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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe various applications of an immunoblot technique which allows the qualitative determination of the specific antibody activity of oligoclonal IgG intrathecally synthesized in infectious diseases of the nervous system. After dilution of sera to the same IgG concentration as the paired CSF samples, 10 microliters of both fluids are applied side by side on agarose gel plates and isoelectrically focused. Precipitated IgG or specific IgG antibodies are then blotted onto a nitrocellulose sheet previously coated with either a rabbit anti-IgG antiserum or the antigen under study, respectively. The immunoblot is successively incubated with biotinylated anti-IgG antiserum and with the streptavidin-biotin-peroxidase complex before staining with 4 chloro-1-naphthol. This method was applied to samples from patients with subacute sclerosing panencephalitis, herpetic encephalitis, meningoradiculitis due to Herpes Zoster, neuro-AIDS, neurobrucellosis, meningoradiculitis or encephalomyelitis due to Borrelia burgdorferi, and tuberculous meningitis. In each case, specific oligoclonal IgG antibodies, superimposed or not on a diffuse polyclonal synthesis were detected in the CSF, but not, or more faintly, in the corresponding serum. This was taken as evidence for an intra-thecal synthesis of these antibodies. In contrast, when a "mirror effect" was observed, i.e. similar oligoclonal bands in both serum and CSF after dilution at the same IgG concentration, an intra-thecal synthesis was ruled out.
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PMID:[Antibody activity of CSF oligoclonal IgG in infectious neurological diseases. Detection using immunoblotting]. 320 96

The murine hepatitis virus, JHM strain, causes a relapsing subacute demyelinating encephalomyelitis in Lewis rats after intracranial infection. The disease process involves both virus persistence within glial cells and the induction of autoimmunological attack of myelin, however, the relative importance of these features involved in chronic relapsing demyelination remains to be determined. In this report, we analyze the tropism of JHM virus to various neural cell types present within primary Lewis rat central nervous system cultures. Infection of primary cultures with JHM virus revealed that type I astrocytes and brain macrophages are the initial target cells of infection and that the myelin-forming oligodendrocytes are comparatively resistant, becoming infected only rarely through virus mediated cell fusion with previously infected cells. In addition, infection of cultures after removal of oligodendrocytes by various means had no effect on the tropism of JHM virus for the cultures. Cytopathic effects of JHM virus proceed rapidly by cell fusion within the astrocyte-macrophage monolayer, leaving the oligodendrocyte population largely unaffected. Therefore, the highly selective infection of type I astrocytes and macrophages appears to form the basis of JHM virus neurotropism in Lewis rats. These results indicate that JHM virus infection of astrocytes and brain macrophages may be more important in inducing chronic relapsing demyelinating processes than direct infection of the myelin-forming oligodendrocytes. Other possible pathways leading to chronic demyelination in rats involving type I astrocytes and brain macrophages are discussed.
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PMID:Analysis of murine hepatitis virus (JHM strain) tropism toward Lewis rat glial cells in vitro. Type I astrocytes and brain macrophages (microglia) as primary glial cell targets. 352 62

Infection with Borrelia burgdorferi was associated with encephalitis in a horse. The horse lived in an area of Wisconsin endemic for B burgdorferi infection. Borrelia burgdorferi was isolated from the brain, but rabies virus was not detected in the brain. Serum obtained from the horse had a B burgdorferi antibody titer of 1:2,048, but was negative for antibodies to eastern and western encephalomyelitis.
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PMID:Encephalitis associated with Borrelia burgdorferi infection in a horse. 369 96

Sera from indicator chicken flocks situated in southern Alberta near Lethbridge were tested by the hemagglutination-inhibition (HI) technique for antibodies to Western, Eastern and St. Louis Encephalitis viruses during the summer and early fall of the four years 1964 to 1967.One chicken in 1964, 90 in 1965 and five each in 1966 and 1967 were positive to Western encephalomyelitis (WE) virus by hemagglutination-inhibition tests. All of the positive sera were confirmed by neutralization test (NT) in infant mice. No antibodies to the Eastern and St. Louis viruses were detected. Infection with WE virus was detected in each of the four years, indicating that WE virus is endemic to southern Alberta with a marked seasonal incidence occurring between the second week in August and the third week in September. An improved technique for filtering sera is described.
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PMID:Western encephalomyelitis virus infection in "indicator" chickens in southern Alberta. 424 74

Viruses have been found to induce inflammatory demyelinating lesions in central nervous system (CNS) tissue of both animal and man, either by natural infections or after vaccination. At least two different pathogenic mechanisms have been proposed for these changes, a cytopathic viral infection of oligodendroglia cells with subsequent cell death, and a host immune reaction against virus and brain antigens. We now report the occurrence of cell-mediated immune reactions against basic myelin proteins in the course of coronavirus infections in Lewis rats. Infection of rats with the murine coronavirus JHM leads to demyelinating encephalomyelitis developing several weeks to months postinfection. Lymphocytes from these diseased Lewis rats can be restimulated with basic myelin protein (BMP) and adoptive transfer of these cells leads to lesions resembling those of experimental allergic encephalomyelitis (EAE) in recipients, which can be accompanied by a mild clinical disease. This model demonstrates that a virus infection in CNS tissue is capable of initiating an autoimmune response which may be of pathogenic importance.
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PMID:Adoptive transfer of EAE-like lesions from rats with coronavirus-induced demyelinating encephalomyelitis. 631 Apr 11

Infection of 21-25-day-old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6-12 days p.i. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14-30 days p.i. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time-course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10-12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.
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PMID:Sequence of murine coronavirus JHM induced neuropathological changes in rats. 633 Jun 3

Infection of rats with the murine coronavirus JHM led to acute or subacute encephalitis. Viral and host factors greatly influenced the outcome of the infection. A number of temperature-sensitive (ts) mutants was obtained which differed widely in their capacity to induce lesions of the central nervous system (CNS) in rats. Under defined conditions a subacute demyelinating encephalomyelitis ( SDE ) with pronounced clinical signs was observed 14-160 days post infection (p.i.). A number of rats, which showed a remission of SDE later developed a relapse of the disease accompanied by neurological symptoms. Neuropathological examination of such animals revealed lesions of active demyelination and extended remyelinated areas. The presence of viral antigen or infectious virus in the CNS of these rats demonstrated that they were persistently infected. Further investigations indicated that this virus infection triggers a cell mediated immune response against basic myelin protein which may contribute to the development of subacute to chronic encephalomyelitides .
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PMID:Virological and immunological aspects of coronavirus induced subacute demyelinating encephalomyelitis in rats. 633 Nov 17

Disease induced by 3 virulent strains of Canine Distemper Virus (CDV) was compared in specific pathogen-free Beagle dogs. All strains produced an encephalomyelitis but variation was observed in the severity, clinical course and resulting neuropathology. Infection with Snyder Hill strain of CDV was consistently acute; dogs either succumbed 14 to 19 days post-inoculation (PI) or recovered. Lesions in the neuraxis were those of a polioencephalomyelitis. In contrast, CDV strain A75-17 produced subacute to chronic disease in which demyelination was the predominant finding. Some dogs succumbed, generally around 28 to 42 days PI. Total recovery was again recorded for some members of the group. Others developed persistent central nervous system (CNS) infection but remained clinically stable until electively killed with barbiturate, up to 62 days PI. CDV strain R252 also induced delayed, predominantly white matter disease with a mixed pattern of mortalities, persistent infections and recoveries, similar to A75-17. Neutralizing antibody responses correlated with the disease course. Dogs which died had low serum titres or lacked serum antibody. Recovering dogs had the earliest and highest titres. A few dogs with persistent CNS infection had antibody in the cerebrospinal fluid also. Current concepts of the pathogenesis of canine distemper encephalomyelitis (CDE) are discussed and a basis for the strain-dependent clinical and pathological expression of CDE is proposed. Viral strain appears to be an important factor in this common disease of the canine CNS.
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PMID:Canine distemper encephalomyelitis: variation with virus strain. 669 31

A 38-year-old woman with encephalitis presented no signs of infectious disease or exanthema. After a remission lasting 10 months, she died during a second attack after demonstrating signs of brain stem lesions. Histological examination revealed lesions, mainly in the brain stem and characterized by intense necrosis, moderate degrees of inflammation, and localized foci of gliosis. In spite of the necrotic lesions, the neurones were relatively spared. An old infarct of the left caudate nucleus was present. Taking other demyelinating diseases into account, it is suggested that this is a clinical form of multiple sclerosis, this enabling a relationship to be established between multiple sclerosis and post-infections perivenous encephalitis or acute disseminated encephalomyelitis.
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PMID:[Encephalitis with necrosis limited to the brain stem: a case report (author's transl)]. 710 Jul 41

A Borna disease virus (BDV)-like agent was isolated from the central nervous system (CNS) of cats with a spontaneous non-suppurative encephalomyelitis ('staggering disease'). In contrast to the rabbit-adapted BDV strain V, which can be propagated in several primary and permanent cell cultures, the cat virus grew only in embryonic mink brain cells. Infection of adult Wistar rats with feline brain tissue material did not result in clinical disease during a period of 5 months, nor in growth of infectious virus in the brain. However, using the brain suspension of a newborn rat inoculated with feline brain tissue material, it was possible to induce typical Borna disease (BD) in four adult rats. This indicates a possible adaptation of the cat virus during passages in rats. By the use of an RT-PCR technique, BDV-specific RNA could be detected in a majority of brain samples from diseased cats. BDV-specific antigen was demonstrated in feline CNS samples both by immunohistochemistry and ELISA. However, the amount of BDV RNA and BDV antigen was less in the cats as compared to horses with BD, providing further support for the notion that a distinct feline BDV strain exists.
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PMID:Staggering disease in cats: isolation and characterization of the feline Borna disease virus. 756 58


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