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PubMed1990

Japanese encephalitis and the traveller.

Japanese encephalitis is a mosquito borne arbovirus disease that is endemic over a wide area of Asia, India, and the south eastern USSR. The disease is associated with a severe encephalitis, a high death rate and a high incidence of neurological sequelae in survivors. While natives of endemic areas may develop immunity, Western travellers are at risk. To date there have been two reported cases of Japanese encephalitis in people returning to Australia from overseas. A vaccine against Japanese encephalitis is available.

Encephalitis, Japanese↗

PubMed1990

[Recurrent herpetic encephalitis].

A 64 year-old woman experienced, at 6 weeks' interval, two episodes of encephalitis with left hemiparesis, coma and signs of meningitis. Paraclinical examinations showed lymphocytic meningitis, right temporal hypodensity at CT and high titers for herpes simplex at blood serology. The spontaneous course was favourable with almost complete recovery. A third recurrence took place 2 months later with left hemiplegia, confusion and meningism. A tentative diagnosis of herpes simplex encephalitis was confirmed by major intrathecal synthesis of herpes virus specific antibodies and by highly suggestive MRI images. Treatment with acyclovir resulted in rapid regression of motor deficit and meningism, but neuropsychological disorders regressed more slowly with persistent visuo-constructive and memory disorders. During a fourth and milder recurrence, a stereotactic temporal brain biopsy was performed, which showed lesions of encephalitis and elevated titers for HSV1 in the temporal fluid. Another course of acyclovir followed by vidarabine produced complete remission. The possibility of recurrent types of herpes simplex encephalitis is discussed.

Acyclovir↗

PubMed1990

[A case of neonatal herpes simplex virus encephalitis with calcifications of thalamus and basal ganglia].

A male infant developed left-sided myoclonus associated with low grade fever at 21 days of age. The course of pregnancy and delivery had been uneventful. Birth weight was 2,240g at 38 weeks of gestation. Physical examination at 26 days of age revealed hyperirritability and incomplete Moro reflex. EEG showed periodic discharges originating in the right central region. Initial brain CT at 26 days of age showed no apparent abnormality. In lumbar CSF protein was 173 mg/dl, and nucleated cells 328/mm3 (polynuclear cells 6 and mononuclear cells 322). Cultures of CSF for bacteria and viruses were negative. Although, the serum titers of CF antibody to herpes simplex virus (HSV) were 1:4 to 1:8 during hospitalization and those in CSF were not increased significantly, ELISA titers for IgG and IgM in serum and CSF rose significantly. The diagnosis of HSV encephalitis was made at 41 days of age. His myoclonus was well controlled with phenobarbital and clonazepam. He was treated with acyclovir and CSF findings returned to normal. On 2nd brain CT (39 days of age), calcification at thalamus, basal ganglia and right frontal lobe, which is extremely rare CT findings for HSV encephalitis, was noticed. His DQ at discharge was about 90. It is emphasized that the early diagnosis of HSV encephalitis can be made by ELISA and serial brain CT examinations, and that HSV encephalitis should be considered when calcification of thalamus and basal ganglia are detected on brain CT.

Basal Ganglia Diseases↗

PubMed1989

Importance of endogenous IFN-gamma for prevention of toxoplasmic encephalitis in mice.

The importance of endogenous IFN-gamma for prevention of toxoplasmic encephalitis was studied in mice chronically infected with Toxoplasma gondii by using a mAb to this lymphokine. Control mice chronically infected with the ME49 strain that received saline or normal IgG had slight inflammation in their brains whereas those that received the mAb developed severe encephalitis. In contrast to control mice, the mAb-treated mice had many areas of acute focal inflammation and infiltration of large numbers of inflammatory cells in the meninges and parenchyma of their brains. In the areas of acute focal inflammation, tachyzoites and Toxoplasma Ag were demonstrated by immunoperoxidase staining with the use of rabbit anti-Toxoplasma antibody, suggesting that the focal inflammation was induced by Toxoplasma organisms. Acute inflammation was also observed around cysts of Toxoplasma. Immunohistologic staining revealed tachyzoites and Toxoplasma Ag surrounding the periphery of these cysts suggesting cyst disruption had occurred. Mice treated with mAb against IFN-gamma had five times the numbers of cysts in their brains as did control mice. These results clearly indicate that endogenous IFN-gamma plays a significant and important role in prevention of encephalitis in mice chronically infected with Toxoplasma. The mAb-treated mice had the same Toxoplasma antibody titers and the same degree of macrophage killing of Toxoplasma as did untreated controls. These results suggest that IFN-gamma may have a direct role in preventing cyst rupture and toxoplasmic encephalitis.

Animals↗

PubMed1989

DNA restriction enzyme analysis of a bovine herpesvirus 1 strain isolated from encephalitis in Hungary.

The DNA of a bovine herpesvirus 1 (BHV-1) strain isolated from calf encephalitis in Hungary was analysed with restriction enzymes. The cleavage pattern of the encephalitis strain Na/67 differed from those of all the other Hungarian BHV-1 isolates investigated so far. The EcoRI and HindIII cleavage patterns of virus strain Na/67 were found to be similar to the patterns of two other encephalitis strains (N569 and A663 from Australia and Argentina, respectively) characterized earlier. Strain Na/67 is the first isolate in Europe which showed the restriction enzyme pattern of BHV-1.3 previously supposed to be characteristic of encephalitis strains.

Animals↗

PubMed1989

[Neuropathology of HIV encephalitis].

Neuropathologic features of HIV encephalitis are described in 8 cases selected among 36 autopsies of AIDS patients. From an epidemiologic point of view, the author remarks that parenteral drug addict patients are as prone as male homosexual patients to get HIV encephalitis. The surprisingly low incidence of this illness, recorded in the epidemiologic bulletin of Health Ministry is pointed out. Clinicopathologically, the complex nosologic problem and terminologic confusion of AIDS dementia are discussed, as well as the different neuropathologic criteria used to define HIV encephalitis. The term "panencephalitis with multinucleated cells" is proposed to name the neuropathologic lesions of those patients with HIV dementia and who show multinucleated cells as histopathologic hall mark of HIV encephalitis on brain examination. Physiopathologic interpretation about how the HIV affects the CNS is analyzed. Recent etiopathogenic interpretations of HIV dementia are included.

AIDS Dementia Complex↗

PubMed1989

[Biochemical and morphological changes in the neuroglia in experimental herpetic encephalitis].

The complex virological, biochemical and morphological study permitted to obtain various characteristics of mice herpes encephalitis. The reaction of astrocyte glia at different stages of herpes encephalitis was revealed and analyzed in detail. New data on the dynamics of desoxyribonuclease activity changes in neuroglia and the glial complex formation were obtained. It was shown that the increased DNA-ase activity in neuroglia and the astrocyte activation which morphological manifestation was the formation of glial complexes, may be referred to as processes dealing with barrier and elimination neuroglia functions in herpes encephalitis. The results presented allows to suppose that the severity of the development and outcome of herpes encephalitis mainly depends on the astrocyte glia condition, its potential abilities in appearing of barrier and eliminative functions.

Animals↗

PubMed1985

The use of the single radial haemolysis technique in the serological diagnosis of dengue and Japanese encephalitis virus infections.

The single radial haemolysis test for the serological diagnosis of suspected dengue and Japanese encephalitis virus infections uses crude virus antigens with a haemagglutinin titre of 1:320 or 1:640. The results, which may be read 3 hours after the addition of a patient's serum, showed a general agreement between this test and haemagglutination-inhibition tests in the number of case diagnoses that were confirmed. The antibody responses of individual patients shown by the two tests, however, were different, which suggests that the two tests may not be measuring the same antibody. The single radial haemolysis test can distinguish between dengue and Japanese encephalitis viruses using specific mouse hyperimmune sera. Tests on a limited number of sera from Japanese encephalitis patients also showed no cross-reactions with dengue virus antigens in those cases having a low-titred but significant fourfold antibody rise to Japanese encephalitis antigen.

Dengue↗

PubMed1985

[Clinical and computer tomographic diagnosis of necrotic encephalitis].

Twenty-five patients with a suspicion of necrotic encephalitis were examined by computer-aided tomography (CT). Brain tumors were detected in 5 patients. Three patients had negative results of CT examination and later other etiology was established in these cases. Fifteen patients showed characteristic foci of diminished density in the cerebral substance; in 3 cases necrosis was verified postmortem. The time-course of the encephalitis process was traced in the majority of patients. The diagnosis based on laboratory findings made it possible to confirm the etiological role of herpes simplex virus in the development of encephalitis in 2 patients with negative results of CT examinations. Possible causes of the negative results are discussed. Possible involvement of the lenticular nuclei, the brain stem and the cerebellum in necrotic encephalitis is demonstrated. The method is recommended for the early diagnosis of necrotic encephalitides.

Adolescent↗

PubMed1985

Acyclovir versus vidarabine in herpes simplex encephalitis.

One hundred and twenty-seven patients with suspected herpes simplex encephalitis were entered in a randomised, controlled comparative study of therapy with acyclovir 10 mg/kg, 8-hourly, versus vidarabine, 15 mg/kg daily, for 10 days. Consecutive patients were included and nearly all diagnosed cases of HSV-encephalitis in Sweden were enrolled in the study. The diagnosis of HSV-encephalitis was verified by demonstration of intrathecal herpes simplex virus (HSV) antibody production and by HSV cultivation, or antigen detection, in brain biopsy or necropsy material. Of 53 confirmed cases of HSV-encephalitis (corresponding to 2.3 cases per million inhabitants per year in Sweden), 51 (27 acyclovir, 24 vidarabine) were evaluable for therapeutic efficacy. The mortality was 19% in the acyclovir-treated group versus 50% in the vidarabine group (p = 0.04). At 12 month of observation 15 of 27 (56%) acyclovir recipients had no, or mild, sequelae compared with 3 of 24 (13%) vidarabine recipients (p = 0.002). Nineteen of 24 (79%) vidarabine-treated patients died or suffered severe sequelae, compared with 9 of 27 (33%) acyclovir-treated patients (p = 0.005). The effect of treatment was influenced by the level of consciousness at the start of therapy. The outcome for 20 vidarabine-treated patients above 30 years of age with HSE was similar to that for the 53 patients reported by an American collaborative study.

Acyclovir↗

PubMed1983

[Effect of ara-A on the experimental herpes simplex virus encephalitis--pathology and fluctuation of the cerebrospinal fluid and serum antibody levels].

The effect of Ara-A treatment on the experimentally induced herpes simplex virus (HSV) encephalitis in rabbits was examined. Simultaneously practical value of enzyme-linked immunosorbent assay (ELISA) for rapid diagnosis was tested to find an early rise of antibody in cerebrospinal fluid (CSF) and serum in connection with an adoption of Ara-A administration. HSV encephalitis was produced by inoculation with type-1 HSV into the bilateral corneas of the eyes. A large amount of pus and typical neurological signs characteristic to encephalitis appeared after several days of infection. Ara-A therapy begun at the 3rd day of infection clearly increased the survival rate (90%) and improved the clinical signs, but the start of the drug at the 6th day could only increase the survival rate (60%) without cure of the clinical symptoms. ELISA could catch the early rise of IgG antibody in CSF from 3-4 days and in serum from 4-6 days after infection. Ara-A didn't interfere the antibody production. Viral antigens were found in the corneal epithelia and propria, neurons and Schwann's cells of trigeminal ganglia, neurons and glial cells of pons and cerebrum, especially in hippocampal nuclei. Typical Cowdry A and full type intranuclear inclusion bodies in the neurons were observed in the above tissues with infiltration of large amount of small round cells. In conclusion, Ara-A therapy in HSV encephalitis at the early stage of infection was quite effective for cure and the ELISA method is a useful tool for detection of early antibody rise in CSF and serum.

Animals↗

PubMed1984

Biological properties of strains of tick-borne encephalitis virus isolated in the natural foci of the eastern part of the Russian plain.

Strains of tick-borne encephalitis virus isolated in the natural foci of infection in the eastern part of the Russian Plain (the Kirov region) were examined for their biological properties. The strains examined were 69 strains isolated from ticks Ixodes persulcatus, 62 strains obtained from patients with the clinically manifest form of tick-borne encephalitis and 56 strains isolated from the blood of patients with the inapparent form of infection. Comparative studies on laboratory animals (albino mice, golden hamsters, suckling guinea pigs and other mammals) as well as comparative serologic studies provided evidence which suggested that all virus isolates from the Kirov region were antigenically identical with the strain "Sofin" isolated in the Far East and represent thus a single causative agent of the tick-borne encephalitis virus infection. This strain of virus is supposed to exist in two variants, in dependence on ecological conditions: one of these variants is the eastern variant (strain Sofin and strains from the Kirov region) and the other one is the western variant of tick-borne encephalitis virus.

Animals↗

PubMed1984

Toxoplasmic encephalitis in patients with acquired immune deficiency syndrome.

An epidemic of cases of toxoplasmic encephalitis is occurring in patients with acquired immune deficiency syndrome (AIDS). Serological or histopathologic studies were performed on 70 cases with AIDS and toxoplasmic encephalitis. In many cases conventional stains of brain-tissue specimens failed to disclose Toxoplasma organisms; all were positive when stained by the peroxidase-antiperoxidase technique. Except for a single patient, serological titers were not indicative of an acute acquired infection. The ratio of titers in the agglutination test to titers in the Sabin-Feldman dye test seemed to be more predictive of active toxoplasmic encephalitis in patients with AIDS than either test alone. Based on histological and serological data, an approach is presented for diagnosis and treatment of suspected toxoplasmic encephalitis in patients with AIDS.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Monocyte adhesion to endothelium in simian immunodeficiency virus-induced AIDS encephalitis is mediated by vascular cell adhesion molecule-1/alpha 4 beta 1 integrin interactions.

Because the mechanisms associated with recruitment of monocytes to brain in AIDS encephalitis are unknown, we used tissues from rhesus monkeys infected with simian immunodeficiency virus (SIV) to examine the relative contributions of various adhesion pathways in mediating monocyte adhesion to endothelium from encephalitic brain. Using a modified Stamper and Woodruff tissue adhesion assay, we found that the human monocytic cell lines, THP-1 and U937, and the B cell line, Ramos, preferentially bound to brain vessels from monkeys with AIDS encephalitis. Using a combined tissue adhesion/immunohistochemistry approach, these cells only bound to vessels expressing vascular cell adhesion molecule-1 (VCAM-1). Furthermore, pretreatment of tissues with antibodies to VCAM-1 or cell lines with antibodies to VLA-4 (CD49d) inhibited adhesion by more than 70%. Intercellular adhesion molecule-1 (ICAM-1)/beta 2 integrin interactions were not significant in mediating cell adhesion to the vasculature in encephalitic simian brain using a cell line (JY) capable of binding rhesus monkey ICAM-1. In addition, selectin-mediated interactions did not significantly contribute to cell binding to encephalitic brain as there was no immunohistochemical expression of E-selectin and P-selectin in either normal or encephalitic brain, nor was there a demonstrable adhesive effect from L-selectin using L-selectin-transfected 300.19 cells on simian encephalitic brain. These results demonstrate that using the tissue adhesion assay, THP-1, U937, and Ramos cells bind to vessels in brain from animals with AIDS encephalitis using VCAM-1/alpha 4 beta 1 integrin interactions and suggest that VCAM-1 and VLA-4 may be integral for monocyte recruitment to the central nervous system during the development of AIDS encephalitis.

Animals↗

PubMedDate not supplied

[Psychopathological symptoms in atypical viral hemorrhagic tick-borne encephalitis].

A 17 year old boy was admitted because of symptoms of a catatonic syndrome. During the diagnosis we ascertained that there was bleeding from the central nervous system of unknown origin. The intensification of neurological and general symptoms/among others-hyperthermia/suggested haemorrhagic encephalitis, which was confirmed by the viral investigation of the cerebrospinal fluid (tick-borne encephalitis). We describe this case because viral encephalitis rarely has haemorrhagic effects. Usually tick-borne encephalitis is of diphasic type with the attacks of "epilepsia partialis continua", which were not observed in this case.

Adolescent↗

PubMed1995

[Value of gene amplification of herpesviruses in the diagnosis and treatment of acute viral encephalitis].

Positive diagnosis of Herpes simplex virus (HSV) encephalitis was rarely obtained in the past, when brain biopsy had been performed. Other tests (HSV antigen and HSV antibodies detection and interferon alpha measurement, in cerebrospinal fluid) failed to prove HSV infection. Polymerase chain reaction has been proposed for accurate and rapid diagnosis of HSV encephalitis. With 35 cycles of a DNA polymerase sequence duplication, sensitivity reaches 95% and specificity 100%. HSV PCR is a useful tool for the diagnosis of acute encephalitis. This should be available in many neurologic clinics. Therapeutic consequences include rapid disruption of aciclovir when clinical features, MRI study and negative PCR suggest non herpetic encephalitis.

Acute Disease↗

PubMed1994

[The clinical picture and pathogenesis of polyradiculoneuropathy in tick-borne encephalitis].

Based on examination of tick-borne encephalitis patients with ascending polyradiculoneuropathy the authors describe the character of the disease, its clinical picture and the results of laboratory studies, etc. Differential diagnosis is made between the indicated syndrome associated with tick-borne encephalitis and sporadic polyradiculoneuropathies. A detailed description is given for the first time of the clinical and pathomorphological picture of that gravest form of tick-borne encephalitis. As regards the character of the clinical and pathomorphological alterations, the ascending polyradiculoneuropathy associated with tick-borne encephalitis is meningoencephalomyelitis with the radicular syndrome which often determines the disease gravity and prognosis.

Adolescent↗

PubMed1976

[Posttraumatic pyogenic and granulomatous encephalitis. An animal experimental contribution on inflammation (author's transl)].

The present studies were performed to elucidate the factors responsible for the relative resistance of the brain to bacterial infections. As a model, group A streptococci were used to produce an experimental brain infection in mice. Attention was focussed on the activity of brain macrophages, the function of which to date is poorly understood. The primary purpose of the experiments was to compare the types of inflammation elicited in the brain by the injection of either killed or living group A streptococci. As a result, two fundamentally different types of encephalitis were observed histologically. A granulomatous inflammation was induced by killed streptococci; when deposited in the brain by intracerebral injection, these were phagocytosed by invading mononuclear macrophages and polymorphonuclear granulocytes during the first day p.i. There was no necrosis of brain tissue excepting the stab wound at the site of injection. The number of granulocytes in the inflammatory infiltrates decreased during the first week p.i. whereas, during the same period, the number of macrophages forming granuloma-like cell accummulations increased. At the beginning of the third week a fading of the granulomatous encephalitis was observed. In contrast, living streptococci produced a pyogenic inflammation of the meninges as well as of the grey and white matter in the region of the stab wound combined with extended tissue necrosis surrounding deposits of bacteria. This pyogenic infection progressed until the end of the first week, forming a brain abscess. A phlegmonous spreading of the pyogenic inflammation predominantly in the white matter and pyocephalus internus was also observed. In contrast to the increase of mononuclear macrophages in the border zone of the abscesses, the granulocytic inflammation decreased. During the second and third weeks p.i. granulation tissue consisting of proliferating connective tissue cells, macrophages and lymphocytes replaced pyogenic necrosis. A secondary purpose was to determine the fate of living and killed streptococci within the pyogenic and granulomatous encephalitis. In these studies immunohistologic, electron microscopic, bacteriologic and serologic methods were employed in addition to the techniques already mentioned. In the majority of the experimental animals streptococci were killed by granulocytes within the first week after injection of the living bacteria. At this time, most of the streptococci were contained within granulocytes and macrophages located to the periphery of the brain abscesses. Corresponding to the granulomatous encephalitis produced by injection of killed streptococci it was possible to detect persistent cell wall material in macrophages by immunohistology. By electronmicroscopy streptococci and their cell walls were found within the phagocytic vacuoles of macrophages. During the course of degradation the group-specific cell wall carbohydrate was enzymatically converted into the group A-variant specific structure...

Animals↗