PubMed HealthSearch

PubMed · 8588829

[Candida vasculitis].

Abstract

Apart from direct skin attacks, yeasts of the Candida group hold a place that is much discussed in the occurrence of immuno-allergic reactions of the skin, because of their usual saprophytic characteristics. We report here on observation of a patient of 62 years who presented with a secondary purpuric maculo-papular eruption making a tri-symptom of Gougerot, for which we have incriminated the role of the immunogenicity of Candida. Skin histology confirmed the presence of an angiitis and necrotising capillarity. An intradermal test with candidine reproduced the skin symptoms and histology, whilst other microbial and fungal tests remained within normal limits. Other examinations showed the transitory presence of circulating immune complexes, although the remainder of the immunity factors were negative. A digestive focus of Candida was present. Recovery occurred after systemic mycological treatment was started, though there was a return of symptoms after a temporary initial check.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J L Bourrain, J C Béani, P Amblard. 1995. [Candida vasculitis].. https://pubmed.ncbi.nlm.nih.gov/8588829/

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

KEEP EXPLORING

Related citations

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

Amphotericin B as an intracellular antioxidant: protection against 2,2'-azobis(2,4-dimethylvaleronitrile)-induced peroxidation of membrane phospholipids in rat aortic smooth muscle cells.

The antifungal activity of amphotericin B (AmB) and its side-effects (e.g. nephrotoxicity and hemolytic action) are suggested to be associated with its prooxidant effects in target cells. To test this hypothesis, we have undertaken studies to examine the role of AmB in oxidative stress in cultured rat aortic smooth muscle cells (SMC) incubated in the absence or in the presence of a lipid-soluble azo-initiator of peroxyl radicals, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). No changes in the pattern of membrane phospholipids could be detected by two-dimensional high performance thin-layer chromatography (HPTLC) after oxidative stress induced by AMVN in which the cells remained viable, as judged by trypan blue exclusion. To improve the sensitivity of detection of oxidative stress in the cells, cis-parinaric acid (PnA) was incorporated biosynthetically into the membrane phospholipids [using PnA-human serum albumin (hSA) complex]. Incubation of the cells under aerobic conditions in the presence of up to 10 microM AmB showed no significant change in the pattern of PnA-labeled phospholipids, suggesting that AmB was not affecting the oxidative state of the cells. In contrast, treatment with AMVN (0.5 mM, incubation in the dark for 2 hr at 37 degrees--conditions in which the viability of the cells was maintained) caused a significant reduction of all fluorescently labeled phospholipid fractions separated by HPLC. When PnA-labeled cells were subjected to oxidative stress by incubation with 0.5 mM AMVN in the presence of AmB, the loss of fluorescent phospholipids was reduced in a concentration-dependent manner over a concentration range of 0.25 to 10 microM. Thus, AmB does not produce any prooxidant effect but rather acts as an intracellular antioxidant.

Amphotericin B