Abstract
Tick-borne encephalitis (TBE) is one of the most dangerous flavivirus infection of the central nervous system in Eurasia. The etiological agent, the TBE virus (TBEV) is transmitted to man by tick bytes. Geographic natural habitat of the TBEV appeared to be discontinuous and extended throughout southern part of Eurasian forest belt from Pacific to Atlantic ocean mainly within distribution areas of the virus vectors – ixodid ticks. TBE outbreaks have been registered in northern China and Japan in the east, through Russia to about 30 European countries including France, northern Italy and Norway in the west with the highest morbidity rates in Russia, Austria, Czech Republic, Slovenia and the Baltics (Latvia, Lithuania and Estonia) (Gritsun et al, 2003; Mansfield et al., 2009). In France, Italy, Greece, Norway and Denmark, TBE is of minor importance. In the United Kingdom, Ireland, Belgium, the Netherlands, Luxembourg, Spain and Portugal, TBE is not indigenous and no TBE cases have been reported yet. Detailed epidemiological statistics from 1990 onwards can be obtained from the website of the International Scientific Working Group on TBE [http://www.isw-tbe.info]. The TBE prevalence is increasing worldwide with spread of the virus to previously non-endemic countries in Europe (France) and Asia (China, Mongolia, Japan and South Korea). TBEV is listed as a category C agent on the Centers for Disease Control and Prevention (USA) list of select biological agents. The TBEV persists in endemic regions or so-called natural foci, where it circulates among vertebrate hosts (mainly small rodents and insectivorous) and the arthropod vectors (ticks). Years of observations of the distribution of TBE incidences suggest that such natural foci are very stable. Formation, development and stability of the TBE natural foci are determined by the coincidence of several ecological factors including temperature, relative air humidity, soil humidity, biotope vegetation, population density and dynamics of ixodid ticks and their hosts, susceptibility of reservoir hosts to the TBEV, proportion of immune hosts as well as the virus prevalence among both ticks and vertebrate hosts (Hofmann, 1973; Plassmann, 1980; L’vov et al., 1989; Korotkov et al., 2007; Tick-Borne Encephalitis (TBE) and its Immunoprophylaxis, 1996 and references therein). Reservoir host species abundance, multiple transmission cycles and adaptation of the TBEV to different hosts cause long-term resistance of the parasitic system in endemic regions.
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