Clonal anergy of CD117+chB6+ B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance.

BACKGROUND: The pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown. RESULTS: In this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies. In congenitally infected chickens, immune organs, particularly the bursa of Fabricius, were poorly developed. Moreover, IgM-and IgG-positive cells and total immunoglobulin levels were significantly decreased in these chickens. Large numbers of bursa follicles with no differentiation into cortex and medulla indicated that B cell development was arrested at the early stage. Flow cytometry analysis further confirmed that ALV-J blocked the differentiation of CD117+chB6+ B cell progenitors in the bursa of Fabricius. Furthermore, both the humoral immunity and the immunological capability of B cells and their progenitors were significantly suppressed, as assessed by (a) the antibody titres against sheep red blood cells and the Marek's disease virus attenuated serotype 1 vaccine; (b) the proliferative response of B cells against thymus-independent antigen lipopolysaccharide (LPS) in the spleen germinal centres; and (c) the capacities for proliferation, differentiation and immunoglobulin gene class-switch recombination of B cell progenitors in response to LPS and interleukin-4(IL-4) in vitro. CONCLUSIONS: These findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J.

Congenital cerebellar dysplasia in White Leghorn chickens (Gallus gallus domesticus).

Congenital cerebellar anomalies have been rarely reported in birds. We examined cerebellums with disorganized folia from seven specific-pathogen-free White Leghorn chickens (Gallus gallus domesticus). Islands of heterotopic cortex were distributed from the deeper cortices to the medulla in the cerebellum. The characteristic lesions were composed of randomly admixed components of the cerebellar cortex, including Purkinje cells, a molecular layer and granular cells. Immunofluorescent analysis revealed Purkinje cells with haphazardly extended dendrites and a lack of Bergmann's glial fibres in the foci. Chicken parvovirus, Aino virus and avian retrovirus were not detected in the affected birds by polymerase chain reaction. This is the first report of cerebellar dysplasia in chickens possibly caused by a genetic abnormality.

Congenital cataract in 1-day-old French Mulard ducklings.

Ocular opacity, associated with reluctance to move and inability to feed properly, was observed in approximately 1% of all newly hatched females from several related flocks of Mulard ducks. A 5-week follow-up study of 10 1-day-old affected females was performed, and they were compared with 10 control animals. Clinical, ocular and ultrasonographic examinations, and a complete necropsy of two animals per group with histological examination of the eye, were performed weekly. A bilateral immature cortical anterior cataract was diagnosed at ocular examination and confirmed by ultrasonography in affected ducks. Dyscoria was occasionally observed in affected animals. Severe cataract, with Morgagnian globules, severe anterior fibre liquefaction and disorganization were observed by photonic microscopy. No retinal or choroidal lesions were observed. No progression or repair of ultrasonographic and microscopic lesions could be detected during the 5 weeks of examination. The female predisposition for the ocular lesions suggests a congenital sex-linked recessive cataract.

Congenital intestinal incarceration in broiler chickens.

The present work describes specific congenital intestinal accidents found in commercial broiler chickens where the affected individuals have their intestinal loops translocated outside the abdomen. These anomalies have been observed in many embryos that failed to hatch, in newly hatched chicks, as well as in broilers at various stages of growth. It appears that these lesions stem from incomplete closure of the abdominal cavity during the last stages of embryonic development.

Two congenital abnormalities in domestic chickens.

During routine necropsies performed in domestic chickens, two abnormalities were noticed in adult White Leghorn female birds; one was of the sternal keel (carina), and the other was of the cecum.

Skeletal abnormalities in domestic chicken.

In 14,891 necropsies performed on domestic poultry during January 1976 to October 1977, two cases of skeletal abnormalities were found. One was a tarsometatarsal spur in an adult female chicken, and the other was a crossed-beak associated with microphthalmia.

Congenital anomalies of domestic fowl: seven cases.

In 13,483 necropsies of domestic fowl, six anomalies were recorded: bifurcation of the metasternum, duplication of the ileum, pancreas divisum (partial), vesica fellea occulta, aplasia of the left cecum, and aplasia of the right kidney (2 cases).

The effect of experimental turkey embryo infection with Mycoplasma meleagridis on weight, weight gain, feed consumption, and conversion.

Turkey poults were obtained from an earlier trial where hatchability performance of a group of embryos experimentally infected with Mycoplasma meleagridis [MM(+)] was compared with that of a group of uninfected cohorts [MM(-)]. In the present trial, post-hatch production parameters compared were weight, weight gain, feed consumption, feed conversion, culling, and mortality. Both toms and hens were monitored for 16 weeks, and a group of randomly selected toms was monitored for 22 weeks. Final liveweights and dressweights of hens were compared at 17 weeks, and those of the toms were compared at 23 weeks. Hens showed no significant (P less than 0.05) differences in the measured parameters during the 16-week period, nor did the initial population of toms, except in weight gain during the final period (weeks 12-16) and in final weight at week 16, which were significantly (P less than 0.05) greater in the MM(+) toms than in their MM(-) cohorts. Dressweights at slaughter of MM(+) hens were significantly greater than those of MM(-) hens, but liveweights of hens at slaughter and both liveweights and dressweights of toms at slaughter did not differ significantly. This inability of MM(-) turkeys to demonstrate a comparative advantage over MM(+) birds agrees with an earlier trial (4), in which MM(+) poults had weights superior to those of MM(-) cohorts during the first 3 to 4 weeks of life (4). These data indicate that the theory of superior performance in association with MM(-) birds must be reevaluated before the benefits derived from an M. meleagridis eradication program can be measured.

Brain lesions in mallard ducklings from parents fed methylmercury.

Methylmercury dicyandiamide was fed to mallard ducks at 3 ppm mercury. Mercury accumulated in the eggs to an average of 7.18 and 5.46 ppm on a wet-weight basis in 2 successive years. Mercury in the eggs is believed to have caused brain lesions in the hatched ducklings. Lesions included demyelination, neuron shrink-age, necrosis, and hemorrhage in the meninges overlying the cerebellum. Brains of dead ducklings contained an average of 6.17 and 5.19 ppm mercury on a wet-weight basis in 2 successive years.

Vertical transmission of reticuloendotheliosis virus in breeder turkeys.

Epizootiological studies were conducted on a commercial turkey breeder flock naturally infected with nondefective reticuloendotheliosis (RE) virus. Although RE virus was isolated from 27 (46%) of the 59 hens studied, only 4 of the 45 hens tested transmitted RE virus to progeny during a 6-week observation period and the overall transmission rate was 1.8%. The transmitter hens were of two types: three hens were consistently viremic and antigenemic and lacked antibody; one hen was viremic but lacked detectable viral antigen and possessed antibody. Toms appeared to play no role in vertical transmission of the infection. Of several tests evaluated for detection of transmitter hens, the direct enzyme-linked immunosorbent assay on albumen was probably best, since it detected three of four transmitter hens, detected relatively few nontransmitter hens, and had the best consistency of any test. No significant differences in hatchability were found between eggs from viremic and non-viremic hens. These findings can be utilized in the development of programs for eradication of RE virus from turkey breeding flocks.

Teratogenic activity of Arasan fed to broiler breeder hens.

Tetramethylthiuramdisulfide (TMTD), the active ingredient in Arasan, fed to broiler breeder hens at 10, 20, or 40 ppm depressed egg production, reduced hatchability, and resulted in soft-shelled eggs. The progeny of these hens had anomalies manifested by bilaternal medial deviation of the toes, exophthalmia, and shortened femurs. Broiler breeder hens that consumed a ration containing 80 ppm of TMTD produced only soft-shelled eggs.

Genetic cellular resistance to subgroup E avian leukosis virus in slow-feathering dams reduces congenital transmission of an endogenous retrovirus encoded at locus ev21.

The gene ev21, which encodes an infectious endogenous subgroup E avian leukosis virus (ALV-E), designated EV21, is closely linked to the sex-linked, slow-feathering (SF) gene K. To address the relationship between congenital transmission of EV21 and host susceptibility to ALV-E infection, SF roosters that were heterozygous for the dominant gene for susceptibility to ALV-E were mated with ev-negative rapid-feathering (RF), subgroup E-resistant dams to produce SF and RF progeny. The SF female progeny that were heterozygous ALV-E susceptible were viremic at hatch and, when mature, consistently shed the ALV group-specific antigen, p27, in the egg albumen they produced. In contrast, SF females that were homozygous ALV-E resistant were neither viremic at hatch nor shedders of ALV p27. Infectious ALV-E assays of progeny from susceptible and resistant SF dams confirmed that maternal cellular resistance to ALV-E limited congenital transmission of EV21. It is proposed that, in progeny, immunologic tolerance toward exogenous ALV infection due to congenital transmission of antigenically related endogenous viruses may be abrogated by selection for cellular resistance to ALV-E in SF lines used as female parents of feather-sexed crosses.

Influence of congenital transmission of endogenous virus-21 on the immune response to avian leukosis virus infection and the incidence of tumors in chickens.

After contact exposure to Strain RPL-40 avian leukosis virus-infected hatchmates, a dilatory neutralizing antibody response and prolonged RPL-40 viremia was found among most pullets that were congenitally infected with endogenous virus 21 (EV21). Conversely, most of the hatchmates that were not congenitally infected seroconverted within 10 wk after exposure to Strain RPL-40 virus. Compared with noncongenitally infected hatchmates, EV-21 infection-induced tolerance to pathogenic avian leukosis viruses was reflected in a significantly higher incidence of lymphomas in congenitally infected hens. The rate of seroconversion and the incidence of RPL-40 virus-induced tumors among noncongenitally infected daughters from slow-feathering dams homozygous resistant to EV were similar to those found among daughters of rapid-feathering dams that lacked genetic locus ev21. Results suggest that selection for resistance to EV may eliminate tolerance toward oncogenic field strains of avian leukosis viruses and may improve the performance of progeny from a feather-sex cross.

Ectopic feather follicles in a chicken teratoma or malformation.

At necropsy of an 8-week-old pullet a 0.75 X 5.0 cm. yellowish, moderately firm cigar-shaped object was seen in the greater abdominal air sac lying parallel to the border of the right hepatic lobe. A capsule of 5 tissue layers (from inside outward-stratified squamous epithelium fibrous tissue, longitudinal muslce, fibrous tissue and circular muscle) enclosed featherlike structures which had developed from the stratified squamous epithelial layer. This combination of tissue components constituted ectopic follicles and feathers in a malformation or teratoma.

First report of polymelia and a rudimentary wing in a Nigerian Nera black chicken.

A case of polymelia with a rudimentary wing is described in an eight-week-old Nera black chicken (Gallus domesticus). It is a rare disorder with chromosomal aberrations, which are associated with congenital limb malformations. The condition was observed during routine physical examination of a flock of 2000 poultry birds in the month of February 2008 in Ibadan, Nigeria. After physical examination, the bird was found to have two extra well-developed legs, which were shorter than the normal legs. These extra legs were also found to be non-functional. Similarly, a rudimentary wing, which was highly vestigial, was found on the left lateral side of the bird very close to the cloaca. The bird died at the age of eight weeks. This is the first reported case of polymelia with a rudimentary wing in a domestic chicken in Nigeria.