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Tick-borne Encephalitis

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Tick-borne encephalitis (TBE) — caused by TBE virus (Flavivirus, family Flaviviridae), transmitted by Ixodes tick bites — is a potentially life-threatening neurological infection endemic across a broad arc from Central Europe to the Far East, including the Caucasus region and Georgia, where TBE virus has been documented in ticks and animals and human cases occur in rural and forested areas (ECDC). TBE causes a characteristic biphasic illness (initial flu-like phase → 7-10 day remission → neurological phase with meningitis, encephalitis or meningoencephalomyelitis in 30% of symptomatic patients), with no specific antiviral treatment available and long-term neurological sequelae in 10-30% of those who develop CNS disease. Highly effective TBE vaccines (FSME-IMMUN, Encepur) are available and WHO-recommended for residents and travellers to endemic areas — with particular importance for the Georgian and broader Caucasus public health context.

Key messages

Endemic in Caucasus — no specific treatment
TBE virus is endemic in the Caucasus region including Georgia, where it circulates in Ixodes ticks in forested and rural areas. No specific antiviral treatment exists; care is entirely supportive. Prevention through vaccination is critical (ECDC).
Biphasic illness — the 10-day trap
TBE causes a characteristic two-phase illness: Phase 1 (viremia — flu-like, 4-5 days); apparent recovery (5-7 days — the deceptive “remission”); Phase 2 — in approximately 30% of symptomatic patients — meningitis, encephalitis or meningoencephalomyelitis.
ECDC mandatory surveillance — rising incidence
TBE is an ECDC notifiable disease. European TBE incidence has been rising for decades, with geographic expansion into new areas (UK, Netherlands, Scandinavia) linked to climate change and land-use changes expanding tick habitats.
TBE vaccine — highly effective, underused
TBE vaccines (FSME-IMMUN, Encepur) achieve approximately 99% protection after the primary 3-dose series and are highly safe. Despite excellent efficacy, vaccination coverage remains low in many endemic areas including the Caucasus.
10-30% develop long-term neurological sequelae
Neurological complications from TBE Phase 2 include meningitis (best prognosis), encephalitis (memory impairment, behavioural change) and meningoencephalomyelitis (spinal cord involvement — limb weakness, paralysis, respiratory failure). Approximately 10-30% of encephalitis patients develop lasting neurological deficits.
Three TBE subtypes — different severity
European subtype (I. ricinus): lowest case fatality (0.5-2%). Siberian subtype (I. persulcatus): intermediate (2-3%). Far Eastern/Russian Spring-Summer subtype (I. persulcatus): highest case fatality (5-20%) and chronic progressive encephalitis. The Caucasus region harbours both European and Siberian subtypes.

Key statistics

~10K
TBE cases reported to ECDC annually in EU/EEA
ECDC
~30%
of symptomatic TBE patients develop neurological Phase 2
ECDC/WHO
10-30%
of Phase 2 patients develop permanent neurological deficits
ECDC
~99%
protection from 3-dose TBE vaccine series
ECDC/WHO
Rising
TBE incidence and geographic expansion across Europe (ECDC)
ECDC 2024
0
specific antiviral treatment for TBE — supportive care only
WHO/ECDC

TBE endemic countries in Europe and Caucasus — ECDC risk zones

Source: ECDC. Risk zones expanding northward and westward with climate change. Georgia in Caucasus endemic zone.

Glossary of key terms

TBE virus (TBEV)
WHO/ECDC
Tick-borne encephalitis virus — family Flaviviridae, genus Flavivirus (related to dengue, Zika, West Nile, yellow fever). Three subtypes: European (TBEV-Eu), Siberian (TBEV-Sib) and Far Eastern (TBEV-FE). RNA virus. Transmitted by Ixodes tick bite (main route) or by ingestion of unpasteurised milk from viremic animals (ruminants — rare).
Ixodes ricinus (European tick)
ECDC
The sheep tick (castor bean tick) — the primary TBE vector in Europe. Also transmits Borrelia burgdorferi (Lyme disease) and other pathogens. Three-stage life cycle (larva → nymph → adult). Nymphs (spring-summer) are the most important human-biting stage. Active when temperatures >7°C.
Biphasic illness
ECDC/Clinical
Phase 1 (viremic, 4-5 days): fever, headache, myalgia, nausea — clinically indistinguishable from influenza. Apparent remission (5-7 days, temperature normalises — deceptive). Phase 2 (neurological — in approximately 30%): aseptic meningitis (least severe); meningoencephalitis (confusion, impaired consciousness); meningoencephalomyelitis (spinal cord — flaccid paralysis of upper limbs, respiratory involvement). The remission interval distinguishes TBE from other viral encephalitides.
FSME-IMMUN and Encepur
Pfizer/GSK
FSME-IMMUN (Pfizer): inactivated TBEV grown on chick embryo fibroblasts. Primary schedule: 0, 1-3 months, 5-12 months (3 doses); accelerated (0, 14 days, 5-12 months). Encepur (GSK): similar composition and schedule. Both achieve approximately 99% protection after 3 doses. Boosters every 3-5 years thereafter (every 3 years for >60 years — reduced immune response with age).
Immunoglobulin controversy
ECDC/Austria
Passive immunisation with TBE hyperimmune globulin (FSME-Bulin) was historically used post-exposure in Austria but was withdrawn in 1999 after evidence it might worsen disease severity (antibody enhancement). Post-exposure prophylaxis with immunoglobulin is no longer recommended — this reinforces the importance of pre-exposure vaccination.
Alimentary (milk-borne) TBE
ECDC
Ingestion of raw (unpasteurised) milk or dairy products from viremic goats, sheep or cows can cause TBE — without any tick bite. Alimentary TBE clusters are reported, particularly in rural Europe. Pasteurisation eliminates the risk. This route accounts for approximately 1-5% of TBE cases in some endemic areas.

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Lyme disease (same tick vector)Tick-borne rickettsiaCCHF (tick-borne)TBE vaccinationClimate/tick range expansionNeurological emergency

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