Evidence map›Paper›PMID 9564569›Full record

ReviewClinical microbiology reviews1998

Clinical, cellular, and molecular factors that contribute to antifungal drug resistance.

T C White, K A Marr, R A Bowden

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical microbiology reviews, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 428 papers.

0numbers the graph read from it
0cells of the map it votes in
428citing papers in PubMed
36.8field-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

428 citing papers in PubMed, 1,343 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
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  6. Review
  7. Microbiology and molecular biology reviews : MMBR · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Does the use of topical azoles have an impact on antifungal resistance?The Journal of antimicrobial chemotherapy · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Genome research · 2025
    Article
  18. Review
  19. Article
  20. Review

368 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 3 countries.

T C WhiteDepartment of Pathobiology, School of Public Health and Community Medicine, University of Washington, Seattle Biomedical Research Institute, Washington, USA. tedwhite@u.washington.edu
K A Marr
R A Bowden
Cape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZACenter for Infectious Disease Research · US

Funding

ORAL CANDIDIASIS IN LENTIVIRUS INFECTED MACAQUESR01DE011367 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI WHITE, THEODORE C. · 1994 to 2007
$2.5M
NIDCR NIH HHS R01 DE011367NIDCR NIH HHS R01 DE-11367
6 · The paper itself

Abstract

In the past decade, the frequency of diagnosed fungal infections has risen sharply due to several factors, including the increase in the number of immunosuppressed patients resulting from the AIDS epidemic and treatments during and after organ and bone marrow transplants. Linked with the increase in fungal infections is a recent increase in the frequency with which these infections are recalcitrant to standard antifungal therapy. This review summarizes the factors that contribute to antifungal drug resistance on three levels: (i) clinical factors that result in the inability to successfully treat refractory disease; (ii) cellular factors associated with a resistant fungal strain; and (iii) molecular factors that are ultimately responsible for the resistance phenotype in the cell. Many of the clinical factors that contribute to resistance are associated with the immune status of the patient, with the pharmacology of the drugs, or with the degree or type of fungal infection present. At a cellular level, antifungal drug resistance can be the result of replacement of a susceptible strain with a more resistant strain or species or the alteration of an endogenous strain (by mutation or gene expression) to a resistant phenotype. The molecular mechanisms of resistance that have been identified to date in Candida albicans include overexpression of two types of efflux pumps, overexpression or mutation of the target enzyme, and alteration of other enzymes in the same biosynthetic pathway as the target enzyme. Since the study of antifungal drug resistance is relatively new, other factors that may also contribute to resistance are discussed.

Indexed as

Antifungal AgentsCandida albicansCandidiasisDrug Resistance, MicrobialDrug Resistance, MultipleFungiGenes, FungalHumansMicrobial Sensitivity TestsMycosesAntifungal Agents

Identifiers

PMID9564569
PMCPMC106838
OpenAlexW2107013040

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.