Course Of Tick-borne Encephalitis Research Articles

A fatal case of tick-borne encephalitis in an immunocompromised patient: case report from Northeastern Poland and review of literature

Tick-borne encephalitis (TBE) is an infectious illness of the central nervous system caused by the TBE virus, which is commonly transmitted through a tick-bite. TBE is endemic in Europe and mid-Asia. In this study, we report a case of a 36-year-old woman, living in Northeastern Poland, with a history of double corneal transplantation and post-transplant immunosuppressive therapy who was admitted to hospital because of progressive weakness, acute headache, nausea, vertigo, vomiting, and fever. The patient was diagnosed with TBE. However, the diagnosis was challenging as the initial serological tests for antibodies against the TBE virus were negative. We want to raise the awareness among the clinicians that the course of TBE is often unpredictable and that it tends to be more severe in immunocompromised individuals.. Delayed production of antibodies against TBE virus, which might inhibit the diagnosis of the disease, is observed in some immunocompromised patients.

The thick-borne encephalitis caused by alimentary transmission - case series report.

Tick-borne encephalitis (TBE) is a central nervous system zoonotic disease transmitted by ticks. Tick-borne encephalitis virus (TBEV) is one of the main causes of lymphocytic meningitis in the areas of its endemic occurrence. A mode of transmission of TBEV which is rarely observed in clinical practice is an alimentary transmission through consumption of unpasteurised dairy products from infected animals. The following article contains detailed description of the clinical course of TBE among five family members, for whom the occurrence of TBE was temporarily associated with the consumption of unpasteurised goat's milk from the same source. The epidemiological outbreak presented in this article is the fifth ever described case of the milk-borne TBE in Poland. More so, the clinical course of the disease has shown differences from the typical course characterised so far in the literature. Clinical cases of TBE described in this study were similar to infections caused by tick bites in humans. The following article discusses available methods of preventing TBE, with emphasis on alimentary transmission of TBEV, since possibility of serious detrimental long-term neurological complications resulting from TBE was stressed in prior literature.

Chapter 9: Immunology of TBEV infection

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.

Nature of pathological changes on magnetic resonance imaging of the CNS in patients with focal forms of acute tick-borne encephalitis

Introduction. Tick-borne encephalitis (TBE) is a widespread natural focal viral neuroinfection in Russia and the Sverdlovsk region. The high level of morbidity, leading to disability, and the annual registration of focal forms and lethal cases determine the relevance of the search for early differential diagnostic criteria for acute tickborne encephalitis (TBE). A promising direction in the early diagnosis of TBE is acquired by magnetic resonance imaging (MRI).The aim of the study was to study the features of the MRI picture in patients with focal forms of TBE.Material and methods. The study included 38 patients with focal forms of OKE who were treated in the neurological department of Sverdlonsk regional clinical hospital № 1 since 2009 to 2019.Results. In the acute period of focal forms of TBE, pathological changes of an inflammatory nature during MRI of the CNS were more often detected in the cerebral hemispheres (mainly in the white matter) in 40.4 % and subcortical structures in 36.8 %, in the brainstem in 16.7 %, less often in 6.1 % – in the region of the cerebellum and spinal cord. Bilateral nature and combined lesions of the CNS structures were detected 2 times more often. Discussion A detailed analysis of the localization and nature of MRI changes in the CNS in patients with severe focal forms of the disease, in contrast to single descriptions of the MRI picture of TBE according to the literature, made it possible to identify combined lesions of the frontal and parietal lobes characteristic of TBE in combination with pathological changes in the region of the thalamus and basal ganglia.Conclusion. Identification of typical MRI changes in the CNS in patients with a clinical picture of viral encephalitis in the spring-summer period contributes to the early diagnosis of a severe course of TBE.

Chapter 9: Immunology of TBEV-Infection

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 (meningoencephalitic) 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.

Tick Borne Encephalitis

Tick-borne encephalitis (TBE) is the medically most common tick-borne viral disease in Europe and Asia. The TBE virus (TBEV) is a member of the family Flaviviridae. Transmission mainly to humans occurs by ticks of the Family Ixodidae, mainly the castor bean tick (Ixodes ricinus) in Europe and the taiga tick (Ixodes persulcatus) in Asia. Rarely TBEV is also transmitted by contaminated milk of infected ungulates (goat, sheep, cow). The clinical course of TBE is variable and may range from subclinical to fatal encephalomyelitis. Probably host and viral factors are involved in the pathogenesis of disease. So far, no specific treatment of the disease is available. The only effective prevention of TBE is vaccination. A number of different vaccines are available worldwide. In Europe two vaccines are licensed which contain inactivated European subtype TBEV. Probably the European vaccines protect also against infections with other subtypes of TBEV.

Chapter 9: Immunology of TBEV-Infection

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.

Comparison of Clinical, Laboratory and Immune Characteristics of the Monophasic and Biphasic Course of Tick-Borne Encephalitis.

The biphasic course of tick-borne encephalitis (TBE) is well described, but information on the monophasic course is limited. We assessed and compared the clinical presentation, laboratory findings, and immune responses in 705 adult TBE patients: 283 with monophasic and 422 with biphasic course. Patients with the monophasic course were significantly (p ≤ 0.002) older (57 vs. 50 years), more often vaccinated against TBE (7.4% vs. 0.9%), more often had comorbidities (52% vs. 37%), and were more often treated in the intensive care unit (12.4% vs. 5.2%). Multivariate logistic regression found strong association between the monophasic TBE course and previous TBE vaccination (OR = 18.45), presence of underlying illness (OR = 1.85), duration of neurologic involvement before cerebrospinal fluid (CSF) examination (OR = 1.39), and patients’ age (OR = 1.02). Furthermore, patients with monophasic TBE had higher CSF levels of immune mediators associated with innate and adaptive (Th1 and B-cell) immune responses, and they had more pronounced disruption of the blood–brain barrier. However, the long-term outcome 2–7 years after TBE was comparable. In summary, the monophasic course is a frequent and distinct presentation of TBE that is associated with more difficult disease course and higher levels of inflammatory mediators in CSF than the biphasic course; however, the long-term outcome is similar.

Epidemiology, diagnosis, and prevention of tick-borne encephalitis in Poland and selected European countries - a position statement of the Polish group of experts

Tick-borne encephalitis (TBE) is one of the most common viral neuroinfections in Poland. Detection of specific IgM and IgG anti- TBE antibodies in the serum or cerebrospinal fluid with enzyme-linked immunosorbent assay (ELISA) is a method of choice in TBE diagnostics. No effective antiviral treatment is available for TBE. Increased intracranial pressure, epileptic seizures, and other neurological symptoms in the course of TBE are managed with standard procedures. A routine use of corticosteroids is not recommended. Adults with TBE-related neurological sequelae should undergo physical mobilization and periodic neurological assessments. All patients ought to control their psychological condition and visit a physician in case of worrisome symptoms. Additionally, children need to undergo regular psychological and otolaryngologic consultations. Notably, TBE cases are reported across Poland; therefore, the entire country must be considered as a TBE risk region. The degree of endemicity can be variable in particular parts of the country. Immunization against TBE containing a European subtype of the virus is the most effective prophylactic method. In areas where the disease is highly endemic (according to the WHO definition of ≥5 cases/100 000 population/year), immunization needs to be offered to all ages. Vaccination is recommended in the communities living in areas of moderate TBE endemicity (1-5 cases/100 000/ year), in particular for individuals at high risk of a TBE infection as well as children and the elderly. Vaccination should also be offered to subjects living in areas where TBE occurrence is rare (<1 case/100 000/year) but who are at high risk of infection. A TBE vaccine is recommended to the following populations at high risk of TBE: a) individuals undertaking outdoor leisure activities, b) all professionals working outdoors, particularly in green areas, and c) individuals traveling to endemic areas, if activities during their visit may pose a risk of a tick bite. Post-exposure immunization is not recommended. Med Pr. 2021;72(2):193-210.

CHAPTER 9: Immunology of TBEV-Infections

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.

Analysis of CCL-4, CCL-17, CCL-20 and IL-8 concentrations in the serum of patients with tick-borne encephalitis and anaplasmosis

PurposeTick-borne co-infections are a serious epidemiological and clinical problem. Only a few studies aimed to investigate the effect of tick-borne encephalitis (TBE) and human granulocytic anaplasmosis (HGA) co-infection in the course of the inflammatory process and the participation of chemokines in the pathomechanism of these diseases. The aim of the study was to evaluate CCL-4, CCL-17, CCL-20, and IL-8 serum concentrations in patients with HGA, TBE and HGA + TBE co-infection. MethodsEighty-seven patients with HGA (n = 20), TBE (n = 49) and HGA + TBE (n = 18) were included to the study. The control group (CG) consisted of 20 healthy people. Concentrations of cytokines were measured in serum using commercial ELISA assays. In patients with TBE and HGA + TBE inflammatory markers were assessed during the acute and convalescent period. The results were analyzed using non-parametric tests with p < 0.05 considered as significant. ResultsBefore treatment, significantly higher concentrations of IL-8, CCL-4 and CCL-20 were observed in HGA patients. CCL-4 and CCL-20 concentrations were significantly higher in TBE patients compared to CG. Concentrations of IL-8, CCL-4, and CCL-20 were significantly higher in HGA + TBE than in CG. After treatment, a significant reduction of IL-8, CCL-4, and CCL-20 concentrations in TBE patients and IL-8 in HGA + TBE co-infection was observed. CCL-4 concentration was higher in HGA + TBE co-infection in comparison to patients with TBE after treatment. ConclusionsOur study confirms that concentrations of IL-8, CCL-4, and CCL-20 are increased in the course of HGA and TBE. Their concentrations in serum may be used to monitor the course of TBE and HGA, as well as possibly detect co-infections with the diseases.

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.

Seroprevalence of tick-borne encephalitis and Lyme borreliosis in a defined Czech population

Purpose: The South Bohemian Region of the Czech Republic is an endemic area of tick-borne encephalitis (TBE). In 2017, the inhabitants of Římov municipality developed a serious course of TBE and Lyme borreliosis (LB). This led experts to research and serology examinations of the inhabitants of Římov in order to detect the seroprevalence of TBE and LB. Methods & Materials: Římov is situated on the Malše river. A water dam has been built on the river, there are extensive deciduous and mixed forests around the waterways and the biotope allows for the development of ticks. A questionnaire was distributed to all the inhabitants of the municipality to get the basic information (life span, occupation, experience with TBE and LB, vaccinations against TBE, number of tick bites per year and the interest in detection of antibodies of TBE and LB). The questionnaires have been evaluated and participants, who gave their consent, were blood tested and serological tests have been done. A total of 114 people participated in the study. Results: From the questionnaires and the serological examination, it appeared that 4 persons (3.5%) experienced the manifest form of TBE and 5 people (4.4%) experienced the latent form of TBE. In total, 7.9% of the sample experienced the manifest or the latent form of TBE. 80% of the sample confirmed sufficient antibody levels after vaccination. 12.1% of the population remain vulnerable. 32.5% of the sample experienced Lyme disease (9 people, i.e. 7.9% manifested the disease, 22 people (19.3%) had latent disease, early phase of the infection was confirmed in 6 people (5.3%). 77 people (67.5%) remain vulnerable. Conclusion: A serological examination of the population's research sample revealed that of the people living in the focus point of TBE in Římov, approximately 8% have developed antibodies after being diagnosed the disease or having experienced the latent form and 80% have created antibodies after vaccination. Anamnestic antibodies after being diagnosed or having experienced the latent form of LB, or the early phase of the infection was demonstrated in 32.5% of the study sample. Further research will be focused on testing the ticks of the given site.

Chapter 9: Immunology of TBEV-Infection

• 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 (meningoencephalitic) 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.

A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection

BackgroundTick-borne encephalitis is caused by the neurotropic, positive-sense RNA virus, tick-borne encephalitis virus (TBEV). TBEV infection can lead to a variety of clinical manifestations ranging from slight fever to severe neurological illness. Very little is known about genetic factors predisposing to severe forms of disease caused by TBEV. The aims of the study were to compile a catalog of human genes involved in response to TBEV infection and to rank genes from the catalog based on the number of neighbors in the network of pairwise interactions involving these genes and TBEV RNA or proteins.ResultsBased on manual review and curation of scientific publications a catalog comprising 140 human genes involved in response to TBEV infection was developed. To provide access to data on all genes, the TBEVhostDB web resource (http://icg.nsc.ru/TBEVHostDB/) was created. We reconstructed a network formed by pairwise interactions between TBEV virion itself, viral RNA and viral proteins and 140 genes/proteins from TBEVHostDB. Genes were ranked according to the number of interactions in the network. Two genes/proteins (CCR5 and IFNAR1) that had maximal number of interactions were revealed. It was found that the subnetworks formed by CCR5 and IFNAR1 and their neighbors were a fragments of two key pathways functioning during the course of tick-borne encephalitis: (1) the attenuation of interferon-I signaling pathway by the TBEV NS5 protein that targeted peptidase D; (2) proinflammation and tissue damage pathway triggered by chemokine receptor CCR5 interacting with CD4, CCL3, CCL4, CCL2. Among nine genes associated with severe forms of TBEV infection, three genes/proteins (CCR5, IL10, ARID1B) were found to have protein-protein interactions within the network, and two genes/proteins (IFNL3 and the IL10, that was just mentioned) were up- or down-regulated in response to TBEV infection. Based on this finding, potential mechanisms for participation of CCR5, IL10, ARID1B, and IFNL3 in the host response to TBEV infection were suggested.ConclusionsA database comprising 140 human genes involved in response to TBEV infection was compiled and the TBEVHostDB web resource, providing access to all genes was created. This is the first effort of integrating and unifying data on genetic factors that may predispose to severe forms of diseases caused by TBEV. The TBEVHostDB could potentially be used for assessment of risk factors for severe forms of tick-borne encephalitis and for the design of personalized pharmacological strategies for the treatment of TBEV infection.

Usefulness of copeptin as a potential biomarker in TBE

Objective: The aim of the study was to evaluate the usefulness of copeptin for differentiation of hyponatremia in the course of tick-borne encephalitis (TBE) and for being a prognostic marker of the severity of TBE.Materials and methods: One hundred and fourteen patients with TBE were included in the study. The control group consisted of 62 patients diagnosed with viral meningitis.Results: Copeptin concentration did not differ in patients with hyponatremia and normonatremia. Urinary sodium excretion to plasma copeptin (copeptin/UNa Secretion) ratio was significantly lower in Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion patients than in patients with hyponatremia of other origin. Mean copeptin concentration in TBE patients was higher than in control group (VM) patients. There were no differences between patients with severe and mild course of TBE.Conclusions: Copeptin/UNa ratio may be used as a potential biomarker of SIADH in patients with TBE. Copeptin concentration is significantly higher in patients with TBE than in viral meningitis of other origin, especially in patients aged 18–34 and >49 years old. Copeptin does not differentiate TBE of mild and severe course.

The expression of the chemokine receptor CCR5 in tick-borne encephalitis.

BackgroundChemokine receptor 5 (CCR5) is hypothesized to drive the lymphocyte migration to central nervous system in flavivirus encephalitis, and the non-functional CCR5Δ32 genetic variant was identified as a risk factor of a West Nile virus infection and of tick-borne encephalitis (TBE). We have attempted to investigate how CCR5 expression corresponds to the clinical course and severity of TBE.MethodsWe have repeatedly studied CCR5 expression in 76 patients during encephalitic and convalescent TBE phase, analyzing its association with clinical features, cerebrospinal fluid (csf) pleocytosis, and concentrations of CCR5 ligands (chemokines CCL3, CCL4, and CCL5) and CCR5 genotype. Fifteen patients with neuroborreliosis, 7 with aseptic meningitis, 17 in whom meningitis/encephalitis had been excluded, and 18 healthy blood donors were studied as controls. Expression of CCR5 was measured cytometrically in blood and csf-activated Th lymphocytes (CD3+CD4+CD45RO+). Concentrations of chemokines in serum and csf were measured immunoenzymatically, and CCR5Δ32 was detected with sequence-specific primers. Data were analyzed with non-parametric tests, and p < 0.05 was considered significant.ResultsThe blood expression of CCR5 did neither differ between the groups nor change in the course of TBE. The CCR5 expression in the inflammatory csf was several-fold increased in comparison with blood but lower in TBE than in neuroborreliosis. The csf concentration of CCL5 was increased in TBE, the highest in the most severe presentation (meningoencephalomyelitis) and correlated with pleocytosis. The CCR5Δ32/wt genotype present in 7 TBE patients was associated with a decreased CCR5 expression, but enrichment of csf Th population in CCR5-positive cells and the intrathecal inflammatory response were preserved, without a compensatory increase of CCL5 expression.ConclusionsWe infer CCR5 and CCL5 participate in the response to TBE virus, as well as to other neurotropic pathogens. The intrathecal response to TBE is not hampered in the bearers of a single copy of CCR5Δ32 allele, suggesting that the association of CCR5Δ32 with TBE may be mediated in the periphery at the earlier stage of the infection. Otherwise, a variability of the CCR5 expression in the peripheral blood lymphocytes seems not to be associated with a variable susceptibility to TBE.

MRI-imaging and clinical findings of eleven children with tick-borne encephalitisand review of the literature.

The incidence of tick-borne encephalitis (TBE) is increasing in many countries. Magnetic resonance imaging (MRI) in the course of TBE is not regularly performed in children. The aim of our study was evaluating MRI-findings of children and adolescents with TBE. Retrospective evaluation of the charts and MRIs of patients who had been treated for TBE in the four participating hospitals in the last twenty years. 11 patients (5 male; age at TBE 3 weeks-15 9/12 years; mean 104.9 months) were included. MRI (within the first week after admission) revealed symmetric or asymmetric T2-hyperintensities in both thalami in 7/11 patients with additional bilateral lesions in putamen and/or caudate nucleus in 3 patients, and additional cortical lesions in 2 patients. Our youngest patient presented with T2-hyperintensities affecting the whole left cerebral hemisphere including white and grey matter and both cerebellar hemispheres. One patient had a minimal reversible T2-hyperintensity in the splenium of the corpus callosum (RHSCC). 3/11 patients had a normal MRI. 4/11 patients showed complete neurological recovery (2/4 with a normal MRI, RHSCC patient). 6/11 children survived with significant sequelae: hemiparesis (n=4); cognitive deficits (n=4); pharmacoresistant epilepsy (n=2). One patient died of a malignant brain edema. A spectrum of MRI findings can be found in children with TBE, often showing involvement of the subcortical deep grey matter structures. In children presenting with a meningoencephalitis and bilateral thalamic involvement TBE should be included in the differential diagnosis.

THE COURSE OF TICK-BORNE ENCEPHALITIS IN PERSONS OF ADVANCED AGE

The article describes a course of tick-borne encephalitis in patients of advanced age. We rarely met two-wave fever in these patients; quite long period of apyrexia is specific for them Eyeball pain and meningeal symptoms were seen in these patients less often than in other age groups. Concurrent infection is most typical and high risk of lethal outcomes is common for this group of patients. It can be explained by existence of serious comorbid conditions, lack of specific prevention and by late initiation of specific treatment .All these factors have to be taken into account during hospitalizing elderly persons with neurologic symptoms, especially in endemic regions on TBE from May till September.

Evaluation of hyponatraemia in patients with tick-borne encephalitis – A preliminary study

Hyponatraemia is one of the most frequently observed, but sometimes overlooked, electrolyte disorder. Patients with meningitis are predisposed to develop hypovolaemic hyponatraemia. However, hyponatraemia in meningitis may also be caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Proper differentiation of these pathomechanisms is crucial in patient's treatment as dehydration requires fluid supplementation, while SIADH is treated with fluid restriction. The aim of the present study was the evaluation of frequency, potential causes, and risk factors of hyponatraemia in patients with tick-borne encephalitis (TBE). A total of 61 patients (22 women, 39 men) aged 18–80 years, with a history of TBE was included in the study. Hyponatraemia was diagnosed when sodium concentration was below 135mmol/l. Hyponatraemia was considered mild when sodium concentration was 130–134mmol/l, moderate when 125–129mmol/l, and severe when <125mmol/l. Among the 61 patients, hyponatraemia was observed in 41% (25 patients). In 20 patients (33%), hyponatraemia was mild, in 3 (5%) it was moderate, and in 2 (3%) severe. Two patients with severe hyponatraemia and one with moderate hyponatraemia fulfilled the SIADH criteria. In the non-SIADH patients, sodium concentration normalized within 1–2 (1.1±0.2) days while in the SIADH group, the disturbances lasted for 4–8 (6±2) days. Sodium concentration correlated with patients age (R Spearmann – 0.27, p<0.05). There were no significant differences as far as gender or clinical form of the disease are concerned. Hyponatraemia, usually mild, is a common disorder in the course of TBE, although it is not significantly more frequent than in other hospitalized patients. Dehydration seems to be the main cause of hyponatraemia in the course of TBE. SIADH is a less common cause of hyponatraemia in the course of TBE, although it should be taken into consideration as the treatment differs significantly. Patients >60 years of age with TBE are more susceptible to hyponatraemia than younger patients.