Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Encephalitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

[Successfully treated case with microscopic polyangiitis complicated severe varicella zoster virus infection including encephalitis and disseminated varicella zoster].

We report a case with microscopic polyangiitis (MPA) complicated by varicella zoster encephalitis. A 60-year-old woman caught a common cold and had acute otitis media in April 1998. Proteinuria and hematuria with hyaline cast were noted at the routine medical check in May, and she was referred to our hospital because of high fever and chest pain. MPA was diagnosed with acute progressive renal failure, pleuritis and elevated anti-neutrophil cytoplasmic myeloperoxidase antibody (MPO-ANCA). Corticosteroid therapy was administered under hemodialysis but MPA was flared several times with various symptoms including interstitial pneumonitis, alveolar hemorrhage and erythema multiforme exudativum. During the course of the disease she developed disseminated varicella zoster and encephalitis. Positive polymerase chain reaction to varicella zoster in cerebrospinal fluid helped to differentiate her encephalitis from central nervous system symptoms due to microscopic angiitis and herpes simplex encephalitis. Combination of corticosteroid and acyclovir therapies for MPA and varicella zoster encephalitis under hemodialysis were successful. The diagnostic process and therapies to these complicated contexts were thought to be very important.

Acute Kidney Injury↗

[A case of non-herpetic acute encephalitis with autoantibodies for ionotropic glutamate receptor delta2 and epsilon2].

We report a 45-year-old woman admitted to our hospital due to fever, consciousness disturbance, and severe seizures. Based on her signs and symptoms and clinical course, a diagnosis of non-herpetic acute encephalitis was made. She received antibiotic drugs, acyclovir, gamma-globulin, and steroid pulse therapy (methylprednisolone 1 g/day, 3 days). The patient's signs, symptoms and severe seizure showed marked improvement, but she still showed monthly seizure attacks and both anterograde and retrograde amnesia Viral infection and autoimmune response after viral infection may have been involved in non-herpetic acute encephalitis in our patient. Recently, autoantibodies to GluRepsilon2 and VGKC were reported in cases of non-herpetic acute limbic encephalitis (NHALE). In our patient, we detected IgM type autoantibody to GluRdelta2 and epsilon2 in both the CSF and serum, and these antibodies normalized in the CSF with the clinical course. Autoantibodies to GluRdelta2 and epsilon2 may be involved in the clinical symptoms and pathogenesis of non herpetic acute limbic encephalitis. This is the first report of MRI-positive non-herpetic acute encephalitis with autoantibodies to GluRdelta2 and epsilon2.

Acute Disease↗

Update on herpes simplex encephalitis.

Herpes simplex encephalitis is the most common identified cause of sporadic viral encephalitis in the United States. Early diagnosis is critical because treatment with the antiviral drug acyclovir dramatically decreases morbidity and mortality. The use of polymerase chain reaction (PCR) techniques to amplify the genome of herpes simplex virus (HSV) from cerebrospinal fluid (CSF) has become the diagnostic procedure of choice. False-positive CSF HSV PCR results are rare when testing is performed in experienced laboratories. Negative CSF HSV PCR results should always be interpreted in the context of the timing of specimen collection and the likelihood of disease. Negative CSF HSV PCR tests can occur within the first 72 hours of illness, with subsequent tests becoming positive. Patients with HSV encephalitis will typically have a negative CSF HSV PCR after 14 days of acyclovir treatment, and a persisting positive PCR should prompt consideration of additional or revised antiviral therapy. Quantitative PCR testing provides information about HSV viral load in CSF, but the potential correlation of viral load with prognosis or other clinical features of disease remains uncertain. Although the neuroimaging abnormalities seen in HSV encephalitis are not unique, more than 90% of patients with proven HSV encephalitis will have magnetic resonance imaging (MRI) abnormalities involving the temporal lobes. Special MRI techniques, including fluid-attenuated inversion recovery and diffusion-weighted imaging, might reveal abnormalities not seen with conventional imaging sequences. Neuroimaging patterns in infants and children differ significantly from those seen in adults and include a higher frequency of extratemporal lesions.

Acyclovir↗

[Characteristics of the response of mice with temporary immunodepression to the administration of live or inactivated vaccine against tick-borne encephalitis].

Mice with immunity defects caused by administration of cyclophosphane were inoculated with an inactivated vaccine or Langat virus (TP-21 strain) considered to be an approximate model of the vaccine against tick-borne encephalitis. In mice with depressed immune response, the asymptomatic infection caused by Langat virus turns into acute form and encephalitis with a fatal outcome develops in 86--100%. Pre-treatment with inactivated tick-borne encephalitis vaccine did not protect the animals with the immunity defect against neuroinfection induced by subsequent inoculation with Langat or tick-borne encephalitis virus. The experimental results suggest that the use of a live vaccine against tick-borne encephalitis in specimens with immunity defects is very dangerous because of the possibility of affection of the central nervous system.

Animals↗

[Immune response and reactions to simultaneous administration of hepatitis B vaccine with routine vaccine in children. II. Immune response and reactions to simultaneous administration of hepatitis B vaccine with Japanese B encephalitis vaccine and measles vaccine].

This paper reports the result of the immune response and reactions to simultaneous administration of Japanese B encephalitis vaccine, measles and hepatitis B vaccine. 215 children (0-9 months of age) were divided into three groups. Group one was vaccinated with hepatitis B vaccine alone, group two was vaccinated with Japanese B encephalitis vaccine, measles vaccine, and group three was Vaccinated with hepatitis B vaccine, Japanese B encephalitis vaccine and measles vaccine simultaneously. The result of the immune response to the combination of hepatitis B vaccine with Japanese B encephalitis vaccine were similar to that observed after immunization with each vaccine alone. But the result of the immune response to the combination of hepatitis B vaccine with measles vaccine were lower than to that observed after immunization with measles vaccine alone. The general reaction of all vaccine were mild, no significant difference between each group was noted. The study demonstrated that children can not be immunized with hepatitis B vaccine and measles vaccine simultaneously but can be immunized with hepatitis B Vaccine and Japanese B encephalitis vaccine.

Encephalitis Virus, Japanese↗

Toxoplasmic encephalitis in patients with AIDS.

Toxoplasmic encephalitis has been recognized as a major CNS complication in patients with AIDS and is the most frequent cause of focal intracerebral lesions in these patients. This complication of AIDS is almost always observed in patients who have a chronic (latent) infection with Toxoplasma gondii. Therefore, patients who from the outset of their HIV infection or AIDS are known to have antibodies to T. gondii should be considered at risk for development of toxoplasmic encephalitis. Although serologic tests cannot distinguish active from latent infection, a patient who is seronegative for Toxoplasma antibodies is unlikely to have toxoplasmic encephalitis. Neuroradiologic studies may be highly suggestive of toxoplasmic encephalitis, but, at present, the definitive diagnosis can be made only by demonstration of Toxoplasma in brain tissue. The unique pathogenesis of toxoplasmic encephalitis in patients with AIDS makes intensive primary therapy followed by a lifelong suppressive regimen necessary. We recommend 6 weeks of high doses of pyrimethamine and sulfadiazine (or trisulfapyrimidines) as primary therapy for the acute disease followed by daily administration of reduced doses of these drugs. The use of clindamycin as an alternative drug for primary therapy, at least at present, must be regarded as investigational and should be reserved for patients who suffer severe reactions to the sulfonamides. As most patients will respond to their primary therapy, those who fail to improve clinically and radiologically to therapy within 10 days should be evaluated for additional or alternative causes of their intracerebral pathology. This will often necessitate brain biopsy.

Acquired Immunodeficiency Syndrome↗

Viral encephalitis in children: detection with technetium-99m HMPAO brain single-photon emission CT and its value in prediction of outcome.

PURPOSE: To assess the role of regional cerebral blood flow measured by technetium-99m hexamethyl propyleneamine oxime (HMPAO) brain single-photon emission CT (SPECT) in viral encephalitis of children. METHODS: Eighteen children diagnosed as having viral encephalitis (12 Epstein-Barr virus, 4 herpes simplex virus, and 2 Japanese B virus) underwent Tc-99m HMPAO brain SPECT and brain MR and/or CT. RESULTS: During the acute episode, 4 (22%) of the 18 patients had localized abnormality on brain MR and/or CT. Tc-99m HMPAO brain SPECT in the acute phase showed that 17 (94%) of the 18 patients had increased regional cerebral blood flow and 1 (6%) of the 18 children had a normal brain SPECT. Follow-up brain SPECT was performed at least 15 days after the acute episode. In 17 patients with abnormal first brain SPECT, 12 (71%) had normal second brain SPECT and 5 (29%) had decreased regional cerebral blood flow. The group of patients with normal regional cerebral blood flow on the follow-up brain SPECT had a better outcome than the group of patients with decreased regional cerebral blood flow. CONCLUSIONS: (a) The Tc-99m HMPAO brain SPECT was abnormal more often than CT or MR in children with acute viral encephalitis and provided better location. (b) In acute episodes of encephalitis, most patients showed locally increased regional cerebral blood flow. (c) After acute episodes, the regional cerebral blood flow returned to normal in most cases. (d) A normal Tc-99m HMPAO brain SPECT in the subacute phase usually indicates a good clinical outcome (no neurologic defect) 1 year after the acute illness in children with viral encephalitis.

Adolescent↗

[Complicated febrile convulsion vs herpes-encephalitis].

Since Acyclovir is available a sufficient treatment of herpes simplex virus (HSV) encephalitis exists. Febrile convulsions may occur as the initial manifestation of an encephalitis, particularly of an HSV encephalitis. Within 25 months out of 151 children with febrile convulsions five children with complicated febrile convulsions were admitted at the pediatric department of Graz. In all children HSV antibodies in serum and cerebrospinal fluid (CSF) were negative and the diagnosis of an HSV encephalitis was made by positive CSF HSV polymerase chain reaction (PCR). Therefore, in any suspected case, i.e. in any case of a complicated febrile convulsion, CSF should be investigated including a HSV PCR to rapidly confirm or exclude HSV encephalitis.

Acyclovir↗

Expression of pro- and anti-apoptosis gene products in brains from paediatric patients with HIV-1 encephalitis.

We have previously demonstrated the presence of DNA fragmentation in neurons, macrophages and microglia consistent with apoptosis, but not in reactive astrocytes in brain tissue from paediatric patients with HIV-1 encephalitis (HIVE). To further understand the underlying mechanism(s) for these findings as they relate to gene-directed neural cell death, we studied the in-situ expression of the Bcl-2 family of proteins, including the pro-apoptosis gene product Bax, the anti-apoptosis gene product Bcl-2, and Bcl-x. We demonstrate significantly elevated numbers of Bax-positive microglia and macrophages immunoreactive in basal ganglia and cerebral cortex of children who had HIVE, in comparison to HIV-1 infected children without encephalitis or children who were seronegative for HIV-1. In contrast, patients with HIVE, but not HIV-1 without encephalitis, or seronegative controls, had increased expression of Bcl-2 and Bcl-x in reactive astrocytes in cortex and basal ganglia. In vitro studies using Western blot analysis demonstrated an up-regulation in the levels of Bax, and phosphorylated (i.e. inactive) Bcl-2 in HIV-1 infected macrophages, and in LPS-activated macrophages, relative to levels in virus-negative unstimulated macrophages. These results suggest that productive HIV-1 infection, or cellular activation, renders macrophages more vulnerable to apoptosis. Taken together, these findings suggest that brain-resident macrophages and microglia in patients with HIV-1 encephalitis are more prone to undergo apoptosis and that astrocytes in contrast may be resistant to apoptosis. This may represent a mechanism to limit microglial activation and the spread of productive HIV-1 infection in the CNS of children with HIV-1 encephalitis.

Adolescent↗

Early intrathecal synthesis of interferon in herpes encephalitis.

Large quantities of type I interferon were detected in the cerebrospinal fluid (CSF) collected at the onset of herpes encephalitis. This interferon was synthesized intrathecally and disappeared about 10 days after the beginning of neurological signs. In 12 cases of post-eruptive measles encephalitis and in four post-rubella encephalitis, type I interferon was present only in low amounts, or not found at all, even in the CSF collected early. The existence of an intrathecal synthesis of interferon during encephalitis provides a valuable contribution to both the early diagnosis of herpes encephalitis and the study of the pathogenesis of virus infection of the central nervous system (CNS).

Adolescent↗

Enzyme-linked immunosorbent assay using recombinant antigens expressed in mammalian cells for serodiagnosis of tick-borne encephalitis.

A recombinant plasmid that expresses the tick-borne encephalitis (TBE) virus premembrane (prM) and envelope (E) proteins in mammalian cells was constructed. Recombinant proteins retained antigenic and conformational structures similar to those of native virus proteins, and transfected cells released virus-like particles (VLPs), which were 1.13-1.14 g/ml in density and 20-30 nm in diameter, into the culture medium. Recombinant E proteins were used for the development of an enzyme-linked immunosorbent assay (ELISA) to detect TBE virus-specific IgM and IgG antibodies in serum. The results of this ELISA correlated well with the results of commercial ELISA, when tested with 95 serum samples from clinically TBE-suspected patients. In addition, ELISA using recombinant antigens showed no cross-reactivity against serum from Japanese encephalitis (JE) patients, despite the cross-reactivity shown by commercial ELISA systems. These observations indicated that this newly developed ELISA system could distinguish tick-borne encephalitis from Japanese encephalitis infection, and that it constitutes a useful and safe alternative to conventional ELISA systems.

Animals↗

The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis.

Japanese encephalitis and postmeasles encephalomyelitis represent two important forms of acute encephalitis in the developing world. Japanese encephalitis accounts for 20,000 acute illnesses per year, and measles encephalomyelitis accounts for as many as 100,000. Both are accompanied by mortalities of 20%-30%, and in both forms, approximately one-half of the survivors have neurological sequelae. Therefore, these two diseases are responsible for a considerable proportion of worldwide mental and motor disabilities. Furthermore, both diseases are preventable with use of safe vaccines. Despite these similarities, their very different pathologies appear to be based on different mechanisms of pathogenesis (table 2). In Japanese encephalitis there is direct invasion of the virus into the nervous system, selective infection and destruction of neurons, and evidence that both humoral and cellular immune responses attenuate the infection. In measles encephalomyelitis there is little evidence that the virus invades the nervous system. Rather, measles virus infects lymphoid cells and causes abnormalities in immune regulation. Humoral immune responses are not found within the nervous system, and the cellular immune response may be inappropriately directed against host antigens. In measles encephalomyelitis, the inflammatory cells entering the nervous system may be the effector cells of autoimmune disease.

Animals↗

Antibodies to arthropod-borne encephalitis viruses in small mammals from southern Florida.

From 1987 through 1991, blood samples were collected from 10 species of small mammals in Indian River Country, Florida (USA). Sera from 1,347 animals were analyzed for hemagglutination-inhibition (HI) antibody to St. Louis encephalitis (SLE) and eastern equine encephalitis (EEE) viruses. Of these, 75 (5.6%) were positive for HI antibody to SLE virus and 121 (9.0%) were positive for EEE antibody. Sera from five mammalian species were tested for neutralizing (NT) antibody to SLE, EEE, Highlands J (HJ a member of the western equine encephalitis virus complex), or Everglades (EVE, a member of the Venezuelan equine encephalitis complex) viruses. By serum neutralization tests, 26 (46%) of 57 had SLE antibodies, 14 (24%) of 58 had EEE antibodies, two (3.2%) of 63 had HJ antibodies, and 9 (14%) of 63 had EVE antibodies. One Sigmodon hispidus and one Peromyscus gossypinus had NT antibodies both to EEE and HJ viruses. Blood samples from 512 mammals were tested for virus. Isolations of one EVE virus and two unidentified arenaviruses were made from P. gossypinus and one EVE virus isolate was made from a S. hispidus.

Animals↗

Encephalitis in Kern County. California, 1941-1950.

Encephalitis is a challenging public health problem in Kern County and in the San Joaquin Valley area. During the last ten years the authors have studied the epidemiology of encephalitides due to arthropod-borne viruses and the methods used in the differential dignosis of these conditions. To incriminate a virus it is necessary to demonstrate a rise in antibody titer in the blood over a period of seven to fourteen days, the first specimen to be taken as soon as possible after onset of symptoms. A variety of tests may be necessary in some cases. Among the patients included in this presentation the greater number of those with encephalitis and also of those with poliomyelitis were under 30 years of age. The age range was five weeks to 49 years. The median annual mortality rate was 4.3 deaths per 100 cases for poliomyelitis and 3.9 for encephalitis. The greatest incidence occurred during the summer months.The clinical manifestations usually observed in encephalitis are described, but it is emphasized that wide variations and even completely atypical clinical phenomena are encountered. Four representative cases are reported and treatment is discussed. Vaccination and vector control are considered as the most promising means of combating the disease.

Biometry↗

The effect of vaccination with a live attenuated strain of Japanese encephalitis virus on stillbirths in swine in Taiwan.

Since an excellent candidate strain (M) for live virus vaccination of swine against Japanese encephalitis was developed, a number of large vaccination programmes have been implemented in Japan with the aim of controlling Japanese encephalitis epidemics in man by reducing the population size of nonimmune swine. Encouraging results have been obtained but no studies have been made on the benefits of live-virus vaccination to the industry. In order to determine the effect of vaccination upon the number of stillbirths occurring in the Japanese encephalitis post-emergence season, a total of 74 vaccinated, and subsequently mated, gilts at a large breeding farm in subtropical Taiwan were subjected to follow-up observations in comparison with a control group. The total incidence of litter stillbirths in the vaccinated group (1/74) was significantly lower than that in the control group (21/68). Over 92% of the newborn piglets from the vaccinated gilts were healthy, while 31.6-54.1% of the newborn piglets in the control groups were stillborn. The litter size of vaccinated gilts was larger than that of the control gilts. The vaccine was shown by tests in 22 swine to have an adequate degree of safety. Four weeks after vaccination with either 10(5.6) or 10(8.0) smicLD(50) of virus, all the swine developed an adequate level of antibody. The results indicate that live virus vaccination could benefit the industry in addition to achieving the main aim of controlling Japanese encephalitis viraemia in swine.

Animals↗

Human infection with tick-borne encephalitis virus in the Tribec region.

The isolation of tick-borne encephalitis (TBE) virus from the spinal fluid of a patient with a clinical diagnosis of meningo-encephalitis and the demonstration of virus-neutralizing antibodies in sera from inhabitants of the Tribec region have shown this area to be an active natural focus of tick-borne encephalitis. Of healthy people from the villages of Jarok and Kostolany, 26% had antibodies to TBE virus. Children from Kostolany had no such antibodies, whereas in Jarok 7% of children less than 15 years old were serologically positive. This finding, together with the generally higher antibody titres of sera from inhabitants of Jarok, suggests that this elementary focus of tick-borne encephalitis has been active more recently than that in Kostolany. In both villages the frequency of antibodies was high in persons over 55 years old (50% in Jarok and 63% in Kostolany); the highest frequency was found in those working regularly within the natural focus, i.e., forest workers and housewives.

Adolescent↗

La Crosse encephalitis: occurrence of disease and control in a suburban area.

Fifteen (6.4%) of 233 residents sampled in State Road Coulee (SRC) during 1972-73 had antibodies neutralizing La Crosse (LAC) virus, 9 (3.9%) trivittatus (TVT), 12 (5.2%) Jamestown Canyon (JC) and 2 (0.9%) Bunyamwera serogroup virus. Six of seven youths who had antibodies to LAC virus had been ill: three were serologically confirmed as cases of LAC encephalitis and three had possibly related illnesses. The other reported no illness. Possibly related illnesses were reported by 1 of 10 adults with antibody to LAC; also by 3 of 6 youths who had antibodies to TVT or JC viruses, and by 4 of 39 youths who did not have these antibodies. In prospective studies, 4 of 132 sampled again during 1977 had acquired antibodies, including 2 to LAC and 2 to JC virus. The LAC disease-infection rate was 50%. One of those with antibody to LAC virus was a girl with encephalitis who had a serologically confirmed infection a year after she had moved away from SRC. Her exposure to mosquitoes was not in SRC. The other was a boy who remained a resident but did not have encephalitis or other severe illness. The two who had acquired antibody to JC virus were boys who reported histories of undiagnosed febrile illnesses while attending summer camps in central Wisconsin. Control measures, including closure of treeholes, removing old tires and education, were applied. LAC infections in SRC were reduced from six during 1965 thru 1972, to only one during 1973 thru 1977. No cases have been found in SRC since 1977. Following expansion to a county-wide control program, LAC encephalitis in La Crosse County has been reduced from seven and eight cases during 1978 and 1979 to only one and two during 1980 and 1981. No cases have been found in La Crosse County so far during 1982.

Adolescent↗

New Thoughts on Pathogenesis and Diagnosis of Encephalitis.

Knowledge regarding the pathogenesis of viral encephalitis, defined as inflammation and destruction of the central nervous system (CNS) from viral infection and the resulting immune response, has improved with advances in molecular biology techniques and recent advances in immunology and neuroscience research. An increasingly complex understanding has developed with regard to viral CNS infection. In addition to advances in viral genetics exploring increased viral spread and neurovirulence, improved understanding from research on neurochemistry, neurodevelopment, and cytokine expression in the CNS has led to new hypotheses regarding the mechanism of CNS damage during viral CNS infection. This review explores three advances in the understanding of viral encephalitis in the past few years: 1) the relationship between viral load and extent of viral CNS disease, 2) chemokines and their role in the CNS inflammatory response as well as in the pathogenesis of encephalitis, and 3) secondary damage from the release of neurotoxins during encephalitis. By examining this research, the reviewers intend to introduce novel therapeutic modalities that are developing for the management of patients with viral encephalitis beyond the timely use of antiviral therapy.

Journal Article↗