scholarly journals Assessment of the YKL-40 concentration in patients with tick-borne encephalitis

2022 ◽  
pp. 101895
Author(s):  
Piotr Czupryna ◽  
Agnieszka Kulczyńka-Przybik ◽  
Barbara Mroczko ◽  
Mulugeta A. Wondim ◽  
Sambor Grygorczuk ◽  
...  
Author(s):  
Kuulo Kutsar

The first cases of tick-borne encephalitis (TBE) in Estonia were identified in 1949. Today, Estonia is a TBE-endemic country. A TBE-endemic area in Estonia is defined as an area with circulation between ticks and vertebrate hosts as determined by detection of TBEV or the demonstration of autochthonous infections in humans or animals within the last 20 years.


Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.


Even though tick-borne encephalitis (TBE) has been a notifiable disease in Croatia since 2007, there are no or only limited data available on the occurring tick species in the endemic areas, on the prevalence of TBE virus (TBEV) in ticks, its distribution in Croatia, and its genetic characteristics. Reporting of human cases also is very scarce. The Central European subtype of virus (TBEV-EU) appears to be present in Croatia


Author(s):  
Joon Young Song

Although no human case of tick-borne encephalitis (TBE) has been documented in South Korea to date, surveillance studies have been conducted to evaluate the prevalence of tick-borne encephalitis virus (TBEV) in wild ticks.


Author(s):  
Jana Kerlik

The former Czechoslovak Republic was one of the first countries in Europe where the tick-borne encephalitis virus (TBEV) was identified.


Author(s):  
Katarzyna Pancer ◽  
Włodzimierz Gut

Clinical symptoms of tick-borne encephalitis (TBE) were first described in Poland in 1948 by Demiaszkiewicz. All patients had been living in the Białowieża region (in northeastern Poland). Similar infections were described to those that had been diagnosed in the same region before World War II as complicated cases of typhoid fever or influenza.


Author(s):  
Wilhelm Erber ◽  
Tamara Vuković Janković

Although there are no reliable data on the number of tick-borne encephalitis (TBE) cases or the percentage of infected ticks, based on the geography and the presence of TBE virus (TBEV) in all neighboring countries, it must be assumed that TBEV is present anywhere in Moldova.


Author(s):  
Valentina Tagliapietra ◽  
Flavia Riccardo ◽  
Giovanni Rezza

Italy is considered a low incidence country for tick-borne encephalitis (TBE) in Europe. Areas at higher risk for TBE in Italy are geographically clustered in the forested and mountainous regions and provinces in the north east part of the country, as suggested by TBE case series published over the last decade.


Tick-borne encephalitis virus (TBEV) was isolated for the first time in Sweden in 1958 (from ticks and from 1 tick-borne encephalitis [TBE] patient).1 In 2003, Haglund and colleagues reported the isolation and antigenic and genetic characterization of 14 TBEV strains from Swedish patients (samples collected 1991–1994).2 The first serum sample, from which TBEV was isolated, was obtained 2–10 days after onset of disease and found to be negative for anti-TBEV immunoglobulin M (IgM) by enzyme-linked immunosorbent assay (ELISA), whereas TBEV-specific IgM (and TBEV-specific immunoglobulin G/cerebrospinal fluid [IgG/CSF] activity) was demonstrated in later serum samples taken during the second phase of the disease.


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