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Biomedical subjects

W G Powderly

Publications and source records attributed to W G Powderly.

120 records · Page 7Linked to original sources
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↗
PubMed1986

In vitro T cell-mediated killing of Pseudomonas aeruginosa. IV. Nonresponsiveness in polysaccharide-immunized BALB/c mice is attributable to vinblastine-sensitive suppressor T cells.

We reported previously that BALB/c mice immunized with a polysaccharide (PS) antigen isolated from immunotype 1 Pseudomonas aeruginosa and vinblastine sulfate develop T cell-mediated protective immunity, despite their failure to produce specific antibody. In vitro, Lyt-1-,2+, I-J+ T cells from vinblastine- and PS-immunized mice kill P. aeruginosa by secretion of a bactericidal lymphokine. BALB/c mice immunized with PS alone generate neither protective antibodies nor a protective T cell response. The current studies indicate that T cells from mice immunized with PS alone significantly suppress the bactericidal activity of T cells from mice immunized with vinblastine and PS. The suppressor T cells are of the same Lyt-1-,2+, I-J+ phenotype as the bactericidal T cells. Suppression is mediated by a soluble product of these suppressor T cells which both inhibits T cell proliferation and interferes with the production or release of the bactericidal lymphokine. Cyclophosphamide, used in other systems to remove suppressor T cells, fails to enhance bacterial killing and does not inhibit suppressor cell activity. These studies indicate that immunization with PS elicits responses in two functionally distinct subgroups of Lyt-1-,2+, I-J+ T cells, and that these cells are distinguishable by their sensitivity to vinblastine sulfate.

Animals↗
PubMed1986

T lymphocyte-mediated protection against Pseudomonas aeruginosa infection in granulocytopenic mice.

BALB/c mice immunized with Pseudomonas aeruginosa immunotype 1 polysaccharide develop protective T cell immunity to bacterial challenge. In vitro, T cells from immunized mice kill P. aeruginosa by production of a bactericidal lymphokine. The present study demonstrates that adoptive transfer of T cells from immunized BALB/c mice to granulocytopenic mice resulted in 97% survival on challenge with P. aeruginosa, compared with 17% survival with adoptive transfer of T cells from nonimmune BALB/c mice. This protection is specifically elicited by reexposure to the original immunizing antigen; adoptive recipients cannot withstand challenge with immunotype 3 P. aeruginosa. However, the adoptive recipients do survive simultaneous infection with both P. aeruginosa immunotypes 1 and 3. Adoptive transfer of T cells from the congenic CB.20 mice, which are unable to kill P. aeruginosa in vitro, provides only 20% protection to granulocytopenic mice. These studies indicate that transfer of specific immune T lymphocytes can significantly enhance the resistance to P. aeruginosa infection in granulocytopenic mice.

Agranulocytosis↗
PubMed1986

In vitro T cell-mediated killing of Pseudomonas aeruginosa. III. The role of suppressor T cells in nonresponder mice.

T lymphocytes from immune BALB/c mice can adoptively transfer protection against infection with the extracellular Gram-negative bacterium Pseudomonas aeruginosa to nonimmune recipients, and in vitro, immune T cells are able to kill these bacteria. Earlier studies indicated that this killing is mediated by a bactericidal lymphokine. The current studies demonstrate that T cells from immunized CB.20 mice, a strain congenic with BALB/c, fail to kill Pseudomonas aeruginosa in vitro. This nonresponsiveness is attributable to the activity of suppressor T cells of the Lyt-1-, 2,3+, I-J+ phenotype. CB.20 mice are known to differ from BALB/c mice only at a single locus, which includes the Igh-1 allotype CH genes. These results suggest a critical role for this locus or closely linked genes in the control of T cell killing of this extracellular bacterium.

Animals↗
PubMed1985

Renal glomerulopathies associated with Hodgkin's disease.

From a series of 138 patients with Hodgkin's disease seen over a 17-year period, 2 developed the nephrotic syndrome. One patient developed hematuria unrelated to cytotoxic chemotherapy or thrombocytopenia. All three patients had evidence of glomerulopathy on histologic examination of renal tissue, but none had the more usually associated minimal-change glomerular histologic features. The patients with nephrotic syndrome had effective clinical regression with systemic chemotherapy. The significance of renal glomerular disease in association with Hodgkin's disease is discussed.

Adult↗
PubMedDate not supplied

Pneumococcal endocarditis: report of a series and review of the literature.

Pneumococcal endocarditis has declined sharply in incidence since the advent of penicillin but remains a potentially lethal infection. From 1980 to 1984, pneumococcal endocarditis was diagnosed in seven patients--four adults and three infants. Apart from one patient who had had a splenectomy, there were no recognizable predisposing factors to infection due to Streptococcus pneumoniae, although all three children were younger than 15 months of age. Congenital heart disease was present in two patients, calcific aortic disease in one, and mitral valve prolapse in a fourth. The remaining three patients had previously normal hearts. Meningitis occurred in five (71%) of the seven patients. Five patients were cured of their infection: four by medical therapy alone (penicillin or vancomycin), and a fifth, by medical therapy plus valvular debridement. Two patients died: one with intractable heart failure, and the second, from the complications of cardiac surgery. Penicillin alone is effective therapy for pneumococcal endocarditis. Patients unable to tolerate penicillin may be treated with vancomycin.

Adult↗
PubMedDate not supplied

Prophylaxis and treatment of opportunistic infection in patients on HAART.

Opportunistic infections (OIs) are the hallmark of the immunodeficiency associated with HIV infection. Prophylaxis strategies have improved the morbidity and mortality associated with AIDS. The widespread use of highly active antiretroviral therapy (HAART) has brought about a change in the natural history and clinical manifestations of OIs; a decline in the incidence of most OIs; and an improvement in the clinical outcome of many OIs. The possibility of immune reconstitution raises questions about whether withdrawal or prophylaxis is safe and, in some cases, whether certain diseases may be curable without lifelong maintenance prophylaxis. Ongoing studies should provide information about the safety of removing primary and secondary prophylaxis in patients who respond to HAART. This review will update clinicians on the current state of the art of prophylaxis and treatment of OIs in patients taking HAART.

AIDS-Related Opportunistic Infections↗