Cutaneous mast cell tumor in a great horned owl (Bubo virginianus).
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Biomedical subjects
Publications and source records attributed to D E Swayne.
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The presence of vasogenic brain oedema and its distribution in Marek's disease virus (MDV)-induced transient paralysis (TP) were determined in genetically resistant and susceptible inbred White Leghorn chickens. MDV-inoculated TP-susceptible chickens with nervous signs (9 days post-inoculation) had severe vacuolation of cerebellar white matter and associated diffuse leakage of albumin and IgG. The serum protein leakage was associated morphologically with a vasculitis and intramural pseudocyst formation in the walls of blood vessels cuffed by mononuclear cells. This transient vasculitis and resulting vasogenic oedema coincided with the temporary neurological signs seen in TP-susceptible chickens. The vasculitis and vasogenic oedema were not present in brain tissue from recovered MDV-inoculated TP-susceptible chickens, MDV-inoculated TP-resistant chickens, or uninoculated control chickens from either line.
Ultrastructural findings in a feline ventral abdominal vascular tumour showed lack of basal lamina, few micropinocytotic vesicles and intercellular junctions and a discontinuous endothelial cell layer. A splenic cyst had a continuous basal lamina, numerous micropinocytotic vesicles and intercellular junctions and a continuous endothelial cell layer. These findings were compatible with diagnosis of lymphangiosarcoma (ventral abdomen and metastases) and haemangiosarcoma (splenic cyst).
The presence of brain edema and its distribution in Marek's disease virus (MDV)-induced transient paralysis (TP) was determined in genetically resistant and susceptible inbred White Leghorn chickens. Density measurements on samples from the cerebellum, cerebral cortex, optic chiasm, and optic lobe were determined on continuous density Percoll gradients. At 9 days post inoculation of MDV, the cerebellums from the susceptible line of chickens were significantly less dense than cerebellums from the resistant line or the controls of either line. The cerebellar edema, as measured by tissue density, coincided with the transient neurological symptoms and was not present in brain tissue from clinically recovered TP birds.
The intermediate filament desmin was present in three canine botryoid rhabdomyosarcomas. The use of desmin as a diagnostic tool may, as in these tumours in man, be of value in the classification of canine sarcomas where the origin of the tumour is not always apparent from routine histological sections.
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A poorly differentiated cutaneous lymphosarcoma with delayed multicentric anatomical distribution was diagnosed in a dog. The neoplasm had cells with chromosome numbers of 58 or 67 and the former cells lacked the subtelocentric marker chromosome seen in cells of canine transmissible venereal tumour with 58 chromosomes.
Generally accepted criteria were used to identify typical nucleated thrombocytes and typical small lymphocytes in chicken-blood smears subjected to modified-Wright staining. Other cells, here referred to as "intermediate cells," were difficult to classify because in some aspects they resembled thrombocytes while they also had features typical of small lymphocytes. The "intermediate cells" had small, round or oval nuclei with coarsely condensed chromatin, characteristic of both thrombocytes and small lymphocytes. In addition, "intermediate cells" had moderately abundant cytoplasmic volumes, typical of thrombocytes but blue cytoplasm lacking both granules and vacuoles, which is characteristic of small lymphocytes. It made little difference to the thrombocyte count whether these cells were classified as thrombocytes or small lymphocytes; however, this decision made a substantial difference to the lymphocyte count in some chicken-blood smears. Most "intermediate cells" (351 of 410 cells examined) were nonfluorescent after treatment with formaldehyde gas. Furthermore, most "intermediate cells" failed to acquire characteristic pigments when subjected to either Grimelius staining (179 of 204 cells examined) or periodic acid-Schiff staining (173 of 206 cells examined). Typical small lymphocytes reacted in the same way, failing to fluoresce after gaseous formaldehyde treatment (65 of 65 cells examined) and failing to react during Grimelius staining (41 of 44 cells examined) or periodic acid-Schiff staining (21 of 21 cells examined). In contrast, almost all typical thrombocytes became fluorescent in response to gaseous formaldehyde (709 of 718 cells examined) and gave positive reactions when subjected to Grimelius staining (381 of 382 cells examined) or periodic acid-Schiff staining (322 of 326 cells examined). These findings suggested that "intermediate cells" should be classified as lymphocytes in differential cell counts.
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Four Basset Hound littermates, each 4 weeks old, with predominantly mahogany coats, had congenital focal alopecia especially affecting the head and dorsal pelvic region. Two predominantly black-coated female littermates were clinically normal. Histologic diagnosis was hypotrichosis.
Added phospholipid failed to accelerate chicken-plasma coagulation, induced by high concentrations of crude Russell's viper venom; however, similarly induced coagulation of canine and human plasma proceeded more rapidly when phospholipid was added. Phospholipid reduced clotting times of canine, human and also chicken plasma when partially purified factor X-activating enzyme from Russell's viper venom was the inducing agent. In the absence of added phospholipid, preincubation of chicken plasma with factor V-activating enzyme from Russell's viper venom accelerated factor X-activating-enzyme-induced coagulation. Preincubation of chicken plasma with the factor V-activating enzyme slowed factor X-activating-enzyme-induced coagulation in the presence of added phospholipid.
Exudative diathesis, a condition caused by a selenium (Se)/vitamin E deficiency, was studied in chicks. Trios of chicks that showed clinical signs of exudative diathesis were matched for severity. One was injected subcutaneously with 0.5 mL distilled water, and the other two received 15 microg of Se in 0.5 mL distilled water. A chick fed a diet with supplemental Se also received 0.5 mL distilled water. Blood was collected from three chicks 2 d after injection, and from the other chick, 6 d after injection. After blood was collected, pectoral muscle and bone marrow were collected. Deficient chicks showed varying degrees of necrosis in pectoral muscle, whereas recovering chicks had extensive fibrosis in pectoral muscle. An analysis of blood showed differences in CO2, glucose, Se, glutathione peroxidase, alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Heterophils and monocytes were increased in deficient chicks; lymphocytes, basophils, and hemoglobin decreased. After 6 d of recovery, all of the changes noted above were correcting toward normal. Eosinophils, in contrast, were unaffected by a deficiency, but increased in recovering chicks. It is hypothesized that cytokines associated with the inflammatory response accentuate the clinical signs of exudative diathesis.
During 1999 and 2000, a disease outbreak of West Nile (WN) virus occurred in humans, horses, and wild and zoological birds in the northeastern USA. In our experiments, WN virus infection of young domestic geese (Anser anser domesticus) caused depression, weight loss, torticollis, opisthotonus, and death with accompanying encephalitis and myocarditis. Based on this experimental study and a field outbreak in Israel, WN virus is a disease threat to young goslings and viremia levels are potentially sufficient to infect mosquitoes and transmit WN virus to other animal species.
Vaccines against mildly pathogenic avian influenza (AI) have been used in turkeys within the United States as part of a comprehensive control strategy. Recently, AI vaccines have been used in control programs against highly pathogenic (HP) AI of chickens in Pakistan and Mexico. A recombinant fowl pox-AI hemagglutinin subtype (H) 5 gene insert vaccine has been shown to protect specific-pathogen-free chickens from HP H5 AI virus (AIV) challenge and has been licensed by the USDA for emergency use. The ability of the recombinant fowl pox vaccine to protect chickens preimmunized against fowl pox is unknown. In the current study, broiler breeders (BB) and white leghorn (WL) pullets vaccinated with a control fowl poxvirus vaccine (FP-C) and/or a recombinant fowl poxvirus vaccine containing an H5 hemagglutinin gene insert (FP-HA) were challenged with a HP H5N2 AIV isolated from chickens in Mexico. When used alone, the FP-HA vaccine protected BB and WL chickens from lethal challenge, but when given as a secondary vaccine after a primary FP-C immunization, protection against a HP AIV challenge was inconsistent. Both vaccines protected against virulent fowl pox challenge. This lack of consistent protection against HPAI may limit use to chickens without previous fowl pox vaccinations. In addition, prior exposure to field fowl poxvirus could be expected to limit protection induced by this vaccine.
In the fall of 1999, West Nile virus (WNV) was isolated during an outbreak of neurologic disease in humans, horses, and wild and zoological birds in New York, Connecticut, and New Jersey. Turkeys could potentially be a large reservoir for WNV because of the high-density turkey farming and the presence of large wild turkey populations in the eastern seaboard of the United States. Little is known about the pathogenicity of WNV in domestic or wild turkeys. Specific-pathogen-free 3-wk-old turkeys were inoculated subcutaneously with 10(3.3) mean tissue culture infective doses of a WNV strain isolated fromthe index case in a New York crow. No clinical signs were observed in the turkeys over the 21 days of the experiment. One turkey died abruptly at 8 days postinoculation (DPI). Many turkeys developed viremia between 2 and 10 DPI, but the average level of virus was very low, less than needed to efficiently infect mosquitos. Low levels of WNV were detected in feces on 4 and 7 DPI, but no virus was isolated from oropharyngeal swabs. WNV wasnot transmitted from WNV-inoculated to contact-exposed turkeys. All WNV-inoculated poults seroconverted on 7 DPI. In the turkey that died, WNV was not isolated from intestine, myocardium, brain, kidney, or cloacal and oropharyngeal swabs, but sparse viral antigen was demonstrated by immunohistochemistry in the heart and spleen. Turkeys in contact with WNV-inoculated turkeys and sham-inoculated controls lacked WNV specific antibodies,and WNV was not isolated from plasma and cloacal and oropharyngeal swabs. These data suggest that WNV lacks the potential to be a major new disease of turkeys and that turkeys will not be a significant amplifying host for infecting mosquitos.
In 1997, highly pathogenic (HP) H5N1 avian influenza virus (AIV) caused infections in poultry in Hong Kong and crossed into humans, resulting in a limited number of infections including 18 hospitalized cases and six associated deaths. The unique ability of this, AIV to infect both poultry and people raised a concern for the potential of humans to be biological as well as mechanical vectors of this AIV to poultry. The current study was undertaken to determine if existing vaccines and their technologies could be used during an outbreak to protect poultry. Commercial and experimental inactivated whole H5 AIV and baculovirus-expressed AIV H5 hemagglurinin protein vaccines provided protection from clinical signs and death in chickens after lethal challenge by human-origin HP H5N1 Hong Kong strains 156/97 and 483/97. The commercial and experimental inactivated vaccines had mean protective doses ranging from 0.25 to 0.89, which represents the milligrams of viral protein in the vaccines that provided protection from death in half of the birds. Furthermore, the vaccines reduced the ability of the challenge AIV to replicate in chickens and decreased the recovery of challenge AIV from the enteric and respiratory tracts, but the use of a vaccine will nor totally prevent AI virus replication and shedding. Existing vaccines will protect poultry from mortality and reduce virus replication from the new HP AIV strain that can infect both poultry and humans.
The in situ hybridization assay was developed for the detection of infectious bursal disease virus (IBDV) infections in chickens. Bursal tissue samples were harvested 4 days following infection with the ST-C, MD, E, IN, or SAL IBDV strain. The cDNA clones STC-243, located on genome segment A, and STC-119, located on genome segment B, were used to prepare non-radioactive probes. Probes were labeled with digoxigenin and detected the homologous ST-C virus and also heterologous viruses in bursal tissue sections. No positive cells were observed in tissue sections from uninfected control chickens.
Feces-stained eggshells, diarrhea, and typhlitis were identified in two commercial laying flocks in Ohio. Hens with diarrhea had spirochetes in cecal lumina and crypts. On culture, the spirochetes were motile and non-hemolytic, did not produce indole, had 12 to 15 axial filaments, were 9.2 to 11.7 microns in length and 240 to 370 nm in diameter, and had a wavelength of 5.1 to 6.5 microns on transmission electron microscopy.