Cited by 170Antifungal resistance and susceptibilityFungal and yeast genetics researchYeasts and Rust Fungi Studies

The DOI matches its Crossref record; 117 of the 120 references it cites were found in a registry or an index; none of the 112 sources its claims cite is checked for support yet.

Candida glabrata: Pathogenicity and Resistance Mechanisms for Adaptation and Survival

Open access

Published version of a preprint

Abstract

Candida glabrata is a yeast of increasing medical relevance, particularly in critically ill patients. It is the second most isolated Candida species associated with invasive candidiasis (IC) behind C. albicans. The attributed higher incidence is primarily due to an increase in the acquired immunodeficiency syndrome (AIDS) population, cancer, and diabetic patients. The elderly population and the frequent use of indwelling medical devices are also predisposing factors. This work aimed to review various virulence factors that facilitate the survival of pathogenic C. glabrata in IC. The available published research articles related to the pathogenicity of C. glabrata were retrieved and reviewed from four credible databases, mainly Google Scholar, ScienceDirect, PubMed, and Scopus. The articles highlighted many virulence factors associated with pathogenicity in C. glabrata, including adherence to susceptible host surfaces, evading host defences, replicative ageing, and producing hydrolytic enzymes (e.g., phospholipases, proteases, and haemolysins). The factors facilitate infection initiation. Other virulent factors include iron regulation and genetic mutations. Accordingly, biofilm production, tolerance to high-stress environments, resistance to neutrophil killings, and development of resistance to antifungal drugs, notably to fluconazole and other azole derivatives, were reported. The review provided evident pathogenic mechanisms and antifungal resistance associated with C. glabrata in ensuring its sustenance and survival.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

This review summarizes virulence and antifungal resistance mechanisms that enable *Candida glabrata* to colonize, evade host immunity, and survive therapy. It highlights adhesion, biofilm formation, stress adaptation, replicative ageing, iron acquisition, and azole/echinocandin resistance as key contributors to its clinical persistence.

Key findings

  • *C. glabrata* is the second most frequently isolated *Candida* species in invasive candidiasis after *C. albicans*, accounting for approximately 15–25% of invasive clinical cases; invasive candidiasis due to *C. glabrata* has an estimated morbidity and mortality of approximately 40–60%.
  • Virulence factors include hydrolytic enzymes (phospholipases, proteases, haemolysins), epithelial adhesin (EPA)-family adhesins, sparse yeast-cell biofilms, cell wall/chitin remodeling, iron acquisition, environmental stress adaptation, and replicative ageing; *C. glabrata* lacks hyphal formation and provokes a weaker host immune response than *C. albicans*.
  • Resistance mechanisms include intrinsic and acquired fluconazole resistance, azole resistance via *ERG11* mutations, *PDR1* gain-of-function mutations, efflux pumps, aneuploidy, and mitochondrial dysfunction; echinocandin resistance is around 4% in *C. glabrata* and less than 1% in *C. albicans*, primarily through *FKS1* and *FKS2* hotspot mutations.
  • Biofilm formation on medical devices contributes to drug tolerance, and the review states that an estimated 65% of all human infections are of biofilm aetiology.

Methods

  • Narrative review of published research articles related to *C. glabrata* pathogenicity, retrieved from four credible databases: Google Scholar, ScienceDirect, PubMed, and Scopus.
  • The paper synthesizes cited studies on virulence factors, host–pathogen interactions, and antifungal resistance mechanisms; it reports no primary experiments or new data.
  • No systematic search dates, inclusion/exclusion criteria, or quality appraisal methods are described in the text.

Limitations

  • The paper has no formal limitations section; it states that the exact azole resistance mechanism is not entirely clear, iron homeostasis mechanisms in *C. glabrata* remain unknown, it is unclear how *Candida* biofilm structure affects mucosal infection and host immunity, and acid stress tolerance has not been extensively investigated.
  • Evident from the text: as a narrative review, it lacks a systematic search strategy, quantitative synthesis, and formal risk-of-bias assessment.
  • Evident from the text: many cited findings derive from in vitro assays or murine models, which may limit direct clinical generalizability.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.3390/jof7080667

Cites

117 of 117 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

0 of 112 cited sources checked · 0 supported · 0 flagged

Show all 78 claims

  • It may state two separate claims as one. 36
  • Probably not a substantial claim. 27
52 of 52
  • The authors state this as an assumption.

    The mechanisms of biofilm resistance include elevated cellular density, exopolymeric protective effect, differential upregulation of resistance genes and efflux pumps, and a subpopulation within the biofilm community.

    “The resistance development due to biofilm is complex and multifactorial; among the assumed mechanisms are (i) the elevated cellular density within the biofilm, (ii) the exopolymeric protective effect of the biofilm, (iii) differential upregulation of genes linked to resistance and those encoding efflux pumps, and (iv) the presence of a subpopulation within the biofilm community.”
  • The paper relies on this without support.

    The four databases Google Scholar, ScienceDirect, PubMed, and Scopus cover the relevant published research on C. glabrata pathogenicity.

    “The available published research articles related to the pathogenicity of C. glabrata were retrieved and reviewed from four credible databases, mainly Google Scholar, ScienceDirect, PubMed, and Scopus.”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 120 references

3 of the 120 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Molina, 2000, Protein Localisation Approaches for Understanding Yeast Cell Wall Biogenesis, Histol. Stud. Yeast, 612, 601
  2. Walker, 2009, Methods in Molecular Biology. TM Series Editor, Life Sci., 531, 588

Cited by

Sorted by citations

Metadata

Authors
Hassan, Y., Chew, S. Y., & Than, L. T. L.
Affiliations
Universiti Putra Malaysia (MY)
Corresponding author
Than, Leslie Thian Lung
Venue
Journal of Fungi
Publisher
MDPI AG
Published
2021-08-17
Volume
7
Issue
8
Pages
667
ISSN
2309-608X (ISSN-L)
OpenAlex
W3194477778
Cited by
170
References
120
Citations by year
2026: 35 · 2025: 41 · 2024: 42 · 2023: 26 · 2022: 20 · 2021: 6
FWCI
2.75
Type
journal article
Language
en
Open access
Locations
  • Journal of Fungi (publishedVersion, cc-by)
  • Preprints.org (acceptedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Universiti Putra Malaysia Institutional Repository (Universiti Putra Malaysia) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Greater South Information System
Funders
Universiti Putra Malaysia (GP-IPS/2018/9612400)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Life Sciences › Immunology and Microbiology › Microbiology › Yeasts and Rust Fungi Studies
Keywords
Candida glabrata, invasive candidiasis, virulence factors, antifungal resistance, fluconazole resistance, azole resistance, biofilm formation, host defense evasion, iron regulation, hydrolytic enzymes, phospholipase, proteolytic enzymes, hemolysin, critically ill patients

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