SUMMARY. Severity of the tracheal histologic inflammatory response induced in broilers by ocular inoculation of two infectious bronchitis (IBV) and three Newcastle disease virus (NDV) commercial vaccines were evaluated. The vaccine was delivered by eye drop with a coarse spray to day-old chicks. The vaccines were given individually or in various combinations and were evaluated relative to nonvaccinated controls. Evaluations were performed on postvaccination (PV) days 7 and 14. Histologic endpoints included semiquantitative severity scoring of inflammatory components and quantitative morphometric determinations of inflammatory cell concentration, mucosal thickness, and percentage of ciliated mucosal surface. Strong positive correlations were observed between routine severity scoring and morphometric inflammatory parameters, whereas a negative correlation was present between inflammation severity and the percentage of mucosal ciliation. Variable, sometimes extensive, and often statistically significant differences in inflammatory responses were observed between the various vaccines. One IBV Massachusetts strain vaccine (IBV-A) produced the greatest overall inflammatory response when given alone or in combination with the NDV vaccines. Enhancement of tracheitis was seen on PV day 14 by covaccination of IBV-A with the NDV vaccines, but not by covaccination of another IBV Massachusetts strain vaccine (IBV-B) with NDV. Reduction in cilia percentage was observed for all vaccine groups relative to controls on PV day 7. However, although reactive cilia regeneration occurred on PV day 14 for most vaccine groups, a cilia regenerative response was not apparent for individual or NDV combination vaccination for IBV-A. The study also demonstrates that substantial microscopic trachea pathology may be present in vaccinated birds not exhibiting apparent clinical respiratory signs.

SUMMARY. Histologic and bacteriologic features for groups of average 31-day-old broilers displaying three gross categories of femoral head alterations were documented. Categories included simple femoral head separation (FHS), femoral head transitional changes (FHT), and femoral head necrosis (FHN). Groups with grossly normal (NORM) femoral heads and cull birds with FHN and having gross signs of sepsis (Cull-FHN) were also included in the study. There was a 10% occurrence of positive bacterial cultures for all birds tested. Most positive cultures (33%) were found in the Cull-FHN group, while only a 12% occurrence was seen in the FHS group, and no positives were present in the FHT or FHN groups. A 14% total occurrence of femoral bacterial chondronecrosis with osteomyelitis or simple osteomyelitis (BCO-O) was observed. A progressive increase in the prevalence of BCO-O was apparent between groups going from NORM (0%), FHS (4%), FHT (14%), FHN (13%), and reaching a maximum of 67% in the Cull-FHN group. Minimal to mild femoral head cartilage necrosis was present in 40% of NORM broilers and 100% of the FHS, FHT, and FHN groups, but at moderate severity in 20% of the Cull-FHN group. Thus, the majority of FHN cases were associated with aseptic cartilage necrosis rather than BCO-O. These findings suggest that aseptic cartilage necrosis may be as important as septic necrosis as a cause of gross femoral head disease. A 26% overall occurrence was seen for hip synovitis–arthritis, but group differences were not statistically significant. Synovitis was not seen in the NORM group and was present in some (12%) of the FHS group but was observed at a high rate in both the FHN (43%) and the Cull-FHN (50%) groups. Morphometric measurements demonstrated that the area size of femoral fibrous cortical defects or “cutback zones” were generally larger for all gross categories relative to NORM, with a significant difference between NORM and FHS groups. This study underscores the multifactorial etiology of FHN and the importance of conducting both histologic and bacteriologic evaluations in which gross evidence of FHN or BCO-O occurs.

SUMMARY Routine and quantitative histologic studies on femoral head separation (FHS) associated with coxofemoral joint disarticulation at necropsy were conducted on 125 femoral heads collected from 21- to 50-day-old clinically normal broilers. The study compared groups demonstrating grossly detached femoral heads (DFHs) with those having attached femoral heads (AFHs). Marked microscopic lesions compatible with osteochondrosis (OCD) consistently occurred along the separation surface in the DFH population. The histologic changes consisted of cartilage degeneration and necrosis sometimes forming small clefts or microfractures. Hemorrhage and less frequent inflammatory cells were often present along the separation surfaces. Small foci of OCD in the femur occurred in the AFH group with lesser frequency and severity. The histologic changes were mainly found within the proximal proliferative zone of the physis near the epiphyseal junction. Histomorphometry disclosed significant quantitative reductions in chondrocyte density with increased pyknosis occurring adjacent to the separation site and to a lesser extent in deeper regions of the growth plate for the DFH compared with AFH. Measurements made along the separation surface of the percentage length occupied by osteochondrotic defects and actual separated cartilage disclosed significant differences between evaluation groups. However, determinations of vascular canal areas present within two or more regions of the growth plate revealed a slight and significant increased area for DFH compared with AFH. Severity scores for the occurrence of microthrombi within the growth plate showed no difference between the groups. The pathogenesis of FHS in broilers is related to defective cartilage production or degeneration resulting in increased fragility. This contrasts with the proposed pathogenesis of OCD in mammals, which involves ischemic necrosis due to underlying vascular defects. The results for the FHS-disarticulation model also differ from those reported for glucorticoid-induced femoral head necrosis in broilers. The FHS-associated lesions occurred without histologic evidence of bacterial chondritis or osteomyelitis.

Even though males represent only 8%–12% of the birds of a breeder flock, their role in infectious bronchitis virus (IBV) dissemination is largely unknown. We first assessed the effect of IBV replication in the chicken testes. Ten-week-old males were inoculated with Arkansas (Ark) or Massachusetts (Mass) IBV virulent strains. Seven days postinoculation (DPI) IBV RNA was detected in testicles of 100% of M41- and in 96% of Ark-infected males. Marginal nonsynonymous variation was detected in spike (S) gene of the predominant population of IBV replicating in the testes compared to the S gene of the predominant population of viruses prior to inoculation. IBV M41 and Ark were detected in spermatogonia and Sertoli cells of testicles of infected roosters by immunofluorescence, without evident histopathological changes. We next assessed venereal transmission of IBV by artificially inseminating 54-wk-old hens either with semen from IBV-infected roosters or with IBV suspended in naïve semen. IBV RNA was detected in the trachea of all hens inseminated with IBV-spiked semen and in 50% of hens inseminated with semen from IBV-infected males. The egg internal and external quality was negatively affected in hens inseminated with semen containing IBV. These results provide experimental evidence for IBV venereal transmission.

Chickens, turkeys, and other poultry in a production environment can be exposed to stressors and infectious diseases that impair innate and acquired immunity, erode general health and welfare, and diminish genetic and nutritional potential for efficient production. Innate immunity can be affected by stressful physiologic events related to hatching and to environmental factors during the first week of life. Exposure to environmental ammonia, foodborne mycotoxins, and suboptimal nutrition can diminish innate immunity. Infectious bursal disease (IBD), chicken infectious anemia (CIA), and Marek's disease (MD) are major infectious diseases that increase susceptibility to viral, bacterial, and parasitic diseases and interfere with acquired vaccinal immunity. A shared feature is lymphocytolytic infection capable of suppressing both humoral and cell-mediated immune functions. Enteric viral infections can be accompanied by atrophic and depleted lymphoid organs, but the immunosuppressive features are modestly characterized. Some reoviruses cause atrophy of lymphoid organs and replicate in blood monocytes. Enteric parvoviruses of chickens and turkeys merit further study for immunosuppression. Hemorrhagic enteritis of turkeys has immunosuppressive features similar to IBD. Other virulent fowl adenoviruses have immunosuppressive capabilities. Newcastle disease can damage lymphoid tissues and macrophages. Avian pneumovirus infections impair the mucociliary functions of the upper respiratory tract and augment deeper bacterial infections. Recognition of immunosuppression involves detection of specific diseases using diagnostic tests such as serology, etiologic agent detection, and pathology. Broader measurements of immunosuppression by combined noninfectious and infectious causes have not found general application. Microarray technology to detect genetic expression of immunologic mediators and receptors offers potential advances but is currently at the developmental state. Control methods for immunosuppressive diseases rely largely on minimizing stress, reducing exposure to infectious agents through biosecurity, and increasing host resistance to infectious immunosuppressive diseases by vaccination. A longer term approach involves genetic selection for resistance to immunosuppressive diseases, which has shown promising results for MD but equivocal results for IBD and CIA. Abbreviations: BF = bursa of Fabricius; CAV = chicken anemia virus; CIA = chicken infectious anemia; FAV = fowl adenovirus; HE = hemorrhagic enteritis; HEV = hemorrhagic enteritis virus; HVT = turkey herpesvirus; IBD = infectious bursal disease; IBDV = infectious bursal disease virus; IBV = infectious bronchitis virus; MD = Marek's disease; MDV = Marek's disease virus; MHC = major histocompatibility complex; NDV = Newcastle disease virus; ORT = Ornithobacterium rhinotracheale ; PEMS = poultry enteritis and mortality syndrome; REV = reticuloendotheliosis virus; RSS = runting stunting syndrome; SE = Salmonella enterica serovar Enteritidis; ST = Salmonella Typhimurium

Our previous genetic characterization of chicken anemia virus (CAV) in commercial broiler chickens in Alabama revealed a previously undetected polymorphism: a glutamine codon at VP1 position 22, in 7 of the 14 sequences. The novel glutamine codon was always found in association with a VP1 “hypervariable region” identical to CAV field isolates that replicate poorly in culture. The complete genome of CAV73, representative of the sequences with the novel polymorphism, was generated from cloned polymerase chain reaction (PCR) fragments amplified directly from naturally infected tissues. CAV73 had been detected in 31-day-old broilers submitted for examination for reasons unrelated to anemia. After electroporation of the cloned genomes into MDCC-CU147 lymphoblastoid cells, the regenerated CAV caused the culture to fail within 9 days, and the medium contained 5 × 10 6 TCID 50 CAV/ml. Use of MDCC-CU147 cells was essential, as identical electroporation of MDCC-MSB1 cells failed to generate CAV able to destroy the culture within 8 wk. Regenerated CAV73 produced anemia and severe lymphocytic depletion of the thymus when inoculated into susceptible 3-day-old chickens and was reisolated from these chickens. Furthermore, it replicated in low- and high-passage MDCC-MSB1 cells similarly to a low-passage CAV field isolate that contains a different VP1 “hypervariable region.” The regeneration of CAV from PCR products directly from naturally infected carcasses, as performed in this study, provides a tool for the evaluation of distinct genetic polymorphisms that may be detected in specimens where infective virions are no longer available. Our results also provide some insight into the differential susceptibility of cell lines for low-passage CAV field isolates.