PubMed Health⌕ Search

Biomedical subjects

T J Bagust

Publications and source records attributed to T J Bagust.

At least 19 recordsLinked to original sources
PubMed2004

Detection of subgroup J avian leukosis virus infection in Australian meat-type chickens.

OBJECTIVE: To determine the extent of avian leukosis virus subgroup J (ALV-J) infection in Australian broiler breeder flocks, using virus isolation and molecular biological detection. Any resultant ALV-J viral isolates to be characterised by neutralisation cross testing in order to determine antigenic relationships to overseas isolates of ALV-J. STUDY DESIGN: Samples of blood, feather pulp, albumen and tumours were obtained from broiler breeder flocks which represented four genetic strains of meat chickens being grown in Victoria, South Australia, NSW and Queensland. Dead and ailing birds were necropsied on farm and samples were collected for microscopic and virological examinations. Virus isolation was carried out in C/O and DF-1 CEF cultures and ALV group specific antigen was detected in culture lysates using AC-ELISA. Micro-neutralisation assay was used for antigenic characterisation of selected isolates. Genomic DNA was isolated from cultured cells, tumours and feather pulp. ALV-J envelope sequences were amplified by PCR using specific ALV-J primers while antibodies against ALV-J were detected by ELISA. RESULTS: A total of 62 ALV-J isolates were recovered and confirmed by PCR from 15 (31.3%) of 48 breeder flocks tested. Antibody to ALV-J was detected in 20 (47.6%) of the 42 flocks tested. Characteristic lesions of myeloid leukosis caused by ALV-J were found in affected flocks. The gross pathological lesions were characterised by skeletal myelocytomas located on the inner sternum and ribs, neoplastic enlargement of the liver, and in some cases gross tumour involvement of the spleen, kidney, trachea, skeletal muscles, bone marrow, skin and gonads. Microscopically, the tumours consisted of immature granulated myelocytes, and were present as focal or diffuse infiltrations in the affected organs. Virus micro-neutralisation assays demonstrated antigenic variation among Australian isolates and to overseas strains of ALV-J. CONCLUSION: ALV-J infection was prevalent in Australian broiler breeder flocks during 2001 to 2003. Australian isolates of ALV-J show a degree of antigenic variation when compared to overseas isolates.

Animals↗
PubMed2000

Avian infectious laryngotracheitis.

Avian infectious laryngotracheitis (ILT) herpesvirus continues to cause sporadic cases of respiratory disease in chickens world-wide. Sources of transmission of ILT infection are three-fold, namely: chickens with acute upper respiratory tract disease, latently infected 'carrier' fowls which excrete infectious laryngotracheitis virus (ILTV) when stressed, and all fomites (inanimate articles as well as the personnel in contact with infected chickens). Infectious laryngotracheitis virus infectivity can persist for weeks to months in tracheal mucus or carcasses. Rigorous site biosecurity is therefore critical in ILT disease control. Furthermore, while current (modified live) ILT vaccines can offer good protection, the strains of ILTV used in vaccines can also produce latent infections, as well as ILT disease following bird-to-bird spread. The regional nature of reservoirs of ILTV-infected flocks will tend to interact unfavourably with widely varying ILT control practices in the poultry industry, so as to periodically result in sporadic and unexpected outbreaks of ILT in intensive poultry industry populations. Precautions for trade-related movements of chickens of all ages must therefore include an accurate knowledge of the ILT infection status, both of the donor and recipient flocks.

Animals↗
PubMed1986

Responses of cattle, sheep and poultry to a recombinant vaccinia virus expressing a swine influenza haemagglutinin.

Groups of cattle, sheep and poultry were inoculated with a recombinant vaccinia virus expressing the haemagglutinin of the swine influenza virus A/NJ/11/76. No adverse clinical responses were recorded and none of the animals developed a viraemia when inoculated with the recombinant or wild-type vaccinia virus. Recombinant virus reisolated from lesions in cattle was stable, maintaining its thymidine kinase negative phenotype and ability to express the swine influenza haemagglutinin. Antibodies to the influenza haemagglutinin were detected in cattle, sheep and poultry inoculated with the recombinant virus. While no animals inoculated with wild-type virus developed these antibodies, there was no detectable spread of either recombinant or wild-type virus from the inoculation sites or to in-contact uninoculated animals. The results indicate that recombinant vaccinia viruses can induce immune responses in cattle, sheep and poultry demonstrating their potential as vaccine vectors in a variety of important veterinary species.

Animals↗
PubMed1985

Antibody to the 32K structural protein of infectious bursal disease virus neutralizes viral infectivity in vitro and confers protection on young chickens.

Chicken sera containing IgG antibodies specific for the 32 000 (32K) mol. wt. structural polypeptide of infectious bursal disease (IBD) virus, as assessed by Western blotting, neutralized the in vitro infectivity of tissue culture-adapted IBD virus. When injected into young chickens, the serum passively protected them from challenge with pathogenic IBD virus. Chickens immunized with the 32K structural polypeptide of IBD virus, prepared by electroelution from SDS-PAGE gels, produced antibody detectable by ELISA and the virus neutralization assay, while chickens immunized with the 37K or 41.5K viral polypeptides synthesized antibody detectable by ELISA, but only very low levels of virus-neutralizing antibody. The immunoglobulin fraction of sera obtained from chickens immunized with the 32K polypeptide, but not the 41.5K polypeptide, passively protected chickens from infection with IBD virus. It is concluded that the 32K polypeptide is a major protective immunogen of IBD virus.

Animals↗
PubMed1985

Variation in susceptibility to avian sarcoma viruses and expression of endogenous avian leukosis virus antigens in specific pathogen-free chicken lines.

Five lines of chickens maintained as specific pathogen-free flocks in Australia were characterized in relation to endogenous antigens and endogenous avian leukosis virus expression. Embryos of line N were predominantly of C/E phenotype, uniformly positive for group-specific antigen and chick helper factor (gs+chf+) and 38% expressed endogenous virus at a very low titre. Embryos of line M4 were uniformly of C/ABE phenotype and were either gs+chf+ or gs-chf+. Line W19 embryos segregated for susceptibility to viruses of subgroup A, B and D and were either of C/E or C/ABE phenotype. The majority of W19 embryos were gs+chf+ with a small proportion being gs+chf-. Line I13 embryos were either of C/0 or C/ABE phenotype, uniformly gs-chf- and 44% of embryos expressed endogenous virus at a low titre. Line S segregated for susceptibility to subgroup E virus and embryos were either of C/E or C/0 phenotype, while the majority of embryos from line S were gs-chf- with some embryos being gs+chf+ or gs-chf+. The degree of interference of gs+chf+ and gs-chf+ phenotypes with subgroup E virus infection was identical with the interference patterns of classical gs+chf+ and gs-chf+ phenotypes. The resistance to infection with avian sarcoma viruses of subgroups E in lines N and M4, and to a degree in line W19, was highly associated with the presence of chf. Resistance to subgroup E virus was independent of chf in lines S and I13, probably being under the control of an independent locus. Cellular restriction of endogenous virus replication existed in all subgroup E virus-susceptible cells of line I13 in contrast to cells of line S which supported replication of endogenous virus. The phenotype of chicken cells for the expression of endogenous gs antigen and chf could accurately be predicted from the test performed on whole blood cells.

Animals↗
PubMed1984

Development of the normal gastrointestinal microflora of specific pathogen-free chickens.

The development of the normal intestinal microflora of the small intestine, caecum and large intestine of specific pathogen-free (SPF) chickens, was studied in the period from hatching to 84 days of age. No bacteria were detected in any of the sites at hatchery (day 1), but by day 3 significant levels of faecal streptococci and coliforms were isolated from all sites. The flora of the small intestine was limited to faecal streptococci and coliforms for the first 40 days and then lactobacilli became established and dominated the flora. A large variety of facultative and strictly anaerobic organisms colonized the caecum. Many of these species were transient and were only present for a limited period; after 40 days the flora stabilized to consist predominantly of faecal streptococci, Escherichia coli, Bacteroides spp. and Lactobacillus sp. The flora of the large intestine was composed of organisms also present in the small intestine or the caecum. These findings differ from previously published studies on conventionally reared chickens in that the number of species isolated and the population levels of organisms are much lower. This probably reflects the absence of continuous environmental challenge to the chickens because of the housing and feeding facilities in which the chickens were maintained.

Animals↗
PubMed1983

Inhibition of glycosylation by corynetoxin, the causative agent of annual ryegrass toxicity: a comparison with tunicamycin.

The biological activities of corynetoxins, the causative agents of annual ryegrass toxicity, were compared with those of the closely related tunicamycins and found to be essentially identical. Both showed similar antibiotic activity against Newcastle disease virus and a range of gram-positive bacteria. In preparations of rat liver rough microsomes they also strongly inhibited the uridine diphospho-N-acetylglucosamine (UDP-GlcNAc):dolichol-P N-acetylglucosamine-1-phosphate (GlcNAc-1-P) transferase, an enzyme essential for N-glycosylation of glycoproteins. Pretreatment of rats with corynetoxins resulted in dose- and time-related reduction in the level of activity of this transferase in liver microsomal preparations. The implications of this reduction are discussed with reference to annual ryegrass toxicity, the only field disease known to be caused by tunicamycin-related compounds. Both corynetoxin and tunicamycin produced similar neurological effects and increased vascular permeability in nursling rats and they showed similar LD50-values of 137 and 132 micrograms/kg, respectively, in the nursling rats.

Animals↗
PubMed1979

Infection studies on a reticuloendotheliosis virus contaminant of a commercial Marek's disease vaccine.

Reticuloendotheliosis virus (REV) was isolated in cell cultures from commercial Marek's disease (herpesvirus of turkeys) vaccine and re-isolated from the organs of vaccinated chickens. Runting and feathering abnormalities were produced when 1-day-old specific pathogen free chickens were inoculated with REV. Histopathological lesions in infected chickens were hypoplasia of the thymus, bursa and spleen, and inflammation of the proventriculus, kidneys and liver. Serological responses to REV were detected by the indirect immunoflorescence test in chickens directly inoculated with contaminated vaccine, and spread of REV infection to in-contact chickens was demonstrated by histopathological and serological investigations.

Animals↗
PubMed1975

Coital exanthema in stallions.

Equine coital exanthema can be produced experimentally in stallions by inoculation with an equine herpesvirus (strain 65/61) and be transmitted during coitus with an infected mare. Serological responses to this infection include the production of complement-fixing and serum-neutralizing antibodies which reach maximum levels 14 to 21 days after infection. Complement-fixing antibodies decline rapidly and are usually not detectable by 60 days after infection, whereas serum-neutralizing antibody activity is maintained for at least 1 year. This disparity provides a useful method for the diagnosis of recent infections and estimation of the temporal incidence of infection in groups of mares. It seems likely that clinically normal carrier mares spread the virus on studs where the disease has previously not occurred.

Animals↗