Background: Lyme neuroborreliosis (LNB) is a disease caused by spirochaete Borrelia burgdorferi, involving the nervous system. It usually manifests as lymphocytic meningoradiculitis, but in rare cases it can also lead to cerebrovascular complications. We aimed to perform a systematic review of all reported cases of LNB complicated by central nervous system vasculitis and stroke or transient ischemic attack (TIA). Material and Methods: We conducted a systematic review of literature between May 1987 and December 2016 with patients who presented with cerebrovascular course of LNB. Results: This study included 88 patients with a median age of 46 years. The median interval from onset of symptoms suggesting Lyme disease to first symptoms of cerebrovascular manifestations of LNB was 3.5 months. The most common cerebrovascular manifestation of LNB was ischemic stroke (76.1%), followed by TIA (11.4%). The posterior circulation was affected alone in 37.8% of patients, the anterior circulation in 24.4% of patients, and in 37.8% of cases posterior and anterior circulation were affected simultaneously. The most common affected vessels were middle cerebral artery – in 19 cases, basilar artery – in 17 cases and anterior cerebral artery – in 16 cases. A good response to antibiotic treatment was achieved in the vast number of patients (75.3%). The overall mortality rate was 4.7%. Conclusions: Cerebral vasculitis and stroke due to LNB should be considered, especially in patients who live in or have come from areas with high prevalence of tick-borne diseases, as well as in those without cardiovascular risk factors, but with stroke-like symptoms of unknown cause.

Lyme neuroborreliosis (LNB) is a rare cause of vasculitis and stroke. It may manifest as subarachnoid hemorrhage, intracerebral hemorrhage, and most often ischemic stroke due to cerebral vasculitis. The vast majority of reported cases have been described by European authors. A high index of suspicion is required in patients who live or have traveled to areas with high prevalence of tick-borne diseases, and in the case of stroke-like symptoms of unknown cause in patients without cardiovascular risk factors. In this review, we also present four illustrative cases of vasculitis and stroke-like manifestations of LNB.

Aim: The aim of the study was to evaluate the clinical course and effectiveness of diagnostics tools for Babesia spp. infection in patients bitten by ticks. Materials and methods: Five hundred and forty-eight patients hospitalised or seen in outpatients department because of various symptoms after a tick bite were included in the study. PCR, nucleotide sequencing of Babesia 18S rRNA gene fragment, blood smears and serological tests for Babesia spp., TBEV, A. phagocytophilum and B. burgdorferi were performed in all patients. Six patients infected with Babesia were included in the final analysis. They had PCR, Babesia 18S rRNA gene fragment nucleotide sequencing, blood smears and serological tests for Babesia spp., TBEV, A. phagocytophilum and B. burgdorferi performed twice. Results: Tick-borne infection with Babesia microti in six immunocompetent patients with non-specific symptoms was confirmed for the first time in Poland. No severe course of the disease was seen. No piroplasm forms were noticed within erythrocytes on blood smear. Three patients developed a serological response. Conclusions: 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.

Herpes zoster is a viral disease caused by the reactivation of varicella–zoster virus (VZV) which remained latent in the cranial nerve or dorsal root ganglia. Cell-mediated immunity is known to decline with age as part of immunosenescence and can lead to the reactivation of VZV. Whereas herpes zoster is usually mild in healthy young persons, older patients are at increased risk for complications. In the present study we investigated the serum cytokine profile (IL-17, IL-23, IL-21, IL-4, IL-12), representing cellular and humoral immunity and assessed the level of VZV IgG antibodies in patients with herpes zoster. We investigated the serum concentrations of IL-17, IL-23, IL-21, IL-4, IL-12 and the level of VZV IgG antibodies in 23 patients with herpes zoster who did not develop superinfection. The control group was represented by 21 individuals in similar age with no inflammatory and infectious diseases. Cytokine and antibodies levels were measured by ELISA method. Statistical analysis was performed using the ROC curve (receiver operating characteristic), t-test, Welch’s t-test, and nonparametric tests with STATISTICA 10 software. In patients with herpes zoster, the serum level of IL-17, IL-23, IL-21, IL-4 and IL-12 as well as VZV IgG antibodies titer were statistically significantly increased compared to control group. Our results confirm the broad activation of the immune system involving humoral and cell-mediated immunity.

Systemic sclerosis (SSc) is a connective tissue disease characterized by fibrosis in skin and internal organs, progressive vascular obliteration, and the production of autoantibodies. Diagnostic imaging is irreplaceable in both diagnosing and monitoring patients suffering from systemic sclerosis. In addition to routinely used methods, such as comparative X-ray of the hands or a contrast-enhanced examination of the upper gastrointestinal tract or chest, there is an array of less widespread examinations, with an emphasis on magnetic resonance imaging (MRI) and ultrasonography, not only in the evaluation of the musculoskeletal system. This article will review the various imaging modalities available for SSc imaging and assessment, focusing on their utility as tissue-specific diagnosis and treatment monitoring.

Tick-borne encephalitis (TBE) is caused by a virus that belongs to the Flaviviridae family and is transmitted by tick bites. The disease has a biphasic course. Diagnosis is based on laboratory examinations because of non-specific clinical features, which usually entails the detection of specific IgM antibodies in either blood or cerebrospinal fluid that appear in the second phase of the disease. Neurological symptoms, time course of the disease, and imaging findings are multifaceted. During the second phase of the disease, after the onset of neurological symptoms, magnetic resonance imaging (MRI) abnormalities are observed in a limited number of cases. However, imaging features may aid in predicting the prognosis of the disease.