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  • 11
    Electronic Resource
    Electronic Resource
    Early T cell response in the central nervous system in canine distemper virus infection (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 45-56 
    Details
    ISSN: 1432-0533
    Keywords: Key words Canine distemper virus ; T cells ; Acute demyelination ; Immunosuppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The initial demyelinating lesions in canine distemper virus (CDV) infection develop during a period of severe immunosuppression in the absence of inflammation. In vitro and in vivo studies suggest that early demyelination is due to directly virus-induced oligodendroglial changes. In the present spatiotemporal study in experimentally CDV-infected dogs we observed diffuse up-regulation of T cells throughout the central nervous system (CNS) and T cell invasion in early demyelinating lesions. Invasion of T cells in the CNS occurred despite severe immunosuppression and without any perivascular cuffing. However, the major fraction of invading T cells correlated with sites of viral replication and coincided with the demonstration of an early immune response against the nucleocapsid protein of CDV. Activation of microglial cells was thought to have elicited the migration of T cells to the CNS by secretion of chemokines: marked IL-8 activity was found in the CSF of dogs with acute lesions. In areas of early demyelination, large numbers of CD3+ cells accumulated in the tissue in the absence of any morphological sign of inflammation. Whether the T cells at lesion sites contribute to the development of acute demyelination remains uncertain at this stage. Antiviral cytotoxicity was not apparent since viral clearance in demyelinating lesions is only effective when B cells and concurring antiviral antibody production appeared in the subacute and chronic inflammatory stage of the disease. CD3+ cells appear to persist for several weeks after infection since they were also found in recovered dogs that did not develop demyelination. Accumulation of immune cells, including a significant proportion of resting T cells (CD45RA+) in the CNS in the early stages of the disease may facilitate the later development of the intrathecal immune response and associated immunopathological complications.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050954
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  • 12
    Electronic Resource
    Electronic Resource
    Validation of a Western immunoblotting procedure for bovine PrPSc detection and its use as a rapid surveillance method for the diagnosis of bovine spongiform encephalopathy (BSE) (1999)
    Springer
    Acta neuropathologica 98 (1999), S. 437-443 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this report we document the results of several independent studies testing the sensitivity, specificity and reliability of the Prionics Western blotting (PWB) procedure to detect bovine and ovine disease-specific, protease-resistant prion protein (PrPSc). Validation of the technique was obtained by blind analysis of samples from cattle affected with bovine spongiform encephalopathy (BSE), clinically normal animals or cattle with neurological diseases unrelated to BSE. Overall, very high sensitivity, specificity and reliability was observed. It became clear that sampling of the correct brain region and the method used for protein extraction are important factors for correct diagnosis. Furthermore, we tested the usefulness of the PWB technique as an instrument for surveillance purposes. We analyzed animals from a culling scheme as well as older animals from abattoirs to determine the number of subclinical BSE cases detectable by histopathological examination, immunohistochemistry for PrPSc and PWB. In both studies, BSE-affected animals with no overt clinical symptoms were detected. These results demonstrate the usefulness of the PWB procedure in surveillance systems serving as a rapid diagnostic tool to identify animals subclinically infected with BSE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051106
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  • 13
    Electronic Resource
    Electronic Resource
    Canine distemper virus-immune complexes induce bystander degeneration of oligodendrocytes (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 402-407 
    Details
    ISSN: 1432-0533
    Keywords: Brain cell cultures ; Bystander demyelination ; Canine distemper virus ; Oligodendrocytes ; Immune complexes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Demyelination in chronic canine distemper encephalitis may be the result of a bystander effect in which the antiviral immune response is involved. In the present report we demonstrate that canine distemper virus-antiviral antibody immune complexes induce oligodendroglial degeneration in mixed brain cell cultures, particularly at the level of the cell processes. The involvement of macrophages as effector cells in this process was confirmed by depletion of these cells from the cultures which prevented the immune complex-mediated oligodendroglial degeneration. Canine distemper virus-immune complex-induced oligodendroglial pathology is thought to be mediated by toxic factors released from stimulated macrophages. this bystander effect demonstrated here in vitro may be relevant to the mechanisms of demyelination in vivo, in which virus persistence plays an important role.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00713532
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  • 14
    Electronic Resource
    Electronic Resource
    Peripheral and central distal axonopathy of suspected inherited origin in Birman cats (1991)
    Springer
    Acta neuropathologica 82 (1991), S. 143-146 
    Details
    ISSN: 1432-0533
    Keywords: Cat ; Distal axonopathy ; Dying-back neuropathy ; Heredodegeneration ; Neurological disorder
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three female cats, littermates born from clinically normal parents, were examined at 8 to 10 weeks of age because of a slowly progressive posterior ataxia. Another cat from a previous litter from the same parents suffered from similar neurological symptoms. Histopathological examination of the nervous tissues of these animals revealed degeneration of axons and myelinopathy in a distal distribution pattern. Both peripheral nerves and central nervous system were involved. The central nervous system lesions were most prominent in the lateral pyramidal tracts of the spinal cord, the fasciculi gracili of the dorsal column in the cervical spinal cord and the cerebellar vermian white matter. In the PNS numerous degenerating nerve fibers were found in the sciatic nerves but not in the spinal nerve roots. Our findings show that these cats were suffering from a hereditary multisystem degeneration with a distribution pattern of the lesions suggestive of a distal axonopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293957
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  • 15
    Electronic Resource
    Electronic Resource
    Antibody-induced generation of reactive oxygen radicals by brain macrophages in canine distemper encephalitis: a mechanism for bystander demyelination (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 396-403 
    Details
    ISSN: 1432-0533
    Keywords: Brain macrophages ; Canine distemper encephalitis ; Demyelination ; Oxygen radicals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of inflammatory demyelination in canine distemper encephalitis (CDE) is uncertain but macrophages are thought to play an important effector role in this lesion. Serum and cerebrospinal fluid (CSF), containing anti-canine distemper virus and anti-myelin antibodies from dogs with CDE were tested for their ability to generate reactive oxygen species (ROS) in macrophages in primary dog brain cell cultures using a chemiluminescence (CL) assay. The majority of serum samples and several CSF samples from animals with inflammatory demyelination elicited a CL signal in infected dog brain cell cultures. In contrast, none of these samples induced a positive response in uninfected cultures which contained large numbers of myelin antigen-presenting cells, although defined anti-myelin antibodies lead to a marked secretion of ROS in this system. It was concluded that antiviral antibody-induced secretion of ROS, known to be highly toxic for brain tissue, may play an important role in white matter damage in inflammatory lesions supporting a previous hypothesis of bystander demyelination in CDE. No evidence was found for a similar antibody-dependent cellular cytotoxicity-like mechanism mediated by anti-myelin antibodies in CDE, which does not support the concept of autoimmunity in this disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688176
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  • 16
    Electronic Resource
    Electronic Resource
    Ultrastructural and biochemical findings in brain cell cultures infected with canine distemper virus (1990)
    Springer
    Acta neuropathologica 80 (1990), S. 59-67 
    Details
    ISSN: 1432-0533
    Keywords: Brain cell culture ; Canine distemper virus ; Cerebroside sulfotransferase ; Electron microscopy ; Oligodendrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the pathomechanism of demyelination in canine distemper (CD), dog brain cell cultures were infected with virulent A75/17-CD virus (CDV) and examined ultrastructurally. Special attention was paid to the oligodendrocytes, which were specifically immunolabelled. In addition, cerebroside sulfotransferase (CST), an enzyme specific for oligodendrocyte activity was assayed during the course of the infection. Infection and maturation as well as CDV-induced changes were found in astrocytes and brain macrophages. Infection of oligodendrocytes was rarely seen, although CST activity of the culture markedly decreased and vacuolar degeneration of these cells occurred, resulting in their complete disappearance. We concluded that the degeneration of oligodendrocytes and demyelination is not due to direct virus-oligodendrocyte interaction, but due to CDV-induced events in other glial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294222
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  • 17
    Electronic Resource
    Electronic Resource
    Oligodendroglial pathology in canine distemper (1997)
    Springer
    Acta neuropathologica 95 (1997), S. 71-77 
    Details
    ISSN: 1432-0533
    Keywords: Key words Canine distemper virus ; Oligodendrocytes ; In situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Canine distemper virus (CDV) causes a multifocal demyelinating disease in dogs. The mechanism of acute demyelination in distemper is still poorly understood. The initial demyelinating lesion in distemper is directly virus induced, since there is a clear correlation between the occurrence of demyelination and CDV replication in the cells of the white matter. Yet, there is little evidence for oligodendroglial infection. Changes of these cells have been reported in vitro and in vivo. The in vitro studies showed that – in contrast to other cells such as astrocytes and macrophages – oligodendrocytes hardly express CDV protein. However, we could show that these cells underwent a restricted infection with transcription of CDV RNA and that this phenomenon correlated with down-regulation of myelin gene transcription. The extension of these in vitro findings in vivo was obscured by the lack of reliable oligodendrocyte labelling techniques in canine brain tissue sections. In this study we combined immunohistochemistry with in situ hybridization to examine oligodendrocytes in demyelinating lesions and to investigate the question of oligodendrocyte infection in vivo. We could demonstrate that CDV infection leads to massive down-regulation of myelin gene expression in demyelinating lesions and that this effect correlates in part with a restricted infection of oligodendrocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050767
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  • 18
    Electronic Resource
    Electronic Resource
    Oligodendroglial degeneration in distemper: apoptosis or necrosis? (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 279-287 
    Details
    ISSN: 1432-0533
    Keywords: Key words Canine distemper virus ; Oligodendrocytes ; Apoptosis ; Necrosis ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Canine distemper virus (CDV) causes a multifocal demyelinating disease in dogs. It was previously shown that the initial demyelinating lesions are directly virus induced since a correlation between the occurrence of demyelination and CDV replication in white matter cells was observed. During the course of infection oligodendrocytes undergo distinct morphological alterations, partly due to a restricted CDV infection of these cells, and eventually disappear from the lesions. This phenomenon has been described in vivo as well as in vitro. However, the reason for the morphological alterations and the following oligodendroglial depletion remained unclear. Since virus infection can induce cell death, it was investigated whether apoptosis or necrosis plays a role in the pathogenesis of demyelination in canine distemper. In brain tissue sections from dogs with acute distemper apoptotic cells were not detected within the demyelinating lesions using morphological and biochemical cell death criteria. In chronic distemper, apoptotic cells – presumably inflammatory cells – were seen within the perivascular cuffs. These in vivo findings were correlated to the in vitro situation using CDV-infected primary dog brain cell cultures as well as Vero cells. Infection with culture-adapted CDV lead to massive necrosis but not to apoptosis. After infection with virulent CDV neither apoptosis nor necrosis was a predominant feature in either culture system. These findings suggest that virus-induced demyelination in canine distemper is not the direct consequence of apoptosis or necrosis. It is speculated that another mechanism must be responsible for the observed morphological alterations of oligodendrocytes, ultimately leading to demyelination.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050986
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  • 19
    Electronic Resource
    Electronic Resource
    Canine distemper virus-induced glial cell changes in vitro (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 51-58 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper virus ; Brain tissue culture ; Astrocyte ; Oligodendrocyte ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In vitro studies on glial cell changes in canine distemper virus (CDV) infection could be useful for the understanding of the pathogenesis of demyelination in vivo in this disease. Mixed glial cell cultures derived from neonatal mice and dogs were infected with CDV and examined using immunocytochemical techniques demonstrating specific oligodendroglial and astroglial cell markers. Astrocytic changes were similar in both murine and canine cultures and consisted of loss of processes, cell fusion, and cell necrosis. Marked oligodendroglial lesions were apparent in the canine brain cultures and were characterized by focal perikaryal protrusions, swelling and loss of cell processes, and cell necrosis. Fusion between oligodendrocytes was not observed. Fusion between astrocytes and oligodendrocytes could not be documented with double labeling techniques. In contrast to the canine cultures, murine oligodendrocytes remained relatively unaffected by the infection. These findings were discussed with respect to cell pathology and mechanisms of demyelination in vivo. The exact nature of the canine oligodendroglial lesions in vitro needs to be studied in further experiments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00684920
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  • 20
    Electronic Resource
    Electronic Resource
    Demyelination in experimental canine distemper virus infection: Immunological, pathologic, and immunohistological studies (1982)
    Springer
    Acta neuropathologica 56 (1982), S. 285-293 
    Details
    ISSN: 1432-0533
    Keywords: Canine distemper encephalitis (CDE) ; Immunopathology ; Demyelination ; Immunoglobulin ; Local immune response
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary White matter lesions were induced in the brains of eight of nine dogs by means of experimental canine distemper virus (CDV) infection. Dogs were killed at 21, 24, 31, and 42 days after infection. Lymphocyte responsiveness to Con A and PHA stimulation in vitro was severely suppressed up to 31 days post infection (p.i.), followed by partial recovery as tested at 42 days p.i. Anti-CDV neutralizing antibody response was very weak in most dogs. There was a weak increase in antimyelin and antimyelin basic protein antibodies in most dogs during the course of the experiment. Dogs killed up to 31 days p.i. developed non-inflammatory demyclinating lesions in which no immunoglobulin could be detected. One of the three dogs that were killed at 42 days p.i. developed severe inflammatory demyelination. This was the only dog with a strong anti-MBP antibody response in the CSF and immunoglobulin demonstrated in demyelinating lesions. The present study supports previous observations that demyelination in acute CDV infection is not an immune mediated lesion but that these lesions may progress as a result of the local immune response. It is uncertain at this stage whether the local immune reaction specifically causes myelin destruction or whether bystander demyelination occurs in chronic CDE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691260
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