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PubMed2005

Reduced nuclear translocation of nuclear factor (NF)-kappaB p65 in the footpad epidermis of dogs infected with distemper virus.

Infection of canine footpads with the canine distemper virus (CDV) can cause massive epidermal thickening (hard pad disease), as a consequence of increased proliferation of keratinocytes and hyperkeratosis. Keratinocytes of canine footpad epidermis containing detectable CDV nucleoprotein antigen and CDV mRNA were shown previously to have increased proliferation indices. Because various proteins that play a role in the proliferation of epidermal cells are viral targets, the potential participation of such proteins in CDV-associated keratinocyte proliferation was investigated. Transforming growth factor-alpha (TGF-alpha), cell cycle regulatory proteins p21, p27 and p53, and nuclear factor (NF)-kappaB transcription factor components p50 and p65 were studied in the footpad epidermis from the following groups of dogs inoculated with CDV: group 1, consisting of seven dogs with clinical distemper and CDV in the footpad epidermis; group 2, consisting of four dogs with clinical distemper but no CDV in the footpad epidermis; group 3, consisting of eight dogs with neither clinical distemper nor CDV in the footpad epithelium. Group 4 consisted of two uninoculated control dogs. The expression of TGF-alpha, p21, p27 and p53, and p50 in the basal layer, lower and upper spinous layers, and in the granular layer did not differ statistically between CDV-positive (group 1) and CDV-negative (groups 2-4) footpad epidermis. However, there were differences in the levels of nuclear and cytoplasmic p65 expression between group 1 dogs and the other three groups. Thus, footpads from group 1 dogs had more keratinocytes containing p65 in the cytoplasm and, conversely, fewer nuclei that were positive for p65. These findings indicate that p65 translocation into the nucleus is reduced in CDV-infected footpad epidermis. Such decreased translocation of p65 may help to explain increased keratinocyte proliferation in hard pad disease and suggests interference of CDV with the NF-kappaB pathway.

Animals↗

PubMed2006

Evaluation of ELISA based on the conserved and functional middle region of nucleocapsid protein to detect distemper infection in dogs.

A 287bp fragment from the middle region of the nucleocapsid protein of canine distemper virus (CDV) was amplified from the conjunctival samples of distemper-infected dogs and was cloned into pRSET B vector. The recombinant protein was expressed as a 16-kDa-fusion protein with histidine tag in E. coli. Sera of distemper-infected and vaccinated dogs contained IgG antibodies against the purified recombinant protein as observed by enzyme linked immunosorbent assays (ELISA) and showed a strong correlation (r=0.882, p<0.0001 at 95% CI) and good agreement (kappa=0.718) with the conventional tissue culture viral antigen based ELISA. Further, the results of recombinant protein based ELISA and Western blotting with the sera from the infected and vaccinated dogs correlated well (kappa=0.8226). These findings recommend the use of the recombinant protein in the serodiagnosis of canine distemper virus infection in dogs.

Animals↗

PubMed1999

Identification of CD4+ and CD8+ T cell subsets and B cells in the brain of dogs with spontaneous acute, subacute-, and chronic-demyelinating distemper encephalitis.

CD4 and CD8 antigen expression of T cells as well as B cell and canine distemper virus (CDV) antigen distribution were immunohistologically examined in the cerebellum of dogs with spontaneous distemper encephalitis. Cellular and viral antigen expression were evaluated at intralesional and extralesional sites and in the perivascular space. Histologically, acute and subacute non-inflammatory encephalitis and subacute inflammatory and chronic plaques were distinguished. Demyelination was a feature of all subacute and chronic lesions, although the majority of plaques exhibited no or only a low level of active demyelination as demonstrated by single macrophages with luxol fast blue positive material in their cytoplasm. CDV antigen expression, observed in all distemper brains, was reduced in chronic plaques. CD4+, CD8+, and B cells were absent in controls and in some brains with acute encephalitis. A mild infiltration of CD8+ cells was noticed in the neuropil of the remaining brains with acute and all brains with subacute non-inflammatory encephalitis. Single CD4+ cells were found in two brains with acute and in all brains with subacute non-inflammatory encephalitis. Numerous CD8+ and CD4+ cells and few B cells, with a preponderance of CD8+ cells, were detected in subacute inflammatory and chronic lesions. In contrast, in perivascular infiltrates (PVI) of subacute and chronic lesions a dominance of CD4+ cells was detected. The dominating CD8+ cells in acute and subacute non-inflammatory encephalitis might be involved in viral clearance or contribute as antibody-independent cytotoxic T cells to early lesion development. In subacute inflammatory and chronic lesions CD8+ cells may function as cytotoxic effector cells and CD4+ cells by initiating a delayed-type hypersensitivity reaction. The simultaneous occurrence of perivascular B and CD4+ cells indicated that an antibody-mediated cytotoxicity could synergistically enhance demyelination. Summarized, temporal and spatial distribution of CD4+, CD8+ and B cells and virus antigen in early and late lesions support the hypothesis of a heterogeneous in part immune-mediated plaque pathogenesis in distemper demyelination.

Animals↗

PubMed2002

Natural distemper in vaccinated and unvaccinated dogs in Warsaw.

Two hundred and twenty-four dogs with clinical signs of distemper were examined for the presence of canine distemper virus (CDV) in mucous membranes by direct immunofluorescence assay. The study showed that 22% of the animals were CDV-positive. Most (33/50; 66%) of the infected dogs had never been vaccinated against distemper, whereas only 11 of 50 (22%) CDV-positive animals were immunized at least once. The difference in the infection rate between vaccinated and unvaccinated animals was statistically significant (P < 0.001), as assessed by the chi2 test. It is concluded that distemper is an important disease among dogs in Warsaw and the vaccination significantly reduces the risk of this disease.

Age Factors↗

PubMed1961

Subclinical infection of dogs by canine-adapted measles virus evidenced by their subsequent immunity to canine distemper virus.

Moura, Roberto A. (Chas. Pfizer and Company, Inc., Terre Haute, Ind.) and Joel Warren. Subclinical infection of dogs by canine-adapted measles virus evidenced by their subsequent immunity to canine distemper virus. J. Bacteriol. 82:702-705. 1961.-Young dogs were inoculated with virulent measles virus which had been adapted to canine kidney or human amnion cell culture. None of the animals showed any clinical symptoms nor could virus be isolated from the blood, although measles-neutralizing and complement-fixing antibodies developed during convalescence. All dogs failed to develop antibody to canine distemper. However, when these and normal control animals were subsequently inoculated intracerebrally with virulent distemper virus, each of the controls succumbed to typical symptoms, whereas all of the measles-immune dogs survived. These results suggest that the cross-protection conferred by measles against canine distemper virus infection involves factors other than humoral antibody. The immunity persists for a considerable length of time.

Animals↗

PubMed1997

Canine distemper virus (CDV) infection of ferrets as a model for testing Morbillivirus vaccine strategies: NYVAC- and ALVAC-based CDV recombinants protect against symptomatic infection.

Canine distemper virus (CDV) infection of ferrets causes an acute systemic disease involving multiple organ systems, including the respiratory tract, lymphoid system, and central nervous system (CNS). We have tested candidate CDV vaccines incorporating the fusion (F) and hemagglutinin (HA) proteins in the highly attenuated NYVAC strain of vaccinia virus and in the ALVAC strain of canarypox virus, which does not productively replicate in mammalian hosts. Juvenile ferrets were vaccinated twice with these constructs, or with an attenuated live-virus vaccine, while controls received saline or the NYVAC and ALVAC vectors expressing rabies virus glycoprotein. Control animals did not develop neutralizing antibody and succumbed to distemper after developing fever, weight loss, leukocytopenia, decreased activity, conjunctivitis, an erythematous rash typical of distemper, CNS signs, and viremia in peripheral blood mononuclear cells (as measured by reverse transcription-PCR). All three CDV vaccines elicited neutralizing titers of at least 1:96. All vaccinated ferrets survived, and none developed viremia. Both recombinant vaccines also protected against the development of symptomatic distemper. However, ferrets receiving the live-virus vaccine lost weight, became lymphocytopenic, and developed the erythematous rash typical of CDV. These data show that ferrets are an excellent model for evaluating the ability of CDV vaccines to protect against symptomatic infection. Because the pathogenesis and clinical course of CDV infection of ferrets is quite similar to that of other Morbillivirus infections, including measles, this model will be useful in testing new candidate Morbillivirus vaccines.

Animals↗

PubMed2004

Genetically distant American Canine distemper virus lineages have recently caused epizootics with somewhat different characteristics in raccoons living around a large suburban zoo in the USA.

BACKGROUND: Mortality rates have differed during distemper outbreaks among free-ranging raccoons (Procyon lotor) living around a large Chicago-area zoo, and appeared higher in year 2001 than in 1998 and 2000. We hypothesized that a more lethal variant of the local Canine distemper virus (CDV) lineage had emerged in 2001, and sought the genetic basis that led to increased virulence. However, a more complex model surfaced during preliminary analyses of CDV genomic sequences in infected tissues and of virus isolated in vitro from the raccoons. RESULTS: Phylogenetic analyses of subgenomic CDV fusion (F) -, phosphoprotein (P) -, and complete hemagglutinin (H) - gene sequences indicated that distinct American CDV lineages caused the distemper epizootics. The 1998 outbreak was caused by viruses that are likely from an old CDV lineage that includes CDV Snyder Hill and Lederle, which are CDV strains from the early 1950's. The 2000 and 2001 viruses appear to stem from the lineage of CDV A75/17, which was isolated in the mid 1970's. Only the 2001 viruses formed large syncytia in brain and/or lung tissue, and during primary isolation in-vitro in Vero cells, demonstrating at least one phenotypic property by which they differed from the other viruses. CONCLUSIONS: Two different American CDV lineages caused the raccoon distemper outbreaks. The 1998 viruses are genetically distant to the 2000/2001 viruses. Since CDV does not cause persistent infections, the cycling of different CDV lineages within the same locale suggests multiple reintroductions of the virus to area raccoons. Our findings establish a precedent for determining whether the perceived differences in mortality rates are actual and attributable in part to inherent differences between CDV strains arising from different CDV lineages.

Amino Acid Sequence↗

PubMed2001

Serologic response of maned wolves (Chrysocyon brachyurus) to canine and canine parvovirus vaccination distemper virus.

This study evaluated the immune response of 47 (22 males, 25 females) captive maned wolves (Chrysocyon brachyurus) to modified-live canine parvovirus and canine distemper virus (Onderstepoort and Rockborn strains) vaccines. Sera were collected from 33 adults and 14 pups, including five free-ranging pups captured at 1 yr of age or younger. All the adults and four captive-born pups had been vaccinated prior to this first blood collection. Virus neutralization and hemagglutination-inhibition assays were performed for quantitating antibodies against canine distemper and canine parvovirus, respectively. Distemper antibody titers > or = 100 were present in 57% of adults and 14% of pups. All adults and 29% of pups had parvovirus antibody titers > or = 80. After vaccination, 72% of the wolves developed antibody titers > or = 100 against distemper and 98% developed titers > or = 80 against parvovirus. Both vaccines used were safe and immunogenic to juvenile and adult maned wolves, regardless of prior vaccination history.

Animals↗

PubMed1989

[The prevention of distemper in zoo animals].

The distemper virus infection of different non-domestic carnivorous zoo animals is known since long. All species involved belonged to the suborder Fissipedia. In 1988 a distemper or morbillivirus-like infection occurred in harbour seals, a member of the suborder pinnipedia. For the prophylaxis of distemper in dogs attenuated live vaccines are commonly used. In zoo animals, however, these vaccines caused distemper several times. In contrast, an inactivated virus vaccine proved both its safety and efficacy in more than hundred zoo animals of various species.

Animals↗

PubMed1995

Generation of multinucleated osteoclast-like cells from canine bone marrow: effects of canine distemper virus.

Recent evidence has implicated canine distemper virus (CDV) as a possible aetiologic agent in Paget's disease of bone and the canine bone disorder, metaphyseal osteopathy. We have therefore examined the effects of CDV on the formation of multinucleated osteoclast-like cells in cultures of canine bone marrow mononuclear cells. Marrow cells from a distemper-infected dog and from five uninfected dogs were cultured in the presence of 1 alpha, 25-(OH)2 vitamin D3 and the number of tartrate resistant acid phosphatase positive multinucleated cells (MNCs) was determined. The presence of calcitonin (CT) receptors was confirmed by autoradiography with 125I-labeled human CT. Cultures from the distemper-infected dog contained a higher level of MNCs than those from the normal dogs. The in vitro addition of CDV to the cultures from all the dogs produced a dose-dependent increase in the number of MNCs, and an increase in size of these cells in the cultures from the infected dog. Cells infected with CDV were hyperresponsive to 1 alpha,25-(OH)2 vitamin D3. The presence of the virus in the relevant samples was confirmed using molecular techniques. In situ hybridization studies also revealed a significant increase in the level of infection following in vitro addition of the virus to the culture from the distemper-infected dog, suggesting that further infection had taken place. Resorption pits were formed on bone slices, although the number of pits was not significantly altered by viral infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗

PubMed1997

Abundant expression of viral nucleoprotein mRNA and restricted translation of the corresponding viral protein in inclusion body polioencephalitis of canine distemper.

Brain and other tissues of three dogs aged 4-21 months with inclusion body polioencephalitis caused by canine distemper virus (CDV) were examined for CDV nucleoprotein (N) antigen and mRNA distribution. Two animals (nos 3 and 1) had suddenly shown central nervous system (CNS) signs 4 days and 5 months, respectively, after vaccination with a modified live CDV vaccine; animal no. 2 had shown similar signs 4 weeks after vaccination with an unknown product. Lesions in the CNS, which were restricted to the grey matter, occurred most frequently in the diencephalon, mesencephalon, medulla oblongata and, in one animal, in the cerebral cortex. Changes were characterized by mild to moderate perivascular lymphohistiocytic cuffs, loss of neurons, neuronal necrosis, glial nodules, and oedema. Intranuclear and cytoplasmic inclusion bodies, especially prominent in neurons, were observed. By in-situ hybridization, CDV N mRNA expression was confirmed with a non-radioactively labelled N-specific mRNA probe. The corresponding RNA translation product was detected immunohistochemically with a proteinspecific monoclonal antibody. Viral antigen and mRNA were observed in the same cell types and brain compartments. However, the number of cells expressing N mRNA exceeded the number of cells containing viral antigen greatly in two animals and slightly in one. Some areas with abundant viral mRNA expression were almost completely devoid of viral antigen. mRNA and the corresponding translation product were demonstrated in neurons and less frequently in astrocytes, but not in perivascular inflammatory cells. It would appear that distemper inclusion-body polioencephalitis may be due to a non-productive CDV infection of neurons, characterized by abundant expression of CDV N mRNA and reduced translation of the corresponding viral protein. These findings suggest that in distemper the pathogenesis of grey-matter lesions differs substantially from that of white-matter lesions, which constitute the most common manifestation of distemper encephalitis.

Animals↗

PubMed1976

Genesis and maintenance of a persistent infection by canine distemper virus.

Vero cells were persistently infected with canine distemper virus by continuous undiluted passage of virus harvests. The cells were refractory to superinfection by both measles virus and canine distemper virus. These persistently infected cells produced and released into the medium a labile component which had a potent and selective inhibitory effect on the replication of canine distemper and measles virus. The inhibitory agent was not inactivated by u.v.-irradiation or sedimented by ultracentrifugation. Antisera against canine distemper virus or SSPE sera were able to block this inhibitory effect. We propose that these persistently infected cells produce an excess of a virus-induced regulatory protein.

Antiviral Agents↗

PubMed1975

The adverse effect of environment on the response to distemper vaccination.

Three standard batches of combined distemper and hepatitis vaccine tested in pups housed indoors during a constantly hot summer failed to elicit antibody to distemper virus or to protect the pups against challenge with virulent virus. The response to hepatitis vaccination was normal. When tested in pups housed outdoors, the same batches of vaccine produced antibodies to distemper and protection against the disease. It appears that high relative humidity combined with high environmental temperature caused an increase in body temperature of the pups which was deleterious to the distemper vaccine but did not affect the more heat resistant hepatitis vaccine.

Animals↗

PubMed1973

Myelin-specific autoantibodies associated with central nervous system demyelination in canine distemper virus infection.

Sera from dogs with spontaneously occurring and experimentally produced canine distemper virus-associated demyelinating encephalitis were examined for antibodies to central nervous system myelin by the complement fixation and indirect immunofluorescent methods. Complement-fixing immunoglobulin M antibodies and non-complement-fixing immunoglobulin G antibodies were found in 97% of the spontaneous cases. In comparison, only 28% of control sera contained these antibodies; furthermore, mean antibody titers in the control groups were significantly lower (P < 0.005) when compared to the distemper group. Complement-fixing antimyelin antibodies were also demonstrated in gnotobiotic dogs with experimentally induced distemper virus-associated demyelination. The antibody response could be correlated with clinicopathological features of the disease produced. Results of this study indicate that demyelination in canine distemper may proceed by immune mechanisms.

Absorption↗

PubMed1981

Canine distemper virus-associated cardiac necrosis in the dog.

An age-related canine distemper virus-associated cardiomyopathy characterized by multifocal myocardial degeneration necrosis and mineralization with minimal inflammatory cell response was found in gnotobiotic Beagle pups. Of the 30 dogs infected experimentally at 5 to 7 days of age with virulent R252 strain of canine distemper virus, 11 had gross or microscopic cardiac involvement as early as 16 days post-infection. The 25 dogs similarly infected at 10 to 21 days of age, the uninfected age-matched controls, and pups infected at 5 to 7 days of age with avirulent R252 canine distemper virus had no cardiac lesions. Although the lesions are attributed to a direct viral effect, they occur against a background of other canine distemper virus-related changes including immunosuppression, anemia and encephalomyelitis. All these factors may have a modifying role in the development of this age dependent susceptibility to virus-associated myocardial necrosis.

Animals↗

PubMed1995

Canine distemper virus-specific antibodies in multiple sclerosis.

Current postulates support the idea that MS is triggered by an infectious agent or agents through an autoimmune reaction directed against brain antigens in genetically susceptible individuals. Evidence for an infectious etiology of MS is indirect. We have proposed that MS may, in some instances, be due to a zoonotic infection and that canine distemper virus, a measles-like virus in dogs, is a likely candidate in the causation of this disorder. The high homology between canine distemper and measles virus proteins has made it extremely difficult to distinguish distemper from measles antibodies serologically. We now provide evidence that humans can be infected with this neurotropic dog virus. Furthermore, a high titer of canine distemper virus antibodies is significantly associated with MS. Identification of the etiologic agent in MS may lead to the elucidation of disease pathogenesis and to disease prevention through appropriate public health and vaccination programs.

Adolescent↗

PubMed2003

Incidence of adverse events in ferrets vaccinated with distemper or rabies vaccine: 143 cases (1995-2001).

OBJECTIVE: To determine the incidence of adverse events in ferrets vaccinated with a modified-live avian cell culture canine distemper virus vaccine licensed for use in ferrets, an inactivated rabies vaccine licensed for use in ferrets, or both. DESIGN: Retrospective study. ANIMALS: 143 ferrets. PROCEDURE: Medical records were reviewed to identify ferrets that had an adverse event after vaccination. RESULTS: Adverse events developed within 25 minutes after vaccination in 13 ferrets. One ferret developed an adverse event after receiving a distemper and a rabies vaccine simultaneously and developed a second adverse event the following year after receiving the rabies vaccine alone. Therefore, a total of 14 adverse events were identified. All adverse events were an anaphylactic reaction characterized by generalized hyperemia, hypersalivation, and vomiting. Ten of the 14 anaphylactic reactions occurred after ferrets received both vaccines, 3 occurred after ferrets received the distemper vaccine alone, and 1 occurred after a ferret received the rabies vaccine alone. Incidences of adverse events after administration of both vaccines, the distemper vaccine alone, and the rabies vaccine alone were 5.6, 5.9, and 5.6%, respectively. Ferrets that had an anaphylactic reaction were significantly older at the time of vaccination than were ferrets that did not. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that there may be a high incidence of anaphylactic reactions after vaccination of domestic ferrets. Ferrets should be observed for at least 25 minutes after vaccination, and veterinarians who vaccinate ferrets should be prepared to treat anaphylactic reactions.

Age Factors↗

PubMed2001

Rabies and canine distemper in an arctic fox population in Alaska.

Two oil field workers were attacked by a rabid arctic fox (Alopex lagopus) in the Prudhoe Bay oil field (Alaska, USA) prompting officials to reduce the local fox population. Ninety-nine foxes were killed during winter 1994. We tested foxes for prevalence of rabies and canine distemper. Exposure to rabies was detected in five of 99 foxes. Of the five, only one fox had rabies virus in neural tissue as determined by the direct fluorescent antibody test. The other four foxes had been exposed to rabies, but had apparently produced antibodies and did not have an active infection. No evidence of canine distemper was detected as determined by the absence of distemper antibodies in serum and distemper virus in neural tissue.

Alaska↗