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

Tick-borne encephalitis (TBE) is a viral infection of the central nervous system (CNS) caused by tick-borne encephalitis virus (TBEV). It might take several clinical courses such as: meningitis, meningoencephalitis or meningoencephalomyelitis. The aim this study was to compare the YKL-40 concentration in cerebrospinal fluid (CSF) of patients with different clinical presentations of TBE and patients with excluded meningitis (control group). The concentration of YKL-40 in CSF was determined using Fujirebio tests (Ghent, Belgium) in 32 patients with TBE: Group I-patients with meningoencephalitis (n = 16); Group II-patients with meningitis (n = 16). The control group (CG) consisted of 17 patients in whom any inflammatory process in central nervous system was excluded. The concentration of YKL-40 was significantly higher in encephalitis group than in the CG after 7 days from the last dose of treatment. The concentration in patients with neuroinflammation had a significantly different concentration of YKL-40 compared to patients from the neuroinflammation control group. The ROC curve analysis indicates that CSF YKL-40 concentration at cut-off 783.87 differentiated TBE patients from CG with 100% specificity and 70% sensitivity and CSF YKL-40 concentration at cut-off 980.11 differentiated meningitis from meningoencephalitis with 87.5% specificity and 62.5% sensitivity. YKL-40 takes part in TBE pathogenesis, its concentration is the highest at the early stage of CNS involvement and decreases in the convalescent period. As YKL-40 was significantly higher in the meningitis than in the meningoencephalitis group, it might be used as biomarker in differentiation of these clinical forms of TBE.

Assessment of Coxiella burnetii presence after tick bite in north-eastern Poland.

PURPOSE: The aim of the study is to assess anti-Coxiella burnetii antibodies presence in inhabitants of north-eastern Poland, to assess the risk of Q fever after tick bite and to assess the percentage of co-infection with other pathogens. METHODS: The serological study included 164 foresters and farmers with a history of tick bite. The molecular study included 540 patients, hospitalized because of various symptoms after tick bite. The control group consisted of 20 honorary blood donors. Anti-Coxiella burnetii antibodies titers were determined by Coxiella burnetii (Q fever) Phase 1 IgG ELISA (DRG International Inc. USA). PCR was performed to detect DNA of C. burnetii, Borrelia burgdorferi and Anaplasma phagocytophilum. RESULTS: Anti-C. burnetii IgG was detected in six foresters (7.3%). All foresters with the anti-C. burnetii IgG presence were positive toward anti-B. burgdorferi IgG and anti-TBE (tick-borne encephalitis). Anti-C. burnetii IgG was detected in five farmers (6%). Four farmers with anti-C. burnetii IgG presence were positive toward anti-B. burgdorferi IgG and two with anti-TBE. Among them one was co-infected with B. burgdorferi and TBEV. Correlations between anti-C. burnetii IgG and anti-B. burgdorferi IgG presence and between anti-C. burnetii IgG presence and symptoms of Lyme disease were observed. C. burnetii DNA was not detected in any of the 540 (0%) patients. CONCLUSIONS: C. burnetii is rarely transmitted by ticks, but we proved that it is present in the environment, so it may be a danger to humans. The most common co-occurrence after tick bite concerns C. burnetii and B. burgdorferi.

Assessment of the tau protein concentration in patients with tick-borne encephalitis.

There have been suggestions that tick-borne encephalitis (TBE) may cause neurodenenerative changes in the brain. The aim of this study was the assessment of the tau protein concentration in cerebrospinal fluid (CSF) of patients with different clinical forms of TBE. The concentration of tau protein in CSF was determined using Fujirebio tests (Ghent, Belgium) in 35 patients with TBE: group I-patients with meningitis (n = 16); group II-patients with meningoencephalitis (n = 19). None of the patients reported any neurodegenerative disorder that could affect the results of the study. The control group (CG) consisted of 10 patients in whom inflammatory process in central nervous system was excluded. Tau protein concentration in CSF before treatment did not differ significantly between the examined groups, while its concentration was significantly higher in encephalitis group than in CG after 14 days of treatment. Significant increase in tau protein concentration after treatment was observed in both examined groups. The comparison between the group of patients who fully recovered and patients who presented with persistent symptoms on discharge showed significant differences in tau protein concentration before and after treatment. ROC curve analysis indicates that CSF tau protein concentration before treatment may predict complicated course of the disease with 90.9% specificity and 80% sensitivity, while after treatment, specificity became 72.7% and 71.4% for sensitivity. Correlation analysis showed that in TBE patients (both meningoencephalitis and meningitis groups), CSF pleocytosis before treatment correlated negatively with tau protein concentration in CSF. (1) Neurodegeneration process is present in TBE encephalitis. (2) Tau protein concentration may be used as a predictor of complicated course of TBE.