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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.

Avian reoviruses are ubiquitous among poultry flocks. Although infection is usually present without disease, reoviruses may occasionally be involved in several disease syndromes of which viral arthritis/tenosynovitis in chickens is the most important, particularly in broiler breeds. While reoviruses have been isolated from turkeys and several other species of birds with various conditions, the presence of the virus has been conclusively linked with disease in relatively few instances. In chickens in particular, avian reoviruses with a wide spectrum of pathogenic capability have been isolated and several antigenic types exist. Diagnosis is dependent on the detection of the virus in clinical samples, although the presence of the virus does not necessarily confirm that this is the cause of the disease, except where reoviruses are detected in affected joints. Serological tests are usually difficult to interpret in view of widespread and frequently harmless reovirus infection. The principal approach to control of viral arthritis/tenosynovitis is by vaccination using attenuated vaccines in young birds, followed by inactivated preparations for breeders intended to protect chicks by maternal antibodies. Many vaccines are based on the S1133 strain isolated in the United States of America, but these may not be effective against antigenic variants.

Heterophil function was evaluated in 16 healthy chickens and in 46 chickens with experimentally induced staphylococcal tenosynovitis. In paired blood samples, heterophils from chickens with tenosynovitis had a significant increase in adherence, chemotaxis, phagocytosis, and bacterial killing of Staphylococcus aureus compared to heterophils from healthy chickens. The percent adherence of heterophils to nylon fiber columns increased significantly from a 78.4% mean +/- 6.6% standard deviation to 87.6% +/- 3.2% after induction of staphylococcal tenosynovitis. Heterophil movement following in vitro exposure to saline or endotoxin was increased in chickens with tenosynovitis; 3 +/- 1 heterophils/0.25 mm2 to 10 +/- 6 heterophils/0.25 mm2 and 136 +/- 29 heterophils/0.25 mm2 to 340 +/- 74 heterophils/0.25 mm2, respectively. Endotoxin-activated serum was chemoattractive for heterophils from all chickens. Flow cytometry was used to define the heterophil population on light scatter histograms, evaluate individual cell phagocytosis of latex beads, and quantitate the number of beads phagocytosed per heterophil. When incubated with increased numbers of beads, only heterophils from chickens with tenosynovitis phagocytosed higher numbers of beads. At heterophil to bead ratios of 1:10, the percentage of heterophils that phagocytosed beads increased from baseline values of 37.8% +/- 9.0% to post-infection values of 67.3% +/- 7.5%. Using 1:20 heterophil to bead ratios, heterophil phagocytosis increased from 38.7% +/- 9.9% to post-infection values of 79.8% +/- 7.3%. Heterophils from all chickens were able to phagocytose and kill log phase staphylococcal bacteria. After phagocytosis, the heterophils from chickens with staphylococcal tenosynovitis rapidly decreased the number of viable bacterial colony forming-units per milliliter by approximately one log.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunization of breeder chickens by eyedrop with viral arthritis/tenosynovitis vaccine strain S1133 (73rd egg passage) gave no immunity against day-old oral challenge of their progeny at 1 week postvaccination of the breeders, but progeny immunity was observed at 3, 4, 5, 6, and 7 weeks postvaccination of the breeders. Oral cross-challenge of immune progeny with viral isolates from Connecticut, West Virginia, California, Indiana, Pennsylvania, and Minnesota showed that in vitro neutralization of an isolate by anti-S1133 antiserum correlated with in vivo immunity of the progeny against oral day-old challenge with such an isolate.

A viral agent that was isolated from livers of commercial turkey poults that died at approximately two weeks of age was characterized as a reovirus. Experimental infection of day-old chickens with this reovirus isolate resulted in the development of tenosynovitis, hepatitis, and myocarditis. In vitro neutralization of the turkey reovirus isolate by antiserum against chicken reovirus correlated with in vivo protection of maternally immune chickens from day-old oral challenge with the turkey reovirus isolate.

The effect of cyclosporine A on reovirus-infected male broiler chickens was studied. Beginning at 1 or 10 days of age, 3 groups of 15 broilers were injected in the pectoral muscle with 50 mg of cyclosporine A (CSA) in oil per kg body weight every 3 days until 28 days. Controls were injected with olive oil. Two CSA-injected groups and one untreated group were orally infected with 1000 TCID50 of reovirus at 1 day of age. Cell-mediated immunity was evaluated at 17 and 24 days by a delayed-wattle-response test to injected phytohemagglutinin (PHA-M). Cyclosporine A and reovirus significantly (P less than 0.001) depressed the wattle response following the first injection of PHA-M but not the second. At necropsy 28 days postinoculation (PI), no gross lesions were apparent. Histologic lesions in birds infected with reovirus were lymphocytic pericarditis and tenosynovitis; synovial cells were hyperplastic, and heterophils and fibrin were in synovial spaces. Thymic medullary diameters were significantly (P less than 0.001) smaller in all CSA-treated birds. Although CSA suppressed cell-mediated immunity somewhat, there were no apparent differences in severity of microscopic lesions among reovirus-infected groups.

Previously untreated chicks and those treated neonatally with either cyclophosphamide (CY) or infectious bursal disease virus (IBDV) were subcutaneously inoculated with viral arthritis virus ( VAV ) to determine whether suppression of humoral immunity would affect VAV pathogenicity. No difference was apparent in the disease process that occurred in the immunosuppressed versus the nonimmunosuppressed chickens. However, in the immunosuppressed birds, VAV was recovered from the heart and tendon tissues earlier in the postinoculation (PI) period. Also, VAV inoculated immunosuppressed birds carried higher levels of serum gamma globulins at certain PI intervals than the VAV inoculated positive controls or the untreated negative control chickens. It is suggested that the suppression of the bursa of Fabricius (BF) by CY or IBDV did not interfere in the antibody production to VAV , but the antibody produced was qualitatively defective.

Two viruses serologically related to the tenosynovitis virus of chickens were isolated from two flocks of turkeys experiencing outbreaks of tenosynovitis. Both viruses produced a tenosynovitis when injected into the foot pad of young turkeys. Staphylococcus aureus was not isolated from either flock, nor was there any evidence of Mycoplasma synoviae antibody in either flock.

When chicks with maternal antibodies against infectious tenosynovitis (viral arthritis) virus were inoculated orally at 1 day old with tenosynovitis virus, they were protected against developing active tenosynovitis lesions 3 weeks later. They were not protected against subcutaneous inoculation, however. Breeder vaccination against tenosynovitis resulted in immunity of the progeny against oral infection at 1 day old, whereas progeny from unvaccinated breeders were susceptible to such a challenge.