title: Heterophil function and resistance to staphylococcal challenge in broiler chickens naturally infected with avian leukosis virus subgroup J.
abstract: Avian leukosis virus subgroup J has a high tropism for myeloid lineage cells and frequently induces neoplastic transformation of myelocytes. The impact of congenital avian leukosis virus subgroup J infection on the function of circulating heterophils and susceptibility to staphylococcal infection was investigated. Six-week-old broiler chickens negative for exogenous avian leukosis viruses or congenitally infected with avian leukosis virus subgroup J were inoculated intravenously with 10(6) colony-forming units of Staphylococcus aureus, and pre- and postinoculation heterophil function was assessed. All chickens developed a leukocytosis with heterophilia after inoculation, but total leukocyte and heterophil counts were significantly higher in leukosis-negative chickens than in virus-infected chickens. Tenosynovitis was more severe in leukosis-negative chickens, and 2/10 (20%) of the virus-infected chickens had no histologic evidence of tenosynovitis. Osteomyelitis in the tibiotarsus or tarsometatarsus developed in 5/10 (50%) of the chickens in each group. S. aureus was recovered from the hock joint of 6/10 (60%) of the chickens in each group. Heterophils from all chickens exhibited similar phagocytic ability pre- and postinoculation. Heterophils from virus-infected chickens exhibited less bactericidal ability preinoculation than did heterophils from leukosis-negative chickens. However, postinoculation bactericidal ability was similar in both groups. Avian leukosis virus subgroup J provirus was present in heterophils isolated from congenitally infected chickens. Heterophils isolated from broiler chickens congenitally infected with avian leukosis virus subgroup J exhibit no significant functional deficits, and infected and uninfected chickens exhibit similar susceptibility to staphylococcal infection.
authors.affiliation: Department of Veterinary Pathology, College of Veterinary Medicine, University of Georgia, Athens, 30602, USA.
authors.forename: N L
authors.initials: NL
authors.lastname: Stedman
authors.forename: T P
authors.initials: TP
authors.lastname: Brown
authors.forename: R L
authors.initials: RL
authors.lastname: Brooks
authors.forename: D I
authors.initials: DI
authors.lastname: Bounous
mesh_terms: D000818:Animals; D001353:Avian Leukosis / Q000151:congenital* / Q000276:immunology / Q000382:microbiology; D001354:Avian Leukosis Virus / Q000145:classification; D002645:Chickens; D015169:Colony Count, Microbial / Q000662:veterinary; D004198:Disease Susceptibility / Q000662:veterinary; D005260:Female; D006098:Granulocytes / Q000276:immunology / Q000502:physiology*; D007958:Leukocyte Count / Q000662:veterinary; D008297:Male; D010019:Osteomyelitis / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D010587:Phagocytosis; D011201:Poultry Diseases / Q000151:congenital* / Q000276:immunology / Q000382:microbiology; D013203:Staphylococcal Infections / Q000276:immunology / Q000662:veterinary*; D013211:Staphylococcus aureus / Q000472:pathogenicity*; D013717:Tenosynovitis / Q000276:immunology / Q000382:microbiology / Q000662:veterinary