Richard A. Griesemer
Ohio State University
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Featured researches published by Richard A. Griesemer.
Veterinary Pathology | 1966
L.G. Wolfe; Richard A. Griesemer
Infectious peritonitis, a previously undescribed disease entity, was studied in 16 cats. The clinical disease was characterized by fever, ascites, lack of response to therapy, and high mortality. The principal lesion was a diffuse fibrinous peritonitis. The disease was experimentally produced in germ-free and conventional cats. Thus far, no etiologic agent has been demonstrated.
Veterinary Pathology | 1967
M. W. Rohovsky; Richard A. Griesemer
In the absence of other microorganisms the virus of feline infectious enteritis produced a mild, non-fatal clinical disease in germfree cats. A biphasic temperature rise occurred on post inoculation day (PID) 2 and 4. All of the germfree cats began to recover by PID 7. Absolute lymphopenia occurred on the first day followed by absolute neutropenia on PID 4. The leucocyte counts were within the normal range by PID 10. Severe atrophy of the thymus was the only macroscopic lesion produced. Depletion of mature lymphocytes and reticuloendothelial cell hyperplasia occurred in all other lymphocytic tissue. No inclusion body considered to be of diagnostic significance could be demonstrated. There was no evidence of enteritis grossly or microscopically in germfree cats.
Veterinary Pathology | 1965
John P. Gibson; Richard A. Griesemer; Adalbert Koestner
Distemper was produced experimentally in 12 gnotobiotic dogs with the Snyder Hill and Lederle strains of virus. Eight gnotobiotic dogs served as uninoculated controls. In the absence of other microorganisms, the only signs of disease were mild transient fever and leukopenia. The only macroscopic lesion was severe atrophy of the thymus. Microscopically all the lymphoid tissues underwent lymphoid depletion and reticular cell hyperplasia. Lesions appeared in the brain eight days after inoculation. The virus caused direct neuronal degeneration in the frontal cortex, only minimal lesions in the vicinity of the fourth ventricle and no demyelination. Infrequent inclusion bodies were found in neurons and in the reticular cells of the lymphoid tissues. No lesions were found in the lungs, stomach, urinary bladder, or skin.
Veterinary Pathology | 1967
Louis Kasza; Richard A. Griesemer
The cytopathic effect of more than 30 viruses and Toxoplasma gondii and Histoplasma capsulatum was determined in established canine thyroid adenocarcinoma and canine melanoma cell lines. Marked effect was observed with the viruses of canine hepatitis, pseudorabies, and canine distemper, and reo type 1 and vaccinia viruses in both cell lines. Moderate effect was found with human adenovirus type 1, swine adenovirus and the viruses of swine influenza and Newcastle disease. Cytopathic changes were produced with the virus of herpes simplex in the thyroid adenocarcinoma cells. A transient giant cell formation was produced by the virus of measles in the thyroid cell line. Hemadsorption was demonstrated in both cell lines with vaccinia virus. Toxoplasma gondii multiplied in both cell lines and produced cellular degeneration and necrosis. Histoplasma capsulatum grew in the thyroid adenocarcinoma cell line with little cellular degeneration.
Journal of the National Cancer Institute | 1980
Walden E. Dalbey; Paul Nettesheim; Richard A. Griesemer; John E. Caton; Michael R. Guerin
American Journal of Pathology | 1970
E. A. Hoover; M. W. Rohovsky; Richard A. Griesemer
American Journal of Pathology | 1971
Edward A. Hoover; Richard A. Griesemer
Journal of the National Cancer Institute | 1972
Edward A. Hoover; C. Bruce McCullough; Richard A. Griesemer
American Journal of Pathology | 1972
Gary J. Kociba; Richard A. Griesemer
Archive | 1959
Richard A. Griesemer