Fluconazole and Echinocandin resistance of Candida glabrata correlates better with antifungal drug exposure rather than with MSH2 mutator genotype in a French Cohort of patients harboring low rates of resistance.

Dellière, Sarah; Healey, Kelley; Gits-Muselli, Maud; Carrara, Bastien; Barbaro, Alessandro; Guigue, Nicolas; Lecefel, Christophe; Touratier, Sophie; Desnos-Ollivier, Marie; Perlin, David S.; Bretagne, Stéphane; Alanio, Alexandre

doi:10.3389/fmicb.2016.02038

Cited by 77Antifungal resistance and susceptibilityFungal and yeast genetics researchFungal Plant Pathogen Control

Fluconazole and Echinocandin resistance of Candida glabrata correlates better with antifungal drug exposure rather than with MSH2 mutator genotype in a French Cohort of patients harboring low rates of resistance.

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Dellière, Sarah, Healey, Kelley, Gits-Muselli, Maud, Carrara, Bastien, Barbaro, Alessandro, Guigue, Nicolas, Lecefel, Christophe, Touratier, Sophie +4 more·2016·Frontiers in Microbiology

DOI 10.3389/fmicb.2016.02038PMC PMC5179511

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Abstract

Candida glabrata is a major pathogenic yeast in humans that is known to rapidly acquire resistance to triazole and echinocandin antifungal drugs. A mutator genotype (MSH2 polymorphism) inducing a mismatch repair defect has been recently proposed to be responsible for resistance acquisition in C. glabrata clinical isolates. Our objectives were to evaluate the prevalence of antifungal resistance in a large cohort of patients in Saint-Louis hospital, Paris, France, some of whom were pre-exposed to antifungal drugs, as well as to determine whether MSH2 polymorphisms are associated with an increased rate of fluconazole or echinocandin resistance. We collected 268 isolates from 147 patients along with clinical data and previous antifungal exposure. Fluconazole and micafungin minimal inhibition concentrations (MICs) were tested, short tandem repeat genotyping was performed, and the MSH2 gene was sequenced. According to the European Committee on Antimicrobial Susceptibility breakpoints, 15.7% of isolates were resistant to fluconazole (MIC > 32 mg/L) and 0.7% were resistant to micafungin (MIC > 0.03 mg/L). A non-synonymous mutation within MSH2 occurred in 44% of the isolates, and 17% were fluconazole resistant. In comparison, fluconazole resistant isolates with no MSH2 mutation represented 15% (P=0.65). MSH2 polymorphisms were associated with the short tandem repeat genotype. The rate of echinocandin resistance is low and correlates with prior exposure to echinocandin. The mutator genotype was not associated with enrichment in fluconazole resistance but instead corresponded to rare and specific genotypes.

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44-50% of investigated isolates (n = 625) were carrying MSH2 defects, which indicates that the MSH2 defect may confer some selective advantage in C. glabrata.
“It has been observed that 44–50% of investigated isolates (n = 625) were carrying MSH2 defects which thus indicates that the MSH2 defect may confer some selective advantage in C. glabrata (Dellière et al. 2016; Healey et al. 2016a,b).”
From Comparative Genomics of Two Sequential Candida glabrata Clinical Isolates (2017) · cites this paper as Dellière et al. 2016

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Clinical and Laboratory Development of Echinocandin Resistance in Candida glabrata: Molecular Characterization
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Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance.
Healey, K. R., Zhao, Y., Perez, W. B., Lockhart, S. R., Sobel, J. D., Farmakiotis, D., Kontoyiannis, D. P., Sanglard, D., Taj-Aldeen, S. J., Alexander, B. D., et al. (2016) · Nature Communications · doi:10.1038/ncomms11128 · Cited by 276 · see citing works
Self-citation

Authors: Dellière, S., Healey, K., Gits-Muselli, M., Carrara, B., Barbaro, A., Guigue, N., Lecefel, C., Touratier, S., Desnos-Ollivier, M., Perlin, D. S., Bretagne, S., & Alanio, A.
Affiliations: Assistance Publique – Hôpitaux de Paris (FR)
Rutgers Health (US)
Centre National de la Recherche Scientifique (FR)
Corresponding author: Alanio, Alexandre
ORCID: Dellière, Sarah
Healey, Kelley
Barbaro, Alessandro
Touratier, Sophie
Perlin, David S.
Bretagne, Stéphane
Alanio, Alexandre
Venue: Frontiers in Microbiology
Publisher: Frontiers Media SA
Published: 2016-12-23
Volume: 7
Pages: 2038-2038
ISSN: 1664-302X (ISSN-L)
DOI: 10.3389/fmicb.2016.02038
PMC: PMC5179511
OpenAlex: W2565723463
Cited by: 75
References: 41
Citations by year: 2026: 5 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 9 · 2021: 6 · 2020: 6 · 2019: 10 · 2018: 11 · 2017: 11
FWCI: 9.85
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Microbiology (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (2r01ai109025-11)
National Institute of Allergy and Infectious Diseases (R01AI-109025)
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 › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
Keywords: Candida glabrata, fluconazole resistance, echinocandin resistance, micafungin, DNA mismatch repair, short tandem repeat genotyping, minimum inhibitory concentration, triazole resistance, clinical isolates

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Fluconazole and Echinocandin resistance of Candida glabrata correlates better with antifungal drug exposure rather than with MSH2 mutator genotype in a French Cohort of patients harboring low rates of resistance.

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