Publications by authors named "Gilka F"

Chicks were infected at 1 day of age with highly pathogenic AC-1 or RB-1B isolates of Marek's disease virus and 14 to 36 days post-exposure they were bled for haematocrits and euthanized. At necropsy, specimens were collected for light and electron microscopy. Both viruses caused significant reductions in packed cell volume (P<0.

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The AC-1 strain of Marek's disease herpesvirus (MDV), recently isolated from an outbreak of Marek's disease in vaccinated chickens, was used for intraperitoneal inoculation of one-day-old Single Comb White Leghorns. Chicks were necropsied 12 to 32 days post inoculation and skin was collected for electron microscopic studies. This paper focuses on early stages of MDHV development in feather follicle epithelial cells and on cytoplasmic changes that occur in formation and release of virus particles.

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Meat-type and White Leghorn chickens were inoculated with the RAV-1 strain of avian leukosis virus at 1 day of age and the severity of infection was assessed by clinical illness, haematology and post-mortem findings. The following were examined from selected birds: histological section for chronic mononuclear myocarditis, immunohistochemically-stained sections of myocardium, spleen, bursa of Fabricius and kidney for group-specific viral antigen, and ultrathin sections of these tissues for virus particles by electron microscopy. The experiment was terminated at 115-122 days.

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Specific-pathogen-free white leghorn chickens were inoculated at 1 day of age with avian leukosis virus (ALV, RAV-1). All chickens in Expt. 1, killed 33 or 64 days postinoculation, had focal chronic lymphocytic or lymphoplasmacytic myocarditis.

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Electron microscopy and immunocytochemistry were used to study the development of lymphoid leukosis virus infection in the bursa of Fabricius of experimentally infected chicken embryos and chickens. In embryos infected at 7 days of incubation and killed 10 days later, virus particles and group-specific viral antigen were confined mainly to the connective tissue of the lamina propria of the bursal mucosal folds; a few developing follicles had discrete virions and group-specific antigen between cells. In chickens infected at 1 day of age, infection (as determined by use of electron microscopy and immunocytochemistry) was maximal in 1- to 4-month-old birds, and the greatest concentration of virus and group-specific viral antigen was in the medulla of the follicles.

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The purpose of this study was to improve in vitro procedures for detecting cellular resistance to the avian leukosis-sarcoma group of viruses. Four feather pulp organ cultures (FPOC) were prepared from each chicken by placing pulp squeezed from feathers in wells of microtitre plates that contained culture medium. Two of the four FPOC were inoculated with Rous sarcoma virus (RSV) of subgroup A and 5 to 6 days later the fluids from all four cultures were assayed for virus by inoculating chicken embryo fibroblasts (CEF) and examining for development of foci of transformed cells.

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Chicken embryos and healthy adult chickens naturally infected with lymphoid leukosis virus were used to investigate viral inclusion bodies in myocardial cells by light and electron microscopies and by immunocytochemical technique. Intracytoplasmic viral matrix inclusion bodies frequently appeared in the myocardium of adult chickens, but not in that of embryos. In light microscopic preparations, inclusions were irregularly distributed, were basophilic, and contained ribonucleic acid.

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An indirect immunoperoxidase method was employed in the detection of the group specific antigen of avian leukosis virus in the oviduct, spleen, myocardium and bursae of Fabricius of chickens. In the magnum of the oviduct the group specific antigen was detected at the base and in the lumina of glands. In the spleen the group specific antigen was found in and around the arterioles, sheathed capillaries, and in the capsular tissue.

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In order to gain insight into transmission and pathogenesis of infection, specimens from laying hens that had been naturally exposed to lymphoid leukosis virus (LLV) were tested for group-specific antigen (gsa) of the virus by immunofluorescence (IF), complement fixation (CF), and the enzyme-linked immunosorbant assay (ELISA). Electron microscopic examinations determined the distribution of C-type virus particles in tissues, and the phenotypic-mixing test served as a biological assay for exogenous LLV. The IF gsa was found in all organs tested, and fluorescence was usually found where virus particles were concentrated.

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The influence of a high phosphorus (1.5%) and high calcium (2.2%) diet on ectopic mineralization in boars was examined over a four month period.

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Exogenous lymphoid leukosis virus (LLV) and group-specific antigen (gsa) were detected in feather pulp and other specimens from naturally or experimentally infected chickens by phenotypic mixing or complement fixation tests, respectively. Electron microscopic studies on the calamus of plucked feathers revealed numerous C-type virus particles in intercellular spaces of the epidermis and pulp. LLV and gsa were detected in feather pulp from approximately 90% of 47 newly-hatched chicks that were shown to be congenitally infected.

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Tonsils of 25 adult swine with inflamed crypts were screened for the presence of radiating clubs, and five were selected for electron microscopic study of pathogenesis of clubs. Radiating clubs in crypts were surrounded by an exudate which principally contained neutrophils. Clubs were present on the outer surface of bacterial microcolonies; they also were present on the outer surface of plant particles wedged in crypts or on the cell walls of these particles near bacterial microcolonies.

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Monospecific antiserum obtained from rabbits hyperimmunized against homogeneous p27 group specific protein purified from avian myeloblastosis virus was commercially procured and was then conjugated with fluorescein isothiocyanate. The conjugate was applied to spleens from naturally or experimentally infected chickens that had no evidence of lymphoid tumors. Fluorescence was usually localized in connective tissue of sheathed capillaries giving it a ring-like appearance.

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A method used to calculate the number of Pasteurella haemolytica reaching the lungs of calves during an aerosol exposure is described. This method is based on a linear relationship of bacterial deposition in lungs of mice and calves when exposed to the same bacterial aerosol.

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Discrete mineralized foci and granulomatous inflammation occurred in the lamina propria mucosae of respiratory mucous membranes of adult pigs. Lesions were present in clinically healthy pigs of both sexes, including castrated males, fed various pelleted or non-pelleted diets. They were mainly in longitudinally corrugated mucosae of the dorsal wall of the trachea.

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Young boars supplemented orally with 800, 500,300 and 100 IU of vitamin D2/kg of feed and control boars not supplemented with vitamin D2 for four months developed mineralization in the left atrial endocardium, lamina muscularis mucosae of the fundic stomach and other sites. Since low levels of supplementation with vitamin D2 did not eliminate the lesions, the levels of vitamin D2 added appeared not to be involved in the pathogenesis. All boars had mild hypercalcemia throughout the experiment, and phosphorus levels in sera were lower in all animals receiving than in those not receiving calciferol.

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Pigs on nutritional studies developed heterotopic calcifications in the left atrial endocardium, submucosa of the gastric fundus and to a lesser extent in other sites. Light and electron microscopy of mineralized tissue showed early edema and connective tissue change, deposition of calcium, granulomatous reaction and repair. There was no alkaline phosphatase activity at the sites of calcification and the distribution of this enzyme activity was normal in other tissues.

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The effects of a preparative dose of the leukocyte egesta containing degraded meningococci and a provocative dose of the meningococcal lipopolysaccharide on development of pathological lesions associated with disseminated intravascular coagulation were studied in tissues of 32 rabbits. These effects were compared with effects of a single dose of meningococcal lipopolysaccharide as well as leukocyte egesta containing degraded Staphylococcus epidermidis. Rabbits injected subcutaneously with egesta containing degraded meningococci followed after 12 h with meningococcal endotoxin (intravenously) exhibited heterophilic leukocytosis and disseminated intravascular coagulation mainly in the pulmonary capillaries and venules; focal necroses occurred in myocardium, lungs, and liver, whereas, cortical renal necrosis developed in lethal cases.

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Leucocyte-egested material was harvested after the quantitative in-vitro phagocytosis of Neisseria meningitidis by rabbit or mouse polymorphonuclear leucocytes. The egested material was injected subcutaneously into rabbits and followed 24 h later with an intravenous injection of what would by itself have been a non-lethal quantity of meningococcal endotoxin, or with an equivalent dose of endotoxin in the form of meningococcal cell-wall blebs. Of 32 rabbits treated in this manner, 12 developed disseminated intravascular coagulation and six of these 12 had renal cortical necrosis.

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The influence of pulmonary edema, hydrocortisone, immunization against Pasteurella hemolytica and concurrent infection with parainfluenza-3 virus upon pulmonary clearance of aerosolized P. hemolytica was studied in 31 calves. Following the various treatments calves were challenged with an aerosol of P.

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