Where does tick‑borne encephalitis come from? - briefly
The disease results from infection with the «tick‑borne encephalitis virus», which is maintained in populations of Ixodes ticks that acquire it from infected rodents in temperate forest habitats of Europe and Asia. These ticks transmit the virus to humans during blood meals.
Where does tick‑borne encephalitis come from? - in detail
Tick‑borne encephalitis (TBE) is caused by a flavivirus transmitted primarily through the bite of infected hard‑ticks. The virus circulates in a natural cycle involving small mammals, especially rodents, which serve as reservoirs. Infected rodents develop viremia sufficient to infect feeding ticks, while the ticks maintain the virus through their developmental stages—larva, nymph, and adult—by transstadial transmission. Two tick species dominate the epidemiology: the castor‑bean tick (Ixodes ricinus) in western and central Europe, and the taiga tick (Ixodes persulcatus) across northern and eastern Eurasia.
Geographic distribution aligns with the habitats of these vectors. Endemic regions include:
- Central, northern, and eastern Europe (Germany, Austria, Czech Republic, Baltic states, Scandinavia);
- The Russian Federation, particularly Siberia and the Far East;
- Parts of Central and East Asia (China, Mongolia, Korea);
- Isolated foci in Japan and the Caucasus.
Human infection occurs when a tick attaches for several hours, delivering the virus into the skin. Direct transmission through unpasteurised dairy products is documented but rare. The disease manifests after an incubation period of 7–14 days, with a biphasic clinical course: an initial flu‑like phase followed by neurological involvement in a subset of patients.
Historical records trace the first recognized outbreak to the 1930s in the Soviet Union, where the disease was initially termed “Soviet encephalitis.” Subsequent surveillance identified the same pathogen in western Europe during the 1950s, prompting the development of inactivated vaccines. Climate change and expanding tick habitats have contributed to the recent increase in incidence across previously low‑risk areas.
Control measures focus on reducing tick exposure (protective clothing, repellents, landscape management) and vaccination of high‑risk populations. Monitoring of rodent reservoirs and tick density provides early warning of rising transmission risk.