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 tick-borne encephalitis virus (TBEV) is the arboviral etiological agent of tick-borne encephalitis (TBE), considered to be one of the most important tick-borne viral diseases in Europe and Asia. In recent years, an increase in the incidence of TBE as well as an increasing geographical range of the disease have been noted. Despite the COVID-19 pandemic and the imposition of restrictions that it necessitated, the incidence of TBE is rising in more than half of the European countries analyzed in recent studies. The virus is transmitted between ticks, animals, and humans. It seems that ticks and small mammals play a role in maintaining TBEV in nature. The disease can also affect dogs, horses, cattle, and small ruminants. Humans are incidental hosts, infected through the bite of an infected tick or by the alimentary route, through the consumption of unpasteurized milk or milk products from TBEV-infected animals. TBEV infections in humans may be asymptomatic, but the symptoms can range from mild flu-like to severe neurological. In Europe, cases of TBE are reported every year. While there is currently no effective treatment for TBE, immunization and protection against tick bites are critical in preventing this disease.

Tick-borne encephalitis virus (TBEV) is a flavivirus commonly found in at least 27 European and Asian countries. It is an emerging public health problem, with steadily increasing case numbers over recent decades. Tick-borne encephalitis virus affects between 10,000 and 15,000 patients annually. Infection occurs through the bite of an infected tick and, much less commonly, through infected milk consumption or aerosols. The TBEV genome comprises a positive-sense single-stranded RNA molecule of ∼11 kilobases. The open reading frame is > 10,000 bases long, flanked by untranslated regions (UTR), and encodes a polyprotein that is co- and post-transcriptionally processed into three structural and seven non-structural proteins. Tick-borne encephalitis virus infection results in encephalitis, often with a characteristic biphasic disease course. After a short incubation time, the viraemic phase is characterised by non-specific influenza-like symptoms. After an asymptomatic period of 2-7 days, more than half of patients show progression to a neurological phase, usually characterised by central and, rarely, peripheral nervous system symptoms. Mortality is low-around 1% of confirmed cases, depending on the viral subtype. After acute tick-borne encephalitis (TBE), a minority of patients experience long-term neurological deficits. Additionally, 40%-50% of patients develop a post-encephalitic syndrome, which significantly impairs daily activities and quality of life. Although TBEV has been described for several decades, no specific treatment exists. Much remains unknown regarding the objective assessment of long-lasting sequelae. Additional research is needed to better understand, prevent, and treat TBE. In this review, we aim to provide a comprehensive overview of the epidemiology, virology, and clinical picture of TBE.

Tick-borne encephalitis (TBE) incidence has been increasing in Europe the last decades, but very few cases in pregnant women have been described. We present two cases and describe the serology of both mother and infant at the time of diagnosis and delivery, as well as at months 3, 6, 9, and 12 of follow-up. In both cases, pregnancies and infants developed normally. The mothers had moderate-to severe symptoms of TBE and were positive for IgM and IgG at the time of diagnosis, and throughout the follow up period whilst both infants were PCR- and IgM-negative and positive for IgG during their first months in life. Declining IgG titres were seen in the infants during follow-up until they became negative at the age of nine months. TBE IgG was vertically transmitted in these two cases of infants born to TBE-infected mothers.

Lyme borreliosis (LB) is a tick-borne infectious disease, endemic in the Northern hemisphere, with a polymorphic clinical spectrum (cutaneous, articular, and neurologic involvement). The variability of clinical manifestations poses LB as a diagnostic challenge. We describe a case of acute Lyme neuroborreliosis (LNB) in an adult female with a history of recent travel in Europe. There are few reports of acute LNB presenting as encephalitis in the literature. Suspicion for the diagnosis and prompt treatment seems to have a positive impact on patient outcomes.

Tick-borne encephalitis (TBE) is an acute disease caused by the tick-borne encephalitis virus. Due to the viral nature of the condition, there is no effective causal treatment for full-blown disease. Current and nonspecific TBE treatments only relieve symptoms. Unfortunately, the first phase of TBE is characterized by flu-like symptoms, making diagnosis difficult during this period. The second phase is referred to as the neurological phase as it involves structures in the central nervous system-most commonly the meninges and, in more severe cases, the brain and the spinal cord. Therefore, it is important that early markers of TBE that will guide clinical decision-making and the choice of treatment are established. In this review, we performed an extensive search of literature reports relevant to biomarkers associated with TBE using the MEDLINE/PubMed database. We observed that apart from routinely determined specific immunoglobulins, free light chains may also be useful in the evaluation of intrathecal synthesis in the central nervous system (CNS) during TBEV infection. Moreover, selected metalloproteinases, chemokines, or cytokines appear to play an important role in the pathogenesis of TBE as a consequence of inflammatory reactions and recruitment of white blood cells into the CNS. Furthermore, we reported promising findings on tau protein or Toll-like receptors. It was also observed that some people may be predisposed to TBE. Therefore, to understand the role of selected tick-borne encephalitis biomarkers, we categorized these factors and discussed their potential application in the diagnosis, prognosis, monitoring, or management of TBE.

Ticks transmit a variety of pathogens affecting both human and animal health. In temperate and cold regions of Europe (Western, Central, Eastern, and Northern Europe), the most relevant zoonotic tick-borne pathogens are tick-borne encephalitis virus (TBEV), Borrelia spp. and Anaplasma phagocytophilum. More rarely, Rickettsia spp., Neoehrlichia mikurensis, and zoonotic Babesia spp. are identified as a cause of human disease. Domestic animals may also be clinically affected by these pathogens, and, furthermore, can be regarded as sentinel hosts for their occurrence in a certain area, or even play a role as reservoirs or amplifying hosts. For example, viraemic ruminants may transmit TBEV to humans via raw milk products. This review summarizes the role of domestic animals, including ruminants, horses, dogs, and cats, in the ecology of TBEV, Borrelia spp., A. phagocytophilum, Rickettsia spp., N. mikurensis, and zoonotic Babesia species. It gives an overview on the (sero-)prevalence of these infectious agents in domestic animals in temperate/cold regions of Europe, based on 148 individual prevalence studies. Meta-analyses of seroprevalence in asymptomatic animals estimated an overall seroprevalence of 2.7% for TBEV, 12.9% for Borrelia burgdorferi sensu lato (s.l.), 16.2% for A. phagocytophilum and 7.4% for Babesia divergens, with a high level of heterogeneity. Subgroup analyses with regard to animal species, diagnostic test, geographical region and decade of sampling were mostly non-significant, with the exception of significantly lower B. burgdorferi s.l. seroprevalences in dogs than in horses and cattle. More surveillance studies employing highly sensitive and specific test methods and including hitherto non-investigated regions are needed to determine if and how global changes in terms of climate, land use, agricultural practices and human behavior impact the frequency of zoonotic tick-borne pathogens in domestic animals.

After the recent description of biphasic disease with herpes simplex virus (HSV) encephalitis followed by anti-N-methyl-d-aspartate receptor encephalitis (anti-NMDARE), anti-NMDARE preceded by non-HSV central nervous system (CNS) infection has been more rarely reported. We report the first case of TBE followed by anti-NMDARE and carry out a systematic literature review on anti-NMDARE preceded by non-HSV CNS infection.

Tick-borne encephalitis (TBE) is an illness caused by tick-borne encephalitis virus (TBEV) infection which is often limited to a febrile illness, but may lead to very aggressive downstream neurological manifestations. The disease is prevalent in forested areas of Europe and northeastern Asia, and is typically caused by infection involving one of three TBEV subtypes, namely the European (TBEV-Eu), the Siberian (TBEV-Sib), or the Far Eastern (TBEV-FE) subtypes. In addition to the three main TBEV subtypes, two other subtypes; i.e., the Baikalian (TBEV-Bkl) and the Himalayan subtype (TBEV-Him), have been described recently. In Europe, TBEV-Eu infection usually results in only mild TBE associated with a mortality rate of <2%. TBEV-Sib infection also results in a generally mild TBE associated with a non-paralytic febrile form of encephalitis, although there is a tendency towards persistent TBE caused by chronic viral infection. TBE-FE infection is considered to induce the most severe forms of TBE. Importantly though, viral subtype is not the sole determinant of TBE severity; both mild and severe cases of TBE are in fact associated with infection by any of the subtypes. In keeping with this observation, the overall TBE mortality rate in Russia is ∼2%, in spite of the fact that TBEV-Sib and TBEV-FE subtypes appear to be inducers of more severe TBE than TBEV-Eu. On the other hand, TBEV-Sib and TBEV-FE subtype infections in Russia are associated with essentially unique forms of TBE rarely seen elsewhere if at all, such as the hemorrhagic and chronic (progressive) forms of the disease. For post-exposure prophylaxis and TBE treatment in Russia and Kazakhstan, a specific anti-TBEV immunoglobulin is currently used with well-documented efficacy, but the use of specific TBEV immunoglobulins has been discontinued in Europe due to concerns regarding antibody-enhanced disease in naïve individuals. Therefore, new treatments are essential. This review summarizes available data on the pathogenesis and clinical features of TBE, plus different vaccine preparations available in Europe and Russia. In addition, new treatment possibilities, including small molecule drugs and experimental immunotherapies are reviewed. The authors caution that their descriptions of approved or experimental therapies should not be considered to be recommendations for patient care.

Tick-borne encephalitis (TBE), which is endemic across large regions of Europe and Asia, is most effectively prevented through vaccination. Three-dose primary TBE vaccination schedules are either rapid (0,7,21-days) or conventional (0,28-84-days, 9-12-months). The second dose can also be administered at 14 days for faster priming and sero-protection). Areas covered: We used a three-step selection process to identify 21 publications comparing the immunogenicity and/or safety of different schedules. Expert commentary: Priming with two or three TBE vaccine doses was highly immunogenic. After conventional priming (0-28 days), 95% adults and ≥95% children had neutralization test (NT) titers ≥10 at 14 days post-dose-2 compared with 92% adults and 99% children at 21 days post-dose-3 (rapid schedule). Most subjects retained NT titers ≥10 at day 300. A single booster dose induced a strong immune response in all subjects irrespective of primary vaccination schedule or elapsed time since priming. GMT peaked at 42 days post-dose-1 (i.e., 21 days post-dose 3 [rapid-schedule], or 14-28 days post-dose-2 [conventional-schedule]), and declined thereafter. Adverse events were generally rare and declined with increasing doses. In the absence of data to recommend one particular schedule, the regimen choice will remain at the physician\'s discretion, based on patient constraints and availability.