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PubMed1990

Occurrence of a canine distemper-like disease in aquarium seals.

Outbreaks of a canine distemper-like acute disease brought high mortalities to seal populations in north-west Europe and Lake Baikal from late 1987 to 1988. During these outbreaks three seals which were introduced from Lake Baikal to an aquarium in Japan developed a distemper-like disease and other seals raised in the same room were similarly affected. Clinical signs of dead seals were anorexia, diphasic fever, dyspnea, and neuromuscular tics. Characteristic microscopic lesions of acute interstitial pneumonia seen in the lung were accompanied with hyperplasia and syncytial giant cell formation of type II pneumocytes. Eosinophilic intranuclear and cytoplasmic inclusion bodies were present in bronchial epithelial cells, type II pneumocytes, epithelial cells of bile ducts and interlobular ducts of pancreas, transitional epithelium of renal pelvis, and reticular cells of lymph nodes. Ultrastructure of inclusion bodies was similar to that seen in cells infected with morbilliviruses. Serum samples from recovered seals had virus-neutralization antibodies against canine distemper virus. The present cases were the first report of morbillivirus infection of aquarium seals in Japan.

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PubMedDate not supplied

Toxoplasma gondii genotyping in a dog co-infected with distemper virus and ehrlichiosis rickettsia.

This paper reports a toxoplasmosis, ehrlichiosis and distemper co-infection in a dog with an exuberant neuropathological clinical picture. Primary involvement was discussed based on information collected in the analysis of the clinical case, such as neurological impairment, epidemiological data, poor immunoprophylactic scheme of the dog affected and the role of these diseases on immunosuppression. Canine distemper and ehrlichiosis were diagnosed based on epidemiologic data, clinical signs, hematological and cytological evaluation. Toxoplasma gondii was isolated and genetically characterized as Type I using restriction analysis (RFLP) with SAG-2 genes. Immunosuppression features of both dogs and human beings are discussed, as well as implications on animal and public health. This is the first report on toxoplasmosis, ehrlichiosis and distemper co-infection in a dog in Brazil, associated with genotyping determination of the T. gondii strain involved.

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PubMed2000

Canine distemper in terrestrial carnivores: a review.

Canine distemper virus is a member of the genus Morbillivirus in the family Paramyxoviridae. Canine distemper has been recorded in domestic dogs for centuries. It is now recognized as a worldwide problem of carnivores and has the second highest fatality rate of any infectious disease, after rabies, in domestic dogs. The importance of this disease in nondomestic animals has become evident with vaccine-induced infections in a variety of species and large-scale epidemics in captive and free-ranging felids. To date, canine distemper has been reported in all families of terrestrial carnivores: Canidae, Felidae, Hyaenidae, Mustelidae, Procyonidae, Ursidae, and Viverridae. Veterinarians, including those working with nondomestic carnivores, should be familiar with the clinical signs, diagnosis, and clinical management of this disease.

Animals↗
PubMed1976

Prophylactic, postinfectious and neonatal vaccination against canine distemper in mink.

Mink were vaccinated against canine distemper and challenged with the Snyder Hill strain of canine distemper virus. Protection was acquired if vaccination took place more than a few days before challenge. If vaccination took place even early during incubation mortality was higher than in the unvaccinated controls. Full protection of kits may be achieved even at an age of 16 to 20 days provided the kits had not passively acquired immunity from their mothers. Kits surviving distemper because of passively acquired immunity may not actively acquire immunity during infection and may die at a later exposure.

Animals↗
PubMed1975

The influence of experimental distemper infection on the distribution of lead in dogs previously subacutely intoxicated with lead carbonate.

The ability of experimental canine distemper infection to mobilize body lead deposits has been studied in Beagle dogs previously subacutely intoxicated with lead carbonate. For comparative purposes dogs were included which had either received lead only or distemper only or remained undosed. It was found that in dogs predosed with lead, distemper infection resulted in a significant increase in lead levels in blood and urine; this coincided with the peak body temperatures reached on the third day post infection. It was also found that the lead content of the liver and bone of these dogs was considerably higher than that of dogs receiving lead alone; at the same time bone phosphorus showed a marked decrease while bone calcium values remained similar to undosed controls.

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PubMed1989

[Macrophages in central nervous canine distemper: friends or foes?].

Brain macrophages play an important role in the CNS. We review some biological aspects of brain macrophages in vivo and in vitro. The criteria and methods used for the identification of these cells are considered. They include some morphological features such as the use of histochemical and immunocytochemical techniques for internal and surface components. In the second part of this review, we describe the role of brain macrophages in canine distemper encephalitis as proposed earlier by us. Studies in cultured dog glial cells infected with canine distemper virus (CDV) have shown that brain macrophages stimulated by anti-CDV antibodies will release reactive oxygen species as measured by chemiluminescence. This response depends on the presence of viral antigens on the surfaces of infected cells and is mediated by the interaction of antigen-bound antibodies with Fc receptors on brain macrophages. These observations support the hypotheses that brain macrophages may contribute to the damage of the white matter observed in canine distemper encephalitis.

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PubMedDate not supplied

Canine distemper myoclonus and sleep: observation of a case.

Evolution of myoclonus was analysed electromyographically throughout quiet wakefulness, NREM sleep and REM sleep in a dog with canine distemper myoclonus. Compared with quiet wakefulness, the frequency of myoclonus was decreased and the intensity of discharges in individual myoclonic bursts was also lowered during NREM sleep. When NREM sleep shifted to REM sleep, neither of these parameters was noticeably altered. However, as REM sleep continued, the former was increased markedly and the latter was further attenuated. In general, violent motor activity was concurrent in the limbs, trunk and/or head. Thus, the increase in the frequency of myoclonus seemed to be similar in nature to the phasic event during REM sleep. This indicated that lower motoneurons producing myoclonic discharges responded well to supraspinal influences. In successive myoclonic bursts, a significant and consistent positive correlation existed between the silent period and the subsequent discharge period throughout the three different levels of consciousness, that is, the longer the silent period, the longer the subsequent episode of myoclonus. Therefore, this feature may be intrinsic to myoclonic firing of lower motoneurons in canine distemper myoclonus. These findings may support the idea that hyperexcitability of the lower motoneurons is primarily responsible for the genesis of canine distemper myoclonus.

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PubMed1980

Chronic canine distemper virus encephalitis in mature dogs.

Five dogs 2 to 8 years old with old dog encephalitis were compared to five other dogs, 4 to 8 1/2 years old, with prolonged multifocal demyelinating distemper encephalitis. The dogs with old dog encephalitis had a diffuse panencephalitis involving most areas of the central nervous system with relative sparing of the cerebellum. The clinical signs were related to the cortical and subcortical lesions. The other dogs had severe focal necrotizing lesions mostly in the cerebellum and in the vicinity of the fourth ventricle; clinical signs were related to brainstem and spinal cord lesions. Viral isolation attempts were unsuccessful in the dogs with old dog encephalitis. In two dogs with multifocal encephalitis, canine distemper virus was isolated in tissue culture. The differences in lesions, clinical signs and observations in vitro indicate differences in pathogenesis between old dog encephalitis and multifocal demyelinating distemper encephalitis although both diseases may be caused by the same agent.

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PubMed1993

Phocine distemper in harbor seals (Phoca vitulina) from Long Island, New York.

The first occurrence of phocine distemper (PD) disease in harbor seals (Phoca vitulina) from the United States is reported. Two seals stranded on Long Island, New York (USA) in February 1992 with clinical signs of respiratory distress, fever, and depression. Pneumonia and diffuse pulmonary congestion were the most significant post mortem findings. On histologic examination one seal had a diffuse broncho-interstitial pneumonia with formation of syncytia. The principal lesion in the second animal was nonsuppurative meningoencephalitis. Using immunoperoxidase staining, PD viral antigen was found in the cytoplasm of bronchiolar epithelium and cerebral cortex neurons. With a differential virus neutralization test, there were higher titers against phocine distemper virus (PDV) than against canine distemper virus. Thus, PDV is the most likely agent responsible for the observed lesions.

Animals↗
PubMed1990

Humoral immune responses in seals infected by phocine distemper virus.

Recently the isolation and characterisation of a morbillivirus which caused high mortality in common seals (Phoca vitulina) in 1988 have been reported. Because of the clinical and pathological similarity of the disease in seals to that of distemper in dogs, the name phocine distemper virus (PDV) has been proposed. There are marked differences in the virus-induced proteins of PDV compared to other morbilliviruses and the humoral immune response of moribund and dead seals to PDV was restricted to some of the internal antigens of PDV, similar to the response described earlier for canine distemper virus infection in dogs.

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PubMed1995

Studies on canine distemper virus persistence in the central nervous system.

Chronic progressive demyelination in canine distemper virus (CDV) infection is associated with persistence of the virus in the nervous system. We studied persistence by examining expression of CDV mRNA corresponding to all genes of the virus as well as genomic CDV RNA in brain sections of dogs with acute and chronic demyelinating disease. All virus mRNAs were expressed in acute demyelinating lesions in a way similar to that seen in lymphoid tissues, the primary replication site of CDV. Their distribution corresponded very well with immunohistochemical detection of virus protein. In contrast, much more CDV mRNA than virus protein was found in gray matter areas suggesting that translation of CDV can be impaired in nervous distemper. Virus protein and RNA were cleared from chronic inflammatory demyelinating lesions. mRNA corresponding to the distal genes (F; H; L) of CDV disappeared first in inflammatory lesions for technical reasons associated with the particular mode of transcription of morbilliviruses. CDV RNA and protein persisted in chronically ill dogs in other areas of the CNS in which inflammation had not occurred. Our results suggest that persistence of CDV is favored by non-cytolytic spread of the virus and restricted infection of certain cells with reduced viral protein expression. Both tend to delay immune recognition of the virus.

Animals↗
PubMed1993

Restricted expression of viral surface proteins in canine distemper encephalitis.

Sixteen dogs with naturally occurring acute and chronic canine distemper virus (CDV) encephalitis were examined immunohistochemically for the presence of the five major CDV-specific proteins in the central nervous system. Monoclonal antibodies (mAbs) directed against two, three, four and five epitopes of the nucleo- (N), phospho- (P), fusion (F), and hemagglutinin (H) protein, respectively, and a polyclonal monospecific antibody recognizing the matrix (M) protein were used. Both core proteins and their epitopes, three F protein epitopes and the M protein were demonstrated in all animals examined. A fourth F protein epitope was found only in 13 animals. The H-2 and H-3 epitope of the H protein were detected in 15, the H-1 and H-5 epitope in 14, and the H-4 epitope in 3 animals. All viral proteins were observed in the same types of brain cells including neurons and astrocytes. The N and P protein were demonstrated in nucleus, cytoplasm and cell processes, whereas M, H and F protein were observed in the cytoplasm only and rarely in cell processes. In addition, the M protein was detected occasionally in the nucleus of neurons and reactive astrocytes. Intralesional distribution of CDV-specific proteins varied between core and surface proteins. In acute and subacute lesions without associated inflammation, expression of the M, H and F protein was only slightly diminished compared to the N and P protein. However, plaques with severe inflammation were either devoid of viral antigen or exhibited N- and P protein-specific immunoreactivity exclusively at the periphery, whereas expression of surface proteins was severely reduced or absent. These results are suggestive of restricted synthesis of CDV envelope proteins in acute, and more prominent in chronic, distemper encephalitis.

Animals↗
PubMed1982

Immunological and pathological findings in demyelinating encephalitis associated with canine distemper virus infection.

Nine dogs with canine distemper encephalitis (CDE) were examined with immunological techniques including demonstration of antibodies against canine distemper virus (CDV) in the serum and against myelin basic protein (MBP) in serum and in CSF. Mitogen stimulation tests of lymphocytes were also done. The brains were examined pathologically and immunoglobulin and C3 were demonstrated in lesions by means of immunohistological techniques. Six dogs with acute CDE had none or low antibody levels against CDV or MBP, and there was no immunoglobulin in demyelinating lesions. Some of these dogs had depressed lymphocyte mitogen responses. Two dogs with chronic CDE showed recovery of lymphocyte mitogen responses. One of these had a significant antibody response against CDV and MBP in the serum. Both dogs with chronic CDE had very high antibody titers against MBP in the CSF and demyelinating lesions contained immunoglobulin. These results suggest that acute demyelination in CDE is probably due to some direct viral activity and that the progression of demyelination in chronic CDE is associated with a local immune response.

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PubMed1977

Observations on the distribution of canine distemper virus in the central nervous system of dogs with demyelinating encephalitis.

The distribution of canine distemper virus in the central nervous system was examined in 11 dogs with demyelinating encephalitis by the direct fluorescent antibody technique on paraffin sections of brain and spinal cord. In the grey matter there was a good correlation between the presence and severity of lesions and presence and amount of viral antigen. Large concentrations of virus were found in neurons and their processes. In most demyelinating lesions only small amounts of viral antigen were found, mostly located in astrocytes. The potential importance of the role of the astrocyte in demyelination in canine distemper virus infection is stressed.

Animals↗
PubMed1991

Canine distemper virus infection and encephalitis in javelinas (collared peccaries).

Canine distemper virus has been isolated in dog lymphocyte cultures from the brains of three javelinas that became moribund with signs of encephalitis. Canine distemper viral antigen was demonstrated predominantly in neurons and morbillivirus-like structures were seen by electron microscopy in brains of diseased animals. Serological studies suggest that CDV infection may be common in javelinas.

Animals↗
PubMed1991

Correlation between humoral immune responses and presence of virus in the CNS in dogs experimentally infected with canine distemper virus.

The role of the humoral immune response in clearance or prevention of canine distemper viral encephalitis of dogs infected with a virulent strain of canine distemper virus has been evaluated. Dogs that have demyelinating lesions, CDV proteins and infectious virus in their brains demonstrate an impaired humoral immune response. In dogs that recover from infection and contain no demyelinating lesions, viral proteins or infectious virus in the brain, antibodies to the internal proteins of CDV are observed early after infection. Later antibodies to primarily the H protein are detectable in sera of these dogs and the appearance of antibodies against the surface glycoprotein (H) correlates with the absence of lesions, CDV antigen and infectious virus in the brains of these dogs. Very late after infection immunoprecipitating antibody to all CDV antigens diminished rapidly so that at about ten weeks post infection antibodies that precipitate CDV antigens are barely detectable.

Animals↗
PubMed2003

Phase-dependent expression of matrix metalloproteinases and their inhibitors in demyelinating canine distemper encephalitis.

Matrix metalloproteinases (MMPs) are zinc- and calcium-dependent enzymes that cleave molecules of the extracellular matrix, and thus are able to open the blood-brain-barrier and affect myelin. Their inhibitors (TIMPs) are important candidates for the therapy of demyelinating diseases. To establish an immunohistochemical profile of MMP and TIMP expression in plaque variants in dogs with spontaneous demyelinating distemper encephalitis, paraffin-embedded cerebella were studied employing the avidin-biotin-peroxidase complex method with a panel of nine polyclonal (anti-MMP-1, -3, -7, -9, -12, -13, -14, -TIMP-1, and -2) and two monoclonal antibodies (anti-latent MMP-2, and -MMP-11). All MMPs and TIMPs were prominently up-regulated in acute and subacute non-inflammatory lesions, and double-labeling techniques showed that they were mainly expressed by astrocytes and brain macrophages/microglia. In subacute inflammatory and chronic plaques, a moderate to strong decrease of MMP and TIMP expression compared to acute lesions was observed. In these phases MMP-11, -12, and -13 were still moderately present. In addition to astro- and microglia, invading perivascular mononuclear cells were positive for MMPs and TIMPs. In summary, there seems to be a phase-dependent expression of MMPs and TIMPs in demyelinating canine distemper encephalitis, and an MMP-TIMP imbalance might account for the lesion progression in this disease.

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