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PubMed2003

Apoptosis in the cerebellum of dogs with distemper.

Canine distemper virus (CDV) may induce multifocal demyelination in the central nervous system of infected dogs. The pathogenesis of this process is not clear. The present work identifies the presence of apoptotic cells in white and grey matter of dogs'cerebellum, naturally infected with CDV. Fifteen dogs with clinical signs of canine distemper that tested positive for CDV nucleoprotein were used. Brain specimens were processed and embedded in paraffin. Sections 5 microm thick were stained with hematoxylin-eosin and Shorr. Other sections were submitted to TUNEL reaction and to immunohistochemistry for CDV nucleoprotein detection. Acute and chronic demyelinated plaques were observed in the white matter, while apoptosis occurred particularly in the granular layer of grey matter. Apoptosis seems to play an important role in the pathogenesis of canine distemper demyelination.

Animals↗
PubMedDate not supplied

Glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes in dogs infected with canine distemper virus.

An experiment based on astrocyte immunoreactivity to glial fibrillary acidic protein (GFAP) was designed to determine whether the astrocyte response in canine distemper encephalitis (CDE) was associated with the age of the animal, type of lesion and the cerebellar region affected. Four histopathological types of CDE lesion were examined, namely acute (11 dogs), acute with necrosis (four dogs), subacute (22 dogs) and chronic (six dogs). The animals were divided into three age groups, namely, 0-2 years (27 dogs), 2.1-4 years (12 dogs), and 4.1-12 years (four dogs). Three different cerebellar regions were evaluated. Cerebellar sections from three healthy dogs were used for control purposes. The highest number of astrocytes occurred in the cerebellar white matter and in dogs with acute distemper encephalopathy. In animals with subacute distemper encephalitis, the numbers of astrocytes appeared to increase with age, but the opposite effect occurred in dogs with acute or chronic encephalitis; age appeared not to influence the astrocyte numbers in dogs suffering from acute encephalitis with necrosis.

Acute Disease↗
PubMed1993

Brain structures selectively targeted by canine distemper virus in a mouse model infection.

Paramyxoviruses such as measles virus or canine distemper virus are etiological agents for acute and chronic encephalitis (measles inclusion body encephalitis, subacute sclerosing panencephalitis and chronic distemper encephalitis or old dog encephalitis). The mechanisms by which viral injury leads to neurological diseases have not yet been fully elucidated. We have developed an experimental model in mice in order to analyze the spatial and temporal distribution of canine distemper virus in the central nervous system. Cerebral target structures for viral replication were examined for the presence of viral material (proteins and mRNA) during the two stages of the biphasic disease. During the acute stage of infection all target areas could be identified by day 6 with a similar anatomical distribution in all the animals examined, which were either intracranially or intracerebroventricularly infected. Viral mRNA and proteins were selectively localized in certain brain structures such as the thalamus, hypothalamus, substantia nigra (pars compacta), locus ceruleus and raphe nuclei (dorsalis and centralis), and limbic system (hippocampus, septum, entorhinal and cingulate cortex, amygdala). The virus was apparently unable to replicate in cerebellum, striatum, a large part of cortex, or endothelial cells. During the subacute disease, viral material was no longer detectable except in a few structures such as hypothalamus up to 4-6 weeks after inoculation. After this time, all target structures were devoid of any labeling in spite of the occurrence of pathology (obesity, paralysis) during this viral quiescent phase. These results suggest that after the initial viral exposure, expression of viral genes in defined structures might disrupt central homeostasis and finally may lead to neurological or neuroendocrine diseases, even in the absence of the hallmarks of the virus.

Amygdala↗
PubMed1999

Rapid and sensitive detection of immunoglobulin M (IgM) and IgG antibodies against canine distemper virus by a new recombinant nucleocapsid protein-based enzyme-linked immunosorbent assay.

Canine distemper morbillivirus (CDV) infection causes a frequently fatal systemic disease in a broad range of carnivore species, including domestic dogs. In CDV infection, classical serology provides data of diagnostic and prognostic values (kinetics of seroconversion) and is also used to predict the optimal vaccination age of pups. Routine CDV serology is still based on time- and cost-intensive virus neutralization assays (V-NA). Here, we describe a new capture-sandwich enzyme-linked immunosorbent assay (ELISA) that uses recombinant baculovirus-expressed nucleocapsid (N) protein of a recent CDV wild-type isolate (2544/Han95) for the detection of CDV-specific antibodies in canine sera. Recombinant antigen was produced with high efficacy in Heliothis virescens larvae. The capture-sandwich ELISA enabled a clear-cut qualitative evaluation of the CDV-specific immunoglobulin G (IgG) and IgM serostatuses of 196 and 35 dog sera, respectively. Inter-rater agreement analysis (kappa = 0.988) indicated that the ELISA can be used unrestrictedly as a substitute for the V-NA for the qualitative determination of CDV-specific IgG serostatus. In an attempt to semiquantify N-specific antibodies, a one-step-dilution (alpha method) IgG-specific ELISA was implemented. Alpha values of >/=50% showed very good inter-rater agreement (kappa = 0.968) with V-NA titers of >/=1/100 50% neutralizing dose (ND50) as measured against the central European CDV wild-type isolate 2544/Han95 in canine sera originating from northern Germany. An ND50 titer of 1/100 is considered a threshold, and titers of >/=1/100 indicate a resilient, protective immunity. CDV N-specific antibodies of the IgM class were detected by the newly developed ELISA in 9 of 15 sera obtained from dogs with symptoms of acute distemper. In leucocytes of 5 of the 15 dogs (all of which were also IgM positive) CDV RNA was detected by reverse transcription (RT)-PCR. The recombinant capture-sandwich ELISA detecting N-specific antibodies of the IgG class provided superior sensitivity and specificity and thus represents a rapid and cost-effective alternative to classical CDV V-NA. By detection of specific IgM antibodies, the ELISA will be complementary to RT-PCR and V-NA in the diagnosis of acute distemper infections.

Animals↗
PubMed1996

Canine distemper virus in Lake Baikal seals (Phoca sibirica).

The virus epizootic which resulted in significant mortality in Siberian seals (Phoca sibirica) in Lake Baikal during 1987/88 was caused by canine distemper virus. Sequence analysis of the virus glycoprotein genes revealed that it was most closely related to recent European field isolates of canine distemper virus. This paper presents evidence that the same virus continued to circulate in seals in Lake Baikal after the initial epizootic. Three out of 45 brain tissue samples collected from seals culled in the spring of 1992 were positive for canine distemper virus-specific nucleic acid by the reverse transcription/polymerase chain reaction and the sequences were closely related to that of the original virus isolated in 1988.

Animals↗
PubMed2004

Distemper virus as a cause of central nervous disease and death in badgers (Meles meles) in Denmark.

During the summer of 2002 a distemper-like disease was observed in the free-ranging badger population in Denmark. It was characterised by grand seizures, abnormal behaviour and death; the badgers all had severe chronic pneumonia and some had non-suppurative encephalomyelitis. In this study, eight of the affected badgers were examined by gross pathological, histological, immunohistological, bacteriological, parasitological and virological methods, and were diagnosed with distemper; canine distemper virus was identified.

Animals↗
PubMed1981

Lesions of the enamel organ of developing dog teeth following experimental inoculation of gnotobiotic puppies with canine distemper virus.

Ten 7-day-old gnotobiotic Beagle puppies were inoculated intraperitoneally with virulent canine distemper virus (R252-CDV). The dogs were killed and perfused with paraformaldehyde/glutaraldehyde from eight to 36 days after inoculation. The developing teeth of the mandibles were examined by light microscopy, and the teeth from three dogs were examined by electron microscopy. Necrosis of individual cells in the stratum intermedium of the developing tooth was the first change, detectable at day 9 post-inoculation. At day 16 post-inoculation, there was disorganization of the ameloblasts. In the stratum intermedium, multinucleate giant cells and large eosinophilic cytoplasmic viral inclusions were prominent. Ultrastructurally, these inclusions consisted of clusters of tubular aggregates typical of canine distemper virus nucleocapsids. At 28 to 36 days post-inoculation, the changes were seen in the reduced enamel epithelium. Multinucleate cells were seen, but no inclusions. Some necrotic cells were seen. In these teeth, ameloblastic cells of the root were morphologically normal. Our results suggest that distemper virus affects developing teeth by direct infection of the enamel organ.

Animals↗
PubMed2006

Interstitial pneumonia in neonatal canine pups with evidence of canine distemper virus infection.

Four dead canine pups (5-12 days old) from 3 litters in Douglas County of north central Colorado were submitted to the Colorado State University Diagnostic Laboratory for necropsy. Pups were originally presented to the referring clinics for respiratory tract illness, with or without diarrhea. At necropsy, the lungs from all pups had similar lesions, including random foci of hemorrhage and failure to collapse on opening of the thoracic cavity. The lungs were histologically characterized by subacute interstitial pneumonia, with alveolar septa expanded by a histiocyte-rich infiltrate with a few lymphocytes and neutrophils. The alveolar spaces were filled with moderate amounts of proteinaceous fluid, foamy macrophages, and a few neutrophils. Lungs from 3 of the 4 pups were test positive for canine distemper virus (CDV) by use of reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Immunohistochemically stained lungs, including those from the pup that were CDV negative, by use of RT-PCR analysis, were test positive for CDV antigen in bronchial and bronchiolar epithelial cells and in a few alveolar macrophages. Central nervous system lesions were not observed in any of the 4 pups. These cases represent an unusual presentation of canine distemper in neonatal pups marked by respiratory tract lesions without central nervous system involvement. Canine distemper should be considered in the differential diagnosis of neonatal canine respiratory tract illness.

Animals↗
PubMed1994

Canine distemper epizootic in lions, tigers, and leopards in North America.

Canine distemper virus (CDV) infection occurred in captive leopards (Panthera pardus), tigers (Panthera tigris), lions (Panthera leo), and a jaguar (Panthera onca) in 1991 and 1992. An epizootic affected all 4 types of cats at the Wildlife Waystation, San Fernando, California, with 17 mortalities. CDV-infected raccoons were thought to be the source of infection in these cats. Two black leopards died at the Naibi Zoo, Coal Valley, Illinois, and 2 tigers died at the Shambala Preserve, Acton, California. Initial clinical signs were anorexia with gastrointestinal and/or respiratory disease followed by seizures. Canine distemper virus was isolated from 3 leopards, 3 tigers, and 3 lions that died or were euthanized when moribund. Monoclonal antibody testing identified the virus isolates as CDV. Gross and histopathologic findings were similar to those found in canids with distemper with a few exceptions. There were fewer lesions in the brain, and there was a pronounced type 2 cell proliferation in the lung, with inclusion bodies and CDV antigen demonstrated by immunohistology. Neutralizing antibody to CDV was found in high titers in serum from most animals but was absent or was found only in low titers in some cats that succumbed after CDV infection. There was a marked difference in neutralizing antibody titers when tests were done with different strains of CDV.

Animals↗
PubMed2006

The 2000 canine distemper epidemic in Caspian seals (Phoca caspica): pathology and analysis of contributory factors.

More than 10,000 Caspian seals (Phoca caspica) were reported dead in the Caspian Sea during spring and summer 2000. We performed necropsies and extensive laboratory analyses on 18 seals, as well as examination of the pattern of strandings and variation in weather in recent years, to identify the cause of mortality and potential contributory factors. The monthly stranding rate in 2000 was up to 2.8 times the historic mean. It was preceded by an unusually mild winter, as observed before in mass mortality events of pinnipeds. The primary diagnosis in 11 of 13 seals was canine distemper, characterized by broncho-interstitial pneumonia, lymphocytic necrosis and depletion in lymphoid organs, and the presence of typical intracytoplasmic inclusion bodies in multiple epithelia. Canine distemper virus infection was confirmed by phylogenetic analysis of reverse transcriptase-polymerase chain reaction products. Organochlorine and zinc concentrations in tissues of seals with canine distemper were comparable to those of Caspian seals in previous years. Concurrent bacterial infections that may have contributed to the mortality of the seals included Bordetella bronchiseptica (4/8 seals), Streptococcus phocae (3/8), Salmonella dublin (1/8), and S. choleraesuis (1/8). A newly identified bacterium, Corynebacterium caspium, was associated with balanoposthitis in one seal. Several infectious and parasitic organisms, including poxvirus, Atopobacter phocae, Eimeria- and Sarcocystis-like organisms, and Halarachne sp. were identified in Caspian seals for the first time.

Animals↗
PubMed1989

Distemper-like disease and encephalitozoonosis in wild dogs (Lycaon pictus).

Clinical signs of a fatal disease resembling those of canine distemper were observed in two groups of captive wild dog (Lycaon pictus) pups 13 days after vaccination with a commercially available combination vaccine for dogs which contained a live attenuated strain of canine distemper virus. Histopathological examination of tissues revealed the presence of intranuclear inclusion bodies in neurons and lesions resembling canine distemper as well as colonies of an Encephalitozoon sp. in the central nervous system and kidneys. Lesions were observed in both organs which resembled those described in other species infected with Encephalitozoon cuniculi.

Animals↗
PubMed1975

Measles vaccine in dogs: efficacy against aerosol challenge with virulent canine distemper virus.

Fifty young Beagle pups were used in studies on the efficacy of measles virus vaccine in providing protection against virulent canine distemper (CD) virus given intranasally. Among 29 dogs vaccinated with measles virus vaccine and subsequently exposed to virulent CD virus, 1 died, 7 developed relatively severe signs of CD, 15 had mild signs of distemper, and 6 remained clinically normal. Of 15 unvaccinated dogs similarly exposed to virulent CD virus, 11 succumbed to distemper. Six pups vaccinated with modified live-virus (MLV) CD virus vaccine remained clinically normal following immunity challenge.

Administration, Intranasal↗
PubMed2004

Canine distemper and related diseases: report of a severe outbreak in a kennel.

An outbreak of canine distemper in a kennel of German shepherds in the province of Bari is reported. Six 42-day-old pups developed typical signs of canine distemper (fever, conjunctivitis, respiratory distress and enteritis) and died within 7-10 days. Neurological symptoms were observed only in one pup. Four additional pups, which had shown no sign of illness, were separated and vaccinated, but two of these developed a severe, fatal nervous form 15 days later. Post-mortem examination, carried out on two pups which died without neurological signs, showed pneumonia and enteritis, more severe in one of the two examined pups. Smears from the brain and the conjunctiva of both dogs tested positive for canine distemper virus (CDV) by an immunofluorescent assay, confirmed by the identification of viral RNA using RT-PCR. Bordetella bronchiseptica and a canine adenovirus strain, characterized as canine adenovirus type 2 by a differential PCR assay, were isolated from the lungs of the pup showing the most pronounced lesions. Furthermore, canine coronavirus was detected by PCR in the intestinal content of this pup, suggesting a multifactorial aetiology of the outbreak.

Adenoviridae Infections↗
PubMed1989

Electrophoretic determination of albumin and gamma globulin concentrations in the cerebrospinal fluid of dogs with encephalomyelitis attributable to canine distemper virus infection: 13 cases (1980-1987).

Thirteen dogs with encephalomyelitis attributable to canine distemper virus infection were classified into 3 groups on the basis of histopathologic evidence of virus-induced lesions in CNS tissue. Analysis of data indicated a similarity within groups when arranged by age, clinical neurologic signs, and alterations in the CSF electrophoretic protein values. Comparison with results in dogs with experimentally induced canine distemper encephalomyelitis suggested that when grouped by age, CSF electrophoretic values are helpful in predicting the CNS histopathologic changes in dogs with naturally acquired canine distemper encephalomyelitis.

Albumins↗
PubMed1981

Vaccination-induced distemper in kinkajous.

Following vaccination for distemper, using a modified live-virus vaccine developed for dogs, 2 young kinkajous (Potos flavus) developed diarrhea, then central nervous system disease. Clinical signs included myoclonus, head trembling, loss of muscular coordination, and convulsions. One kinkajou gradually recovered; the other seemed to recover, then relapsed and was euthanatized. Microscopic lesions included those of interstitial pneumonia and enteritis and multifocal lymphocytic inflammation, gliosis, spongiosis, and swollen and degenerating axons in the cerebral, cerebellar, and brain stem white matter. Similar lesions were found at all caudally, as exemplified by complete destruction of the dorsal funiculi and dorsal horns of the gray matter of the upper sacral cord segments. Eosinophilic intranuclear inclusions were seen histologically in the glia in the spinal cord, midbrain, and cerebellum, and were confirmed as canine distemper viral inclusions by the fluorescent antibody method. It was concluded that modified live canine distemper virus vaccines should be used with caution or not at all in kinkajous.

Animals↗
PubMed1976

Failure of attenuated canine distemper virus (Rockborn strain) to suppress lymphocyte blastogenesis in dogs.

The attenuated Rockborn strain of canine distemper virus is commonly used in commercial vaccines. Since immunosuppression is a common feature of virulent (Snyder Hill) distemper virus infection of the dog, an evaluation of the cellular immune functions of dogs given inoculums of the less virulent Rockborn strain was done using lymphocyte blastogenesis responses to various mitogens. Unlike the viruslent Snyder Hill strain, the attenuated distemper virus did not alter lymphocyte blastogenesis responses to phytohemaglutinin (PHA) and pokeweed mitogen (PWM) which are considered in vitro correlates of T and B cell immunity.

Animals↗
PubMed1976

Vaccine-induced canine distemper in a lesser panda.

A fatal disease occurred in a lesser panda (Ailurus fulgens) 2 weeks after vaccination with modified live distemper vaccine. The disease clinically resembled canine distemper. Pathologically there was giant cell pneumonia, with canine distemper viral inclusion bodies in pulmonary and digestive tract epithelium. Viral isolates were indicative of an attenuated strain rather than virulent types.

Animals↗