Evidence map›Paper›PMID 26567278›Full record

ArticleClinical infectious diseases : an official publication of the Infectious Diseases Society of America2015

Echinocandin Resistance in Candida.

David S Perlin

Open access · bronzeAbstract read
In one paragraph

Article in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed
12.2field-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

186 citing papers in PubMed, 347 citations in OpenAlex.

  1. Trial
  2. Article
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  5. Review
  6. Emergence and Comparative Analysis ofJournal of fungi (Basel, Switzerland) · 2026
    Article
  7. Micafungin exposure drives multidrug resistance inbioRxiv : the preprint server for biology · 2026
    Article
  8. Recent Outbreaks, Resistance Trends, and Control Measures inJournal of fungi (Basel, Switzerland) · 2026
    Review
  9. Escalating Antifungal Resistance AmongPathogens (Basel, Switzerland) · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Profound cell wall remodeling inMicrobiology spectrum · 2026
    Article
  14. Microbiology and molecular biology reviews : MMBR · 2026
    Review
  15. Article
  16. Journal of medical microbiology · 2026
    Review
  17. Drug susceptibility ofIranian journal of microbiology · 2026
    Article
  18. Article
  19. Review
  20. Decoding resistance inFrontiers in cellular and infection microbiology · 2026
    Article

126 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

1 author at 1 institution in 1 country.

David S PerlinPublic Health Research Institute, New Jersey Medical School-Rutgers Biomedical and Health Sciences, Newark.
Rutgers Health

Funding

Critical Factors Influencing Echinocandin Resistance in CandidaglabrataR01AI109025 · NIAID · RBHS-NEW JERSEY MEDICAL SCHOOL · PI PERLIN, DAVID S · 2014 to 2025
$9.8M
Mechanism of clinical resistance to echinocandin antifungal drugsR01AI069397 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PERLIN, DAVID S · 2007 to 2011
$2.0M
NIAID NIH HHS AI069397NIAID NIH HHS AI109025NIAID NIH HHS R01 AI069397NIAID NIH HHS R01 AI109025
6 · The paper itself

Abstract

Invasive fungal infections are an important infection concern for patients with underlying immunosuppression. Antifungal therapy is a critical component of patient care, but therapeutic choices are limited due to few drug classes. Antifungal resistance, especially among Candida species, aggravates the problem. The echinocandin drugs (micafungin, anidulafungin, and caspofungin) are the preferred choice to treat a range of candidiasis. They target the fungal-specific enzyme glucan synthase, which is responsible for the biosynthesis of a major cell wall polymer. Therapeutic failure involves acquisition of resistance, although it is a rare event among most Candida species. However, in some settings, higher-level resistance has been reported among Candida glabrata, which is also frequently resistant to azole drugs, resulting in difficult-to-treat multidrug-resistant strains. The mechanism of echinocandin resistance involves amino acid changes in "hot spot" regions of FKS-encoded subunits of glucan synthase, which decreases the sensitivity of enzyme to drug, resulting in higher minimum inhibitory concentration values. The cellular processes promoting the formation of resistant FKS strains involve complex stress response pathways that yield a variety of adaptive compensatory genetic responses. Standardized broth microdilution techniques can be used to distinguish FKS mutant strains from wild type, but testing C. glabrata with caspofungin should be approached cautiously. Finally, clinical factors that promote echinocandin resistance include prophylaxis, host reservoirs including biofilms in the gastrointestinal tract, and intra-abdominal infections. An understanding of clinical and molecular factors that promote echinocandin resistance is critical to develop better diagnostic tools and therapeutic strategies to overcome resistance.

Indexed as

Drug Resistance, Multiple, FungalAnidulafunginAntifungal AgentsAzolesCandidaCandida glabrataCandidiasisCaspofunginEchinocandinsGlucosyltransferasesHumansIntraabdominal InfectionsLipopeptidesMicafunginMutationAnidulafunginAntifungal AgentsAzolesCaspofunginEchinocandinsglucan synthaseGlucosyltransferasesLipopeptidesMicafunginCandidacaspofunginechinocandinFKSmicafungin

Identifiers

PMID26567278
PMCPMC4643482
OpenAlexW2231020609

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.