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PubMed2005

Demyelination in canine distemper virus infection: a review.

Canine distemper virus (CDV) causes severe immunosuppression and neurological disease in dogs, associated with demyelination, and is a model for multiple sclerosis in man. In the early stage of the infection, demyelination is associated with viral replication in the white matter. In acute demyelinating lesions there is massive down-regulation of myelin transcription and metabolic impairment of the myelin-producing cells, but there is no evidence that these cells are undergoing apoptosis or necrosis. Oligodendroglial change is related to restricted infection of these cells (transcription but no translation) and marked activation of microglial cells in acute lesions. Concomitant with immunological recovery during the further course of the disease, inflammation occurs in the demyelinating plaques with progression of the lesions in some animals. A series of experiments in vitro suggests that chronic inflammatory demyelination is due to a bystander mechanism resulting from interactions between macrophages and antiviral antibodies. Autoimmune reactions are also observed, but do not correlate with the course of the disease. The progressive or relapsing course of the disease is associated with viral persistence in the nervous system. Persistence of CDV in the brain appears to be favored by non-cytolytic selective spread of the virus and restricted infection, in this way escaping immune surveillance in the CNS. The CDV Fusion protein appears to play an important role in CDV persistence. Similarities between canine distemper and rodent models of virus-induced demyelination are discussed.

Animals↗
PubMed1996

Up-regulation of major histocompatibility complex class II antigen expression in the central nervous system of dogs with spontaneous canine distemper virus encephalitis.

Major histocompatibility complex class II (MHC II) and canine distemper virus (CDV) antigen expression were compared by immunohistochemistry in the cerebellar white matter of ten dogs with naturally occurring canine distemper encephalitis. In addition, infiltrating mononuclear cells were characterized by employing poly- and monoclonal antibodies directed against human CD3, canine MHC II, CD5, B cell antigen and CDV-specific nucleoprotein. Positive antigen-antibody reaction was visualized by the avidin-biotin-peroxidase complex method on frozen sections. Histologically, neuropathological changes were categorized into acute, subacute, and chronic. In control brains, MHC II expression was weak and predominantly detected on resident microglia of the white matter and on endothelial, perivascular and intravascular cells. In CDV antigen-positive brains, MHC II was mainly found on microglia and to a lesser extent on endothelial, meningeal, choroid plexus epithelial, ependymal and intravascular cells. In addition, virtually all of the perivascular cells expressed MHC II antigen. CDV antigen was demonstrated most frequently in astrocytes. Of the perivascular lymphocytes, the majority were CD3-positive cells, followed by B cells. Only a small proportion of perivascular cells expressed the CD5 antigen. In addition, B cells and CD3 and CD5 antigen-positive cells were found occasionally in subacute and frequently in chronic demyelinating plaques. In acute encephalitis, CDV antigen exhibited a multifocal or diffuse distribution, and MHC II was moderately up-regulated throughout the white matter and accentuated in CDV antigen-positive plaques. In subacute encephalitis, moderate multifocal CDV antigen and moderate to strong diffuse MHC II-specific staining, especially prominent in CDV antigen-positive lesions, were observed. In chronic encephalitis, CDV antigen expression was restricted to single astrocytes at the edge of the lesions or was absent, while MHC II expression, especially prominent on microglia, was strongly up-regulated throughout the white matter, most pronounced in demyelinated plaques. In summary, in acute and subacute lesions without perivascular cuffs, MHC II expression correlated with the presence of CDV antigen. In contrast, in chronic lesions, MHC II expression on microglial cells was the most prominent despite a few CDV antigen-positive astrocytes, indicating that nonviral antigens may play an important role as triggering molecules for the process of demyelination.

Animals↗
PubMed2002

Demyelination precedes oligodendrocyte loss in canine distemper virus-induced encephalitis.

Canine distemper virus (CDV), a negative-stranded RNA morbillivirus, causes a persistent infection within the central nervous system resulting in a progressive, multifocal demyelinating disease. Demyelination is thought to be caused by a selective alteration of the myelin-producing oligodendrocytes. Metabolic impairment and morphological changes of the oligodendrocytes after CDV infection have previously been observed in vitro as well as in vivo. Until now it has been suggested that the oligodendrocytes completely disappear from CDV-induced demyelinating lesions. However, ultrastructural analysis in brain tissue sections and immunohistochemical examination of oligodendrocytes in dog brain cell cultures contradicted these observations. In this study oligodendrocytes from different categories of CDV-induced lesions were examined by in situ hybridization for proteolipid protein mRNA and--as a new tool employed on canine brain tissue sections--by immunohistochemistry using a monoclonal antibody against 2',3'-cyclic nucleotide 3'-phosphodiesterase, a myelin-specific enzyme. A down-regulation in the myelin gene transcription was detected already before demyelination occurred. However, a decrease in the number of oligodendrocytes was not observed until demyelination became evident. Although there was further depletion of oligodendrocytes in plaques with progressive demyelination, we demonstrated for the first time that these cells were still present in a significant amount even in chronic, completely demyelinated distemper lesions.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed2003

Sequence analysis of the fragment of the phosphoprotein gene of Polish distemper virus isolates.

The nucleotide sequence analysis of the 429 bp fragment of the P gene of 11 Polish field isolates of Canine distemper virus (CDV), reference strains and other virus isolates available in the GenBank was the aim of the studies. High homology between all dog strains from east-southern region of Poland and reference strains of CDV was demonstrated. It was estimated as 97-100 % for CDV-OND; 96.7-99.8 % for CDV-Rock; 96.7-99.8 % for CDV-LED and 96.3-97.9 % for A75-17. The 100 % homology of the nucleotide sequence was observed between CDV Pulawy 92, CDV Pulawy 97 and the reference CDV-OND. The homology between CDV-OND and viruses isolated from the mink and ferret was estimated as 97.7 % and 98.4 %, respectively. Virus strains isolated from blue foxes demonstrated the highest homology to CDV-OND - equal to 97.7 % for DV 79 and 99.5 % for DV 92. The fox isolate from 1992 had higher level of homology to dog isolates (96.5-99.5 %) than the strain isolated from the fox in 1979 (97.2-98.8 %). The phylogenetic tree has two main lineages representing two separated genetic groups: I containing PDV and II containing all distemper virus strains isolated from terrestrial carnivores. CDV strains isolated from dogs from Pulawy region between 1992-1998 and from the fox (DV 92) formed the separate lineage containing also reference strains. They differed from the native isolates from the mink and ferret as well as from Japanese strains of CDV.

Amino Acid Sequence↗
PubMed1984

Canine distemper encephalomyelitis: variation with virus strain.

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.

Animals↗
PubMed1985

Canine distemper virus does not infect oligodendrocytes in vitro.

Dissociated canine brain cell cultures were infected with virulent canine distemper virus (CDV). Double immunofluorescent labelling was done to simultaneously demonstrate viral antigen and specific glial cell markers. Virus containing oligodendrocytes were not found at any stage of the infection. A certain proportion of the infected cells were shown to be astrocytes. It was concluded that CDV has no obvious tropism for oligodendrocytes which could explain the mechanism of demyelination in distemper in vivo.

Animals↗
PubMed1987

Establishment of central nervous system infection by canine distemper virus: breach of the blood-brain barrier and facilitation by antiviral antibody.

Morphologic, immunologic and virologic data implicating antiviral antibody in promoting entry of canine distemper virus (CDV) into brain and reticuloendothelial tissues are reviewed. Infection of central nervous system (CNS) endothelium precedes invasion of virus-positive and -negative leukocytes into Virchow-Robin spaces and central nervous system (CNS) parenchyma by 1-3 days. Platelets are implicated in initiation of endothelial infection in that: CDV-infected dogs are thrombocytopenic; platelets from CDV-infected dogs contain IgG-virus complexes on their plasma membranes; platelet microthrombi were observed adjacent to foci of endothelial infection, and; CDV-susceptible ferrets rendered thrombocytopenic by antiplatelet antibody exhibit delayed viral entry into CNS tissues. Renal glomerular-bound IgG, IgM and occasionally CDV antigen were demonstrated in CDV-infected dogs by immunocytochemical techniques. Distemper-infected dogs with inherited C3 deficiency exhibited enhanced renal glomerular disease associated chiefly with deposition of IgM in mesengial regions vs. their homozygous normal CDV-infected littermates. Direct infusion of virus-positive leukocytes, plasma and platelets into the CNS capillary bed via the right carotid artery should establish the primacy of each in the initiation of CNS vascular endothelial infection by CDV.

Animals↗
PubMed1986

Studies on the intrathecal humoral immune response in canine distemper encephalitis.

Albumin and IgG were quantitated in paired cerebrospinal fluid (CSF) and serum samples from dogs with demyelinating canine distemper virus (CDV) infection by means of rocket immunoelectrophoresis. The IgG index as indicator for intrathecal immunoglobulin synthesis was normal in animals with non-inflammatory demyelinating lesions and elevated in dogs with inflammatory myelin lesions. Specific antibodies against CDV and myelin were quantitated in CSF and serum from 8 dogs with an elevated IgG index. Eight of these dogs had significant amounts of antimyelin antibody and 4 dogs had neutralizing anti-CDV antibody in the CSF. Whereas the pathogenetic significance of antimyelin antibodies remains uncertain, the intrathecal antiviral immune response provides a plausible explanation for immunopathologic destruction of myelin in distemper.

Albumins↗
PubMed1988

Hyperinsulinemia induced by canine distemper virus infection of mice and its correlation with the appearance of obesity.

1. Weanling Swiss mice surviving an acute infection with canine distemper virus were persistently infected. Among these mice, up to 30% had hyperinsulinemia and this was followed by an obesity syndrome. 2. Analysis of the lipid composition of various organs revealed that compared to control animals, the obese had an accumulation of triglycerides in both liver and adipose tissue. 3. Studies on the lipid metabolism using a number of radioactive lipid precursors showed a specific accumulation of the triglycerides of the obese animals. 4. A decrease of lipogenesis was observed in white adipose tissue of obese mice. Glycogenesis and serum glucose levels were unaffected during obesity. 5. The model of canine distemper virus-induced obesity is compared with other experimental models.

Adipose Tissue↗
PubMed2004

Microglial cell activation in demyelinating canine distemper lesions.

Microglia cells are the principal immune effector elements of the brain responding to any pathological event. To elucidate the possible role of microglia in initial non-inflammatory demyelination in canine distemper virus (CDV) infection, microglia from experimentally CDV infected dogs were isolated ex vivo by density gradient centrifugation and characterized immunophenotypically and functionally using flow cytometry. Results from dogs with demyelinating lesions were compared to results from recovered dogs and two healthy controls. CDV antigen could be detected in microglia of dogs with histopathologically confirmed demyelination. Microglia of these dogs showed marked upregulation of the surface molecules CD18, CD11b, CD11c, CD1c, MHC class I and MHC class II and a tendency for increased expression intensity of ICAM-1 (CD54), B7-1 (CD80), B7-2 (CD86), whereas no increased expression was found for CD44 and CD45. Functionally, microglia exhibited distinctly enhanced phagocytosis and generation of reactive oxygen species (ROS). It was concluded that in CDV infection, there is a clear association between microglial activation and demyelination. This strongly suggests that microglia contribute to acute myelin destruction in distemper.

Animals↗
PubMed2004

Effective primary isolation of wild-type canine distemper virus in MDCK, MV1 Lu and Vero cells without nucleotide sequence changes within the entire haemagglutinin protein gene and in subgenomic sections of the fusion and phospho protein genes.

Canine distemper virus (CDV) is an important pathogen of many carnivores. We are developing a field-based model of morbillivirus virulence and pathogenesis through a study of distemper in naturally infected free-ranging raccoons. The isolation of CDV from raccoon tissues is essential for this work. CDV has often been isolated from animals only after co-cultivation of infected tissues with peripheral blood mononuclear cells derived from specific pathogen-free dogs or similar methods. We explored the utility and consequences of a simpler and cheaper alternative: CDV isolation in Vero, MDCK, and MV1 Lu cells. Virus growth was detected first in MDCK cells, whereas viral cytopathic effects were most obvious in Vero cells. CDV growth in MV1 Lu cells was relatively protracted and occurred without the formation of cytopathic effects. In primary CDV isolates, the entire nucleotide sequence of the receptor binding haemagglutinin (H) gene, and subgenomic fusion (F) and phospho (P) protein gene sequences corresponding to nt 5399-5733 and 2132-2563 of CDV reference strain Onderstepoort, respectively, were identical to those in matched infected tissues. Virus isolation confirmed the presence of CDV in instances where RT-PCR failed to detect CDV in infected tissues. Different viral phenotypes and genotypes were detected. The conservation of H gene sequences in primary CDV isolates suggests that MDCK, MV1 Lu, and Vero cells express proper receptors for wild-type CDV.

Amino Acid Sequence↗
PubMed1995

Immunohistochemical analysis of the lymphoid organs of dogs naturally infected with canine distemper virus.

The pathogenesis of acute canine distemper in three naturally infected dogs was investigated. The lymphoid organs showed atrophy without secondary follicles. The distribution of canine distemper virus (CDV) antigens was examined immunohistochemically with monoclonal antibodies specific for canine Thy-1, immunoglobulin (Ig) M, CD4, CD8, CD21 and CD45RB, and anti-measles virus nucleocapsid protein serum. The viral antigens were located in the T-cell-dependent areas and in the follicles of lymphoid organs; they were observed mainly in the Thy-1, or CD4-positive cells, but also in the CD8-, CD21-, or IgM-positive cells. The results indicated that Thy-1-positive and CD4-positive T cells serve as major target cells for CDV during the acute stage of infection.

Animals↗
PubMed1991

Viral expression in experimental canine distemper demyelinating encephalitis.

We have characterized the relationship between the expression of canine distemper virus (CDV) and demyelinating lesions in the white matter of the cerebellum of experimentally infected dogs. In animals which had demyelinating lesions, CDV proteins (N, P, F and H) were expressed and infectious virus could be recovered from brain tissue. Viral proteins (N, P, F and H) were detected by monoclonal antibodies and immunocytochemistry within demyelinating lesions as well as in scattered glial cells in areas of the white matter which lacked detectable lesions. Many cell types, including astrocytes, neurons, ependymal cells, choroid plexus cells, meningeal cells and perivascular inflammatory cells were labelled for viral antigen. We conclude from our results that the mechanism of demyelination in canine distemper virus-induced encephalitis involves expression of viral gene products at the lesion site.

Animals↗
PubMed1997

Determinants of persistence in canine distemper viruses.

Viral persistence in the central nervous system is the driving force behind the chronic progressive disease caused by natural canine distemper virus (CDV) infection in dogs. Persistence of CDV is associated with non-cytolytic spread and impaired viral budding. Since budding is to a large extend dependent on the nucleocapsid-(N) and matrixproteins (M) of the virus, we analyzed the nucleotide- and deduced amino acid sequences of the corresponding genes of a spectrum of CDV strains, that differ with respect to virulence and persistence in vivo and in vitro. The wild type CDV (A75/17), which is capable of causing a persistent infection in vivo was compared to two tissue culture adapted CDV strains (passaged A75/17-CDV and Rockborn-CDV), which CDV strains, that differ with respect to virulence and persistence in vivo and in vitro. The wild type CDV (A75/17), which is capable of causing a persistent infection in vivo was compared to two tissue culture adapted CDV strains (passaged A75/17-CDV and Rockborn-CDV), which retain a residual virulence and the capacity to spontaneously persist in vitro. A modified distemper virus (Snyder Hill-CDV), which is neurovirulent but not capable of causing a persistent infection in vivo, and an avianized virus (Onderstepoort-CDV) which is completely apathogenic and spreads by budding in cell cultures were also examined. Differences were found in the C-terminal of the nucleocapsid protein, which--comparing the two extremes of the spectrum (wild A75/17-CDV and OP-CDV)--lead to changes of the predicted protein structure. Such changes could affect the budding process and thus play a role in persistence. Marked changes in the M-gene were found in its non-coding region: the nucleotide sequences of the SH-CDV and OP-CDV differed considerably from the other three strains. Moreover, an additional second open reading frame was detected in the 'non-coding' region of the M gene in the wild A75-CDV, the two tissue culture adapted CDV strains and SH-CDV, but not in OP-CDV. The presence of this additional open reading frame correlated with the ability to cause a spontaneous persistent infection in vitro. Our findings support the notion that both N- and M-genes of CDV harbor determinants of viral persistence.

Amino Acid Sequence↗
PubMed1999

Restricted virus protein translation in canine distemper virus inclusion body polioencephalitis.

In this study, inclusion body polioencephalitis, an uncommon form of canine distemper virus (CDV)-induced encephalitis, was investigated for viral protein and mRNA expression by immunohistochemistry (IH) and in situ hybridization and, in addition, infiltrating cells were characterized by IH. Lesions were predominantly found in the grey matter of the brain stem and the immune response, dominated by T cells, was associated with a strong MHC II upregulation. Abundant expression of all viral protein mRNAs and reduced or lacking protein translation, especially of the matrix protein were the most important findings, indicating that restricted virus infection in the grey matter might represent a mechanism for viral persistence in distemper polioencephalitis.

Animals↗
PubMed2001

Comparison of immunoperoxidase plaque staining and neutralizing tests for canine distemper virus.

The use of immunoperoxidase plaque staining (IP) in the antibody test for canine distemper virus (CDV) and its diagnostic value were investigated. Antibody titres by the IP test and neutralizing test (NT) against CDV were compared in 114 specific pathogen-free (SPF) dogs, including 84 CDV-vaccinated and 30 unimmunized dogs. All of the unimmunized dogs, which had negative NT titres, also showed negative IP titres, and all of the CDV-vaccinated dogs, which had positive NT titres, showed positive IP titres. Furthermore, the IP titres showed similar changes with time after vaccination to the NT titres in five CDV-vaccinated SPF dogs. These findings indicate that the IP test has similar specificity to the NT. Next, the IP and NT titres were compared in 190 clinically suspected cases of canine distemper (CD), including 107 dogs with neurological signs and 83 dogs without neurological signs, and also in 50 clinically healthy dogs. Among the suspected cases of CD, of 46 dogs with neurological signs and 29 dogs without neurological signs, and which had negative NT titres, 33 (72%) and 19 (66%), respectively, showed positive IP titres. Many suspected cases of CD showed a high IP titre despite a low NT titre. In contrast, among healthy dogs, none of 9 NT-negative dogs showed positive IP titres. The difference in the IP and NT titres (log10) [reciprocal of IP titre] - log10) [reciprocal of NT titre]) was measured to investigate the agreement between IP test and NT. The differences were 1.488 +/- 0.867, 1.245 +/- 0.833, 0.595 +/- 0.351 and 0.594 +/- 0.372, respectively, in the suspected cases of CD with neurological signs, the suspected cases of CD without neurological signs, the healthy dogs and the SPF dogs. The differences in the suspected cases of CD were significantly high compared to those for the SPF dogs (p < 0.001). Furthermore, in 8 dogs diagnosed as cases of CD from their paired sera, whose initial sera showed a markedly low NT titre compared to the IP titre, 5 dogs without neurological signs developed neurological signs later. These findings suggest that the IP test can detect CD during its early phases and in dogs with low antibody levels, undetectable by NT, and so would be useful for serological diagnosis.

Animals↗
PubMedDate not supplied

Canine distemper in a genet (Gennetta gennetta), associated with endogenous lipid pneumonia.

This report describes the histological and immunohistochemical findings in an adult male genet (Gennetta gennetta) which died a few hours after being found lying in a forest in Lugo (north-western Spain). Subpleural, yellowish, firm foci were found in the lung. Histopathological examination confirmed a diagnosis of endogenous lipid pneumonia. Microscopical lesions that gave rise to a suspicion of canine distemper virus (CDV) infection included lymphoid depletion, non-suppurative encephalitis and demyelination in the central nervous system, and the presence of inclusion bodies in renal tubules. Immunohistochemical examination was performed with the streptavidin-biotin-complex method and a monoclonal antibody against the nucleocapsid protein (NP) of CDV. Antigen was detected in epithelial, nervous and lymphoid cells in several organs. This would appear to be the first report of distemper-like infection in a genet.

Animals↗
PubMed2002

Distribution of 3beta-hydroxysteroid dehydrogenase in the cerebellum in canine distemper virus infection.

The cerebella of eight dogs naturally infected with canine distemper virus (CDV) and two normal dogs were examined immunohistochemically for glial fibrillary acidic protein (GFAP) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD). The clinical diagnosis of canine distemper was confirmed histopathologically and by the immunohistochemical demonstration of CDV antigen. In all dogs (healthy and infected), the Purkinje cells of the cerebellum were immunolabelled for 3beta-HSD activity. In infected dogs, 3beta-HSD labelling was prominent in astrocytes (particularly in areas of astrocytosis) whereas in healthy dogs such immunolabelling was weak. Double immunolabelling demonstrated that all GFAP-positive cells (especially in demyelinating areas) were also positive for 3beta-HSD. The results suggest that 3beta-HSD expression by astrocytes is associated with demyelination in CDV infection.

3-Hydroxysteroid Dehydrogenases↗