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At least 19 recordsLinked to original sources
PubMed1975

Serologic response to canine distemper viral antigens in gnotobiotic dogs infected with canine distemper virus.

The humoral immune response to canine distemper viral antigens in gnotobiotic dogs experimentally infected with canine distemper virus was studied by the complement fixation and serum neutralization tests. Antibody titers measured by both serologic methods varied inversely with the severity of disease produced. Recovered dogs demonstrated the highest titers of antibody, whereas fatally infected dogs had little or no antibody activity in their sera. A third group of dogs, characterized by chronic persistent infection, had intermediate levels of anitbody to canine distemper virus. Preliminary characterization of the viral antigens involved in the complement fixation test indicated that at least two antigenic components were involved. One antigen was soluble in ether and was heat-labile, whereas the other was relatively heat-stable and was unaffected by treatment with ether. No evidence for serologic cross-reaction between viral and central nervous system components was found. A vigorous antibody response to envelope antigen determinants in addition to core determinants distinguished immune dogs from persistently infected dogs. The results of this study suggest that the inability to produce antibodies to envelope antigens may be a crucial factor in the establishment of a persistent infection with canine distemper virus in these dogs.

Animals↗
PubMed1979

Immune mechanisms against canine distemper. I. Identification of K cell against canine distemper virus infected target cells in vitro.

Canine peripheral blood lymphocytes, polymorphonuclear leucocytes (PMN) and monocytes (macrophages) were obtained by various cell separation techniques and were tested for their cytotoxic capacity against antibody-sensitized canine distemper virus (CDV) infected Vero cells by an in vitro chromium release assay. Canine lymphocytes were found to destroy CDV infected target cells effectively, while neither PMN nor monocytes (macrophages) could do so. The active lymphocyte was characterized by various rosetting techniques to be a non-T and a non-B lymphocyte. These cells bear no surface immunoglobulin (SIg-) but possessed both Fc receptors (Fc+) and complement receptors (EAC+) suggesting that these cells are neither classical T nor B cells. The possible roles of this K cell in the resistance against canine distemper are discussed.

Animals↗
PubMed1979

Immune mechanisms against canine distemper. II. Role of antibody in antigen modulation and prevention of intercellular and extracellular spread of canine distemper virus.

Specific antibody was shown to be highly effective in neutralizing extracellular canine distemper virus (CDV) as well as preventing the intercellular spread of this virus. Thus, relatively low levels of antibody neutralized 1 x 10(5) TCID50 of extracellular CDV and the development of plaques or CPE in Hep-2 and Vero cells respectively could be prevented even when up to 5% of the cells were infected. This inhibition of CPE and virus spread was most pronounced when antibody was added early but could still limit the degree of CPE if added as late as 48 h post-infection. This anti-viral activity was observed in different cell types including canine macrophages, cells normally infected with CDV in vivo. Prolonged exposure of infected target cells to high concentrations of antibody led to redistribution of surface viral antigens and their subsequent disappearance. The possible role of antibody in the defence against, and/or recovery from CDV and the mechanism(s) by which antibody may aid in recovery are discussed.

Animals↗
PubMed1979

Lymphocyte-associated immune responses to canine distemper and measles viruses in distemper-infected gnotobiotic dogs.

Cellular immune responses of peripheral blood lymphocytes to canine distemper virus and measles virus were determined in vaccinated or infected gnotobiotic dogs, using the technique of syncytia inhibition. Cross-reactivity between viruses was detected in both groups of dogs. Peak responses in vaccinated dogs occurred 11 days after vaccination and declined to base-line levels by 3 weeks, whereas responses in infected dogs were present 30 days after inoculation. Fractionation experiments with peripheral blood lymphocytes indicated that synctia inhibition is probably mediated by T lymphocytes.

Animals↗
PubMed1979

A new plaque system for canine distemper: characteristics of the green strain of canine distemper virus.

A Vero cell adapted Green strain of canine distemper virus (CDV) was tested for its plaque-forming capacity in different cell lines. Plaque formation was observed in HEp-2, BS-C-1, and HeLa cells but not in Vero or dog kidney cells even though replication and cytopathology were observed in the latter cell types. In the cells in which the virus was capable of producing plaques, the plaques were observed within 24 h post infection and continued to increase in size with subsequent cellular destruction such that by 72 h postinfection the size of the plaques approached 0.5 mm. With the use of the plaquing technique, it was possible to demonstrate the thermal lability of the virus as well as the kinetics of adsorption. Thus, it was shown that the half-life of the virus was 125 min at 25 degrees C, 75 min at 35 degrees C, and 65 min at 37 degrees C. The rate of adsorption of CDV to HEp-2 cells was 17.2% in 30 min at 37 degrees C and continued slowly for 4 h before completion. Application of this rapid plaque-forming assay to plaque-reduction tests for CDV antibody and for CDV-infected cells by the infectious center assay are described.

Animals↗
PubMed1976

Cell-mediated immunity and age at vaccination associated with measles inoculation and protection of dogs against canine distemper.

The antibody-mediated immune response (AMIR) of dogs to measles and canine distemper viruses has been described. However, there is little information on the cell-mediated immune response (CMIR). The AMIR and the CMIR of dogs to canine distemper and to measles were examined. The CMIR was determined for 6 weeks by measuring the 3H-thymidine uptake by immune lymphocytes in the lymphocyte transformation test. Concurrently, canine distemper and measles virus serum-neutralization antibodies were measured by a microtitration serum-neutralization test. Dogs vaccinated with canine distemper virus had a CMIR and an AMIR to canine distemper. However, measles virus-vaccinated dogs had only a CMIR to canine distemper. A CMIR in the absence of an AMIR indicates that cell-mediated immunity is the most important immune mechanism in protecting measles virus-vaccinated dogs against canine distemper. Development of CMIR and AMIR to canine distemper and measles antigens depended on the age of the dog at the time of vaccination. Adult and juvenile dogs had immune responses to both canine distemper and measles. Neither virus, however, elicited an immune response in neonates.

Age Factors↗
PubMed1992

Canine distemper virus transcripts sequenced from pagetic bone.

Paget's disease is a chronic disease of the skeleton which is believed to be caused by a persistent virus of the paramyxovirus family. There is still conflict as to the precise identity of the virus(es) involved in causing this disease. Our previous results using in situ hybridisation have implicated distemper as a possible cause of this disease. In order to confirm these results, we have reverse transcribed RNA from pagetic bone and have specifically amplified for distemper and measles sequences using the polymerase chain reaction (PCR) technique. We have found that 8/13 of the patients examined had distemper and 1/10 cases had measles nucleic acids sequestered within their bone cells. One individual was found to have both viruses sequestered in his bone cells. Dideoxy sequencing of the distemper virus PCR products revealed 2% base pair changes in the nucleic acid sequences relative to the Onderstpoort strain of canine distemper. We can conclude that in Paget's disease, canine distemper and possible other paramyxoviruses reside in bone cells and that the persistent nature of the virus may be due to mutations in the viral genome.

Animals↗
PubMed1975

[Antibody formation and resistance in dogs vaccinated intravenously and subcutaneously against distemper and Rubarth's disease].

The results of the vaccination of dogs with Canivac F (distemper vaccine) and Canivac FH (distemper) hepatitis vaccine, are presented. The Canivac F vaccine was injected intravenously (i.v.) to 8 dogs, intramuscularly (i.m.) to 1 dog and subcutaneously (s.c.) to 1 dog. The Canivac FH was administered i.v. to 19 dogs, i.m. to 1 dog and s.c. to 18 dogs. All the dogs displayed no-postvaccination signs. Distemper antibodies were observed in blood sera of all dogs vaccinated with Canivac F after 9-10 and 20-21 days. In sera of dogs vaccinated with Canivac FH, distemper, antibodies were present in 14 of 18 serum samples after 9-10 days and in 26 of 27 samples after 20-21 days. The antibody titre did not depend on the vaccination route. The peak of antibody titre was observed after 37 to 51 days after vaccination. The hepatitis antibodies in dogs vaccinated with Canivac FH were found in 15 of 17 animals after 9-10 days, and in all 27 dogs examined after 20-21 days. On the basis of an intracerebral challenge with virulent distemper virus and by intraperitoneal challenge with virulent dog's hepatitis virus (Rubarth's disease), it was demonstrated that all the vaccinated dogs acquired the full immunity. In addition, it was found that vaccinated dogs kept in the environment contaminated naturally with Rubarth's disease virus were also resistant to the disease. All the non-vaccinated dogs were still susceptible to distemper or hepatitis infections. On the strength of the analysis of the obtained results and our previous studies, it can be assumed that Canivac F and FH vaccines produced in Poland are harmless and show a high immunogenic activity.

Adenoviridae↗
PubMed1978

Multiple sclerosis and canine distemper in Iceland.

Iceland offers a favourable opportunity to examine the suggested relationship between canine distemper and multiple sclerosis. Distemper is not enzootic in Iceland and distemper immunisation is not practised. However, importations result in occasional epizootics, three of which have occurred since 1909. Careful enumeration of multiple sclerosis indicates that there were 129 cases during the period 1946--65. When these cases are subdivided into six regions, by place of birth, regional period-prevalence rates were highest in two regions partially involved by distemper only once in the past 70 years. Also, there was substantial prevalence in a third region, encompassing Reykjavik, where the dog population has been kept very low for over 50 years. The Icelandic experience indicates that multiple sclerosis can occur at high incidence in the virtual absence of canine distemper or in the presence of a very small dog population.

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↗
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↗
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↗
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↗
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↗