J. Kisary
Hungarian Academy of Sciences
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Featured researches published by J. Kisary.
Avian Pathology | 1984
J. Kisary; Béla Nagy; Z. Bitay
Small viral particles of 19 to 24 nm in diameter with a buoyant density in CsCl of 1.43 g/ml were detected electron microscopically in samples taken from the gut of 10-day-old chickens suffering from a stunting syndrome. The viral particles are suggested to belong to the Parvoviridae and their possible role in the stunting syndrome is discussed.
Avian Pathology | 1985
J. Kisary
Specific pathogen free (SPF) White Leghorn chicken embryos and day-old chickens and day-old commercial broiler chickens were infected with a parvovirus (strain ABU) isolated from chickens with stunted growth. As a result, egg hatchability was significantly decreased and hatched chickens had enteritis and low vitality. Serious growth retardation, bad feathering and bone disorders were observed in infected broiler chickens. Similar signs were not seen in SPF White Leghorn chickens.
Avian Pathology | 2008
L. Zsak; K. O. Strother; J. Kisary
Poult enteritis mortality syndrome (PEMS) of turkeys and runting-stunting syndrome (RSS) of chickens are significant viral enteric diseases of poultry. Although a number of different viruses, including avian reoviruses, rotaviruses, astroviruses and coronaviruses, have been isolated from the intestinal contents of birds in affected poultry flocks, their role in PEMS and RSS is not yet understood. Here, we report the application of a molecular screening method to detection of novel viruses in intestinal samples of chickens and turkeys exhibiting characteristic signs of enteric disease. The technique is based on random amplification of particle-associated nucleic acids in clinical samples. Using this method we successfully identified parvovirus DNA sequences in intestinal homogenates of affected birds. This is the first time partial genomic sequences of autonomously replicating chicken and turkey parvoviruses have been described. Sequence analysis of the left end of the genome, including the complete non-structural gene, demonstrated that the chicken and turkey parvoviruses were closely related to each other and were representative of a novel member of the Parvovirus family. These parvoviruses may play a significant role in the aetiology of PEMS and RSS.
Avian Pathology | 1975
L. Stipkovits; A.A. El‐Ebeedy; J. Kisary; Lea Varga
This paper presents data about the isolation of members of the order Mycoplasmatales from material of goose origin. Acholeplasma laidlawii strains were isolated from 2 to 8 day old goslings with heavy fibrinous airsacculitis, peritonitis and perihepatitis. Losses reached 30% of the flock by the end of the 8th week of age. Acholeplasma axanthum strains were detected in goose-embryos that died on the 13th day of incubation. A significant loss (up to 60%) of embryos was observed in the flock and some layers died showing fibrinous peritonitis, salpingitis and abdominal airsacculitis. Mycoplasma gallinarum also was isolated from goose-embryo fibroblast tissue cultures. All strains except A. laidlawii caused cytoplasmic vacuolization and intracytoplasmic inclusion bodies in goose-embryo fibroblast tissue cultures. The alteration observed in chicken-embryo fibroblast cell cultures were similar; in addition, the A. laidlawii caused a marked pycnosis of the cells.
Avian Pathology | 1978
J. Kisary; D. Derzsy; J. Mészáros
Serial transfer of the goose parvovirus strain B, causal agent of Derzsys gosling disease, in cultured goose-embryo fibroblast (GEF) resulted in a mutant (designated as Bav) apathogenic for both goose embryos and susceptible goslings. Goose embryos inoculated with the 38th or higher passages of strain B survived the infection, although the virus replicated in their organs. Susceptible goslings survived challenge with the Bav strain without showing symptoms, and developed normally. Only 4.2% of gosling progeny of parents vaccinated twice with strain Bav died after challenge with the virulent strain B goose parvovirus compared with 95% of gosling progeny of unvaccinated parents. Progeny of vaccinated and unvaccinated geese were placed on a farm on which Derzsys disease was present. During the first month of life mortality was 7.7% in the progeny of vaccinated geese compared with 59.8% in the progeny of the unvaccinated geese. At 8 weeks of age the mean weight of the vaccinated goslings was 20% greater than for the unvaccinated goslings. These results indicate that the attenuated apathogenic Bav mutant is suitable for the immunisation of layers to protect their progeny by passive immunisation against Derzsys disease.
Avian Pathology | 1984
L. Zsák; J. Kisary
Viruses isolated from liver and gut of dead 2- to 4-week-old goslings were identified as adenoviruses. The main characteristics of the strains were: development of intranuclear inclusion bodies in virus-infected cells; a buoyant density of the infective particles in CsC1 of 1.33-1.34 g/ml; icosahedral virions measuring 78-83 nm in diameter which had no envelope; a linear duplex DNA genome with a molecular weight of 25-29 x 10(6) daltons. These adenoviruses did not cross-react in neutralisation tests with 11 fowl, two turkey and two duck adenovirus serotypes, however, they shared a common complement-fixing antigen with fowl adenoviruses. Based on the results of the cross-neutralisation tests and on the cleavage pattern of DNAs by BamHI and Hind III restriction endonucleases, the seven adenovirus strains studied represent three distinct goose adenovirus serotypes. The goose adenoviruses caused neither clinical symptoms nor pathological lesions after infection of 3-day-old goslings.
Avian Pathology | 1974
J. Kisary
The Hungarian, French and Dutch goose parvovirus isolates proved to be closely related to each others in the cross-neutralization test performed lin tissue culture system. The results differed from those obtained earlier in embryonated goose eggs and gosling-protection test.
Avian Pathology | 1977
J. Kisary
Laying geese naturally infected by the parvovirus agent of Derzsys disease transmit IgG type maternal immunoglobulins through the eggs to their offsprings. The passively acquired yolk antibodies persisted at a relatively high level until about 12-14 days of age, but were eliminated from the birds during the 3rd week of life. The IgG type immunoglobulins present in the specific hyperimmune sera used for preventive treatment have a half-life, about 6 days, and their blood level falls to a minimal value during the 2nd week following administration. The primary humoral immune response of geese to parvovirus is characterised by the production of initially IgM and then IgG type immunoglobulins. Gosling less than 20 days old began to produce antibodies later after antigenic stimulation and in lower titre than did older birds. The presence of passively acquired antibodies also interfered with the development of an active immune response. It follows that the most efficient approach to the protection of susceptible goslings against Derzsys disease is to boost their levels of maternal antibodies through active immunisation of the laying flocks.
Avian Pathology | 1982
L. Zsák; A. Székely; J. Kisary
Of 19 large flocks of geese in Hungary 15 were serologically positive to the egg drop syndrome 1976 (EDS-76) avian adenovirus strain B8/78. Sixty-five to 100% of the samples taken from each flock were positive with haemagglutination inhibition (HI) titres between 1:8 and 1:256. All the progeny of geese with HI antibodies had maternally derived antibodies. After infection per os of 8-, 19- and 29-day-old goslings with the B8/78 strain of EDS-76 adenovirus clinical signs of disease and mortality were not seen although the birds developed antibodies and shed the virus in the faeces. No lesions were noted using light microscopy. Egg production was unaffected in geese experimentally infected with B8/78 virus strain and there was no change in egg quality. The layers developed antibodies to EDS-76 adenovirus and shed the virus in the faeces. Contact-controls responded in the same way. The results of these experiments suggest that when investigating the origin of EDS-76 avian adenovirus infection not only ducks but also geese should be considered as a potential source of infection.
Avian Pathology | 1976
J. Kisary; A.A. El‐Ebeedy; L. Stipkovits
Of various mycoplasma strains of goose original, axanthum strains (609 and 612) caused the death both of goose and chicken embryos, A. laid-lawii strain (606) killed only goose embryos, whereas M. gallinarum (598) failed to kill either. Infection of 3-day-old goslings with these mycoplasmas resulted in no mortality but lesions were produced with A. axanthum in 9 of 10 birds. Less severe lesions were seen in fewer birds infected with other strains. Dual infection of 3-day-old goslings, with maternal antibody to goose parvovirus, with M. gallinarum (598) or A. axanthum (612) and a virulent parvovirus resulted in some death and all birds showed lesions.