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Biomedical subjects

E A Hoover

Publications and source records attributed to E A Hoover.

At least 19 recordsLinked to original sources
PubMed1979

Enhancement of feline leukemia virus-induced leukemogenesis in cats exposed to methylnitrosourea.

The effect of methylnitrosourea (MNU), a potent resorptive carcinogen, was evaluated for its influence on the susceptibility of adult cats to infection and induction of oncornavirus disease by feline leukemia virus (FeLV). Young adult cats at an age previously demonstrated to be highly resistant to FeLV, were injected intravenously with moderately toxic doses (15-20 mg/kg) of MNU alone or with infections FeLV (Rickard strain). Following exposure to virus and chemical, cats were monitored for antibody to the feline oncornavirus-associated cell membrane antigen (FOCMA), viremia by direct infectivity and the presence of gsa in peripheral blood leukocytes, and for toxic effects of MNU by hemogram analyses on peripheral blood. Of 8 cats injected with MNU + FeLV, 6 developed persistent viremia, 5 of which became debilitated from thymic lymphoma. Only 1 of 6 non-MNU-treated and infected cats of the same age became transiently viremic. FOCMA antibody development was markedly depressed in MNU + FeLV inoculated cats compared with cats inoculated with FeLV alone. Results show that MNU was apparently responsible for the obliteration of age-related susceptibility in cats to FeLV infection and induction of FeLV-related disease, and suggest that in nature exposure to toxic chemical carcinogens may act as factors which determine susceptibility to feline oncornaviruses in the cat.

Age Factors↗
PubMed1979

The effects of methylnitrosourea on the immune system and hematopoietic system of adult specific pathogen free cats.

The effects of a single non-carcinogenic dose of 15 mg/kg methylnitrosourea (MNU) on the immune and hematopoietic systems of adult specific-pathogen-free (SPF) cats were determined. The cell-mediated-immune (CMI) system was markedly suppressed, as evidenced by: (i) Prolonged cutaneous allograft retention time (41-84 days); (ii) Decreased lymphocyte blast transformation response to mitogens (2% of pretreatment response to pokeweed mitogen or concanavalin A) and antigen (12% of untreated control cat response to keyhole limpet hemocyanin); (iii) Reduced number of absolute erythrocyte-rosetting T-cells in the peripheral blood. This immunosuppression lasted at least 3 months, the duration of the experiment. Suppression of the hematopoietic system was also noted as evidenced by: (i) Peripheral lymphopenia lasting 3 months and neutropenia lasting 3 weeks; (ii) Bone marrow hypocellularity lasting 3 weeks; (iii) Hypoplasia of neutrophilic precursors lasting 3 weeks and erythroid precursors lasting 4 days. It was concluded that a single non-carcinogenic dose of MNU induces a prolonged suppression of the CMI system and a brief suppression of hematopoiesis in adult SPF cats. The immunosuppression may in part be responsible for the previously observed increased susceptibility to feline leukemia virus infection and disease of adult SPF cats treated with MNU.

Animals↗
PubMed1979

Immunosuppressive properties of a virion polypeptide, a 15,000-dalton protein, from feline leukemia virus.

The 15,000-molecular-weight polypeptide (p15) of feline leukemia virus (FeLV) was shown to impair normal lymphocyte function in vitro and to abrogate immunity to feline oncornavirus disease in vivo. FeLVp15 suppressed concanavalin A-induced blast transformation of normal feline lymphocytes by 68%, while other virion proteins had no effect. p15 suppression was not due to toxicity, nor was p15 a competitive inhibitor of concanavalin A binding. Capping of receptors for concanavalin A on normal feline lymphocytes also was inhibited by either inactivated FeLV or FeLV p15. Groups of cats were immunized with either killed feline oncornavirus-associated cell membrane antigen bearing tumor cells or tumor cells plus FeLV p15. After challenge with feline sarcoma virus, three of four p15-treated cats developed progressive fatal fibrosarcoma as compared to one of five non-p15-treated cats. The cats receiving p15 also had lower cytotoxic antibody titers against feline oncornavirus-associated cell membrane antigen (mean peak titer, 1:6) than did the non-p15 group (1:74). These data support the hypothesis that the immunosuppression in cats infected with FeLV is mediated by FeLV p15.

Animals↗
PubMed1979

Influence of adrenal corticosteroids on the susceptibility of cats to feline leukemia virus infection.

The natural resistance of adult specific-pathogen-free cats to feline leukemia virus (FeLV) was abrogated by treatment with various doses of a synthetic corticosteroid, methylprednisolone acetate (MPA), prior to either oral-nasal or i.p. inoculation of FeLV. Persistent viremia was induced in 82% (18 of 22) of MPA-treated cats versus 11% (1 of 9) of age-matched control cats. MPA-treated FeLV-inoculated cats developed prolonged lymphopenia (2 to 8 weeks postinoculation) and a delayed antibody response to the feline oncornavirus-associated cell membrane antigen. The distribution of FeLV group specific antigen in tissues of MPA-treated, FeLV-inoculated cats suggested that corticosteroids enhanced susceptibility to FeLV by impairing early viral containment in the reticuloendothelial and lymphoid tissues.

Animals↗
PubMed1979

Elaboration of chemotactic substances by alveolar cells: possible mechanisms for the initial neutrophilic response in feline caliciviral pneumonia.

In vitro experiments established that the interaction of feline calicivirus (FCV) with alveolar macrophages and pneumocytes results in the generation of chemotactic factors that produce directed migration of neutrophils in Boyden chambers. Factors were produced independent of immune mechanisms and of discernible serum factors. Lysates of noninfected alveolar macrophages and pneumocytes did not possess chemotactic activity, indicating that chemotactic factors were not preformed in these cells. Noninfected alveolar macrophages also elaborated neutrophil chemotactic factors in culture; however, activity was greater when macrophages were infected with FCV. The results of this study suggested that the neutrophilic response in the peripheral portion of the lung of cats exposed to aerosols of FCV was the result of the elaboration of complete chemotactic factors from FCV-infected alveolar cells.

Animals↗
PubMed1978

Induced paragonimiasis in cats: clinical signs and diagnosis.

Twenty-eight specific-pathogen-free cats were inoculated with 14 to 50 metacercariae of Paragonimus kellicotti obtained from the hearts of naturally infected crayfish. Young flukes excysted in the intestine of cats and appeared in the peritoneal cavity from 1 to 14 days after inoculation (DAI) and in the pleural cavity from 5 to 23 DAI. Flukes penetrated the pulmonary parenchyma and formed hemorrhagic subpleural lesions within 5 weeks after inoculation. Marked eosinophilia developed between 2 and 12 weeks after inoculation. Fluke-containing pulmonary lesions were detected by radiography 3 to 4 weeks after inoculation. Lesions developed most frequently in the right caudal lung lobe. Clinical signs were mild and did not appear until 4 weeks after inoculation. Thereafter, cats appeared dull and coughed intermittently. One cat became dyspneic due to pneumothorax. Paragonimus eggs were first detected at the 34th DAI, using a fecal sedimentation technique.

Animals↗
PubMed1978

In vitro interaction of alveolar macrophages and pneumocytes with feline respiratory viruses.

Feline alveolar macrophages and feline pneumocytes were inoculated in vitro with low multiplicities of either feline calicivirus or feline viral rhinotracheitis virus. Pneumocytes were permissive for both viruses. High titers were attained, and characteristic cytopathic effects developed. Alveolar macrophages were permissive for feline viral rhinotracheitis virus, although the cycle of replication was delayed. Infection of macrophages with feline calicivirus resulted in the production of viral antigens and cytopathic effects; however, viral particles were not detected by electron microscopy, and viral infectivity titers rose only slightly and then fell to undetectable levels by 96 h. The differences in viral susceptibility between these two peripheral pulmonary cell populations that were demonstrated in vitro probably contribute to the differences in pathogenesis of viral rhinotracheitis and calicivirus infections in cats.

Animals↗
PubMed1978

Increased susceptibility to feline leukemia virus infection in cats exposed to methylnitrosourea.

Exposure of adult specific-pathogen-free cats to methylnitrosourea resulted in increased susceptibility to infection by feline leukemia virus. A greater proportion of cats exposed to methylnitrosourea and feline leukemia virus (69%) became persistently viremic than those exposed to feline leukemia virus alone (17%). Segmented neutrophils were reduced by 90 to 99% within 3 days following exposure to methylnitrosourea, (15 to 20 mg/kg) whereas the effects on lymphocytes and erythrocytes, although less obvious, were also detected.

Animals↗
PubMed1978

Influence of thymectomy on the susceptibility of cats to feline leukemia virus and lymphosarcoma.

Twelve cats were thymectomized at 5 weeks of age. Six of these cats were inoculated at 8 weeks of age and 6 at 4 months of age with the Rickard (R) strain of feline leukemia virus (FeLV), which produces a high incidence of thymic lymphosarcoma. Two groups of age-matched nonthymectomized cats were inoculated with the same FeLV-R stock. Thymectomy prior to FeLV infection had no influence on the induction of viremia or the incidence of lymphosarcoma. In the FeLV-inoculated nonthymectomized cats, lymphosarcoma developed in the thymus. In the thymectomized cats, lymphosarcoma developed in the intestine, mesenteric lymph nodes, and bone marrow, but the malignant lymphoblasts had surface markers characteristic of feline T lymphocytes. It was concluded that the presence of the thymus per se is not required for infection and oncogenesis by FeLV and that feline T lymphocytes may be transformed after peripheralization to other tissues.

Animals↗
PubMed1978

Modifications of the immunofluorescence assay for feline leukemia virus group-specific antigens.

Observations and minor modifications are presented concerning the immunofluorescence assay for feline leukemia virus (FeLV) group-specific antigens (GSA) in blood cells of cats. Data are given regarding absorption of goat FeLV GSA antiserum in vivo in cats, absorption of the antiserum in vitro with feline blood cells, and the comparative efficacy of various chemical fixatives in preservation of FeLV GSA for immunofluorescent staining. The best results were obtained with in vitro absorption of antiserum and methanol fixation of FeLV GSA in blood smears.

Animals↗
PubMed1978

Thymectomy in preweanling kittens: technique and immunologic consequences.

Thymectomy of 5-week-old kittens was accomplished by left parasternal thoracotomy, ligation of the left internal thoracic artery, and removal of the thymus from the mediastinum by traction and blunt dissection. Thymectomy had no adverse clinical effects, and neither the response of peripheral blood lymphocytes to phytomitogens nor the proportions of circulating lymphocytes bearing T- or B-cell markers differed substantially between thymectomized cats and nonthymectomized control cats. Skin allograft rejection times of the thymectomized cats (3 weeks after operation) were slightly longer than those of littermate nonthymectomized controls. We conclude that removal of the thymus in preweanling kittens does not have important physiologic or immunologic consequences.

Animals↗
PubMed1978

Experimentally induced feline chlamydial infection (feline pneumonitis).

Cats exposed to aerosols of feline Chlamydia psittaci developed a disease characterized principally by conjunctivitis. Signs of conjunctivitis appeared between postexposure days (PED) 5 and 10, were often unilateral initially, and persisted for 22 to 45 days. Fever followed the onset of conjunctivitis (PED 11 to 15) and persisted for 3 to 8 days. Signs of mild rhinitis (occasional sneezing and mild serous nasal discharge) occurred in some cats between PED 8 and 37. Neither signs of lower respiratory tract disease nor significant pulmonary lesions were produced by the feline pneumonitis agent. Small foci of pneumonia were detected microscopically in 3 of 6 cats examined between PED 7 and 14. Chlamydiae were identified between PED 7 and 14 in the cytoplasm of epithelial cells in stained conjunctival smears. Conjunctivitis persisted for at least 18 days after chlamydiae no longer were detectable in conjunctival smears. Low levels of chlamydial infectivity, however, still were present in conjunctiva and lung on PED 45.

Animals↗
PubMed1978

Albendazole therapy for experimentally induced Paragonimus kellicotti infection in cats.

The effect of albendazole therapy was studied in 6 cats with pulmonary paragonimiasis induced by experimental inoculation of metacercariae (25/cat) of Paragonimus kellicotti. At 76 to 101 days after they were inoculated, 5 cats were administered an oral aqueous suspension of albendazole in 2 divided doses totaling 20 mg (2 cats), 50 mg (1 cat), or 100 mg (2 cats)/kg of body weight each day for 14 to 21 days. The 6th cat (control) was not administered albendazole. Nine days after cats were given the 50- and 100-mg/kg dosages, Paragonimus ova were not seen in the feces of 3 cats. There was marked reduction in ova production in the feces of the 2 cats administered 20 mg/kg of albendazole. Live flukes were not recovered from the lungs of 3 cats necropsied 4 or 5 weeks after dosing with 50 or 100 mg/kg, but the lungs of the 2 cats administered 20 mg of albendazole/kg yielded 9 and 7 apparently viable flukes. Seventeen live flukes were recovered from the control cat not treated with albendazole. In 4 noninoculated normal cats administered 20 mg (1 cat), 100 mg (1 cat), and 200 mg (2 cats) of albendazole/kg of body weight each day for 14 days, there were no gross or microscopic lesions attributable to the drug.

Animals↗
PubMed1978

Ultrastructural morphogenesis of acute viral pneumonia produced by feline calicivirus.

The ultrastructural morphogenesis of acute viral pneumonia was studied in pathogen-free cats exposed to aerosols of a virulent strain of feline calicivirus. Electron microscopy and fluorescence microscopy indicated that the virus had a marked tropism for alveolar pneumocytes. Viral-induced necrosis of pneumocytes was observed as early as 12 hours after exposure and was associated with acute serofibrinous and neutrophilic inflammation in the distal air exchange tissue. The acute exudative phase abated by 168 hours after exposure. The regenerative phase that followed was characterized by hyperplasia of type II pneumocytes; influx of monocytes, lymphocytes, and plasma cells; and interalveolar and intraalveolar proliferation of fibroblasts. The decrease in pneumocyte injury coincided with the increase in alveolar macrophages and immunocytes. With minor exceptions, feline calicivirus-induced alveolar damage and the subsequent repair resembled toxic alveolar injury produced by oxidant gases. Feline caliciviral pneumonia, therefore, is a naturally occurring example of viral-induced diffuse alveolar damage.

Animals↗