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PubMed2004

Dog distemper: imported into Europe from South America?.

According to Charles Frédéric Heusinger (1853), dog distemper had been imported from Peru into Spain in the course of the 17th century. The disease was well described in 1746 by Ulloa in his work Relación histórica del viaje a la América meridional. During the course of the 1760s, the disease was reported in Spain, followed by England, Italy (1764) and Russia (1770). In 1763, 900 dogs died in a single day in Madrid. In 1844, Karle succeeded in the first experimental transmission of the disease by brushing the lips of young dogs with the discharge from sick animals. The causal agent of the disease was only discovered in 1905, when the virus was isolated by Henri Carré. In the meantime, Edward Jenner, who thought that the disease was a pox-like affection, claimed that it could be prevented by inoculation of the vaccinia virus.

Animals↗
PubMed2005

Induction of castration by immunization of male dogs with recombinant gonadotropin-releasing hormone (GnRH)-canine distemper virus (CDV) T helper cell epitope p35.

Immunocastration is a considerable alternative to a surgical castration method especially in male animal species for alleviating unwanted male behaviors and characteristics. Induction of high titer of antibody specific for gonadotropin-releasing hormone (GnRH) correlates with the regression of testes. Fusion proteins composed of canine GnRH and T helper (Th) cell epitope p35 originated from canine distemper virus (CDV) F protein and goat rotavirus VP6 protein were produced in E. coli. When these fusion proteins were injected to male dogs which were previously immunized with CDV vaccine, the fusion protein of GnRH-CDV Th cell epitope p35 induced much higher antibody than that of GnRH-rotavirus VP6 protein or GnRH alone. The degeneration of spermatogenesis was also verified in the male dogs immunized with the fusion protein of GnRH-CDV Th cell epitope p35. These results indicate that canine GnRH conjugated to CDV Th cell epitope p35 acted as a strong immunogen and the antibody to GnRH specifically neutralized GnRH in the testes. This study also implies a potential application of GnRH-based vaccines for immunocastration of male pets.

Amino Acid Sequence↗
PubMedDate not supplied

[The persistence of the distemper virus in continuous human cells].

Two cultures chronically infected with distemper virus (HEP-2 and L-41) were obtained. The cultures produced a small-plaque cell-associated virus and a virus-specific antigen which was demonstrated by the fluorescence antibody technique in 40%-60% of the cells. The chronically infected cells produced interferon as judged by their resistance to superinfections with heterologous viruses. The virus-carrier state was characterized by temperature sensitivity.

Antigens, Viral↗
PubMed1991

[Demonstration of viral proteins and RNA in hypothalamus of mice infected by canine distemper virus].

There are a number of reports suggesting that neurological disorders may be due to infectious agents, such as viruses. In order to study the role of viruses on cellular plasticity in the central nervous system, we established a model of virus infection in the mouse. Inoculation of mouse with canine distemper virus (CDV) led to an acute encephalitis, late neurological disorders and an obesity syndrome. To analyse the role of viral replication on the development of this syndrome we studied the cerebral distribution of viral products during the course of infection. Viral proteins and RNA accumulated in mouse brain from the 9th day to the 6th week post-inoculation, particularly in hypothalamus, a cerebral structure implicated in obesity. Such selective viral tropism may explain some of the unexpected features of viral-induced disorders.

Animals↗
PubMed1989

Serologic response of domestic ferrets (Mustela putorius furo) to canine distemper and rabies virus vaccines.

Nine unrelated 12-week-old naive domestic ferrets (Mustela putorius furo) were used to evaluate the serologic responses to commercial canine distemper virus (CDV) and rabies virus (RV) vaccines. Five of the ferrets (group 1) were inoculated 3 times at 2-week intervals with a multivalent modified-live virus vaccine of canine cell-line origin, containing CDV and an inactivated RV vaccine. Four of the ferrets (group 2) were inoculated once with the multivalent modified-live virus vaccine containing CDV and were not inoculated with the RV vaccine. Both group-1 and group-2 ferrets seroconverted to the CDV component of the vaccine. Group-1 ferrets also seroconverted after RV vaccination and maintained serum antibody titers to both CDV and RV for at least 7 months. Domestic ferret sera were found to have IgG epitopes similar to sera of domestic dogs and cats. Domestic ferret sera did not contain antibodies to feline coronavirus or FeLV antigens.

Animals↗
PubMed1988

Cryptosporidiosis associated with immunosuppression attributable to distemper in a pup.

Cryptosporidiosis, giardiasis, trichomoniasis, and distemper were diagnosed in a 6-month-old female Siberian Husky pup. Poor growth rate, mucopurulent ocular and nasal discharges, and diarrhea were observed. Results of immunologic studies revealed decreased serum IgG concentration and undetectable serum IgA concentration. Cultured lymphocytes yielded a less-than-adequate response to mitogen stimulation. The serum also contained a factor that suppressed mitogen stimulation in control cultured lymphocytes.

Animals↗
PubMed1986

Evidence of canine distemper virus infection in skunks negative for antibody against rabies virus.

Between January 1981 and October 1985, brain tissue specimens from 192 skunks that were negative for antibodies against rabies virus were obtained from 2 Illinois Public Health laboratories (A and B). Brain lesions were detected microscopically in specimens from 17 of the 91 (18.7%) skunks from laboratory B and in specimens from 30 of the 101 (29.7%) skunks from laboratory A. Lesions in 3 skunks (1 from laboratory A, 2 from B) were caused by cerebral parasitism. Lesions in the remaining 44 skunks were characterized by perivascular, nonsuppurative, mononuclear cell infiltrates and foci of glial cells of differing severity. The similarity of lesions and the finding of inclusions diagnostic of canine distemper virus (CDV) in some skunks indicated that CDV may be the main cause of neurologic disease in nonrabid skunks. Seventeen of 36 (47.2%) skunks evaluated for antibody against CDV, using an unlabeled antibody-enzyme method, were positive for CDV. Findings in skunks from the 2 laboratories indicated similar annual prevalences of brain lesions in 1982, 1983, and 1984. The highest percentage (40.5%) of nonrabid skunks with encephalitis was found in skunks submitted to laboratory B in 1981, which was concurrent with a rabies epizootic among skunks in Illinois in 1981. The number of skunks from both laboratories with CDV infection peaked during winter-spring. Importance of CDV in skunk population dynamics remains to be elucidated; however, infection with CDV appears to be enzootic and occasionally epizootic in skunks. Because enzootic/epizootic CDV may bias rabies surveillance data, caution in interpretation of surveillance data is necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Canine distemper virus-induced thrombocytopenia.

Effects of canine distemper virus (CDV) infection on circulating platelet values were studied in gnotobiotic dogs inoculated with R252-CDV. Thrombocytopenia (less than 200,000 platelets/microliter) was present on postinoculation day (PID) 5 and persisted through PID 15. Peak thrombocytopenia occurred on PID 10 (less than 85,000 platelets/microliter). Thrombocytopenia was accompanied by lymphopenia, neutropenia, and monocytopenia. Platelet membrane-bound CDV antigen and IgG were present from PID 7 onward; neither the third component of complement nor IgM was detected on platelets from CDV-inoculated dogs. The mean number of megakaryocytes per unit of bone marrow surface area was unchanged. Megakaryocyte infection was present in dogs euthanatized on PID 4 (0.33%), increased slightly in dogs euthanatized on PID 8 (3%), and increased sharply in dogs euthanatized on PID 9 and 10 to 17.8% and 8.3%, respectively. Phagocytosis of platelets by stellate reticuloendothelial (Kupffer's) cells in the liver was prominent in dogs euthanatized from PID 5 onward. Seemingly, CDV-induced thrombocytopenia was mediated by virus-antibody immune complexes on platelet membranes. Decreased platelet production after PID 8 resulting from direct viral infection of megakaryocytes was a likely contributing factor and occurred against a background of profound virus-induced dysfunctions of all hematopoietic cellular elements.

Animals↗
PubMed1985

Encephalitis induced in non-human primates by canine distemper virus adapted to human neural cells.

The Onderstepoort strain of canine distemper virus (CDV) adapted to human oligodendroglioma, neuroblastoma and glioblastoma cells, was intracerebrally inoculated into cynomolgus monkeys. All the three viruses caused periventricular encephalitis involving the brain stem. When the neurovirulence of these viruses were compared in terms of clinical signs and histopathological changes, the oligodendroglioma-adapted virus showed the neurovirulence of the highest degree inducing degeneration of axons and glial cells. Chronic encephalitis was also observed. The neuroblastoma-adapted virus induced predominantly nerve-cell degeneration although clinically this virus showed slightly lower degree of neurovirulence than the oligodendroglioma-adapted viruses. The glioblastoma-adapted virus showed clinically much lower neurovirulence than the other two viruses; all monkeys infected with this virus survived and produced high level of antibody in most cases. Histopathologically degeneration of axons and glial cells was characteristics although the incidence was less frequent than the oligodendroglioma-adapted virus. Predominant involvement of nerve cells by neuroblastoma-adapted virus and predominant involvement of axon and glial cells by oligodendroglioma-adapted virus and by glioblastoma-adapted virus suggest that in vitro tropism of the virus to neural cells is partially reflected on tropism of the virus in the CNS.

Animals↗
PubMed1979

Canine distemper virus-associated hypocalcemia.

A retrospective study was done to correlate serum calcium concentrations and parathyroid gland ultrastructure to clinical, immunologic, and pathologic changes experimentally induced in gnotobiotic dogs by canine distemper virus (CDV). Dogs infected with CDV had significantly reduced serum calcium concentrations associated with ultrastructural evidence of parathyroid gland inactivity, degeneration, and viral inclusions. Although CDV-infected dogs exhibited neurologic signs, minimal lesions were present in the central nervous system. It is suggested that viral-induced parathyroid dysfunction may contribute to neutrologic disturbance of CDV infection.

Animals↗
PubMed1984

In vitro propagation of canine distemper virus: establishment of persistent infection in Vero cells.

Primary cultures of bovine fibroblast (BF) and canine brain cells, persistently infected with virulent R252-canine distemper virus (CDV), were cocultured with African green monkey (Vero) cells. Transfer of persistent CDV from BF to Vero cells varied inversely with the in vitro passage level (age) of the CDV-infected BF cells. Successful transfer of CDV to Vero cells was signaled by the transient appearance of viral syncytia, rapid spread of viral antigen to all Vero cells in the culture, and by recovery of cell-free Vero-infectious virus in culture fluids. With time, viral cytopathic effects in Vero cells containing CDV disappeared, and the infected lines could not be distinguished from noninfected control Vero cells, except by immunoassay for viral antigen.

Animals↗
PubMed1982

Immunoperoxidase labeling of canine distemper virus replication cycle in Vero cells.

An indirect immunocytochemical labeling technique, using horseradish peroxidase-conjugated antibody was used to detect the intracellular and surface membrane localization of canine distemper virus (R252-CDV) antigens during productive virus replication in infected Vero cells. Specific labeling of intracellular viral antigens was restricted to rough nucleocapsid aggregates. Surface membrane labeling correlated directly with the appearances both of virus-specific membrane spikes and buds and of mature virions. Syncytial cell formation was associated with labeled cytoplasmic nucleocapsid, but there was no evidence of productive CDV formation on surface membranes. The immunoperoxidase technique provided precise ultrastructural antigenic localization with concomitant preservation of excellent ultrastructural detail within single virus-infected cells during CDV replication cycle in vitro.

Animals↗
PubMedDate not supplied

[Use of an immunoenzyme method for diagnosing canine distemper].

Analysis of the clinical data and laboratory studies brought the authors to a conclusion on the possibility of using dot solid-phase ELISA on nitrocellulose for rapid (1 h), simple, and specific detection of canine distemper virus. The method is sufficiently specific, helps specify the clinical diagnosis, and may be used in future for the creation of a commercial test system.

Animals↗
PubMed1993

Multiple oral procedures performed on a dog with distemper myoclonus.

A 3-year-old male mixed-breed dog was treated for an oral defect along the rostral portion of the hard palate and an oronasal fistula secondary to a severe mandibular brachygnathism and persistent canine distemper virus associated myoclonus. This report describes the treatment using a bilateral radical premaxillectomy, oronasal fistula repair, and pulpotomy.

Animals↗
PubMed1975

Comparison of canine distemper viral strains: an electron microscopic study.

A canine distemper (CD) viral strain, designated R252, originally obtained from a dog with demyelinating encephalomyelitis has been shown to reproduce this disease in gnotobiotic dogs in a high incidence in contradistinction to other CD viral strains which produce an acute fatal disease. Because comparision of R252 strain with the Snyder Hill (SH) and Onderstepoort (Ond) strains revealed differences in in vitro behavior, the 3 viruses were ultrastructurally investigated. The results revealed differences among the 3 viruses: Cytoplasmic nucleocapsid aggregates were characteristic of R252, diffuse aggregates of nucleocapsids were characteristic of SH, and although budding viral particles were recognized in Ond-infected cells, few nucleocapsids were seen in the cytoplasm. Cytoplasmic fibrillar structures were characteristic of R252- and Ond-infected cells. The budding viral particles observed with R252 and SH were similar, whereas Ond budding particles seemed to contain fewer nucleocapsids. Intranuclear inclusions recognized in R252- and SH-infected cultures appeared as areas of clearing of nucleoplasm along with disruption of the nucleolus. The presence of nucleocapsid-like structures was variable. Ultrastructurally, the cytoplasmic inclusions in cells infected with all 3 viruses progressed from focal aggregates of nucleocapsids to electron-dense bodies.

Animals↗
PubMed1993

Canine distemper virus replication in cells on microcarriers.

Chick embryo and Vero cells were grown on Gelaspher M gelatin microcarriers in suspension culture. The microcarriers had no adverse effects on cell morphology and growth. Microcarrier cell cultures were used for large-scale production of canine distemper virus. Virus yields (TCID50 per ml) were more than 10-times higher as compared to stationary cell culture.

Animals↗