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At least 55 records · Page 3Linked to original sources
PubMed1975

Isolates of California encephalitis (La Crosse) virus from field-collected eggs and larvae of Aedes triseriatus: identification of the overwintering site of California encephalitis.

California encephalitis is caused primarily by La Crosse virus, a mosquito-borne agent of which the vector is the mosquito Aedes triseriatus. Once La Crosse virus has been detected in a given geographical area, observations in the same area during subsequent seasons usually have revealed continuing presence of the virus. Field studies were conducted around the homes of children who had had California encephalitis in an effort to define the mechanism by which the virus survived the winter. Eggs and larvae of A. triseriatus collected from natural breeding sites during the springs and summers of 1972-1974 were processed for viral isolation. Collections made during 1972 and 1973 yielded no virus. Eggs, obtained on April 29, 1974 from a basal tree hole of an American elm located approximately 150 feet from the homes of two children who had had California encephalitis in 1970, contained virus, as did larvae aspirated on May 16, 1974, from the same tree hole. This study in Minnesota confirms previous data from Wisconsin and suggests that La Crosse virus may be passed transovarially in A. triseriatus and may overwinter in the diapause stage of eggs.

Aedes↗
PubMed1973

Possible evidence for interference with Venezuelan equine encephalitis virus vaccination of equines by pre-existing antibody to Eastern or Western Equine encephalitis virus, or both.

During 1971, an epizootic of Venezuelan equine encephalitis (VEE) reached the United States. Laboratory tests were performed on a large number of sick, healthy, unvaccinated, and vaccinated horses. Neutralization (N) tests in cell cultures revealed that 153 of 193 (79.3%) equines outside the state of Texas and 175 of 204 (85.8%) within Texas (82.6% overall) had detectable N antibody to VEE virus a week or more after vaccination. Twenty-six of 40 (65%) non-Texas equines and 18 of 29 (62%) Texas equines which had no detectable antibody against VEE virus a week or more after vaccination had N antibody against Eastern equine encephalitis (EEE) or Western equine encephalitis (WEE) virus or both, whereas only 50 of 153 (32.7%) non-Texas equines and 82 of 175 (46.9%) Texas equines with demonstrable N antibody against VEE also had N antibody against EEE and/or WEE virus. In vaccinated equines, significant negative correlations were found between the occurrence of antibody to VEE and antibody to EEE and/or WEE virus. These findings support the hypothesis that pre-existing antibody to EEE and/or WEE virus may modify or interfere with infection by VEE virus. The epizoologic significance of this possibility is discussed briefly.

Animals↗
PubMed2004

Japanese encephalitis virus (JEV) is an important cause of encephalitis among children in Cuddalore district, Tamil Nadu, India.

BACKGROUND: Japanese encephalitis (JE) is endemic in Cuddalore district, Tamil Nadu (TN), Southern India. The reports of JE cases from the local hospitals did not reflect the actual disease burden. It is likely that these cases were attending the nearby referral hospitals, for want of better treatment facilities. OBJECTIVES: Between July 2002 and February 2003, a pilot study was undertaken to examine whether JE was a component of paediatric acute encephalitis syndrome (AES) reported to two major referral hospitals adjacent to Cuddalore, and to map the distribution of the JE cases. STUDY DESIGN: A total of 58 hospitalized children [0-15 years] with AES were investigated. Other than the routine laboratory investigations, either CSF or sera or both [depending on the availability] collected from these children were analyzed at Center for Research in Medical Entomology, Madurai (TN) for JEV-antigen, antibody detection, virus isolation and virus genome detection by indirect immunofluorescence, MAC enzyme linked immunosorbent assay (ELISA), insect bioassay and by reverse transcriptase polymerase chain reaction (RT-PCR), respectively. RESULTS: JE was established in 17 (29%) of 58 AES cases; half of the AES cases [31/58, 53%] and 59% [10/17] of JE cases were confined to JE-endemic areas in Cuddalore district. The JE confirmation scored by different assays varied according to the clinical phase of the illness. The attack rate was high among the children aged 3-8 years. The monthly distribution of acute encephalitic syndrome cases followed the distribution of JE cases [coinciding with the rainy season in this region] suggesting encephalitis of JE origin. CONCLUSION: In JE-endemic areas, the actual JE burden can be estimated by the collection of JE case reports from the local hospitals and from the referral hospitals. Building of diagnostic facilities in hospitals for JE is necessary to achieve this goal.

Acute Disease↗
PubMed2005

Noncytopathic replication of Venezuelan equine encephalitis virus and eastern equine encephalitis virus replicons in Mammalian cells.

Venezuelan equine encephalitis (VEE) and eastern equine encephalitis (EEE) viruses are important, naturally emerging zoonotic viruses. They are significant human and equine pathogens which still pose a serious public health threat. Both VEE and EEE cause chronic infection in mosquitoes and persistent or chronic infection in mosquito-derived cell lines. In contrast, vertebrate hosts infected with either virus develop an acute infection with high-titer viremia and encephalitis, followed by host death or virus clearance by the immune system. Accordingly, EEE and VEE infection in vertebrate cell lines is highly cytopathic. To further understand the pathogenesis of alphaviruses on molecular and cellular levels, we designed EEE- and VEE-based replicons and investigated their replication and their ability to generate cytopathic effect (CPE) and to interfere with other viral infections. VEE and EEE replicons appeared to be less cytopathic than Sindbis virus-based constructs that we designed in our previous research and readily established persistent replication in BHK-21 cells. VEE replicons required additional mutations in the 5' untranslated region and nsP2 or nsP3 genes to further reduce cytopathicity and to become capable of persisting in cells with no defects in alpha/beta interferon production or signaling. The results indicated that alphaviruses strongly differ in virus-host cell interactions, and the ability to cause CPE in tissue culture does not necessarily correlate with pathogenesis and strongly depends on the sequence of viral nonstructural proteins.

Amino Acid Sequence↗
PubMed2004

Nonsuppurative encephalitis in piglets after experimental inoculation of Japanese encephalitis flavivirus isolated from pigs.

Nonsuppurative encephalitis was experimentally induced in 3-week-old piglets by a single intravenous inoculation of either of two strains (IB 2001 or AS-6) of Japanese encephalitis flavivirus (JEV) isolated from field pigs. The lesions, which consisted of neuronal necrosis, neuronophagia, glial nodules, and perivas-cular cuffing, were distributed in the cerebrum, midbrain, pons, medulla oblongata, and cerebellum, particularly in the gray matter of the frontal and temporal lobes and thalamus. The gray matter of the spinal cord of piglets that were given the AS-6 strain also was affected. JEV antigen was immunohistochemically detected in the cytoplasm of the nerve cells in the cortex of the frontal and temporal lobes and in the gray matter of the thalamus and midbrain. Two JEV strains isolated from field pigs exhibited neurovirulence, inducing nonsup-purative encephalitis in piglets.

Animals↗
PubMed2003

Sensitivity of the VecTest antigen assay for eastern equine encephalitis and western equine encephalitis viruses.

VecTest assays for detecting eastern equine encephalitis virus (EEE) and western equine encephalitis virus (WEE) antigen in mosquito pools were evaluated to determine their sensitivity and specificity by using a range of EEE, WEE, St. Louis encephalitis virus (SLE), and West Nile virus (WN) dilutions as well as individual and pooled mosquitoes containing EEE or WEE. The EEE test produced reliable positive results with samples containing > or = 5.3 log10 plaque-forming units (PFU) of EEE/ml, and the WEE test produced reliable positive results with samples containing > or = 4.7 log10 PFU WEE/ml. Both assays detected the respective viral antigens in single virus-positive mosquitoes and in pools containing a single positive mosquito and 49 negative specimens. The SLE and WN assays also contained on the dipsticks accurately detected their respective viruses. No evidence was found of cross reaction or false positives in any of the tests. The VecTest assays were less sensitive than the EEE- and WEE-specific TaqMan reverse transcriptase polymerase chain reaction and Vero cell plaque assay, but appear to be useful for detecting arboviruses in mosquito-based arbovirus surveillance programs.

Animals↗
PubMed2005

[An unusual cause of meningo-encephalitis: Japanese encephalitis].

Two women, 29 and 30 years of age, who had visited Indonesia and Thailand, respectively, during the summer, presented with diarrhoea, headache, fever and later neurological symptoms. The first patient had to be sedated because of restlessness and was admitted to the intensive-care unit for intravenous antimicrobial therapy; the second became comatose and received intravenous rehydration and antipyretics. No diagnosis was made during the acute phase ofthe illness, but later there was serological evidence of Japanese encephalitis. Both patients recovered, but memory and concentration difficulties persisted for a long time. Due to the increase in travelling, we see more and more cases of (rare) imported diseases. Japanese encephalitis is a viral infection that causes 50,000 cases each year in Asia with a mortality of 30%. The risk of transmission for tourists is very low. Most infections with Japanese encephalitis virus do not lead to symptomatic disease; only 0.1-5% of infections lead to clinical disease. The symptoms are initially non-specific, consisting of general discomfort and diarrhoea. After this, patients can develop headache, decreased consciousness and sometimes convulsions. Therapy consists of supportive care. For travellers at high risk of exposure, a formalin-inactivated vaccine is available. For the proper diagnosis of rare imported diseases, it is advisable to consult an infectious-disease specialist or microbiologist at an early stage when evaluating a patient who has recently returned from the tropics.

Adult↗
PubMed1976

Experimental infection of monkeys with viruses of the tick-borne encephalitis complex: degenerative cerebellar lesions following inapparent forms of the disease or recovery from clinical encephalitis.

Rhesus, patas and vervet monkeys were infected i.c. or i.n. with three viruses of the tick-borne encephalitis complex (TBE) as follows: Turkish tick-borne encephalitis virus (TTE), Louping-ill virus and Central European tick-borne encephalitis virus (CETE). The incidence of overt clinical signs of disease varied according to the virus that was used for the inoculations. TTE proved to be more pathogenic for monkeys than the other two members of the complex, whilst CETE was the least pathogenic. Injections of specific antiserum soon after infection tended to increase both the incidence of clinical signs and the moratlity. A proportion of animals with inapparent infections and a number of monkeys that recovered from the acute phase of the disease developed degenerative lesions in the cerebellum, often superimposed on the involuting inflammatory changes. The changes affected either a few only or many folia of the cerebellum and consisted of neuronal and spongy degeneration of the Purkinje and granular layers, usually accompanied by marked astrocytic proliferation and hypertrophy in the granular and molecular layers.

Animals↗
PubMed1980

Western equine encephalitis mimicking herpes simplex encephalitis.

A patient with severe encephalitis had focal findings suggesting herpes simplex encephalitis. After brain biopsy and administration of vidarabine, the patient's condition improved but was ultimately diagnosed as a case of western equine encephalitis. Further complicating laboratory diagnosis, an endogenous murine coronavirus was isolated from newborn mice inoculated with the patient's brain biopsy tissue. This case illustrates the need for caution in attributing therapeutic responses to antiviral agents or in attributing human illness to viruses that are actually endogenous to animals and tissue culture used in diagnostic virology.

Adolescent↗
PubMedDate not supplied

Rasmussen encephalitis: epilepsia partialis continua secondary to chronic encephalitis.

Rasmussen encephalitis is a disease consisting of chronic encephalitis with progressive neurologic deficits and focal intractable seizure activity. The etiology is unknown, but pathologic specimens revealed changes consistent with viral encephalitis. Even though neuro-imaging techniques, such as positron emission tomography and magnetic resonance imaging, offer the prospect of specific, presurgical diagnostic criteria, the initial diagnosis usually is made on a clinical basis. Treatment modalities, including a wide variety of antiepileptic drug therapies and surgical interventions, may result in significant physical and mental impairments. We summarize the clinical presentation, diagnostic considerations, and different treatment protocols in a patient with this rare and debilitating disorder.

Cerebral Cortex↗
PubMed1986

Herpes simplex type II encephalitis in infancy presenting with focal encephalitis.

Herpes virus was recovered from a throat swab, nasopharyngeal washings as well as from brain tissue from a six-month-old infant, who presented with fever, left focal seizures and an enhancing right frontal CT-scan lesion. Cytopathic effect (CPE) as seen with genital herpetic infection was seen, suggesting HSV-2. Immunofluorescent typing of the virus isolate confirmed HSV-2. Early IgM positivity preceding a CF and SN titer rise was observed. The patient received a course of ARA-A and recovered with a left sided hemiparesis. HSV-2 encephalitis occurs beyond the newborn period as a primary infection. In adults however HSV-2 encephalitis occurs predominantly in the immunocompromised host. HSV-1 encephalitis probably is due to reactivation of a latent herpetic infection in previous virus exposed juvenile or adult immunocompetent hosts.

Antibodies, Viral↗
PubMed1980

[Severe and prognostically unfavourable forms of tick-borne encephalitis (early-summer meningo-encephalitis) in Freiburg (author's transl)].

Eight patients with proven tick-borne encephalitis (early-summer meningo-encephalitis; central European encephalitis) were treated in 1979. The disease ran a severe course in four: one died after six weeks of coma and pneumonia with right-heart failure. Another patient is in coma for more than 40 weeks. A third patient had severe flaccid tetraplegia more than 10 weeks after initial coma. The fourth patient still had leg paresis after nine weeks, her left arm also being largely paralysed. This high incidence of severe forms of the disease differs from other published reports.

Adult↗
PubMed2006

Tunicamycin enhances neuroinvasion and encephalitis in mice infected with Venezuelan equine encephalitis virus.

Venezuelan equine encephalitis (VEE) viruses cause natural outbreaks in humans and horses and represent a significant biothreat agent. The effect of tunicamycin on the course of the disease in mice with VEE was investigated, and the combined effects of these agents was characterized. CD-1 mice given 2.5 microg of tunicamycin had >1,000-fold more virus in the brain 48 hours after infection with the virulent VEE strain V3000 and > or =100-fold of the attenuated strain V3034 at all tested times than did untreated mice, indicating enhanced neuroinvasion. Tunicamycin did not alter the viremia profiles of these viruses nor the replication of V3000 in the brain itself. Tunicamycin alone caused ultrastructural blood-brain barrier damage, yet neuroinvasion by V3000 in treated mice appeared to occur via the olfactory system rather than the blood-brain barrier. Tunicamycin-treated, V3000-infected mice also exhibited earlier and more severe weight loss, neurological signs, neuronal infection, neuronal necrosis and apoptosis, and inflammation than untreated, V3000-infected mice. The mean survival time of tunicamycin-treated, V3000-infected mice was 7.3 days versus 9.9 days for untreated, V3000-infected mice. These studies imply that animals that ingest toxins similar to tunicamycin, including the agent of annual ryegrass toxicity in livestock, are conceivably at greater risk from infections by encephalitis viruses and that humans and horses exposed to agents acting similar to tunicamycin may be more susceptible to encephalitis caused by VEE viruses. The exact mechanism of tunicamycin-enhanced neuroinvasion by VEE viruses requires further study.

Animals↗
PubMed2000

Association of herpes simplex virus encephalitis and paraneoplastic encephalitis - a clinico-pathological study.

A 57 year-old woman developed acute limbic encephalitis and brainstem dysfunction. Anti-HU antibodies were repeatedly detected in serum and CSF. Postmortem examination showed necrotic and hemorrhagic lesions in the temporal lobes characteristic of herpes simplex virus encephalitis, which was confirmed by immunocytochemistry, and Purkinje cell loss with proliferation of Bergman glia and myelin loss in the external aspect of the dentate nuclei characteristic of paraneoplastic encephalitis. PCR-assay performed on temporal tissue extracts was positive for HSV-1. There was no identifiable neoplasm. This unusual association raises the possibility of a link between the two diseases.

Antibodies↗
PubMed2001

[A case of brainstem encephalitis associated with Epstein-Barr virus infection: differentiation of acute disseminated encephalomyelitis and Bickerstaff's brainstem encephalitis].

A 28-year-old woman initially suffered high fever and headache (day 1). Aseptic meningitis was diagnosed on day 3. Limb ataxia, however, appeared on day 7, and external ophthalmoplegia and drowsiness were recognized on day 8. Urinary disturbance and orthostatic hypotension appeared on day 13. Cerebrospinal fluid showed moderately high cell counts(mononuclear cells, 51/microliter; polynuclear cells, 9/microliter). MRI T2-weighted images showed high intensity lesions in the pons and mesencephalon. No serum anti-GQ1b IgG antibody was detected on day 4. Epstein-Barr virus (EBV) viral capsid antigen-IgG antibody was positive, and EBV determined nuclear antigen antibody was seroconverted. EBV-DNA was detected in the CSF by PCR. These findings indicate prior infection by EBV. After intravenous dexamethasone therapy, these symptoms rapidly disappeared. Our patient showed external ophthalmoplegia, ataxia, and disturbance of consciousness, which are the cardinal signs in Bickerstaff's brainstem encephalitis. The time course of her neurological symptoms, the presence of meningitis, and the MRI findings, however, indicated the pathogenesis of acute disseminated encephalomyelitis rather than Bickerstaff's brainstem encephalitis. We diagnosed this patient as a brainstem encephalitis associated with EBV infection.

Adult↗
PubMed1990

[Comparative clinical study of herpes simplex encephalitis (HSE) and non-herpes simplex sporadic encephalitis (NHSSE)].

HSV specific antibody IgG was detected in the sera and CSF of 43 patients with sporadic encephalitis by the initial and follow-up tests with ELISA. Twelve cases of HSE were diagnosed, accounting for 27.8% of the cases of sporadic encephalitis, the clinical manifestations of HSE and NHSSE were compared. Differences were observed with regard to the age, general states, mental symptoms, disturbance of consciousness, and fatality rate. The abnormalities in EEG, CSF examination and CT scanning were found to be more severe in the HSE cases. It was concluded that these differences would be of use only as a diagnostic aid where as additional specific tests would be necessary for an accurate diagnosis of herpes simplex encephalitis.

Adolescent↗
PubMed2005

The Golden Agers and Tick-borne encephalitis. Conference report and position paper of the International Scientific Working Group on Tick-borne encephalitis.

The 7th meeting of the ISW TBE had the main topic "Tick-borne encephalitis in the Golden Agers". Data from 14 European countries were presented about incidence and clinical course of Tick borne encephalitis (TBE) in general and especially in the population over 50 years of age. With age immunity is impaired quantitatively and qualitatively, the reactions to vaccinations are generally slower, antibody titres reach lower values and decrease earlier. The incidence of the disease is increasing with age, also the clinical course is more severe, they suffer significantly more sequelae, need a longer rehabilitation and have a higher case fatality. Vaccination as the only efficient protection is needed in endemic areas, considering that mobility has increased very much. For the age group over 50 years regular booster vaccinations according to the recommended vaccination intervals or even shorter intervals are most important.

Age Factors↗
PubMed1995

Nonvascular delivery of St. Louis encephalitis and Venezuelan equine encephalitis viruses by infected mosquitoes (Diptera: Culicidae) feeding on a vertebrate host.

We determined whether mosquitoes infected with the viruses St. Louis encephalitis (SLE) or Venezuelan equine encephalitis inoculate virus extravascularly or directly into the vascular system. Infected mosquitoes fed on the distal 3rd of the tails of suckling mice. Significantly more mice whose tails were amputated at the midpoint within 10 min of mosquito feeding survived than did siblings whose tails remained intact. Even when tails were amputated 1-6 h after SLE virus-infected mosquitoes fed, the median time to death was significantly longer in mice with amputated tails (7.1 d) than in mice with intact tails (5.8 d). We concluded that mosquitoes inoculated virus primarily extravascularly, rather than directly into the vascular system, while feeding on a vertebrate host. Extravascular, rather than intravascular, delivery of pathogens by mosquitoes may affect disease pathogenesis and vaccine efficacy.

Aedes↗