Biomedical subjects

H L Thacker

Publications and source records attributed to H L Thacker.

78 records · Page 5Linked to original sources

PubMedDate not supplied

Erysipelas in domestic white Pekin ducks.

Two epornitics of erysipelas were diagnosed in domestic White Pekin ducks. The first was in 2,000 18-day-old ducklings with a 30% mortality. The other was in 2,400 breeder hens with losses of four or five birds a day. Gross pathologic lesions in birds necropsied from both instances were enlarged swollen livers with occasional subcapsular hemorrhages. Pure isolates of Erysipelothrix insidiosa only were cultured from the livers. Histologic examination revealed congestion and multifocal necrosis in the liver and spleen with associated reticuloendothelial cell proliferation. Special stains demonstrated numerous organisms within the reticuloendothelial cells.

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PubMedDate not supplied

Fatal hepatic trematodiasis in cockatoos due to Platynosomum proxillicens.

Severe hepatic trematodiasis due to Platynosomum proxillicens was diagnosed as the cause of death in two sulfur-crested cockatoos (Cacatua sulfurea). Gross pathologic alterations included hepatomegaly in one bird and hepatic and generalized cyanosis in the other. Microscopic changes included multifocal hepatic necrosis, dilated fibrous bile ducts containing trematode, parasites, bile duct hyperplasia, and hepatic inflammation.

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PubMedDate not supplied

Cellular response of the respiratory tract of chickens to infection with Massachusetts 41 and Australian T infectious bronchitis viruses.

Cellular response of chickens to infection with infectious bronchitis virus (IBV) was investigated by lavage of the respiratory tract of five 2-week-old specific-pathogen-free (SPF) chickens at 2, 8, 24, 48, 72, and 96 hours postinfection (PI) with either Massachusetts 41 (IBV-M41) or Australian T (IBV-T) IBV. Tissue response was monitored by microscopic examination of trachea and lung from five non-lavaged infected chickens collected at the same intervals. The total number of cells recovered by lavage from IBV-M41-infected chickens was dramatically higher than the total number recovered from IBV-T-infected chickens and uninfected controls. By contrast, the total number of cells recovered from IBV-T-infected chickens was no higher than that of the uninfected chickens. Heterophils constituted the majority of inflammatory cells recovered from both IBV-M41-infected and IBV-T-infected chickens. Heterophil numbers in IBV-M41-infected chickens paralleled total cell-number recovery, whereas heterophil numbers in IBV-T-infected birds were no higher than those in uninfected chickens. The number of lymphocytes recovered from IBV-M41-infected chickens increased 72 hours PI and continued to increase for the duration of the study. Lymphocyte numbers in IBV-T-infected chickens exceeded those in uninfected chickens only at 96 hours PI. The number of lavage macrophages in IBV-M41-infected chickens increased earlier than the number of lymphocytes but later reached a plateau. IBV-T macrophage numbers did not exceed those of uninfected chickens. Tissue damage occurred most consistently in the trachea and occurred when lavage heterophil numbers were rising or at their peak. Lavage cell recovery and composition reflected tracheal mucosa inflammatory cell infiltrate.

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PubMedDate not supplied

Cyclophosphamide (Cytoxan)-induced hematologic alterations in specific-pathogen-free chickens.

Cyclophosphamide (Cytoxan) was given at 75 mg/kg body weight via daily intramuscular injections for 4 days to 3-week-old specific-pathogen-free (SPF) chickens in an attempt to determine if heteropenia could be induced in chickens. Control birds were given a like quantity of phosphate-buffered saline, the diluent for Cytoxan. Peripheral blood heterophil numbers were determined and monitored by total leukocyte and differential cell counts. Birds were grouped in pairs on day 0 based on total leukocyte count. The number of heterophils each bird had on day 0 served as a baseline heterophil count for that bird. Thereafter heterophil numbers were determined on the last day of drug treatment and every other day until blood heterophil numbers were 20% of that bird's baseline heterophil count (heteropenia). The effects of Cytoxan on trachea, lung, liver, kidney, bursa of Fabricius, bone marrow, spleen, and thymus were determined by microscopic examination of those tissues collected the day following heteropenia. Cytoxan had no effect on trachea, lung, liver, kidney, and thymus. Bursa of Fabricius and spleen had decreased amounts of lymphoid aggregates. Bone marrow of Cytoxan-treated chickens was hypocellular. The study was then repeated to determine the reversibility of Cytoxan-induced heteropenia. Cytoxan-treated birds were allowed to recover until blood heterophil numbers equaled or exceeded those of control birds. Cytoxan, through bone marrow suppression, induced a reversible heteropenia that developed between treatment days 10 and 12. In addition, Cytoxan induced a reversible lymphocytopenia between days 4 and 10 and a regenerative anemia between days 8 and 10. The ability to produce heteropenia in SPF chickens will allow the use of a heteropenic model for further study of the heterophil's contribution to the inflammatory response.

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PubMedDate not supplied

A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin.

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.

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PubMedDate not supplied

Effect of cytoxan-induced heteropenia on the response of specific-pathogen-free chickens to infectious bronchitis.

Epithelial damage in infectious bronchitis occurs early in the disease process. Heterophil infiltration into the tracheal mucosa is greatest at that time. To determine the contribution of heterophils to tracheal epithelial damage of infectious bronchitis, eight 3-wk-old specific-pathogen-free chickens were made heteropenic by four daily intramuscular injections of cyclophosphamide at 75 mg/kg body weight. Infection with Massachusetts 41 infectious bronchitis virus was timed to coordinate heteropenia with peak tracheal epithelial damage. Heteropenia was monitored by total leukocyte and differential cell counts of peripheral blood. Tissue damage and heterophil infiltrate were monitored by histopathology of tissues taken at termination of the study. Heteropenic birds had lower peripheral blood and tracheal heterophil numbers than nonheteropenic birds. No difference was found in epithelial damage of heteropenic and nonheteropenic birds. Epithelial damage in infectious bronchitis is most likely due to damage by the virus and not due to the infiltrated heterophils.

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