Echinocandin persistence directly impacts the evolution of resistance and survival of the pathogenic fungus Candida glabrata
Open accessAbstract
Recent epidemiological studies documented an alarming increase in the prevalence of echinocandin-resistant (ECR) Candida glabrata blood isolates. ECR isolates are known to arise from a minor subpopulation of a clonal population, termed echinocandin persisters. Although it is believed that isolates with a higher echinocandin persistence (ECP) are more likely to develop ECR, the implication of ECP needs to be better understood. Moreover, replacing laborious and time-consuming traditional approaches to determine ECP levels with rapid, convenient, and reliable tools is imperative to advance our understanding of this emerging concept in clinical practice. Herein, using extensive ex vivo and in vivo systemic infection models, we showed that high ECP isolates are less effectively cleared by micafungin treatment and exclusively give rise to ECR colonies. Additionally, we developed a flow cytometry-based tool that takes advantage of a SYTOX-based assay for the stratification of ECP levels. Once challenged with various collections of echinocandin-susceptible blood isolates, our assay reliably differentiated ECP levels in vitro and predicted ECP levels in real time under ex vivo and in vivo conditions when compared to traditional methods relying on colony-forming unit counting. Given the high and low ECP predictive values of 92.3% and 82.3%, respectively, our assay showed a high agreement with traditional approach. Collectively, our study supports the concept of ECP level determination in clinical settings and provides a robust tool scalable for high-throughput settings. Application of this tool facilitates the interrogation of mutant and drug libraries to further our understanding of persister biology and designing anti-persister therapeutics. IMPORTANCE: Candida glabrata is a prevalent fungal pathogen able to replicate inside macrophages and rapidly develop resistance against frontline antifungal echinocandins. Multiple studies have shown that echinocandin resistance is fueled by the survival of a small subpopulation of susceptible cells surviving lethal concentrations of echinocandins. Importantly, bacterial pathogens that exhibit high antibiotic persistence also impose a high burden and generate more antibiotic-resistant colonies. Nonetheless, the implications of echinocandin persistence (ECP) among the clinical isolates of C. glabrata have not been defined. Additionally, ECP level determination relies on a laborious and time-consuming method, which is prone to high variation. By exploiting in vivo systemic infection and ex vivo models, we showed that C. glabrata isolates with a higher ECP are associated with a higher burden and more likely develop echinocandin resistance upon micafungin treatment. Additionally, we developed an assay that reliably determines ECP levels in real time. Therefore, our study identified C. glabrata isolates displaying high ECP levels as important entities and provided a reliable and convenient tool for measuring echinocandin persistence, which is extendable to other fungal and bacterial pathogens.
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Reports on echinocandin-associated persistence primarily focus on intracellular Nakaseomyces glabratus internalized by macrophages.
“Reports on echinocandin-associated persistence are primarily focused on intracellular Nakaseomyces glabratus (also called Candida glabrata), which internalized by macrophage [38,39].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [39]
The Results section on macrophage infection examines echinocandin persistence in C. glabrata internalized by macrophages. But Fig. 1 also reports in vitro experiments, and the paper does not establish that reports on echinocandin-associated persistence primarily focus on intracellular fungi. The copy provides no page numbers for these passages. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn an N. glabratus systemic infection mouse model, mice infected with high persistent strains had significantly higher fungal burden and echinocandin-resistance mutation rate than those infected with low persistent strains.
“Similarly, in N. glabratus systemic infection mouse model, mice infected with high persistent strains had significantly higher fungal burden and echinocandin-resistance mutation rate than those low persistent strains [39].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [39]
The Results section ('Systemic infection with the HP isolate…') reports significantly higher fungal burdens in mice infected with the high-persister isolate and resistant colonies only in that group. The comparison was made during micafungin treatment, a condition the citing sentence omits. The paper measures the rate of resistant colonies, not a mutation rate directly. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSuch persister cells serve as a reservoir for acquisition of resistance mutations.
“Such persister cells serve as a reservoir for acquisition of resistance mutations (30).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [30]
Time-kill experiments in vitro have shown that most C. glabrata cells die quickly when exposed to high doses of echinocandins, while a small and variable subpopulation dies more slowly, suggesting possible development of long-lived persister cells.
“Time-kill experiments in vitro have shown that most C. glabrata cells die quickly when exposed to high doses of echinocandins, while a small and variable subpopulation dies more slowly (29, 30), suggesting the possible development of long-lived persister cells.”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [30]
A recent survey of CBS138 and dozens of additional C. glabrata strains revealed considerable variation in the number of persister-like cells observed after micafungin exposure.
“Interestingly, a recent survey of CBS138 and dozens of additional C. glabrata strains revealed considerable variation in the number of persister-like cells observed after micafungin exposure (30).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [30]
Echinocandin-tolerant persisters were found in a mouse model of N. glabratus systemic infection.
“For example, echinocandin-tolerant persisters were found in the mouse model of N. glabratus systematic infection [39];”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [39]
A SYTOX-based flow cytometry assay was developed to evaluate persistence level and demonstrated high predictive accuracy compared to traditional CFU counting.
“In another research, a SYTOX-based flow cytometry assay was developed to evaluate the persistence level, demonstrating high predictive accuracy compared to the traditional CFU counting method [39].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [39]
Antifungal persistence has been observed in vivo in a few studies using animal models.
“Antifungal persistence has been observed in vivo in a few studies using animal models [3,39,48].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [39]
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- Authors
- Arastehfar, A., Daneshnia, F., Floyd, D. J., Jeffries, N. E., Salehi, M., Perlin, D. S., Ilkit, M., Lass-Flöerl, C., & Mansour, M. K.
- Affiliations
- Harvard University (US)
- Massachusetts General Hospital (US)
- Center for Regenerative Medicine, Boston, Massachusetts, USA
- K. N. Toosi University of Technology (IR)
- Hackensack Meridian Health (US)
- Division of Mycology, Faculty of Medicine, University of Çukurova, Adana, Türkiye
- Medical University Innsbruck, Institute of Hygiene and Medical Microbiology, Innsbruck, Austria
- Corresponding author
- Arastehfar, Amir
- Mansour, Michael K.
- ORCID
- Venue
- mBio
- Publisher
- American Society for Microbiology
- Published
- 2024-04-10
- Volume
- 15
- Issue
- 4
- Pages
- e0007224-e0007224
- ISSN
- 2150-7511 (ISSN-L)
- PMC
- PMC11005346
- OpenAlex
- W4392953172
- Cited by
- 19
- References
- 39
- Citations by year
- 2026: 11 · 2025: 8
- FWCI
- 6.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- mBio (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UvA-DARE (University of Amsterdam) (publishedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- HHS | National Institutes of Health (RO1AI132638)
- 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, persister cells, antifungal resistance, micafungin, systemic fungal infection, antifungal susceptibility testing, drug resistance evolution, antifungal therapy response, antifungal resistance surveillance
- MeSH terms
- Micafungin, Anti-Bacterial Agents, Antifungal Agents, Microbial Sensitivity Tests, Drug Resistance, Fungal, Candida glabrata, Echinocandins
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