Demyelination in experimental canine distemper virus infection: Immunological, pathologic, and immunohistological studies

Vandevelde, M.; Higgins, Robert; Kristensen, B.; Kristensen, F.; Steck, Andreas; Kihm, U

doi:10.1007/bf00691260

Cited by 67 publications

(58 citation statements)

References 22 publications

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“…Subsequently, CDV-DL follows a certain time course, which strikingly correlates with neuropathological alterations. A well-described histological classification scheme has been used by several authors in order to categorize white matter lesions (Figure 1) [39,40,41]. In this respect, acute, subacute, and chronic lesions are distinguished (Figure 1).…”

Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 99%

“…Immunopathologically, antibody-independent cytotoxicity may be involved in the pathogenesis of acute stages of CDV-DL, whereas delayed type immune-mediated processes with antibody-dependent T cell cytotoxicity are suggested to play a role in chronic stages of CDV-DL [39,49,50]. Demyelination in advanced disease phases is believed to be no longer directly virus-induced, but rather represents an immunopathological bystander phenomenon in a biphasic disease process [9,51].…”

Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 99%

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New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

Lempp

Spitzbarth

Puff

et al. 2014

Viruses

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Canine distemper virus (CDV) is a member of the genus morbillivirus, which is known to cause a variety of disorders in dogs including demyelinating leukoencephalitis (CDV-DL). In recent years, substantial progress in understanding the pathogenetic mechanisms of CDV-DL has been made. In vivo and in vitro investigations provided new insights into its pathogenesis with special emphasis on axon-myelin-glia interaction, potential endogenous mechanisms of regeneration, and astroglial plasticity. CDV-DL is characterized by lesions with a variable degree of demyelination and mononuclear inflammation accompanied by a dysregulated orchestration of cytokines as well as matrix metalloproteinases and their inhibitors. Despite decades of research, several new aspects of the neuropathogenesis of CDV-DL have been described only recently. Early axonal damage seems to represent an initial and progressive lesion in CDV-DL, which interestingly precedes demyelination. Axonopathy may, thus, function as a potential trigger for subsequent disturbed axon-myelin-glia interactions. In particular, the detection of early axonal damage suggests that demyelination is at least in part a secondary event in CDV-DL, thus challenging the dogma of CDV as a purely primary demyelinating disease. Another unexpected finding refers to the appearance of p75 neurotrophin (NTR)-positive bipolar cells during CDV-DL. As p75NTR is a prototype marker for immature Schwann cells, this finding suggests that Schwann cell remyelination might represent a so far underestimated endogenous mechanism of regeneration, though this hypothesis still remains to be proven. Although it is well known that astrocytes represent the major target of CDV infection in CDV-DL, the detection of infected vimentin-positive astrocytes in chronic lesions indicates a crucial role of this cell population in nervous distemper. While glial fibrillary acidic protein represents the characteristic intermediate filament of mature astrocytes, expression of vimentin is generally restricted to immature or reactive astrocytes. Thus, vimentin-positive astrocytes might constitute an important cell population for CDV persistence and spread, as well as lesion progression. In vitro models, such as dissociated glial cell cultures, as well as organotypic brain slice cultures have contributed to a better insight into mechanisms of infection and certain morphological and molecular aspects of CDV-DL. Summarized, recent in vivo and in vitro studies revealed remarkable new aspects of nervous distemper. These new perceptions substantially improved our understanding of the pathogenesis of CDV-DL and might represent new starting points to develop novel treatment strategies.

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Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 99%

Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 99%

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

Lempp

Spitzbarth

Puff

et al. 2014

Viruses

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“…A alta prevalência da desmielinização no cerebelo (88,6%) e tronco encefálico (77,1%), principalmente na ponte (65,7%) e no diencéfalo (61,4%) é relativamente semelhante à observada em outros estudos (Innes & Saunders 1962, Vandevelde et al 1981, Vandevelde et al 1982a,b, Greene & Appel 2006. Além disso, neste estudo pode-se determinar que das cinco regiões (folhas do cerebelo, substância medular do cerebelo, teto do quarto ventrículo, segmento C1-C5 da medula espinhal e tegmento mesencefálico) mais afetadas pela desmielinização, três fazem parte do cerebelo.…”

Section: Quadro 3 Distribuição Da Evolução Das Lesões De Cinomose Deunclassified

Neuropatologia da cinomose canina: 70 casos (2005-2008)

et al. 2009

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643Pesq. Vet. Bras. 29(8):643-652, agosto 2009 RESUMO.-Este estudo teve como objetivo realizar uma investigação anátomo-patológica detalhada das lesões e sua distribuição no sistema nervoso central (SNC) de cães com cinomose. Foram avaliadas secções padronizadas do encéfalo e da medula espinhal de 70 cães. Os casos foram agrupados de acordo com a idade dos cães e classificados conforme a evolução das lesões. Os resultados permitem concluir que: (1) encefalomielite induzida pelo vírus da cinomose canina é mais prevalente em filhotes e adultos; (2) lesões macroscópicas no SNC ocorrem com baixa freqüência; (3) o encéfalo é mais acometido do que a medula espinhal; (4) as cinco regiões anatômicas mais afetadas do encéfalo são, em ordem decrescente de freqüência, o cerebelo, o diencéfalo, o lobo frontal, a ponte e o mesencéfalo; (5) a região anatômica mais afetada da medula espinhal é o segmento cervical cranial (C1-C5); (6) lesões subagudas e crônicas são mais comuns do que lesões agudas; (7) desmielinização é a lesão mais prevalente e ocorre principalmente no cerebelo, na ponte e no diencéfalo, quase sempre acompanhada de astrogliose e inflamação não-supurativa; (8) The current study was performed to determine the pathology and distribution of lesions in the central nervous system (CNS) of 70 dogs naturally affected by canine distemper. Cases were grouped according to the age of the dogs and classified according to the evolution of the lesions. It was possibly to conclude that: (1) the encephalomyelitis induced by canine distemper virus is more prevalent in puppies and adults; (2) gross lesions in the CNS occur infrequently; (3) the brain is more frequently affected than the spinal cord; (4) the five anatomical sites of the rain more frequently affected are, in decreasing order of frequency, cerebellum, diencephalon, frontal lobe of telencephalon, pons and mesencephalon; (5) the anatomical site more frequently affected in the spinal cord is the cervical (C1-C5) segment; (6) subacute and chronic lesions are more common than acute ones; (7) demyelization is the more prevalent lesion and occur mainly in the cerebellum, pons and diencephalons, usually associated with astrogliosis and nonsuppurative inflammation; (8) in most cases with astrogliosis, gemistocytic astrocytes are observed, frequently with syncitia formation; (9) non-suppurative leptomeningitis, malacia and cortical neuronal necrosis are moderately frequent in the brain and less so in the spinal cord; (10) inclusion bodies are frequent in the brain; occur mainly in astrocytes and less frequently in neurons, however independently of the affected cell they occur mainly in the nucleus; (11) a classification of canine distemper encephalitis based in age-related clinical syndromes it is not accurate.INDEX TERMS: Diseases of dogs, neuropathology, canine distemper.

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“…Lytically replicating virus has been isolated from dogs with different forms of CNS disease (32). SSPE in humans and canine distemper in dogs seem to have some distinct features (16), but further evaluation of the latter infection may be of particular value for the understand ing of virus-induced demyelination (113). Cytolytic replication in oli godendroglial cells does not appear to have a central role.…”

Section: Persistent Measles Virus Infection Causes Sspe In Humansmentioning

confidence: 98%