PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 4004313

Neonatal systemic candidiasis.

H Smith·P Congdon
View original source ↗Export metadata ↓

Abstract

Ten babies who required neonatal intensive care developed systemic candidiasis. Eight were extremely preterm (28 weeks' gestation or less) and all received prolonged ventilation, multiple courses of broad spectrum antibiotics, and intravenous hyperalimentation. Diagnosis was established by culture of yeasts from suprapubic urine specimens; venous blood cultures proved unreliable. Initial treatment with 5-flucytosine alone in eight babies and combined with amphotericin B in two, eradicated the infection in nine babies, the treatment failure arising through diagnostic delay and development of resistance to 5-flucytosine. Prophylactic topical antifungal drugs, regular screening of suprapubic urine specimens, and prompt use of systemic antifungal agents before multifocal infection becomes established may reduce the incidence and improve outcome.

Explore related subjects

Amphotericin BAnti-Bacterial AgentsCandidiasisCritical CareDrug Therapy, CombinationFlucytosineHumansInfantInfant, NewbornInfant, Premature, DiseasesRespiration, ArtificialJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Smith, P Congdon. 1985. Neonatal systemic candidiasis.. https://doi.org/10.1136/adc.60.4.365

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↗
PubMed1992

Comparative theoretical study of the conformations of amphotericin methyl ester and amphotericin B polar heads in the presence of water.

Amphotericin methyl ester (AmE) is an interesting derivative of amphotericin B (AmB) because of its enhancement of selectivity against the fungicells. Both AmB and AmE molecules differ by the structure of their polar heads. This work deals with a theoretical study of conformations of the polar head of AmE in the presence of hydration water molecules. The results will be compared with our previous work concerning AmB.

Amphotericin B↗