Higher rates of internal ovulations occur in broiler breeder hens treated with testosterone.

Maximal profit in both the commercial egg and meat industries requires that the quantity of oviposited eggs closely matches the quantity of large yellow follicles maturing in the ovary. While laying hens are genetically selected for maximal egg production and strategies for management of broiler breeders have been constructed to achieve a similar outcome, a percentage of ovarian follicles that are selected into the ovulatory hierarchy in these hens still never make it to oviposition possibly due to atresia of large yellow follicles or internal ovulation of the oocyte into the peritoneal cavity rather than the oviduct. The causes and mechanisms responsible for these processes remain unclear, however, evidence in wild birds suggests that stressful and/or territorial challenges may stimulate oocyte losses. Since testosterone and corticosterone are central to the responses to territorial intrusions and stress, respectively, and since both large yellow follicles and the oviduct that will engulf them are sensitive to hormonal cues, one or both hormones may play a role in the loss of large yellow follicles via atresia and/or internal ovulation in laying hens. To test this, broiler breeder hens were treated with corticosterone or testosterone 5 h prior to ovulation and observed to see whether these treatments influenced the likelihood that a hen would lay an egg 24 h after the predicted ovulation time. A subset of hens that did not lay an egg were killed and dissected to look for evidence of follicle atresia and internal ovulation. Testosterone treatment resulted in significantly more oocyte losses, and 60% of these occurred due to internal ovulations, as was indicated by the presence of yolk in the peritoneal cavity. Corticosterone did not influence the rate of oocyte losses, follicle atresia, or internal ovulation. These results suggest that testosterone can cause disruptions that ultimately prevent the oviduct from capturing the oocyte after ovulation.

Erythrophagocytic multiple myeloma in a cat.

A 7-year-old neutered male domestic shorthair cat was presented to the Veterinary Medical Teaching Hospital at the University of Georgia for further evaluation of a suspected osteolytic lesion of the left 10th rib. Results of a CBC and biochemistry profile revealed mild nonregenerative anemia, hyperproteinemia, hyperglobulinemia, and hypercalcemia. Serum protein electrophoresis was consistent with a monoclonal gammopathy. Marked proteinuria with an increased urine protein to creatinine ratio was found. Cytologic examination of the liver, spleen, and bone marrow revealed numerous plasma cells, many of which were erythrophagocytic. Within the bone marrow, the plasma cells contained phagocytosed metarubricytes in addition to phagocytosed erythrocytes. A diagnosis of erythrophagocytic multiple myeloma was made and treatment with prednisone and melphalan was begun. Four weeks after presentation, the cat was euthanized due to clinical deterioration. A complete necropsy was performed. The distal one-third of the left 10th rib was completely absent. Histologically, there was no evidence for osteolysis or neoplastic cells in the remaining portion of the rib. However, large sheets of plasma cells were found infiltrating the spleen and bone marrow. Moderate erythrophagocytosis by the plasma cells was observed in both organs. The plasma cells, including the erythrophagocytic cells, were positive for CD79alpha by immunohistochemical staining. Erythrophagocytosis by plasma cells as a cause of anemia is uncommon in people with multiple myeloma and is rare in animals. To our knowledge, this is the first report of erythrophagocytic plasma cells in a cat with multiple myeloma.

Protection by recombinant viral proteins against a respiratory challenge with virulent avian metapneumovirus.

Protection by recombinant avian metapneumovirus (aMPV) N or M proteins against a respiratory challenge with virulent aMPV was examined. N, M or N+M proteins were administered intramuscularly (IM) with incomplete Freund's adjuvant (IFA) or by the oculonasal (ON) route with cholera toxin-B (CTB). Each turkey received 40 or 80 microg of each recombinant protein. Birds were considered protected against challenge if the challenge virus was not detectable in the choanal swabs by RT-PCR. At a dose of 40 microg/bird, N protein given with IFA by the IM route protected eight out of nine birds. M protein at the same dose protected three out of seven birds, while a combination of N+M proteins (40 microg each) protected three out of four birds. At a dose of 80 microg of each of N and M proteins per bird given with IFA by the IM route, 100% protection was achieved. ON immunization with a mixture of N and M proteins induced partial protection when the proteins were given with CTB; no detectable protection was noted without CTB. N and M proteins induced anti-aMPV antibodies, although protection against virulent virus challenge did not appear to be associated with the level or presence of antibodies.

Reduced efficacy of hemorrhagic enteritis virus vaccine in turkeys exposed to avian pneumovirus.

Avian pneumovirus (APV) is an immunosuppressive respiratory pathogen of turkeys. We examined the effect of APV infection on the vaccine efficacy of hemorrhagic enteritis virus (HEV) vaccines. APV was inoculated in 2-wk-old turkeys. Two or four days later, an attenuated HEV vaccine (HEVp30) or marble spleen disease virus (MSDV) vaccine were administered. Virulent HEV challenge was given 19 days after HEV vaccination. APV exposure compromised the ability of HEVp30 and MSDV to protect turkeys against virulent HEV. The protective index values were as follows: MSDV (100%) versus APV + MSDV (0%) (P < 0.05); HEVp30 (60%) versus APV + HEVp30 (30%) (P < 0.05) (Experiment I) and HEVp30 (56%) versus APV + HEVp30 (20%) (P < 0.05) (Experiment II). These data indicated that APV reduced the efficacy of HEV vaccines in turkeys.

Pathogenic and immunosuppressive effects of avian pneumovirus in turkeys.

Avian pneumovirus (APV) causes a respiratory disease in turkeys. The virus has been associated with morbidity and mortality due to secondary infections. Our objective was to determine if APV caused immunosuppression in the T-cell or B-cell compartments and to study the pathogenesis of the disease in APV maternal antibody-lacking 2-wk-old commercial turkeys. APV was administered by the eyedrop/intranasal route. Observations were made for gross lesions, viral genome, and T-cell mitogenesis and cytokine secretion at 3, 5, 7, 14, and 21 days postinoculation (DPI). During the acute phase of the disease that lasted for about 1 wk, the turkeys exposed to APV showed clinical signs characterized by nasal discharge and sinus swelling. Virus genome was detected by in situ hybridization in cells of turbinates and trachea at 3 and 5 DPI. At 3 and 5 DPI, spleen cells of the birds infected with APV markedly decreased proliferative response to concanavalin A (Con A). Con A and lipopolysaccharide stimulation of spleen cells from virus-exposed turkeys resulted in accumulation of nitric oxide-inducing factors (NOIF) in the culture fluid. NOIF were not detected in culture fluids of Con A-stimulated spleen cells of virus-free turkeys. APV did not compromise the antibody-producing ability of turkeys against several extraneous antigens such as Brucella abortus and tetanus toxoid.