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PubMed1980

Plasmalogenase and phospholipase A1, A2, and L1 activities in white matter in canine distemper virus-associated demyelinating encephalomyelitis.

Three weeks after inoculation of 24-day-old gnotobiotic dogs with Snyder-Hill canine distemper virus, white matter samples were taken from the primary predilection sites for canine distemper virus-associated demyelination. The plasmalogenase activity in extracts was nearly 6-fold greater than control values for a dog with extensive demyelination and was not detectable in tissue from a dog with non-demyelinating lesions. Acid and neutral phospholipases A1 and A2 were assayed in homogenates and extracts with phosphatidyl ethanolamine substrates. Phospholipase A2 activities at both pH 4.3 and pH 6.8 were less in the dog with severe demyelinating lesions than in dogs with less severe lesions. Phospholipase A1 activities were generally similar for all four dogs. The marked elevation of plasmalogenase activity in demyelinating tissue may be associated with a release from the plasmalogens of arachidonic acid which is converted to oxygenated metabolites that may then be responsible for the inflammation. Phospholipases acting on phosphatidyl ethanolamine do not seem to be involved in the pathogenesis of demyelination associated with canine distemper virus.

Animals↗

PubMed1992

Canine distemper virus-immune complexes induce bystander degeneration of oligodendrocytes.

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.

Animals↗

PubMed1980

Structural polypeptides of canine distemper virus.

The structural polypeptides of two strains of canine distemper virus and the Lec strain of measles virus were analysed by SDS-polyacrylamide-slab-gel electrophoresis. One strain of canine distemper virus derived from a live vaccine (Convac, Dumex), contained six major structural polypeptides with mol.wt. of 85, 78, 59, 43, 41 and 34 x 10(3). The 85K polypeptide was glycosylated. It was interpreted to be equivalent ot the 79K glycoprotein of the measles hemagglutinin. The second strain, a rapidly growing variant of the Onderstepoort strain of canine distemper virus characterized by extensive syncytium forming cytopathic effects in tissue culture, contained the 5, 43, 41 and 34K polypeptides, but the 85 and 78K polypeptides were not present in detectable amounts. The 43K polypeptide was identified as cellular actin by limited proteolysis. By use of monospecific rabbit hyperimmune sera against each of the major structural polypeptides of measles virus, the 59, 41 and 34K structural polypeptides could be identified as nucleocapsid protein (NP), fusion (F) polypeptide, and the membrane (M) polypeptide, respectively. In neutralization tests with rabbit hyperimmune sera against each of the two strains, this Onderstepoort strain, which contained reduced amounts of the hemagglutinin glycoprotein, gave higher neutralization titers than the vaccine strain.

Actins↗

PubMed1987

Demyelination in canine distemper encephalomyelitis: an ultrastructural analysis.

A morphological study of selected white matter lesions was carried out in three dogs with canine distemper encephalomyelitis. Two dogs had experimental infections while the third was a spontaneous case. Two stages were identified in the process of demyelination. The earliest evidence of myelin injury was a ballooning change in myelin sheaths involving single or multiple axons. This was followed by a progressive stripping of compact sheaths by the cytoplasmic fingers of phagocytic cells which infiltrated and removed myelin lamellae. Some axonal necrosis also accompanied these changes. Where demyelination occurred, canine distemper viral nucleocapsids were found in astrocytes, macrophages, ependymal cells and infiltrating lymphocytes. In contrast, oligodendrocytes were conspicuous by their apparent lack of infection. Thus it seems that myelin loss cannot be ascribed to oligodendrocyte infection. Perturbed astrocyte function following canine distemper viral infection may cause oedema of myelin sheaths, leading to ballooning and primary demyelination. Cells which phagocytosed myelin were mainly identified as microglial cells with lesser involvement by astrocytes. Rarely, oligodendrocytes also acted as macrophages. Myelin debris was engulfed in bulk or as small droplets into coated pits. Remyelination was present in established plaques although not in great abundance, perhaps due to the diminished oligodendrocyte numbers and a relative increase in immature forms of these cells. These observations are compared to similar changes observed in other demyelinating diseases of animals and man.

Animals↗

PubMed2000

Up-regulation of the hyaluronate receptor CD44 in canine distemper demyelinated plaques.

CD44 antigen (CD44), the principle cell surface receptor for hyaluronate, is up-regulated in the human demyelinating disease multiple sclerosis on fibrous astrocytes. As astrocytes are the main target cell of canine distemper virus (CDV), the consequences of a CDV infection on the CD44 expression and distribution in brains with spontaneous demyelinating canine distemper encephalitis (CDE) were of interest. Thirteen acute, 35 subacute, and 11 chronic plaques of nine dogs with immunohistologically confirmed CDE and brains of control dogs were included in the study. For light microscopy, 5-micron-thick serial sections were stained with H&E and incubated with monoclonal antibodies (mAbs) against CD44 and canine distemper virus nucleoprotein and polyclonal antibodies (pAbs) against glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP). For immunoelectron microscopy, 90-nm-thick sections were double stained with anti-GFAP and anti-CD44 mAbs to specify CD44-expressing structures. In controls, CD44 was diffusely distributed in the white matter and single meningeal cells exhibited a marginal expression of the antigen. In acute and more prominently in subacute demyelinating encephalitis, there was a plaque-associated up-regulation of CD44 which paralleled GFAP. In chronic demyelinating lesions, a reduction of CD44 associated with a loss of GFAP-positive astrocytes was noted. Additionally, in chronic plaques, CD44 was expressed on the cell membrane of perivascular mononuclear cells. Immunoelectron microscopically, in controls, CD44 was rarely demonstrated on astrocytic cell processes. In contrast, in brains with CDE CD44 was found on the cell membrane of broadened astrocytic cell processes. In summary, CD44 is up-regulated on astrocytes in the early phase of CDE and seems to represent a marker for the activation of immune cells in the late phase of the infection.

Acute Disease↗

PubMed1998

Oligodendroglial pathology in canine distemper.

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.

Animals↗

PubMed1980

Multiple sclerosis and canine distemper encephalitis--an epidemiological approach.

The evolution of the incidence of canine distemper encephalitis in dogs in some areas of Switzerland over the past 30 years was studied from the neuropathological records of the School of Veterinary Medicine at Berne and compared with the incidence of multiple sclerosis, as estimated from the clinical records of the Neurologic Hospital at the same University. Even considering incubation times of up to 10 years no epidemiological relationship was found between the diseases. Whereas canine distemper encephalitis has become a rare disease since the second half of the sixties, the multiple sclerosis rate has remained approximately the same. In view of these findings, a causal link between canine distemper infection in dogs and multiple sclerosis in man seems unlikely.

Animals↗

PubMed1981

A radioimmunoassay search for measles and distemper antigens in subacute sclerosing panencephalitis and multiple sclerosis brain tissues.

Solid-phase direct sandwich radioimmunoassays have been developed which will detect measles antigen in as little as 20 microgram of SSPE brain, measles antigen in 5 x 10(4) pfu/ml of measles virus, and canine distemper antigen in 5 x 10(5) pfu/ml of this virus. Using these assays, a search was carried out for measles and distemper antigens in CNS autopsy tissue from 3 multiple sclerosis (MS) patients. Even in 1000-fol higher concentrations of MS brain (20 mg), antigens of neither virus were detected. Additional studies were carried out using similar radioimmunoassays but employing IgG from 2 MS patients as probe against MS brain specimens, including IgG and acute plaque material from the same individual. However, no reaction between MS IgG and MS brain was detected. Thus no evidence was found for foreign antigen in the MS brain nor for autoantibody which reacted with brain tissue antigens. It is concluded that either measles or distemper are not present in acute MS lesions, or that they are present in such small amounts that their detection will require techniques even more sensitive than those used in the present study.

Animals↗

PubMed1991

Canine distemper viral antigens and antibodies in dogs with rheumatoid arthritis.

Dogs with canine rheumatoid arthritis had significantly elevated levels of antibodies to canine distemper virus. This increase was particularly seen in the synovial fluids, compared with paired sera, and was not found in dogs with infective arthropathies, osteoarthritis or in osteoarthritis secondary to rupture of the cranial cruciate ligament. Analysis of the immune complexes precipitated from synovial fluids showed immunoglobulins in all types of arthropathy. Western blotting analyses showed reactivity with anti-distemper antisera in immune complexes from dogs with rheumatoid arthritis, but not in immune complexes from dogs with other joint diseases. These results suggest that there are increased immune responses to distemper in canine arthritis and that these may be due to the presence of this paramyxovirus in affected joints. The implications for the role of a possible infectious agent in rheumatoid arthritis in the dog are considerable.

Animals↗

PubMed1993

Intestinal lesions in experimental phocine distemper: light microscopy, immunohistochemistry and electron microscopy.

The involvement of the intestinal mucosa and of the gut-associated lymphoid tissue in phocine distemper was studied in six severely diseased harbour seals 11 to 16 days after experimental infection. Five seals exhibited a mild or moderate enteritis in the small or large intestine. In all the seals, a moderate to severe depletion of submucosal lymphoid follicles was found. Likewise, antigen of phocine distemper virus (PDV) was demonstrated immunohistochemically in the intestinal wall of all the seals. Most antigen was found in the submucosal lymphoid follicles, followed by the crypt epithelium and follicle-associated epithelium (FAE). Ultrastructurally, intracytoplasmic tubular structures were detected in the FAE and interpreted as morbilliviral nucleocapsids. The results indicate a direct cytopathogenic effect of PDV on intestinal lymphoid and epithelial cells and suggest an important role of the intestinal tract in phocine distemper and, by analogy, in other morbillivirus infections as a regular site of virus replication, virus shedding and immunosuppression.

Animals↗

PubMed1996

Neural cells from dogs with spontaneous distemper encephalitis express class II major histocompatibility complex molecules.

Expression of class II major histocompatibility complex (MHC) molecules by non-immune cells (e.g., parenchymal cells) leads to the presentation of self-antigens, and may have a role in the pathogenesis of many diseases mediated by autoimmunity. Such diseases, characterized by demyelination of the central nervous system and expression of class II MHC molecules on neural cells, include multiple sclerosis, experimental allergic encephalitis and Theiler's murine encephalomyelitis virus infection. Canine distemper encephalitis probably does not have an autoimmune character, but it shares many similarities with the aforementioned diseases. For this reason, the expression of class II MHC molecules in the brains of dogs with canine distemper encephalitis was investigated immunohistochemically. The results presented here demonstrate that canine microglia and astrocytes "upregulate" class II MHC expression in cases of encephalitis associated with chronic canine distemper.

Animals↗

PubMed2000

Feline infectious pneumonia: a short literature review and a retrospective immunohistological study on the involvement of Chlamydia spp. and distemper virus.

A short literature review of feline infectious pneumonia, feline Chlamydia and Paramyxoviridae is presented. In a retrospective study (from 1987 to 1996) 245 cases of feline pneumonia or conjunctivitis/rhinitis were investigated: histological diagnoses and aetiologies were compared; all lungs were examined immunohistologically for the occurrence of chlamydia and of canine distemper virus (CDV), but neither pathogen could be demonstrated. The results confirm previous reports indicating that feline chlamydia is not a primarily pulmonary pathogen and that CDV is not a causative agent of pneumonia in cats as it is in large felids. The review provides a summary of the known causes and pathology of infectious pneumonia in cats (in order of frequency), although some remain aetiologically uncertain. It focuses on chlamydia and distemper virus - a recognized and as yet unknown cause of feline pneumonia. The role and especially the frequency of chlamydia as a cause of feline pneumonia are controversial but distemper virus, known to cause pneumonia in dogs and large felids, has not as yet been demonstrated in cats. The aims of the retrospective study were to determine the occurrence of chlamydia in 245 cases of feline pneumonia or conjunctivitis/rhinitis, and to investigate the presence of CDV in these lungs.

Animals↗

PubMed1979

Antigenic relationships between measles and canine distemper viruses: comparison of immune response in animals and humans to individual virus-specific polypeptides.

Precipitation with hyperimmune rabbit sera, sera from patients convalescing from measles, and sera from patients with subacute sclerosing panencephalitis, followed by electrophoresis, enabled antigenic relationships between the individual polypeptides of measles and canine distemper viruses to be examined. Virus isolates from patients with acute measles or subacute sclerosing panencephalitis showed no antigenic differences. With rabbit hyperimmune sera, antigenic crossreactivity was present between all polypeptides of measles and canine distemper viruses except H. The N polypeptides showed the highest degree of crossreactivity and were interpreted as group-specific antigens. Both convalescent measles sera and sera from subacute sclerosing panencephalitis showed high antibody titers to all measles polypeptides except L and M. However, these sera contained only low activities to the N and F1 polypeptides from canine distemper virus.

Animals↗

PubMed1987

Autologous and allogeneic antibody responses to canine distemper virus isolates from dogs with chronic neurological diseases.

We describe the antibody responses to three strains of canine distemper virus (CDV) isolated from dogs with chronic neurological disease in the Los Angeles area using the naturally occurring sera and cerebrospinal fluids (CSFs) of these animals as probes for comparison. CDV/CDE-2 was derived from a dog with chronic distemper encephalitis, and CDV/ODE-8 and CDV/ODE-10 were derived from dogs with old dog encephalitis. Sera and CSFs were used in autologous (same dog) and allogeneic (different dog) combinations to immune precipitate the [35S]-methionine-labelled H, P, NP, F1, and M polypeptides of the virus-infected cell cultures. The polypeptides were separated by SDS-PAGE and detected by fluorography. There was decreased recognition by the CSF and sera of the polypeptides of the viral isolates in several autologous as well as allogeneic combinations. It is concluded that the immune responses to the CDV strains are not identical, and it is likely that viral mutations occurred after the animals were infected. Some mutations may have contributed to the pathogenesis of distemper encephalitis in these animals and some may have occurred during subsequent passage of the viruses in cell culture. This may explain the decreased recognition of the polypeptides of the viral isolates by the CSF and sera.

Animals↗

PubMed1989

Morbillivirus infection among seals (Phoca vitulina) during the 1988 epidemic in the Bay of Heligoland. II. Serogological investigations reflecting a previous phocine distemper epidemic in a seal orphanage.

Of 57 seals hospitalized in the Norddeich Orphanage, 37 (65%) had died until 22nd of August, 1988, when the first collection of blood samples from the survivors commenced. All the sera including those obtained at a later date from the remaining animals had invariably higher neutralizing antibody titres against a phocine distemper virus (PDV) isolate than against canine distemper virus (CDV). The difference of mean titres was calculated to be more than 1.5 x log10 serum dilution. Peak titres demonstrated by a direct neutralization peroxidase-linked antibody (NPLA) assay reached 1/90,000. Attempts to isolate PDV in seal kidney cell cultures from heparinized blood samples collected from convalescent animals were not successful. From the increase in antibody titre following the last fatal case it was concluded that the devastating epidemic sweeping through the Norddeich Orphanage was primarily due to phocine distemper.

Animals↗

PubMed1992

Investigations on course and outcome of phocine distemper virus infection in harbour seals (Phoca vitulina) exposed to polychlorinated biphenyls. Virological and serological investigations.

The influence of polychlorinated biphenyls (PCBs) on phocine distemper virus (PDV) infections in harbour seals (Phoca vitulina) was studied. Six out of ten seals had been conditioned with a defined mixture of PCB-congeners for several weeks. Following exposure to the cell culture-propagated PDV isolate 2558/Han 88 the complete clinical picture of "1988 seal plague" was provoked in all ten seals inoculated. Four out of six PCB-conditioned seals and two out of four seals not loaded with PCBs succumbed to the infection within three weeks post inoculation. With regard to the clinical course, duration of cell-associated viremia, PDV-antigen distribution in tissues of fatally infected seals and the humoral immune response to PDV no differences between PCB-loaded and unloaded seals were recognized. Evidence was obtained that the pathogenesis of experimental PDV-infection in harbour seals shares some features with those of canine distemper in terrestrial carnivores. In contrast, however, to experimental distemper infection of gnotobiotic dogs prompt development of high titres of PDV-specific IgG did not correlate with recovery from infection.

Animals↗

PubMed1985

Cloning and characterization of DNA complementary to the canine distemper virus mRNA encoding matrix, phosphoprotein, and nucleocapsid protein.

Double-stranded cDNA synthesized from total polyadenylate-containing mRNA, extracted from monkey kidney cells infected with canine distemper virus (CDV), has been cloned into the PstI site of Escherichia coli plasmid pBR322. Clones containing canine distemper virus DNA were identified by hybridization to a canine distemper virus-specific, 32P-labeled cDNA. Four specific clones containing different classes of sequences have been identified. The cloned plasmids contain inserts of 800 (clone 44-80), 960 (clone 74-16), 1,700 (clone 364), and 950 (clone 40-9) base pairs. The sizes of the mRNA species complementary to these inserts are 1,500, 1,850, 1,850 and 2,500 nucleotides, respectively, as determined by the Northern technique. Three of the cloned DNA fragments were further identified as the reverse transcripts of the mRNA coding for the matrix, phosphoprotein, and nucleocapsid protein of CDV.

Base Sequence↗

PubMed1989

Antiviral antibodies stimulate production of reactive oxygen species in cultured canine brain cells infected with canine distemper virus.

Canine distemper is characterized mainly by respiratory, enteric, and nervous symptoms. Infection of the central nervous system results in demyelination, to which inflammation has been shown to contribute significantly. It has been proposed that macrophages play a major role as effector cells in this process. We report that cultured dog brain cells contain a population of macrophages capable of producing reactive oxygen species as measured by luminol-dependent chemiluminescence. In cultures infected with canine distemper virus, a burst of reactive oxygen is triggered by antiviral antibody. This response depends on the presence of viral antigens on the surfaces of infected cells and is mediated by the interaction of antigen-bound antibody with Fc receptors on the macrophages. Since there is no evidence in vitro or in vivo that oligodendrocytes, the cells forming myelin, are infected, our observation supports the hypothesis that "innocent bystander killing" is important in demyelination caused by canine distemper virus. Reactive oxygen species released from macrophages may contribute to destruction of myelin.

Animals↗