Clinical Characteristics of Patients with Tick-Borne Encephalitis (TBE): A European Multicentre Study from 2010 to 2017.

Tick-borne encephalitis (TBE) virus is a major cause of central nervous system infections in endemic countries. Here, we present clinical and laboratory characteristics of a large international cohort of patients with confirmed TBE using a uniform clinical protocol. Patients were recruited in eight centers from six European countries between 2010 and 2017. A detailed description of clinical signs and symptoms was recorded. The obtained information enabled a reliable classification in 553 of 555 patients: 207 (37.3%) had meningitis, 273 (49.2%) meningoencephalitis, 15 (2.7%) meningomyelitis, and 58 (10.5%) meningoencephalomyelitis; 41 (7.4%) patients had a peripheral paresis of extremities, 13 (2.3%) a central paresis of extremities, and 25 (4.5%) had single or multiple cranial nerve palsies. Five (0.9%) patients died during acute illness. Outcome at discharge was recorded in 298 patients. Of 176 (59.1%) patients with incomplete recovery, 80 (27%) displayed persisting symptoms or signs without recovery expectation. This study provides further evidence that TBE is a severe disease with a large proportion of patients with incomplete recovery. We suggest monitoring TBE in endemic European countries using a uniform protocol to record the full clinical spectrum of the disease.

Magnetic resonance imaging and clinical findings in adults with tick-borne encephalitis.

BACKGROUND: Magnetic resonance imaging (MRI) in tick-borne encephalitis (TBE) is often performed for differential diagnosis, but only a few reports on the morphologic changes in TBE patients and their relation to the disease severity exist. METHODS: We retrospectively searched for all TBE patients who were admitted to the Departments of Neurology of the Medical University of Graz (Austria) and the Paracelsus Medical University of Salzburg (Austria) between 2003 and 2014. We recorded the clinical and demographic variables and rated overall disease severity as mild, moderate, severe or leading to death due to TBE. MRI scans were screened for morphologic abnormalities. RESULTS: Of an initial cohort of 88 patients with TBE, 45 patients with an available MRI of the brain were included in this study (median age 58.0years, range: 18-80; men n=28). Their median time spent in the hospital was 18days (range: 4-174days). 16 patients had a mild, 18 a moderate and 10 a severe disease course. One patient died due to TBE. TBE related brain abnormalities could be identified in 4 cases. They consisted of diffuse areas of T2-signal hyperintensity, which were located in the crura cerebri in three patients and in the right centrum semiovale in one patient. No contrast enhancement was observed in any of the lesions and their presence was not related to specific clinical findings or the severity of TBE. CONCLUSION: MRI brain lesions in TBE are rare and do not correlate with the course of the disease. Diffuse areas of signal hyperintensity in the crura cerebri appear suggestive of TBE.

Genotoxicity and mutagenicity of melanoidins isolated from a roasted glucose-glycine model in human lymphocyte cultures, intestinal Caco-2 cells and in the Salmonella typhimurium strains TA98 and TA102 applying the AMES test.

Melanoidins are formed during household cooking procedures and are part of our daily diet, but data on their toxicological potential are still scarce. Therefore, the mutagenic, cytotoxic and genotoxic activity of the water soluble total fraction (sol A), the water soluble high molecular weight fraction (HMW; Molecular weight>12,400 Da) and the remaining water soluble low molecular weight fraction (LMW) isolated from a glucose-glycine model system roasted at 125 degrees C was comprehensively studied in human lymphocytes (genetic end point: sister chromatid exchange (SCE)), Caco-2 cells (SCE, cell viability, cell proliferation) and in the Salmonella typhimurium strains TA98 and TA102 (Ames test). Tests were performed in a dose- and time-dependent manner. The results indicate a significant increase in SCE formation in human lymphocytes after the exposure to 0.05% and 0.1% of the melanoidin fractions. In Caco-2 cells, only the exposure to LMW increased the SCE formation as a matter of concentration. Cell's proliferation and viability decreased significantly after exposure to melanoidins. In the AMES test, melanoidins did not show a mutagenic potential, neither using the TA98 nor the TA102 strain. These results show that melanoidins isolated from the glucose-glycine mixture exhibited modest but significant genotoxic effects in human lymphocytes and, in particular the LMW, in Caco-2 cells, but they induce neither in low nor in very high concentrations mutagenicity in bacteria strains.