Tick-borne encephalitis

Tick-borne encephalitis (TBE) occurs throughout the northern hemisphere, and mirrors the geographical distribution of the Ixodes species of ticks.

Disease onset is 4 to 28 days after a bite from an infected tick (usually 4 days for foodborne infection).

Diagnosis is made based on immune status; seasonality; geographical, animal, and arthropod exposures; clinical findings; and radiographic abnormalities. TBE is a biphasic illness in most patients.

Treatment consists of supportive care and management of complications. Aciclovir is given empirically until herpes simplex/varicella zoster infection is ruled out.

Most patients recover fully without long-term sequelae, but some patients may experience long-term neurological symptoms or even death.

Vaccines are available for prevention .

Tick-borne encephalitis (TBE) is a flavivirus infection of the central nervous system, characterised by a biphasic meningoencephalitis.[1]Chiffi G, Grandgirard D, Leib SL, et al. Tick-borne encephalitis: a comprehensive review of the epidemiology, virology, and clinical picture. Rev Med Virol. 2023 Sep;33(5):e2470. http://www.ncbi.nlm.nih.gov/pubmed/37392370?tool=bestpractice.com ​ It is caused by the TBE virus, which is usually transmitted by hard ticks of the Ixodes genus. TBE can also be acquired from consumption of raw (unpasteurised) dairy products from infected animals.[2]Taba P, Schmutzhard E, Forsberg P, et al. EAN consensus review on prevention, diagnosis and management of tick-borne encephalitis. Eur J Neurol. 2017 Oct;24(10):1214-e61. http://www.ncbi.nlm.nih.gov/pubmed/28762591?tool=bestpractice.com ​​ This topic focuses on TBE caused by the TBE virus.