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D E ROGERS

Publications and source records attributed to D E ROGERS.

At least 19 recordsLinked to original sources
PubMed1965

THE DYNAMICS OF RETICULOENDOTHELIAL BLOCKADE.

The dynamics of "reticuloendothelial blockade" were studied in living rabbits and isolated, perfused rabbit livers utilizing gelatin as a blockading agent and Au(198) stabilized in gelatin as a tracer. Employing the above experimental model, the following observations were made. (a) RES blockade was specific and dependent on the surface properties of the particle under study. (b) RES blockade was not caused by saturation of hepatic removal mechanisms. (c) RES blockade was not caused by depletion of demonstrable serum opsonins. (d) RES blockade appeared to correlate with high circulating levels of the blockading agent, per se. Thus, under the conditions employed, the term "reticuloendothelial blockade" was a misnomer. Although specificity of liver macrophage-particle interaction was evident and deserves further study, the data suggest that blockade as usually studied is a laboratory phenomenon induced by the continuing circulation of the blockading agent.

Animals↗
PubMed1962

Factors relating to the virulence of Staphylococci. II. Observations on four mouse-pathogenic strains.

Four clumping factor-negative strains of Staphylococcus aureus were found to closely resemble the diffuse colonial variant of the Smith strain. All produced fatal intraperitoneal infections in mice, all grew in diffuse, streaming colonies in plasma or serum soft agar, and all behaved like encapsulated microorganisms in in vitro opsonic systems. These staphylococci were resistant to phagocytosis in the peritoneal cavities of normal mice. When mice were immunized with heat-killed vaccines prepared from the Smith diffuse variant these strains were rapidly ingested by peritoneal leukocytes and the animals survived. This observation suggests that these strains share the same or a similar phagocytosis-retarding antigen. While most pathogenic staphylococci isolated from human material do not behave like these unusual mouse-virulent strains, indirect evidence is cited to support the suggestion that other staphylococci may acquire similar phagocytosis-resisting characteristics during in vivo multiplication. Studies to support or refute this thesis are in progress.

Animals↗
PubMed1962

Factors relating to the virulence of Staphylococci. III. Antibacterial versus antioxic immunity.

Antitoxic and antibacterial immunity have been clearly differentiated in the experimental mouse infection produced by the diffuse colonial variant of the Smith strain of Staphylococcus aureus. Immunization with crude toxoid protected mice from otherwise lethal doses of alpha hemolysin, but did not alter mortality following intraperitoneal infection with living staphylococci. Conversely, animals immunized with heat killed vaccines were readily killed by culture supernates containing alpha hemolysin, but were strikingly protected from otherwise fatal intraperitoneal infection with viable staphylococci. Protection was directly related to the ability of the immunizing substance to promote early intraperitoneal phagocytosis of the infecting inoculum. In these studies with the Smith diffuse variant, rapid intraperitoneal phagocytosis was induced by vaccination with whole cell bacterial vaccines but not by alpha hemolysin toxoid.

Animals↗
PubMed1961

Studies on bacteriemia. V. The effect of simultaneous leukopenia and reticuloendothelial blockade on the early blood stream clearance of staphylococci and Escherichia coli.

Observations are presented on the course of experimental bacteriemia in rabbits modified by thorotrast reticuloendothelial "blockade" and mechlorethamine induced leukopenia, given singly and together. The production of severe granulocytopenia did not impair the clearance of staphylococci from the blood stream and did not enhance the impairment of clearance produced by thorotrast reticuloendothelial "blockade." Neither severe granulocytopenia nor thorotrast blockade alone produced consistent impairment in the removal of circulating E. coli from the blood stream, whereas when these conditions were present together, the early phases of clearance in these animals were virtually prevented. These results indicate that the host mechanisms operative in the control of bacteriemia differ for staphylococci and E. coli. It is suggested that the fate of bacteria within polymorphonuclear leukocytes may in part determine the importance of these cells in the removal of bacteria from the blood stream.

Animals↗
PubMed1960

Fate of staphylococci within human leukocytes.

Direct observations by phase microscopy have demonstrated that small numbers of pathogenic staphylococci survive prolonged periods of time within living human polymorphonuclear leukocytes. Non-pathogenic microorganisms are rapidly destroyed in similar preparations. Leukocytes in which staphylococci remained viable often appeared less vigorous after ingesting microorganisms, but intracellular survival could not be correlated with obvious leukocyte damage with any consistency. Both pathogenic and non-pathogenic cocci were seen to divide within living granulocytes during the first few minutes after ingestion. Occasionally pathogenic staphylococci multiplied in dying cells after long periods of intracellular residence. Phagocytosis of more than one pair of staphylococci by a single leukocyte appeared to act as a stimulus to bacterial destruction. Multiple ingestions of pathogenic staphylococci reduced the incidence of survival of the total microbiol population contained within the cell.

Granulocytes↗
PubMed1960

Further observations on the behavior of staphylococci within human leukocytes.

A specific serum factor was required for rapid phagocytosis of pathogenic staphylococci by human polymorphonuclear leukocytes when the ingestion process was studied in siliconed glass systems and the concentrations of staphylococci were maintained at low levels. In contrast to certain other microbes, the resistance to phagocytosis which characterized pathogenic staphylococci was relative, and phagocytosis was readily accomplished when large populations of staphylococci were present in the test system. A factor promoting phagocytosis was present in eight of eight normal adult sera. In contrast, the sera of twenty-eight of thirty normal rabbits did not promote phagocytosis. Serum obtained from 2 rabbits maintained in the rabbit colony for several months acquired the ability to opsonize pathogenic staphylococci. The phagocytosis-promoting factor was almost completely removed by prior absorption of test sera with the homologous strain. The factor was incompletely removed by absorption with heterologous strains of pathogenic staphylococci and was not significantly reduced by absorption with coagulase-negative staphylococci or unrelated microorganisms. Present evidence suggests that the factor promoting phagocytosis is a thermostable opsonin. While the activity of heated serum could not be restored by the addition of small amounts of fresh serum or complement, the addition of large amounts of complement partially restored opsonic activity. Incubation of staphylococci in fresh serum prior to heat inactivation did not reduce subsequent phagocytosis, further suggesting the heat stability of the phagocytosis-promoting factor. Preliminary studies correlating the presence of antistaphylococcal hemagglutinins and phagocytosis-promoting factor in certain sera suggest that the two factors were not necessarily related. The phagocytosis of staphylococci in fresh human serum was inhibited by the addition of fresh or inactivated rabbit serum. Further studies on the nature of such inhibition are in progress. Once ingestion was accomplished, coagulase-positive staphylococci consistently survived in significant numbers within the cytoplasm of human granulocytes. Coagulase-negative staphylococci appeared to be destroyed within the leukocyte and could not be recultured from the cytoplasm following 3 to 4 hours of intracellular residence.

Adult↗