Biomedical subjects

J B Moe

Publications and source records attributed to J B Moe.

35 records · Page 2Linked to original sources

PubMed1977

Studies of the coagulation and complement systems during experimental Rocky Mountain spotted fever in rhesus monkeys.

We studied the coagulation and complement systems during Rocky Mountain spotted fever in Macaca mulatta experimentally infected with Rickettsia rickettsii. Ninety-one percent of monkeys infected intravenously with a high dose (10(6) plaque-forming units [pfu]) and 56% of monkeys infected with low doses (10(-1)-10(2) pfu) of R. rickettsii died after two to four days of illness. With the onset of fever and rickettsemia, animals developed hyperfibrinogenemia, mild thrombocytopenia, prolonged prothrombin and activated thromboplastin times, and increased serum fibrin/fibrinogen degradation products (FDP). Rickettsemia, thrombocytopenia, and FDP were greater in fatally ill monkeys than in survivors. Hemolytic titers of the second and third components of complement were not depressed except in a single surviving monkey that developed peripheral gangrenous ecchymoses at a time when both rickettsemia and agglutinating antibody were present. Thus, although activation and consumption of complement may occur during Rocky Mountain spotted fever, the hemostatic disturbances in fulminant infections seem to be a direct effect of the infectious vasculitis.

Animals↗

PubMed1977

Fibrosarcoma in a white-tailed deer.

A large, rapidly growing subcutaneous fibrosarcoma was observed on the head of an aged male white-tailed deer (Odocoileus virginianus) from Frederick County, Maryland. Although there was no evidence of distant metastasis, the large neoplastic mass had extensively invaded the osseous supraorbital process, and had several small satellite nodules nearby.

Animals↗

PubMed1976

Therapeutic effects of ribavirin given by the intraperitoneal or aerosol route against influenza virus infections in mice.

Ribavirin (1-beta-d-ribofuranosyl-1,2,4-triazole-3-carboxamide) is an effective antiviral agent against type A influenza infection of mice. Therapy was most effective when administered as a small-particle aerosol early in the infection. Treatment was also effective by either the intraperitoneal or aerosol route in mice with histological evidence of pneumonia. Ribavirin increased the percent survival, lowered lung virus titers, and decreased the development of lung pathology when therapy was initiated at 6 h as a small-particle aerosol. There was no evidence of pulmonary toxicity or immunosuppressive effects.

Aerosols↗

PubMed1976

Pathology of experimental Rocky Mountain spotted fever in rhesus monkeys.

Rhesus monkeys were inoculated intravenously or intraperitoneally with various numbers of Rickettsia rickettsii. Monkeys that were given more than 10(4) organisms intravenously died on days 3-6 after inoculation, whereas those given less than 10(3) intravenously or more than 10(4) intraperitoneally died on day 7 or later. There was no significant difference in incidence of lesions between the early- and late-death groups. Vasculitis and thrombosis occurred most frequently in the nares, pinna of the ear, scrotal skin, and testicle. Adrenal cortical necrosis was caused by capillary thrombosis. Rickettsiae, estimated by plaque formation in culture, were most numerous in the lung and spleen.

Adrenal Cortex↗

PubMed1976

Alterations in plasma copper, zinc, amino acids, and seromucoid during Rocky Moutain spotted fever in guinea pigs.

Guinea pigs inoculated with virulent Rickettsia rickettsii responded with a significant increase in plasma copper concentration within 1 day, preceding fever and detectable rickettsemia by 2 and 4 days, respectively. A decrease in serum zinc concentration coinciding with peak rickettsemia was detectable on Day 5. Evidence of altered host nitrogen metabolism during this illness included a doubling of plasma seromucoid concentration and a significant rise in the plasma phenylalanine/tyrosine ratio.

Amino Acids↗

PubMed1976

Functional and morphologic changes during experimental Rocky Mountain spotted fever in guinea pigs.

Experimental Rocky Mountain spotted fever was studied in guinea pigs following intraperitoneal inoculation of 10(7) Rickettsia rickettsii. After a 2-day incubation period, animals developed fever, progressive emaciation, and scrotal swelling with necrosis. Vasculitis, with increased small vessel permeability for colloidal carbon, was evident in cremaster muscles as early as 1 day after inoculation. Inflammatory changes in vessels became progressively more severe as numbers of circulating rickettsiae increased. Thrombosis and vascular occlusion were first evident on day 4. Mild thrombocytopenia developed, coinciding with the development of vasculitis, and preceding the appearance of either fibrin-split products in blood or thrombi in vessels. Rickettsiae were first detected in blood on day 2; peak rickettsemia occurred on days 5 to 8. Rickettsiae were demonstrated in inflamed vessels on day 5 and later, but not at earlier stages. Serum lysozyme concentration was moderately elevated and hemolytic complement was moderately depressed throughout the illness. Agglutinating antibody was present in low titers on days 3 to 10. Antibody titers increased on days 12 to 16 after the rickettsiae were cleared from blood. These studies indicate that vasculitis seen early in the course of Rocky Mountain spotted fever is the result of rickettsial infection, but is not dependent on the presence of rickettsiae in endothelial cells or other blood vessel components.

Agglutination Tests↗

PubMed1975

Treatment of influenza infection of mice by using rimantadine hydrochlorides by the aerosol and intraperitoneal routes.

Rimantadine hydrochloride was administered for 4 days in a small-particle (95% < 6.5 mum) aerosol (8.8 mg/kg per day) or intraperitoneally (40 mg/kg per day) to mice previously infected with influenza A/Aichi/2/68 (H(3)N(2)), mouse adapted. Mean time to death and incidence of survival were significantly increased in all treated groups of mice. The rate of eventual disappearance of virus from lung tissue was also accelerated by therapy. However, maximal mean virus titer per lung, and lung histopathology, did not reveal any difference between control and either group of treated mice. Aerosol therapy initiated at 72 h postinfection was as effective as that initiated at 6 h, even though lung virus titers of these mice had already peaked by 72 h. In contrast, intraperitoneal therapy initiated at 72 h was not effective in all studies.

Adamantane↗

PubMed1975

Relationship of serum beta-glucuronidase and lysozyme to pathogenesis of tularemia in immune and nonimmune rats.

A temporal study is reported of the febrile responses, tissue bacterial contents, and serum concentration of the lysosomal enzymes, beta-glucuronidase and lysozyme, in nonimmune rats inoculated with virulent or attenuated strains of Francisella tularensis, and in immune rats challenged with either a high or low dose of virulent organisms. The level of serum beta-glucuronidase appears to be an indicator of hepatocyte damage, whereas serum lysozyme correlates with the appearance, frequency, and severity of pyogranulomatous lesions. Survival of nonimmune rats after a challenge with either virulent or attenuated organisms appears to depend on a balance between dose of bacterial inoculum, celerity of irreversible pathologic events, and the ability of the reticuloendothelial and immune systems to collaboratively mount a response to limit or prevent dissemination of the infection. In immune rats, infection of parenchymal hepatic cells does not occur after a low dose (10-4) virulent challenge. Infection of parenchymal hepatic cells, however, does occur in immunized rats when the challenge dose is sufficiently large (10-8) so as to overcome the capacity of the reticuloendothelial to clear opsonized organisms.

Animals↗

PubMed1975

Induced metabolic sequelae of tularemia in the rat: correlation with tissue damage.

Serum and liver zinc concentration, amino acid uptake by liver, seromucoid content, and alpha2-macrofetoprotein production were measured in vaccinated as well as nonimmune rats exposed to either virulent (SCHU S4) or attenuated (LVS) strains of Francisella tularensi. It appears that liver damage (pyogranulomatous lesions) must occur before there is any alteration in the above variables. The presence of bacteria in the liver is not of itself sufficient to lead to the onset of systemic, induced metabolic sequelae (IMS). The occurrence of zinc redistribution in all instances of increased serum protein synthesis may imply a necessary relationship between these two sequelae. Amino acid redistribution does not appear to be linked to serum protein synthesis. An endogenous mediator of systemic IMS can be detected in tularemic rats by injection of the serum of these animals into healthy recipients. The occurrence of zinc redistribution and increased serum protein synthesis in some groups of rats in the absence of amino acids uptake by liver, as well as the apparent differential dose responsiveness of these responses, are suggestive of a multiplicity of endogenous mediators.

Amino Acids↗

PubMed1975

Myxosarcoma in a young rhesus monkey.

A myxosarcoma that arose spontaneously in the ilial region of a young male Rhesus monkey grew rapidly and invaded and lysed the pelvic bones. It consisted of large pleomorphic cells, with single or multiple nuclei and dilated rough endoplasmic reticulum, in abundant intercellular matrix.

Animals↗

PubMed1975

Pathogenesis of tularemia in immune and nonimmune rats.

Pathogenesis of tularemia in nonimmune rats given (intraperitoneal inoculation) virulent strain (SCHU S4) or vaccinal strain (LVS) of Francisella tularensis and in immune rats given SCHU S4 is described. Both LVS and SCHU S4 caused pyogranulomas in liver and spleen of nonimmune rats. Nonimmune rats given 10(4) SCHU S4 organisms did not survive beyond 72 hours, but immune rats given challenge inoculum of 10(8) SCHU S4 organisms developed lesions and survived. Larger doses of LVS resulted in earlier onset of characteristic hepatitis and splenitis in nonimmune rats. Periportal lymphocytic infiltrates were present in the liver 48 hours after SCHU S4 challenge inoculation of immune rats and 96 hours after inoculation of LVS in nonimmune rats and were associated with intense macrophage aggregation. These changes indicate that the pathogenesis of tularemia is a result of the interdependency of the dose and virulence of the causative agent with the immune status of the host and that cellular immunity has a significant role in the response of the rat to tularemia.

Animals↗

PubMed1973