bjöersdorff A: Borreliosis and tick-borne encephalitis. In: Arthropod-borne Diseases. 2002, Sci. Proc. BSAVA Congress, Birmingham, pp 185-6

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