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Biomedical subjects

W G Powderly

Publications and source records attributed to W G Powderly.

At least 109 records · Page 6Linked to original sources
PubMed1992

Failure of prophylactic ganciclovir to prevent cytomegalovirus disease in recipients of lung transplants.

In an effort to prevent cytomegalovirus (CMV) pneumonitis, seven consecutive CMV-seronegative lung transplant recipients of organs from seropositive donors (D+/R-) were given ganciclovir, 2.5-5 mg/kg intravenously twice daily for the first 10-21 days after transplantation, and commercial polyvalent immune globulin, 200-400 mg/kg every 7-14 days intravenously, for the first 2-3 weeks after transplantation. This regimen was followed by oral acyclovir. Six patients developed CMV viremia and all developed CMV pneumonitis. Viremia occurred later in these patients compared with D+/R- patients who received alternative forms of CMV prophylaxis or CMV-seropositive recipients who received no specific prophylaxis (P = .023 and P = .021, respectively). There was no statistical difference in incidence or time to onset of CMV pneumonitis. When given as described, prophylactic ganciclovir and immune globulin followed by oral acyclovir may have delayed CMV viremia but did not prevent it or pneumonitis in high-risk lung transplant recipients.

Acyclovir↗
PubMed1992

Molecular typing of candida albicans isolated from oral lesions of HIV-infected individuals.

OBJECTIVE: To evaluate the epidemiology of Candida albicans infection in HIV-infected patients with oral lesions using molecular techniques. METHODS: Thirty-nine isolates from HIV-positive patients with oral candidiasis were examined using two DNA probes (a Histoplasma capsulatum ribosomal DNA probe that cross-hybridizes with C. albicans and a C. albicans strain-specific probe derived from repetitive sequence DNA). C. albicans obtained from the oral cavity of patients receiving cytotoxic chemotherapy was used as controls. RESULTS: Using the H. capsulatum ribosomal DNA probe, isolates were shown to members of many distinct classes of C. albicans. Forty-nine per cent (19 out of 39) of isolates were members of the same class; however, 46% (6 out of 13) of control C. albicans isolates were also members of this class. Further analysis of the class-restricted isolates from the HIV-infected patients using the C. albicans strain-specific probe showed that these could be further separated into distinct strains. CONCLUSIONS: These data indicate that strains of C. albicans that cause oral candidiasis in HIV-positive individuals are not clonally restricted and are similar to those colonizing the oral cavity of other severely immunocompromised hosts. Most patients appear to be infected with unique strains of C. albicans.

Blotting, Southern↗
PubMed1991

Two cases of blastomycosis from a common source: use of DNA restriction analysis to identify strains.

Two friends, one with AIDS, developed severe pulmonary blastomycosis but differed markedly in clinical course. The human immunodeficiency virus-negative patient responded completely to ketoconazole; the patient with AIDS died of progressive disseminated infection despite treatment with fluconazole and amphotericin B. Epidemiologic investigation suggested a common source of infection, but serologic evaluation and environmental cultures were unrevealing. EcoRI digestion of the Blastomyces dermatitidis isolates showed identical restriction fragment patterns that differed from patterns obtained from other clinical isolates. Analysis using a Histoplasma capsulatum ribosomal DNA probe that cross-hybridizes with B. dermatitidis showed that the isolates from the two patients were identical and different from others. Thus, the patients were probably infected with the same strain, possibly from a common source. These data indicate the critical role of cellular immunity in patients with blastomycosis, show that there are multiple genotypes of B. dermatitidis, and suggest that DNA restriction analysis is a useful epidemiologic tool.

Acquired Immunodeficiency Syndrome↗
PubMed1990

The safety and efficacy of zidovudine (AZT) in the treatment of subjects with mildly symptomatic human immunodeficiency virus type 1 (HIV) infection. A double-blind, placebo-controlled trial. The AIDS Clinical Trials Group.

OBJECTIVE: To evaluate the efficacy and safety of zidovudine early in the treatment of human immunodeficiency virus type 1 (HIV) infection. DESIGN: A double-blind, randomized, placebo-controlled trial with subject stratification by pretreatment CD4 T lymphocyte counts. SETTING: Multicenter trial at AIDS Clinical Trial units. SUBJECTS: Seven hundred eleven subjects with mildly symptomatic HIV infection. INTERVENTION: Three hundred fifty-one subjects were assigned to placebo and 360 to zidovudine, 200 mg orally every 4 hours. The median duration of follow-up was 11 months. MEASUREMENTS AND MAIN RESULTS: Fifty-one subjects developed the acquired immunodeficiency syndrome (AIDS), advanced AIDS-related complex, or death as a first critical event. For the stratum of subjects with more than 200 but less than 500 CD4 T lymphocytes/mm3 before treatment, 34 events occurred in placebo recipients and 12 in zidovudine recipients (P = 0.0002; relative risk [RR] estimate, 3.23 [95% CI, 1.67 to 6.24]). For the stratum of subjects with 500 to 799 CD4 T lymphocytes/mm3 before treatment, 2 events occurred in placebo recipients and 3 in zidovudine recipients. Candidiasis at study entry independently increased the risk for having an event (P = 0.005; RR estimate, 2.3 [95% CI, 1.29 to 4.12]); HIV antigenemia at study entry also increased this risk (P = 0.01; RR estimate, 2.1 [95% CI, 1.2 to 3.8]). Significant differences between the treatment groups in CD4 T-lymphocyte counts occurred in subjects with more than 200 but less than 500 CD4 T lymphocytes/mm3 after 4 weeks of therapy (P = 0.002). Differences persisted through week 52. Less prominent changes occurred in subjects with 500 or more CD4 T lymphocytes/mm3. Serum levels of HIV antigen decreased significantly in zidovudine recipients. Serious anemia and neutropenia occurred in 5% and 4% of zidovudine recipients, respectively, and in 0% and 1% of placebo recipients, respectively. CONCLUSION: Zidovudine delayed progression of HIV disease and produced little toxicity in subjects with mildly symptomatic HIV disease and less than 500 CD4 T lymphocytes/mm3.

AIDS-Related Complex↗
PubMed1990

Fungal infections in patients infected with HIV.

HIV-positive patients are at risk for a number of serious fungal infections. The author reviews the common fungal infections and stresses the importance of early detection and appropriate treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Initial clinical management of the HIV-infected patient.

For the primary care physician, treatment of HIV-infected patients often centers on the stage of illness at which the patient first seeks care. Disease staging, which uses symptoms in its classification scheme, thus leads to evaluation and selection of appropriate therapy. This is the second article in a series from the Washington University AIDS Clinical Trials Unit.

CD4-Positive T-Lymphocytes↗
PubMed1989

Zidovudine.

Zidovudine, or azidothymidine (AZT), is the only drug currently approved for treating patients with HIV infection. Though it effectively inhibits the disease, the drug's use is associated with a number of side effects, some grave. Management of zidovudine therapy and its side effects is highlighted. This is the third article in a series from the Washington University AIDS Clinical Trials Unit.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Human immunodeficiency virus infection. Clinical diagnosis.

Primary care physicians are likely to see HIV-infected individuals well before they develop full-blown AIDS or even AIDS-related complex. The author presents an overview of the symptoms that may appear in so-called "asymptomatic" patients with human immunodeficiency virus infection.

AIDS-Related Complex↗
PubMed1988

Suppressor T cells regulating the cell-mediated immune response to Pseudomonas aeruginosa can be generated by immunization with anti-bacterial T cells.

We previously demonstrated that immunization with low (10 micrograms) doses of high m.w. polysaccharide from the gram-negative bacterium Pseudomonas aeruginosa generates T cells that suppress the ability of antibacterial T cells (Tab) to protect against bacterial infection. The current studies indicate that Ts cells with properties identical to those elicited by low dose polysaccharide immunization can be generated by immunization with Tab. Tab-elicited Ts cells can abrogate in vivo induction and in vitro and in vivo expression of antibacterial T cell activity. Tab-elicited Ts are Ag-specific and H-2 restricted in their suppressor activity. Non-immune T cells fail to elicit suppressor activity. These studies provide additional evidence that the protective T cell response to P. aeruginosa is controlled by a network of T cells that are probably recognizing idiotypic determinants on P. aeruginosa-immune T and B cells.

Animals↗
PubMed1988

T cells recognizing polysaccharide-specific B cells function as contrasuppressor cells in the generation of T cell immunity to Pseudomonas aeruginosa.

The cellular interactions involved in the development of T cell-mediated immunity to Pseudomonas aeruginosa have been examined. T cell immunity can be generated by immunizing mice with 10 micrograms of P. aeruginosa polysaccharide (PS) plus the antimitotic agent vinblastine sulfate. Vinblastine is required to inactivate a population of Ts cells generated by immunization with 10 micrograms of PS alone. Immunization with either live bacteria or with higher dose (50 micrograms) of PS without vinblastine also generates T cell immunity; these protocols activate a population of Lyt-1+, 2-, I-J+ T cells which, like vinblastine, counteract the effect of Ts cells. Immunization with 10 micrograms PS alone fails to activate this T cell subpopulation. When administered at the time of immunization, this subpopulation can render the tolerogenic 10-micrograms immunization protocols immunogenic. Like previously described contrasuppressor T cells, this T cell subpopulation exhibits an affinity for the lectin Vicia villosa. We have determined, however, that the T cells that act as contrasuppressor cells in this system are directly activated by PS-immune B cells and not by PS Ag. Furthermore, their activity can be removed by adsorption to PS-specific B cell hybridomas. Our studies indicate an important role for B cells in the development of T cell immunity to P. aeruginosa and suggest that a complex idiotype network controls the development of this response.

Agranulocytosis↗
PubMed1988

Exposure of mice to live Pseudomonas aeruginosa generates protective cell-mediated immunity in the absence of an antibody response.

In previous studies we have elicited T cell-mediated protective immunity to the extra-cellular Gram-negative bacterium Pseudomonas aeruginosa by administering P. aeruginosa polysaccharide Ag and the anti-mitotic agent vinblastine sulfate to BALB/c mice. The current studies indicate that T cells which inhibit the growth of P. aeruginosa in vitro and protect granulocytopenic mice from P. aeruginosa infection can be generated by exposure of BALB/c mice to as few as 10(2) live bacteria without simultaneous administration of vinblastine. The in vitro inhibition of bacterial growth and mouse protection are P. aeruginosa immunotype specific. Exposure to 10(6) live bacteria is required to elicit a detectable antibody response. These findings indicate a potential role for T cells in resistance to P. aeruginosa infection in the large majority of individuals who lack anti-P. aeruginosa antibody.

Animals↗
PubMed1988

Amphotericin B-resistant yeast infection in severely immunocompromised patients.

Systemic yeast infections are a major cause of morbidity and mortality in severely immunocompromised patients. The in vitro susceptibility to amphotericin B of 29 yeasts causing fungemia was examined in 26 patients undergoing allogeneic or autologous bone marrow transplantation and/or myelosuppressive chemotherapy. The minimal inhibitory concentrations (MICs) of amphotericin B observed with blood isolates from these patients were significantly higher than those observed with blood, sputum, or skin isolates from non-immunocompromised patients (p less than 0.01). All episodes (10 of 10) of bloodstream infection in immunocompromised patients caused by isolates with MICs greater than 0.8 micrograms/ml were fatal, versus eight of 17 episodes of bloodstream infection caused by yeasts with MICs of 0.8 micrograms/ml or less (p = 0.04). Although 15 of 26 patients received empiric treatment with amphotericin B before laboratory evidence of fungemia developed, the amphotericin B susceptibilities of their isolates were not significantly different from those of patients who had not received empiric amphotericin B treatment. It is concluded that yeast fungemia in severely immunocompromised patients is often caused by organisms resistant to the usual concentrations of amphotericin B obtainable in vivo, and that this finding is clinically significant.

Adult↗
PubMed1987

In vitro T cell-mediated killing of Pseudomonas aeruginosa. V. Generation of bactericidal T cells in nonresponder mice.

We have previously reported that BALB/c mice immunized with 10 micrograms of a Pseudomonas aeruginosa polysaccharide antigen (PS) and 100 micrograms vinblastine sulfate develop T cell-mediated protective immunity, but fail to generate an antibody response. Vinblastine functions in this system to remove a suppressor cell that normally inhibits expression of this form of immunity after PS immunization. T cells from CB.20 mice immunized with the 10 micrograms of PS and 100 micrograms vinblastine fail to kill P. aeruginosa in vitro. These mice are allotype congenic with BALB/c mice, differing at loci closely linked to the IgH-1 locus. Immunization of CB.20 mice with 10 micrograms PS and 100 micrograms vinblastine results in the appearance of T cells which suppress in vitro bactericidal activity of BALB/c T cells. In the current study we found that T cell-mediated bactericidal activity can be generated in CB.20 mice by increasing the dose of vinblastine given at the time of PS immunization. The phenotype of the CB.20 bactericidal T cell generated by high dose vinblastine is identical to that of the BALB/c bactericidal T cell, and the CB.20 bactericidal T cell can adoptively transfer protective immunity to granulocytopenic mice. After immunization of BALB/c and CB.20 mice with PS alone, approximately one log fewer CB.20 T cells than BALB/c T cells are required to suppress bacterial killing in vitro. Furthermore, the number of CB.20 T cells required to suppress in vitro bacterial killing is directly correlated with the dose of vinblastine administered at the time of immunization. Increasing the immunizing dose of PS overcomes suppressor activity and allows the generation of bactericidal T cells in BALB/c mice without a requirement for vinblastine. CB.20 mice fail to generate bactericidal T cells after immunization with high doses of PS. These results indicate that CB.20 and BALB/c mice both possess the full repertoire of T cells required to express bactericidal T cell activity and that the differences in their responses reflect only quantitative differences in suppressor cell activity.

Animals↗