PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6828837

[Systemic mycoses in hematologic neoplasms].

R A Stahel·P Vogt·G Schüler·J R Rüttner·P Frick·O Oelz
View original source ↗Export metadata ↓

Abstract

Between July 1973 and June 1981 systemic fungal infections were found in 27 of 270 autopsies of patients with hematologic malignancies: in 16 aspergillosis, in 6 candidiasis, in one aspergillosis and candidiasis, and in 4 mucormycosis. The frequency increased from 6% during the first 6 years to 25% during the last 2 years (p = 0.025). Fever despite antibiotics and new pulmonary infiltrates were the major symptoms. In only 6 of 16 patients did microbiological findings support the clinically suspected diagnosis. Systemic fungal infections were the principal cause of death in 12 patients. Because of the difficulty of establishing the diagnosis, empiric antimycotic therapy should be started promptly on clinical suspicion in patients with neutropenia and fever despite antibiotics.

Explore related subjects

Amphotericin BAspergillosisCandidiasisHumansLeukemiaLymphomaMucormycosisMycosesMyeloproliferative DisordersRetrospective StudiesEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R A Stahel, P Vogt, G Schüler, J R Rüttner, P Frick, O Oelz. 1983-01-15. [Systemic mycoses in hematologic neoplasms].. https://pubmed.ncbi.nlm.nih.gov/6828837/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Multi-Omics Analysis of Experimentally Evolved Candida auris Isolates Reveals Modulation of Sterols, Sphingolipids, and Oxidative Stress in Acquired Amphotericin B Resistance.

Clinical isolates of Candida auris show a high prevalence of resistance to Amphotericin B (AmB)-an uncommon trait in most Candida species. Alterations in ergosterol biosynthesis can contribute to acquired AmB resistance in C. auris laboratory strains but are rarely seen in clinical isolates. In this study, we experimentally evolved two drug-susceptible Clade II isolates of C. auris to develop AmB resistance. The evolved strains displayed a four to eight fold increase in MIC50 compared to the parental cells. We analyzed changes in their karyotype, genome, lipidome, and transcriptome associated with this acquired resistance. In one lineage, AOX2 was upregulated, and its deletion reversed the AmB resistance phenotype. The aox2Δ mutant also failed to evolve AmB resistance under experimental conditions. In the same lineage, restoring the UPC2 S332R and RTG3 S101T mutations to the wild-type allele restored AmB susceptibility. In another lineage, the ergosterol and sphingolipid pathways were observed to play a critical role, and upregulation of the ERG genes elevated the total sterol content, while significant downregulation of HSX11 (glucosylceramide synthase) resulted in lower levels of glucosylceramides. To our knowledge, this study is the first to show that AmB resistance in C. auris can be acquired through mechanisms both dependent on or independent of sterol content modulation, highlighting Aox2 and Upc2 as key regulators of amphotericin resistance.

Amphotericin B↗
PubMed2007

Correlation of Neo-Sensitabs tablet diffusion assay results on three different agar media with CLSI broth microdilution M27-A2 and disk diffusion M44-A results for testing susceptibilities of Candida spp. and Cryptococcus neoformans to amphotericin B, caspofungin, fluconazole, itraconazole, and voriconazole.

We compared the Neo-Sensitabs tablet assay to both reference M27-A2 broth microdilution and M44-A disk diffusion methods for testing susceptibilities of 110 isolates of Candida spp. and Cryptococcus neoformans to amphotericin B, caspofungin, fluconazole, itraconazole, and voriconazole. Neo-Sensitabs assay inhibition zone diameters in millimeters on three agars (Mueller-Hinton agar supplemented with 2% dextrose and 0.5 microg/ml methylene blue [MGM], Shadomy [SHA], and RPMI 1640 [RPMI, 2% dextrose]) were obtained at 24 to 72 h. The correlation coefficient of Neo-Sensitabs results with MICs was similar to that of the disk method for most of the five agents on MGM (R, 0.80 to 0.89 versus 0.76 to 0.89, respectively). Overall, superior correlation was observed at 24 h for most agents. The exception was amphotericin B (R values of 0.68 and 0.5 for disk and tablet, respectively, at 48 h versus 0.68 and 0.48, respectively, at 24 h). In general, Neo-Sensitabs results were less consistent on SHA and RPMI agars. Although agreement by breakpoint category of Neo-Sensitabs and disk results with CLSI method M27-A2 was also similar on MGM (92.7 to 98.2% versus 95.5 to 100%, respectively), the Neo-Sensitabs method failed to identify two of the six isolates with high amphotericin B MICs. These data suggest the potential value of the Neo-Sensitabs assay for testing at least four of the five agents against yeasts evaluated in the clinical laboratory.

Amphotericin B↗