The purpose of this study was evaluation of the prevalence of co-infection with Borrelia species, A. phagocytophilum and Babesia spp. in patients with tick-borne encephalitis (TBE). At total of 110 patients with TBE were included in the study. Serological tests for tick-borne encephalitis virus (TBEV), PCR for Borrelia species, Anaplasma phagocytophilum and Babesia spp., blood smears for A. phagocytophilum and Babesia spp. and BLAST analysis for Babesia spp. were performed. Results showed a significant majority of patients co-infected with Borrelia species (30/110; 27 %), much less with A. phagocytophilum (12/110; 10.9 %) and with Babesia spp. (1/110; 0.9 %). The BLAST analysis of the 18S rDNA sequence obtained with the Babesia spp. specific primers indicated that the patient was infected with Babesia microti. Triple co-infections (TBEV-Borrelia species- A. phagocytophilum) were observed in three (3/110; 2.7 %) patients. Conclusions were such that differential diagnosis in patients after the tick bite, presenting with acute symptoms, should include not only TBE and Lyme disease, but also other diseases transmitted by ticks. In patients with low parasitemia in suspicion of Babesia spp. infection PCR seems to be a more sensitive method than blood smear. Co-infection with various tick-borne pathogens must be always considered, especially in endemic regions.

Immunocompetent patients may be unaware of infection with Babesia microti after a tick bite. It must be included in the differential diagnosis after the tick bite. In patients with low parasitaemia PCR and serology seem useful when blood smear is negative. Self-elimination of Babesia spp. is possible, especially in cases with low parasitaemia.

BackgroundTick-borne encephalitis (TBE) is a clinically variable but potentially severe Flavivirus infection, with the outcome strongly dependent on secondary immunopathology. Neutrophils are present in cerebrospinal fluid (CSF) of TBE patients, but their pathogenetic role remains unknown. In animal models, neutrophils contributed both to the Flavivirus entry into central nervous system (CNS) and to the control of the encephalitis, which we attempted to evaluate in human TBE.MethodsWe analyzed records of 240 patients with TBE presenting as meningitis (n = 110), meningoencephalitis (n = 114) or meningoencephalomyelitis (n = 16) assessing CSF neutrophil count on admission and at follow-up 2 weeks later, and their associations with other laboratory and clinical parameters. We measured serum and CSF concentrations of Th17-type cytokines (interleukin-17A, IL-17F, IL-22) and chemokines attracting neutrophils (IL-8, CXCL1, CXCL2) in patients with TBE (n = 36 for IL-8, n = 15 for other), with non-TBE aseptic meningitis (n = 6) and in non-meningitis controls (n = 7), using commercial ELISA assays. The results were analyzed with non-parametric tests with p < 0.05 considered as significant.ResultsOn admission, neutrophils were universally present in CSF constituting 25% (median) of total pleocytosis, but on follow-up, they were absent in most of patients (58%) and scarce (< 10%) in 36%. CSF neutrophil count did not correlate with lymphocyte count and blood-brain barrier integrity, did not differ between meningitis and meningoencephalitis, but was higher in meningoencephalomyelitis patients. Prolonged presence of neutrophils in follow-up CSF was associated with encephalitis and neurologic sequelae. All the studied cytokines were expressed intrathecally, with IL-8 having the highest CSF concentration index. Additionally, IL-17A concentration was significantly increased in serum. IL-17F and CXCL1 CSF concentrations correlated with neutrophil count and CXCL1 concentration was higher in patients with encephalitis.ConclusionsThe neutrophil CNS infiltrate does not correlate directly with TBE severity, but is associated with clinical features like myelitis, possibly being involved in its pathogenesis. Th17 cytokine response is present in TBE, especially intrathecally, and contributes to the CNS neutrophilic inflammation. IL-8 and CXCL1 may be chemokines directly responsible for the neutrophil migration.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1138-0) contains supplementary material, which is available to authorized users.

The synthesis of chemokines (Il-8, MIP-1alpha and 1beta) is increased in Lyme borreliosis and, at least in the early stages of the disease, is related to the synthesis of Il-1beta. Chemokine concentrations depend on the clinical form of Lyme borreliosis, with a tendency for higher values in early infection (erythema migrans and neuroborreliosis). Of the chemokines studied, Il-8 created a chemotactic gradient towards the inflammation site, and thus might be responsible for leukocyte migration.

IntroductionThe aim of this study was the assessment of neuron‐specific enolase (NSE) and S‐100 concentration in serum and cerebrospinal fluid (CSF) in patients with different clinical forms of tick‐borne encephalitis (TBE).Material and MethodsThe serum and CFS concentrations of S100B and NSE of 43 patients with TBE were measured with ELISA method using commercial kits: NSE and S100B Elisa Kit (DRG, Germany). Subjects were divided into: Group I—patients with meningoencephalitis (n = 17) and Group II—patients with meningitis (n = 26). None of the patients reported any neurodegenerative disorder that could affect the results of the study. The control group (CG) consisted of 13 patients. These patients were admitted to the hospital because of headache, and the CSF examination excluded inflammatory process. Samples were collected on admission (sample 1) and after treatment (sample 2).ResultsNeuron‐specific enolase concentration in CSF was higher in group I than in group II (p = 0.0002) and controls (p = 0.04). NSE concentration was higher in the second serum and CSF sample in both groups. S100B concentration did not differ between TBE patients and controls. NSE concentration in serum after 14 days was higher in the sequelae group (34.3 ± 9.7 vs. 16.7 ± 15, p = 0.04). Also, NSE serum sample 2/serum sample 1 ratio was significantly higher in the sequelae group (3.57 ± 0.92 vs. 1.53 ± 1.99, p = 0.04). Receiver Operating Characteristic curve analysis indicated that NSE concentration in serum II differentiates sequelae group from other meningoencephalitis patients (p = 0.0001). S100B serum sample 2/CSF sample 2 ratio was lower in the sequelae group (0.05 ± 0.1 vs. 0.37 ± 0.28, p = 0.02).Conclusions(a) Neurodegeneration process is present in TBE encephalitis. (b) NSE concentration correlates with inflammatory parameters in CSF in TBE. (c) Neurodegeneration is present even after clinical recovery of TBE. (d) NSE could be used in the prediction of TBE course. (e) S‐100 did not differ between TBE patients and controls.