Azole Resistance in Candida glabrata
Abstract
Candida infections have increased due to the growth and expansion of susceptible patient populations. The azole fluconazole is the most widely prescribed antifungal, but rising rates of clinical resistance among Candida glabrata isolates have greatly limited its utility. A better understanding of the mechanisms of azole antifungal resistance will provide information needed to overcome this clinical problem and reclaim this antifungal class as an option for empiric treatment of Candida infections. By far, the most frequent mechanism of azole resistance in C. glabrata is the overexpression of multidrug transporters due to activating mutations in the gene encoding transcription factor Pdr1. In this review, we will discuss the molecular and genetic basis of azole resistance in C. glabrata with particular attention given to the most recent discoveries in this field.
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The PKC-mediated cell wall integrity pathway is required for the transcriptional activation of multidrug efflux pumps, the most frequent azole resistance mechanism in clinical settings worldwide.
“The PKC-mediated cell wall integrity pathway has been shown to be required for the transcriptional activation of multidrug efflux pumps, which is the most frequent azole resistance mechanism in clinical settings world-wide [91,101,104,105].”
From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [101]
A substantial number of azole-resistant C. glabrata isolates have also been found to be resistant to cell-wall targeting drugs echinocandins, which inhibit the β-glucan synthase enzyme.
“Recently, a substantial number of azole-resistant C. glabrata isolates have also been found to be resistant to cell-wall targeting drugs echinocandins, which inhibit the β-glucan synthase enzyme [101,102,103].”
From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [101]
C. glabrata is intrinsically less susceptible to azoles, which impede ergosterol biosynthesis by inhibiting the cytochrome P450-dependent lanosterol 14α-demethylase enzyme.
“Of three common antifungal drugs, polyenes, azoles and echinocandins, for treatment of systemic Candida infections, C. glabrata is intrinsically less susceptible to azoles which impede ergosterol biosynthesis by inhibiting the cytochrome P450-dependent lanosterol 14α-demethylase enzyme [101].”
From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [101]
Candida glabrata commonly acquires resistance to azole drugs like fluconazole via mutations in a gene encoding a transcription factor called PDR1.
“Second, high level resistant isolates easily arise that contain gain-of-function (GOF) mutations in a transcription factor-encoding gene called PDR1 [7–9].”
From The Candida glabrata Upc2A transcription factor is a global regulator of antifungal drug resistance pathways (2021) · cites this paper as [9]
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References 89 · Cited by 85
- Authors
- Whaley, S. G., & Rogers, P. D.
- Affiliations
- University of Tennessee Health Science Center (US)
- Corresponding author
- Rogers, P. David
- Venue
- Current Infectious Disease Reports
- Published
- 2016-10-19
- Volume
- 18
- Issue
- 12
- Pages
- 41-41
- ISSN
- 1523-3847 (ISSN-L)
- 1534-3146
- OpenAlex
- W2532007534
- Semantic Scholar
- 89345d5bd2cafab1c8c70c5faa1615de2bc7db81
- Cited by
- 85
- References
- 89
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 5 · 2023: 9 · 2022: 16 · 2021: 12 · 2020: 6 · 2019: 17 · 2018: 6 · 2017: 3
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Infectious Disease Reports (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIH NIAID (R01 AI058145)
- 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, azole resistance, fluconazole, antifungal resistance mechanisms, multidrug transporter, drug efflux, candidiasis, empirical antifungal therapy
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