Evidence map›Paper›PMID 38466738›Full record

ArticlePLoS pathogens2024

Candida auris undergoes adhesin-dependent and -independent cellular aggregation.

Chloe Pelletier, Sophie Shaw, Sakinah Alsayegh, Alistair J P Brown, Alexander Lorenz

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
14.0field-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

32 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Insights on molecular drivers of phenotypic plasticity in Candidozyma auris.World journal of microbiology & biotechnology · 2026
    Review
  3. Article
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  6. Microbiology and molecular biology reviews : MMBR · 2026
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  20. Dry Surface Biofilm Formation by Candida auris Facilitates Persistence and Tolerance to Sodium Hypochlorite.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025
    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

5 authors at 2 institutions in 1 country.

Chloe PelletierInstitute of Medical Sciences (IMS), University of Aberdeen, Aberdeen, United Kingdom.ORCID 0000-0002-5581-3442
Sophie ShawCentre for Genome-Enabled Biology and Medicine (CGEBM), University of Aberdeen, Aberdeen, United Kingdom.
Sakinah AlsayeghInstitute of Medical Sciences (IMS), University of Aberdeen, Aberdeen, United Kingdom.
Alistair J P BrownMRC Centre for Medical Mycology, University of Exeter, Exeter, United Kingdom.ORCID 0000-0003-1406-4251
Alexander LorenzInstitute of Medical Sciences (IMS), University of Aberdeen, Aberdeen, United Kingdom.ORCID 0000-0003-1925-3713
University of Aberdeen · GBUniversity of Exeter · GB

Funding

Medical Research Council MR/M026663/1Medical Research Council MR/M026663/2Medical Research Council MR/V033417/1
6 · The paper itself

Abstract

Candida auris is a fungal pathogen of humans responsible for nosocomial infections with high mortality rates. High levels of resistance to antifungal drugs and environmental persistence mean these infections are difficult to treat and eradicate from a healthcare setting. Understanding the life cycle and the genetics of this fungus underpinning clinically relevant traits, such as antifungal resistance and virulence, is of the utmost importance to develop novel treatments and therapies. Epidemiological and genomic studies have identified five geographical clades (I-V), which display phenotypic and genomic differences. Aggregation of cells, a phenotype primarily of clade III strains, has been linked to reduced virulence in some infection models. The aggregation phenotype has thus been associated with conferring an advantage for (skin) colonisation rather than for systemic infection. However, strains with different clade affiliations were compared to infer the effects of different morphologies on virulence. This makes it difficult to distinguish morphology-dependent causes from clade-specific or even strain-specific genetic factors. Here, we identify two different types of aggregation: one induced by antifungal treatment which is a result of a cell separation defect; and a second which is controlled by growth conditions and only occurs in strains with the ability to aggregate. The latter aggregation type depends on an ALS-family adhesin which is differentially expressed during aggregation in an aggregative C. auris strain. Finally, we demonstrate that macrophages cannot clear aggregates, suggesting that aggregation might after all provide a benefit during systemic infection and could facilitate long-term persistence in the host.

Indexed as

Antifungal AgentsCandidaAdhesins, BacterialCandida aurisDrug Resistance, FungalHumansMicrobial Sensitivity TestsVirulenceAdhesins, BacterialAntifungal Agents

Identifiers

PMID38466738
PMCPMC10957086
OpenAlexW4392639057

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.