Evidence map›Paper›PMID 26920879›Full record

ReviewJournal of microbiology (Seoul, Korea)2016

The development of fluconazole resistance in Candida albicans - an example of microevolution of a fungal pathogen.

Joachim Morschhäuser

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of microbiology (Seoul, Korea), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Morphotype-specific susceptibility toMicrobiology spectrum · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Microevolution during Chronic Infection May LeadDermatology research and practice · 2024
    Article
  9. Assessing the In Vitro Potential of Glatiramer Acetate (CopaxoneJournal of fungi (Basel, Switzerland) · 2023
    Article
  10. Article
  11. The Risk Factors and Mechanisms of Azole Resistance ofJournal of fungi (Basel, Switzerland) · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Molecules (Basel, Switzerland) · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Joachim MorschhäuserInstitute for Molecular Infection Biology, University of Würzburg, D-97080, Würzburg, Germany. joachim.morschhaeuser@uni-wuerzburg.de.
University of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The yeast Candida albicans is a member of the microbiota in the gastrointestinal and urogenital tracts of most healthy persons, but it can also cause symptomatic infections, especially in immunocompromised patients. During the life-long association with its human host, C. albicans generates genetically altered variants that are better adapted to changes in their environment. A prime example of this microevolution is the development of resistance to the commonly used drug fluconazole, which inhibits ergosterol biosynthesis, during antimycotic therapy. Fluconazole resistance can be caused by mutations in the drug target, by changes in the sterol biosynthesis pathway, and by gain-of-function mutations in transcription factors that result in the constitutive upregulation of ergosterol biosynthesis genes and multidrug efflux pumps. Fluconazole also induces genomic rearrangements that result in gene amplification and loss of heterozygosity for resistance mutations, which further increases drug resistance. These genome alterations may affect extended chromosomal regions and have additional phenotypic consequences. A striking case is the loss of heterozygosity for the mating type locus MTL in many fluconazole-resistant clinical isolates, which allows the cells to switch to the mating-competent opaque phenotype. This, in turn, raises the possibility that sexual recombination between different variants of an originally clonal, drug-susceptible population may contribute to the generation of highly fluconazole-resistant strains with multiple resistance mechanisms. The gain-of-function mutations in transcription factors, which result in deregulated gene expression, also cause reduced fitness. In spite of this, many clinical isolates that contain such mutations do not exhibit fitness defects, indicating that they have overcome the costs of drug resistance with further evolution by still unknown mechanisms.

Indexed as

AnimalsAntifungal AgentsCandida albicansCandidiasisDrug Resistance, FungalEvolution, MolecularFluconazoleHumansAntifungal AgentsFluconazoledrug resistancefitness costsgain-of-function mutationgenome alterationsloss of heterozygosity

Identifiers

PMID26920879
OpenAlexW2278571227

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.