In addition, demonstration of intrathecal production of anti-TBEV IgM and IgG verified CNS infection with TBEV (Table ?(Table1).1). fluid pleocytosis is not required in encephalitis caused by tick borne encephalitis computer virus. In daily clinical practice, in patients with neurologic symptoms/indicators compatible with tick borne encephalitis and the risk of Triclabendazole exposure to ticks in a tick borne encephalitis endemic region, the search for central nervous system contamination with tick borne encephalitis computer virus is warranted despite the lack of cerebrospinal fluid pleocytosis. Background Tick borne encephalitis (TBE) is the most frequent vector-transmitted infectious disease of the central nervous system (CNS) in Europe and Asia and is considered an emerging disease due to its rising incidence and the spread of endemic areas in recent decades [1]. TBE caused by European subtype of TBE computer virus (TBEV) has typically a biphasic clinical course with the second phase presenting as meningitis, meningoencephalitis, or meningoencephalomyelitis [2]. Cerebrospinal fluid (CSF) pleocytosis is considered a condition sine qua non for the diagnosis of CNS involvement in TBE, which in routine clinical practice is usually confirmed by demonstration of serum IgM and IgG antibodies to TBEV [2]-[4]. Cases of TBE with neurologic involvement but without CSF pleocytosis have been published [5]-[7], however, only the case recently reported by P?schl et al. was convincingly substantiated [5]. Here we present a patient from Slovenia, an area highly endemic for TBE [8], with clinical features of encephalitis, who fulfilled criteria for recent CNS contamination with TBEV although he had no CSF pleocytosis. Case presentation A 79-year-old man with arterial hypertension Triclabendazole and chronic venous ulcers on both shins, fell ill acutely with diarrhea, fatigue and sleepiness in midsummer 2013. After a week, diarrhea halted, but he became febrile up to 38.5C and Triclabendazole was no longer able to walk independently due to general weakness. As a beekeeper he had been exposed to ticks in the past but could not remember having experienced a tick bite during the preceding few months. At admission to hospital on day 8 of his illness, he was lethargic, disoriented, but without indicators of meningeal irritation. His blood pressure was 133/83 mmHg, heart rate 99/min, breathing rate Triclabendazole 30/min Rabbit Polyclonal to TACC1 and axillary heat 38.9C. Program laboratory blood assessments revealed normal blood cell count, moderate hyponatremia (Na 129; normal 135-145 mmol/l), and slightly elevated concentrations of C-reactive protein (32 mg/l; normal 0-5 mg/l), liver enzymes (aspartate aminotransferase 0.73; normal 0.58 kat/l, gamma-glutamyl transpeptidase 1.12 kat/l; normal 0.92 kat/l) and creatinine (101 mol/l; normal 44-97 mol/l). CSF examination yielded elevated protein concentration (1.31 g/l; normal 0.15-0.45 g/l), but normal leukocyte count (3 106/l; normal 5 106/l) and glucose concentration. In the following days the patient remained febrile up to 39.4C. On day 10, tremor of hands and tongue appeared and his mental status deteriorated to somnolence. Computed tomography of the brain showed only moderate periventricular leukopathy. Repeated CSF analyses on day 14 and 23 revealed elevated protein concentrations (1.23, and 2.02 g/l, respectively), but still no pleocytosis (CSF leukocyte count 1, and 2 106/l, respectively). PCR analyses of CSF for the presence of TBEV on day 8 and 23 were negative as were for HSV 1, HSV 2, VZV, and enteroviruses. Based on serological results the patient did not have Lyme neuroborreliosis. However, serum IgM and IgG antibodies to TBEV were exhibited using enzyme linked immunosorbent assay – ELISA (Enzygnost Anti-TBE/FSME Computer virus IgG, IgM; Siemens, Marburg, Germany) (Table ?(Table1).1). The follow-up levels of specific serum antibodies and the avidity of specific serum IgG (12.7%, 15.4%, and 51.6% on day 14, 21, and 65, respectively) indicated recent infection with TBEV. In addition, demonstration of intrathecal production of anti-TBEV IgM and IgG verified CNS contamination with TBEV (Table ?(Table1).1). From day 14 the patient was no longer febrile and his mental and physical status progressively improved. Hospitalization was prolonged because of hospital acquired pneumonia.