Tickborne Encephalitis Virus

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Also Known As: TBEV — TBE — Spanish Sheep Encephalomyelitis — Exotic Encephalitis — Turkish Sheep Encephalomyelitis


Tickborne encephalitis is caused by a Flavivirus infection. Disease can be caused by any one of a large complex of related viruses and can affect a wide range of hosts including ruminants, birds, rodents, carnivores and horses, but clinical disease is most commonly observed in dogs with most other infections remaining subclinical.

These diseases can also be zoonotic. Ruminants and dogs are thought to be the main source of infection for humans.[1]


Louping Ill Virus, Central European Encephalitis Virus, Hanzalova Virus, Hypr Virus, Kumlinge Virus and Neudoerfl Virus are all found in Europe.

Omsk Haemorhhagic Fever Virus, Russian Spring-Summer encephalitis virus, Karshi Virus, Langat Virus, Negishi Virus, Royal Farm Virus and Sofyn Virus are all found in different parts of Asia.

Carey Island Virus is only found on the Malaysian island of the same name and Phnom Penh Bat Virus in Cambodia.

Kyasanur Forest Disease Virus is found in India and the Middle-East.

Powassan Virus is restricted to North America.

The viruses are all spread by tick vectors, more information on the role of ticks can be found at tick disease transmission. Ixodes spp., Dermacentor spp. and Haemaphysalis spp. are all implicated. Transmission is trans-stadial.


A host of species can be affected with ruminants and dogs being the main species for clinical signs to manifest in.

Disease outbreaks tend to occur during the Summer months when the ticks are most active.

Clinical Signs


Dogs exhibit neurological signs including tremors, stupor, tetraparesis, bunny hopping, seizures, blindness, delirium, hyperaesthesia aggression, circling, head pressing, dullness and mortalities.


Ruminants exhibit neurological signs, usually head tilt, facial paralysis, listlessness, blindness, hypermetria, opisthotonus, excess salivation and ataxia. They may bunny hop if weakness is severe. Animals are often anorexic and demonstrating discomfort and bruxism.

Respiratory signs can also occur.


Humans can be infected by ticks or by drinking unpasteurised milk from infected cattle.

TBE results in serious, acute central nervous system disease which may result in death or permanent/longterm neurological deficits. Onset is usually characterised by fever, headache and meningeal irritation followed by convulsions, colic and diarrhoea.


In dogs confirmed with TBE infection, lymphohistiocytic meningitis is seen with neuronal necrosis, glial karyorrhexis and microglial proliferation. Perivascular cuffs can be present in all regions of the brain.

Viral antigen is most consistently found in the neuroparenchyma surrounding the fourth ventricle but also in the cerebellum, mesencephalon, thalamus, hippocampus and neocortex.[2] CSF can also be used. Virus can be detected by immunohistology.[2] Antibodies can be detected in serum and CSF by ELISA.


Palliative care is the only option once infected. There is no cure for TBE.


Humans are protected by vaccines but they are not commercially available in animals.

Reduction of exposure to ticks and tick removal is valuable but difficult.

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  1. Anon (1999) Flaviviridae. In: Murphy, F. A., Gibbs, E. P. J., Horzinek, M. C., Studdert, M. J. eds. Veterinary Virology. San Diego, USA: Academic Press, 556-569
  2. 2.0 2.1 Weissenböck, H (1999) Post-mortem diagnosis of tick-borne encephalitis in dogs. Tierärztliche Umschau, 54(5):249-255; 15


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 6 July 2011.

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