Course Of Tick-borne Encephalitis Research Articles

PP72 - Peroxidative metabolism of fatty acids in the course of tick-borne encephalitis

PP72 - Peroxidative metabolism of fatty acids in the course of tick-borne encephalitis

Mice with different susceptibility to tick-borne encephalitis virus infection show selective neutralizing antibody response and inflammatory reaction in the central nervous system

BackgroundThe clinical course of tick-borne encephalitis (TBE), a disease caused by TBE virus, ranges from asymptomatic or mild influenza-like infection to severe debilitating encephalitis or encephalomyelitis. Despite the medical importance of this disease, some crucial steps in the development of encephalitis remain poorly understood. In particular, the basis of the disease severity is largely unknown.MethodsTBE virus growth, neutralizing antibody response, key cytokine and chemokine mRNA production and changes in mRNA levels of cell surface markers of immunocompetent cells in brain were measured in mice with different susceptibilities to TBE virus infection.ResultsAn animal model of TBE based on BALB/c-c-STS/A (CcS/Dem) recombinant congenic mouse strains showing different severities of the infection in relation to the host genetic background was developed. After subcutaneous inoculation of TBE virus, BALB/c mice showed medium susceptibility to the infection, STS mice were resistant, and CcS-11 mice were highly susceptible. The resistant STS mice showed lower and delayed viremia, lower virus production in the brain and low cytokine/chemokine mRNA production, but had a strong neutralizing antibody response. The most sensitive strain (CcS-11) failed in production of neutralizing antibodies, but exhibited strong cytokine/chemokine mRNA production in the brain. After intracerebral inoculation, all mouse strains were sensitive to the infection and had similar virus production in the brain, but STS mice survived significantly longer than CcS-11 mice. These two strains also differed in the expression of key cytokines/chemokines, particularly interferon gamma-induced protein 10 (IP-10/CXCL10) and monocyte chemotactic protein-1 (MCP-1/CCL2) in the brain.ConclusionsOur data indicate that the genetic control is an important factor influencing the clinical course of TBE. High neutralizing antibody response might be crucial for preventing host fatality, but high expression of various cytokines/chemokines during TBE can mediate immunopathology and be associated with more severe course of the infection and increased fatality.

Peripheral facial palsy in patients with tick-borne encephalitis

Although tick-borne encephalitis (TBE) has been recognized in Europe for more than 70 years and has been the topic of numerous reports, information on the involvement of facial nerves in the course of the disease is limited. Our study conducted at a single medical centre revealed that facial nerve involvement in the course of TBE in Central Europe is (i) infrequent—it was found in only 11 of 1218 (0.9%) consecutive adult patients diagnosed with TBE; (ii) manifests with unilateral or rarely bilateral peripheral facial palsy (PFP) (nine and two patients, respectively); (iii) appears late in the course of acute illness—in our patients 10-20 days after the onset of the meningoencephalitic phase of TBE, and often after defervescence (in 8/11 patients; 6-13 days after normalization of body temperature); (iv) develops more often in patients with more severe illness, i.e. more frequently in those with encephalitic than in those with meningitic clinical presentation, and more commonly in patients with monophasic than biphasic illness; and (v) has a favourable outcome—our patients had a clinically complete recovery from PFP within 7-90 (median 30) days after its onset. Moreover, the finding of Borrelia infection in 3/11 (27.3%) patients (diagnosis of confirmed Lyme neuroborreliosis was established in 1/11 patients and two patients fulfilled criteria for possible Lyme neuroborreliosis) suggests that in countries where TBE and Lyme borreliosis are endemic, concomitant infection with Borrelia burgdorferi sensu lato should be considered and searched for in patients who develop PFP in the course of TBE.

Tick-borne Meningoencephalitis in a 4.5-Month-Old Infant

The course of tick-borne encephalitis (TBE) in children is supposed to be mild though severe neurological sequelae have been reported. Only occasionally infants are affected. Case report, review of literature. We describe the first case of tick-borne encephalitis in a 4.5-month-old male infant in Germany. 11 days after a tick-bite he developed acute illness with fever, focal and generalized seizures. Meningoencephalitis caused by the TBE virus was diagnosed by cerebrospinal fluid (CSF) pleocytosis and detection of TBE-RNA in the CSF. Neurological follow-up showed no abnormalities. The acute meningoencephalitis in the present case and the neurological short and long term morbidity of 3 additional published cases of TBE suggest the considerable burden of this disease in infancy. As parents can transmit the tick to their infant informations about exposure-prophylactic measurements are recommended.

Tick-borne encephalitis in Slovenia from 2000 to 2004: Comparison of the course in adult and elderly patients

To present epidemiological data and clinical characteristics of tick-borne encephalitis (TBE) in adult patients, and to compare findings in the subgroup over the age of 60 years with those aged 60 or under. The information for this retrospective study was obtained by review of medical documentation. All patients over 15 years of age hospitalized at the Department of Infectious Diseases, University Medical Center Ljubljana, Slovenia, between 2000 and 2004 with pleocytosis (cerebrospinal fluid leukocyte count >5 x 10(6) cells/l) and the presence of serum IgM antibodies against TBE virus qualified for inclusion in this report. Patients were divided into two groups according to their age (patients over the age of 60 were classified as seniors and those aged 60 or under as adults); the findings in the two groups were compared. Of 448 patients with TBE, 318 were in the adult group and 130 in the senior group. Males predominated in both groups. A biphasic course of the illness was reported by 56% of patients. There were no significant differences in the majority of clinical parameters in the initial phase of TBE but several distinctions between adults and seniors were found in the second phase of the illness. Adults more often presented with fever, headache, stiff neck and photophobia, whereas seniors more frequently reported fatigue, altered consciousness and decreased muscle strength, these differences indicating a more classic course of TBE in the younger group and a somehow different and more severe acute disease in the older group. More severe acute disease and less favorable outcome in seniors was further corroborated by the occurrence of urine retention (18/318, 5.7% versus 27/130, 20.8%; P < 0.001), frequency of pareses (10/318, 3.1% versus 7/130, 5.4%; P = 0.002) and the need for antiedematous treatment (103/318, 32.4% versus 61/130, 46.9%; P = 0.005), as well as by the duration of treatment, duration of hospital stay and the death rate (0/318 versus 3/130, 2.3%; P = 0.024). Several distinctions were present also in laboratory findings, including higher cerebrospinal fluid leukocyte count in the adults than in the seniors (107 x 10(6) cells/l versus 47 x 10(6) cells/l; P < 0.001). Direct comparison of the course and outcome of TBE revealed several distinctions between patients over 60 years of age and those aged 60 or under and corroborates previous assumptions that TBE is a more serious illness in the elderly population.

Tickborne encephalitis in an area of high endemicity in lithuania: disease severity and long-term prognosis.

Of 250 consecutively admitted patients with central nervous system (CNS) infections who were treated during a 1-year period, all 133 patients with tickborne encephalitis (TBE) were included in a prospective follow-up study. TBE presented as mild (meningeal) in 43.6% of patients and as moderate or severe (encephalitic) in 43.6% and 12.8% of patients, respectively. Paralytic disease was observed in 3.8% of the subjects, and cranial nerve injury was observed in 5.3%. One patient died of TBE. Permanent CNS dysfunction after 1 year was found in 30.8% of patients; in 8.5% of all TBE cases, severe disabilities required adjustment of daily activities. Corticosteroid treatment did not seem to improve outcome. A progressive course of TBE was noted in 2 patients. The risk of incomplete recovery was significantly higher among patients with the encephalitic form of TBE (odds ratio, 4.066; 95% confidence interval, 1.848-8.947). In conclusion, TBE is an important pathogen in CNS infection in the Kaunas region of Lithuania, and it causes long-lasting morbidity in one-third of cases.

Laboratory findings in tick-borne encephalitis--correlation with clinical outcome.

Infection with the tick-borne encephalitis virus (TBEV) can result in various neurological complications. At present, there are little data available on laboratory findings that might help predict the clinical course and prognosis of tick-borne encephalitis (TBE). In the present study 100 patients with TBE were examined in respect to various laboratory parameters potentially characteristic for the disease and indicative for the prognosis in TBE. Pleocytosis, impairment of the blood-CSF barrier and intrathecal synthesis of immunoglobulins (IgM > IgG, IgA) were common findings in most patients. On admission to the hospital, 84% of the patients presented with an intrathecal synthesis of TBEV-specific IgM and/or IgG antibodies in the CSF. At follow-up, intrathecal synthesis of TBEV-specific antibodies was demonstrated in all patients studied within 15 days after the first examination, but changes of CSF parameters did not correlate with the clinical course of disease. In contrast to those with moderate course of disease, patients with severe courses of TBE displayed higher cell counts in the CSF and lower concentrations of neutralizing antibodies in serum, and more frequently revealed an intrathecal synthesis of total IgG. TBE-specific oligoclonal IgG antibodies in the CSF were demonstrated only in three patients with prior, incomplete, vaccination against TBE. The severe course of disease in individual patients with TBE may result from a slow or low production of neutralizing antibodies. In these patients, the more intense damage of the CNS tissue is reflected by higher cell counts in the CSF. At onset of disease the presence of a low concentration of neutralizing antibodies in serum and a high cell count in the CSF might indicate an unfavorable course of TBE.

Severe tick-borne encephalitis following passive immunization

We report on a 5-year-old girl with an unusually severe course of tick-borne encephalitis following passive immunization with specific hyperimmune globulin after a tick bite in an endemic area. Serial investigations of the CSF revealed intrathecal production of specific antibodies paralleled by increasing numbers of B-cells after initial T-cell pleocytosis. Focal central lesions were evident on MRI.ConclusionThe severity of the presented case questions the benefit of passive immunization and rather justifies consideration of vaccine recommendation to residents and travellers to areas endemic for tick-borne encephalitis virus.