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Journal articles on the topic 'Mechanisms of azole resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Sanglard, Dominique, and Alix T. Coste. "Activity of Isavuconazole and Other Azoles against Candida Clinical Isolates and Yeast Model Systems with Known Azole Resistance Mechanisms." Antimicrobial Agents and Chemotherapy 60, no. 1 (2015): 229–38. http://dx.doi.org/10.1128/aac.02157-15.

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ABSTRACTIsavuconazole is a novel, broad-spectrum, antifungal azole. In order to evaluate its interactions with known azole resistance mechanisms, isavuconazole susceptibility among different yeast models and clinical isolates expressing characterized azole resistance mechanisms was tested and compared to those of fluconazole, itraconazole, posaconazole, and voriconazole.Saccharomyces cerevisiaeexpressing theCandida albicansandC. glabrataATP binding cassette (ABC) transporters (CDR1,CDR2, andCgCDR1), major facilitator (MDR1), and lanosterol 14-α-sterol-demethylase (ERG11) alleles with mutations

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Gonzalez-Jimenez, Irene, Jose Lucio, Jorge Amich, et al. "A Cyp51B Mutation Contributes to Azole Resistance in Aspergillus fumigatus." Journal of Fungi 6, no. 4 (2020): 315. http://dx.doi.org/10.3390/jof6040315.

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The emergence and spread of Aspergillus fumigatus azole resistance has been acknowledged worldwide. The main problem of azole resistance is the limited therapeutic options for patients suffering aspergillosis. Azole resistance mechanisms have been mostly linked to the enzyme Cyp51A, a target of azole drugs, with a wide variety of modifications responsible for the different resistance mechanisms described to date. However, there are increasing reports of A. fumigatus strains showing azole resistance without Cyp51A modifications, and thus, novel resistance mechanisms are being explored. Here, we

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3

Ghannoum, Mahmoud. "Azole Resistance in Dermatophytes." Journal of the American Podiatric Medical Association 106, no. 1 (2016): 79–86. http://dx.doi.org/10.7547/14-109.

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Azole antifungal agents (eg, fluconazole and itraconazole) have been widely used to treat superficial fungal infections caused by dermatophytes and, unlike the allylamines (such as terbinafine and naftifine), have been associated with resistance development. Although many published manuscripts describe resistance to azoles among yeast and molds, reports describing resistance of dermatophytes are starting to appear. In this review, I discuss the mode of action of azole antifungals and mechanisms underlying their resistance compared with the allylamine class of compounds. Data from published and

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4

Arikan-Akdagli, Sevtap, Mahmoud Ghannoum, and Jacques Meis. "Antifungal Resistance: Specific Focus on Multidrug Resistance in Candida auris and Secondary Azole Resistance in Aspergillus fumigatus." Journal of Fungi 4, no. 4 (2018): 129. http://dx.doi.org/10.3390/jof4040129.

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Antifungal resistance is a topic of concern, particularly for specific fungal species and drugs. Among these are the multidrug-resistant Candida auris and azole-resistant Aspergillus fumigatus. While the knowledge on molecular mechanisms of resistance is now accumulating, further data are also available for the clinical implications and the extent of correlation of in vitro resistance to clinical outcomes. This review article summarizes the epidemiology of C. auris infections, animal models focusing on the activity of novel antifungal compounds in C. auris infections, virulence factors, and th

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MacCallum, Donna M., Alix Coste, Françoise Ischer, Mette D. Jacobsen, Frank C. Odds, and Dominique Sanglard. "Genetic Dissection of Azole Resistance Mechanisms in Candida albicans and Their Validation in a Mouse Model of Disseminated Infection." Antimicrobial Agents and Chemotherapy 54, no. 4 (2010): 1476–83. http://dx.doi.org/10.1128/aac.01645-09.

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ABSTRACT Principal mechanisms of resistance to azole antifungals include the upregulation of multidrug transporters and the modification of the target enzyme, a cytochrome P450 (Erg11) involved in the 14α-demethylation of ergosterol. These mechanisms are often combined in azole-resistant Candida albicans isolates recovered from patients. However, the precise contributions of individual mechanisms to C. albicans resistance to specific azoles have been difficult to establish because of the technical difficulties in the genetic manipulation of this diploid species. Recent advances have made genet

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6

Marichal, P., and H. Vanden Bossche. "Mechanisms of resistance to azole antifungals." Acta Biochimica Polonica 42, no. 4 (1995): 509–16. http://dx.doi.org/10.18388/abp.1995_4904.

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Until the late eighties, clinical resistance to azole antifungals was a rare phenomenon. Only a few cases of resistance to ketoconazole were found in patients with chronic mucocutaneous candidiasis (CMC). The spread of AIDS and the widespread prophylactic and therapeutic use of the hydrophilic azole compound fluconazole resulted both in the selection and induction of resistant strains and in a shift in the nature of the infecting organisms. Most azole antifungals such as itraconazole, ketoconazole and fluconazole are active against a variety of fungal diseases. However, the concentration neede

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Vandeputte, Patrick, Gérald Larcher, Thierry Bergès, Gilles Renier, Dominique Chabasse, and Jean-Philippe Bouchara. "Mechanisms of Azole Resistance in a Clinical Isolate of Candida tropicalis." Antimicrobial Agents and Chemotherapy 49, no. 11 (2005): 4608–15. http://dx.doi.org/10.1128/aac.49.11.4608-4615.2005.

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ABSTRACT Azole resistance has been insufficiently investigated in the yeast Candida tropicalis. Here we determined the molecular mechanisms responsible for azole resistance in a clinical isolate of this pathogenic yeast. Antifungal susceptibility testing performed by a disk diffusion method showed resistance or markedly decreased susceptibility to azoles, which was confirmed by determination of MICs. Considering the relationship between azole susceptibility and the respiration reported for other yeast species, the respiratory activity of this isolate was investigated. Flow cytometry using rhod

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8

Coste, Alix, Anna Selmecki, Anja Forche, et al. "Genotypic Evolution of Azole Resistance Mechanisms in Sequential Candida albicans Isolates." Eukaryotic Cell 6, no. 10 (2007): 1889–904. http://dx.doi.org/10.1128/ec.00151-07.

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ABSTRACT TAC1 (for transcriptional activator of CDR genes) is critical for the upregulation of the ABC transporters CDR1 and CDR2, which mediate azole resistance in Candida albicans. While a wild-type TAC1 allele drives high expression of CDR1/2 in response to inducers, we showed previously that TAC1 can be hyperactive by a gain-of-function (GOF) point mutation responsible for constitutive high expression of CDR1/2. High azole resistance levels are achieved when C. albicans carries hyperactive alleles only as a consequence of loss of heterozygosity (LOH) at the TAC1 locus on chromosome 5 (Chr

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Perea, Sofia, José L. López-Ribot, William R. Kirkpatrick, et al. "Prevalence of Molecular Mechanisms of Resistance to Azole Antifungal Agents in Candida albicans Strains Displaying High-Level Fluconazole Resistance Isolated from Human Immunodeficiency Virus-Infected Patients." Antimicrobial Agents and Chemotherapy 45, no. 10 (2001): 2676–84. http://dx.doi.org/10.1128/aac.45.10.2676-2684.2001.

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ABSTRACT Molecular mechanisms of azole resistance in Candida albicans, including alterations in the target enzyme and increased efflux of drug, have been described, but the epidemiology of the resistance mechanisms has not been established. We have investigated the molecular mechanisms of resistance to azoles inC. albicans strains displaying high-level fluconazole resistance (MICs, ≥64 μg/ml) isolated from human immunodeficiency virus (HIV)-infected patients with oropharyngeal candidiasis. The levels of expression of genes encoding lanosterol 14α-demethylase (ERG11) and efflux transporters (MD

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10

Meis, Jacques F., Anuradha Chowdhary, Johanna L. Rhodes, Matthew C. Fisher, and Paul E. Verweij. "Clinical implications of globally emerging azole resistance in Aspergillus fumigatus." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1709 (2016): 20150460. http://dx.doi.org/10.1098/rstb.2015.0460.

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Aspergillus fungi are the cause of an array of diseases affecting humans, animals and plants. The triazole antifungal agents itraconazole, voriconazole, isavuconazole and posaconazole are treatment options against diseases caused by Aspergillus . However, resistance to azoles has recently emerged as a new therapeutic challenge in six continents. Although de novo azole resistance occurs occasionally in patients during azole therapy, the main burden is the aquisition of resistance through the environment. In this setting, the evolution of resistance is attributed to the widespread use of azole-b

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Sanguinetti, Maurizio, Brunella Posteraro, Barbara Fiori, Stefania Ranno, Riccardo Torelli, and Giovanni Fadda. "Mechanisms of Azole Resistance in Clinical Isolates of Candida glabrata Collected during a Hospital Survey of Antifungal Resistance." Antimicrobial Agents and Chemotherapy 49, no. 2 (2005): 668–79. http://dx.doi.org/10.1128/aac.49.2.668-679.2005.

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ABSTRACT The increasing use of azole antifungals for the treatment of mucosal and systemic Candida glabrata infections has resulted in the selection and/or emergence of resistant strains. The main mechanisms of azole resistance include alterations in the C. glabrata ERG11 gene (CgERG11), which encodes the azole target enzyme, and upregulation of the CgCDR1 and CgCDR2 genes, which encode efflux pumps. In the present study, we evaluated these molecular mechanisms in 29 unmatched clinical isolates of C. glabrata, of which 20 isolates were resistant and 9 were susceptible dose dependent (S-DD) to

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Wang, Kangji, Zhenying Zhang, Xi Chen, et al. "Transcription Factor ADS-4 Regulates Adaptive Responses and Resistance to Antifungal Azole Stress." Antimicrobial Agents and Chemotherapy 59, no. 9 (2015): 5396–404. http://dx.doi.org/10.1128/aac.00542-15.

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ABSTRACTAzoles are commonly used as antifungal drugs or pesticides to control fungal infections in medicine and agriculture. Fungi adapt to azole stress by rapidly activating the transcription of a number of genes, and transcriptional increases in some azole-responsive genes can elevate azole resistance. The regulatory mechanisms that control transcriptional responses to azole stress in filamentous fungi are not well understood. This study identified a bZIP transcription factor, ADS-4 (antifungaldrugsensitive-4), as a new regulator of adaptive responses and resistance to antifungal azoles. Tra

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Bhattacharya, Somanon, Sutthichai Sae-Tia, and Bettina C. Fries. "Candidiasis and Mechanisms of Antifungal Resistance." Antibiotics 9, no. 6 (2020): 312. http://dx.doi.org/10.3390/antibiotics9060312.

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Candidiasis can be present as a cutaneous, mucosal or deep-seated organ infection, which is caused by more than 20 types of Candida sp., with C. albicans being the most common. These are pathogenic yeast and are usually present in the normal microbiome. High-risk individuals are patients of human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), organ transplant, and diabetes. During infection, pathogens can adhere to complement receptors and various extracellular matrix proteins in the oral and vaginal cavity. Oral and vaginal Candidiasis results from the overgrowth of Can

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14

Brun, Sophie, Thierry Bergès, Pascal Poupard, et al. "Mechanisms of Azole Resistance in Petite Mutants of Candida glabrata." Antimicrobial Agents and Chemotherapy 48, no. 5 (2004): 1788–96. http://dx.doi.org/10.1128/aac.48.5.1788-1796.2004.

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ABSTRACT We previously showed that resistant colonies of Candida glabrata inside the azole inhibition zones had respiratory deficiency due to mutations in mitochondrial DNA. Here, we analyzed the mechanisms of azole resistance in petite mutants of C. glabrata obtained by exposure to fluconazole or induced by ethidium bromide. The respiratory deficiency of these mutants was confirmed by oxygraphy and flow cytometric analysis with rhodamine 123, and its mitochondrial origin was demonstrated by transmission electron microscopy and restriction endonuclease analysis of the mitochondrial DNA. Flow c

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15

Joseph-Horne, Tim, and Derek W. Hollomon. "Molecular mechanisms of azole resistance in fungi." FEMS Microbiology Letters 149, no. 2 (2006): 141–49. http://dx.doi.org/10.1111/j.1574-6968.1997.tb10321.x.

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16

Mortensen, Klaus Leth, Emilia Mellado, Cornelia Lass-Flörl, Juan Luis Rodriguez-Tudela, Helle Krogh Johansen, and Maiken Cavling Arendrup. "Environmental Study of Azole-Resistant Aspergillus fumigatus and Other Aspergilli in Austria, Denmark, and Spain." Antimicrobial Agents and Chemotherapy 54, no. 11 (2010): 4545–49. http://dx.doi.org/10.1128/aac.00692-10.

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ABSTRACT A single mechanism of azole resistance was shown to predominate in clinical and environmental Aspergillus fumigatus isolates from the Netherlands, and a link to the use of azoles in the environment was suggested. To explore the prevalence of azole-resistant A. fumigatus and other aspergilli in the environment in other European countries, we collected samples from the surroundings of hospitals in Copenhagen, Innsbruck, and Madrid, flowerbeds in an amusement park in Copenhagen, and compost bags purchased in Austria, Denmark, and Spain and screened for azole resistance using multidish ag

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17

Silva, A. P., I. M. Miranda, A. Guida, et al. "Transcriptional Profiling of Azole-Resistant Candida parapsilosis Strains." Antimicrobial Agents and Chemotherapy 55, no. 7 (2011): 3546–56. http://dx.doi.org/10.1128/aac.01127-10.

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ABSTRACTHerein we describe the changes in the gene expression profile ofCandida parapsilosisassociated with the acquisition of experimentally induced resistance to azole antifungal drugs. Three resistant strains ofC. parapsilosiswere obtained following prolongedin vitroexposure of a susceptible clinical isolate to constant concentrations of fluconazole, voriconazole, or posaconazole. We found that after incubation with fluconazole or voriconazole, strains became resistant to both azoles but not to posaconazole, although susceptibility to this azole decreased, whereas the strain incubated with

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18

Parent-Michaud, Maxime, Philippe J. Dufresne, Eric Fournier, et al. "Prevalence and mechanisms of azole resistance in clinical isolates of Aspergillus section Fumigati species in a Canadian tertiary care centre, 2000 to 2013." Journal of Antimicrobial Chemotherapy 75, no. 4 (2019): 849–58. http://dx.doi.org/10.1093/jac/dkz534.

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Abstract Objectives Azole resistance among Aspergillus fumigatus isolates is a growing concern worldwide. Induction of mutations during azole therapy, environment-acquired mutations caused by azole fungicides and intrinsic resistance of cryptic Fumigati species all contribute to the burden of resistance. However, there is a lack of data in Canada on this emerging threat. Methods To gain insights into the magnitude and mechanisms of resistance, a 14 year collection of Aspergillus section Fumigati comprising 999 isolates from 807 patients at a Montreal hospital was screened for azole resistance,

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Sanglard, Dominique, Françoise Ischer, David Calabrese, Paul A. Majcherczyk, and Jacques Bille. "The ATP Binding Cassette Transporter GeneCgCDR1 from Candida glabrata Is Involved in the Resistance of Clinical Isolates to Azole Antifungal Agents." Antimicrobial Agents and Chemotherapy 43, no. 11 (1999): 2753–65. http://dx.doi.org/10.1128/aac.43.11.2753.

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ABSTRACT The resistance mechanisms to azole antifungal agents were investigated in this study with two pairs of Candida glabrata clinical isolates recovered from two separate AIDS patients. The two pairs each contained a fluconazole-susceptible isolate and a fluconazole-resistant isolate, the latter with cross-resistance to itraconazole and ketoconazole. Since the accumulation of fluconazole and of another unrelated substance, rhodamine 6G, was reduced in the azole-resistant isolates, enhanced drug efflux was considered as a possible resistance mechanism. The expression of multidrug efflux tra

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Camps, Simone M. T., Jan W. M. van der Linden, Yi Li, et al. "Rapid Induction of Multiple Resistance Mechanisms in Aspergillus fumigatus during Azole Therapy: a Case Study and Review of the Literature." Antimicrobial Agents and Chemotherapy 56, no. 1 (2011): 10–16. http://dx.doi.org/10.1128/aac.05088-11.

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ABSTRACTNine consecutive isogenicAspergillus fumigatusisolates cultured from a patient with aspergilloma were investigated for azole resistance. The first cultured isolate showed a wild-type phenotype, but four azole-resistant phenotypes were observed in the subsequent eight isolates. Four mutations were found in thecyp51Agene of these isolates, leading to the substitutions A9T, G54E, P216L, and F219I. Only G54 substitutions were previously proved to be associated with azole resistance. Using a Cyp51A homology model and recombination experiments in which the mutations were introduced into a su

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Chen, Pao-Yu, Yu-Chung Chuang, Un-In Wu, et al. "Mechanisms of Azole Resistance and Trailing in Candida tropicalis Bloodstream Isolates." Journal of Fungi 7, no. 8 (2021): 612. http://dx.doi.org/10.3390/jof7080612.

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Objectives: Azole-resistant Candida tropicalis has emerged in Asia in the context of its trailing nature, defined by residual growth above minimum inhibitory concentrations (MICs). However, limited investigations in C. tropicalis have focused on the difference of genotypes and molecular mechanisms between these two traits. Methods: Sixty-four non-duplicated C. tropicalis bloodstream isolates collected in 2017 were evaluated for azole MICs by the EUCAST E.def 7.3.1 method, diploid sequence type (DST) by multilocus sequencing typing, and sequences and expression levels of genes encoding ERG11, i

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Rosam, Katharina, Brian C. Monk та Michaela Lackner. "Sterol 14α-Demethylase Ligand-Binding Pocket-Mediated Acquired and Intrinsic Azole Resistance in Fungal Pathogens". Journal of Fungi 7, № 1 (2020): 1. http://dx.doi.org/10.3390/jof7010001.

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The fungal cytochrome P450 enzyme sterol 14α-demethylase (SDM) is a key enzyme in the ergosterol biosynthesis pathway. The binding of azoles to the active site of SDM results in a depletion of ergosterol, the accumulation of toxic intermediates and growth inhibition. The prevalence of azole-resistant strains and fungi is increasing in both agriculture and medicine. This can lead to major yield loss during food production and therapeutic failure in medical settings. Diverse mechanisms are responsible for azole resistance. They include amino acid (AA) substitutions in SDM and overexpression of S

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Sheehan, Daniel J., Christopher A. Hitchcock, and Carol M. Sibley. "Current and Emerging Azole Antifungal Agents." Clinical Microbiology Reviews 12, no. 1 (1999): 40–79. http://dx.doi.org/10.1128/cmr.12.1.40.

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SUMMARY Major developments in research into the azole class of antifungal agents during the 1990s have provided expanded options for the treatment of many opportunistic and endemic fungal infections. Fluconazole and itraconazole have proved to be safer than both amphotericin B and ketoconazole. Despite these advances, serious fungal infections remain difficult to treat, and resistance to the available drugs is emerging. This review describes present and future uses of the currently available azole antifungal agents in the treatment of systemic and superficial fungal infections and provides a b

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Snelders, Eveline, Robert A. G. Huis in 't Veld, Anthonius J. M. M. Rijs, Gert H. J. Kema, Willem J. G. Melchers, and Paul E. Verweij. "Possible Environmental Origin of Resistance of Aspergillus fumigatus to Medical Triazoles." Applied and Environmental Microbiology 75, no. 12 (2009): 4053–57. http://dx.doi.org/10.1128/aem.00231-09.

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ABSTRACT We reported the emergence of resistance to medical triazoles of Aspergillus fumigatus isolates from patients with invasive aspergillosis. A dominant resistance mechanism was found, and we hypothesized that azole resistance might develop through azole exposure in the environment rather than in azole-treated patients. We investigated if A. fumigatus isolates resistant to medical triazoles are present in our environment by sampling the hospital indoor environment and soil from the outdoor environment. Antifungal susceptibility, resistance mechanisms, and genetic relatedness were compared

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Gonzalez-Jimenez, Irene, Jose Lucio, Maria Dolores Menéndez-Fraga, Emilia Mellado, and Teresa Peláez. "Hospital Environment as a Source of Azole-Resistant Aspergillus fumigatus Strains with TR34/L98H and G448S Cyp51A Mutations." Journal of Fungi 7, no. 1 (2021): 22. http://dx.doi.org/10.3390/jof7010022.

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Azole-resistant Aspergillus fumigatus is an emerging worldwide problem with increasing reports of therapy failure cases produced by resistant isolates. A case of azole-resistant A. fumigatus hospital colonization in a patient is reported here. Investigations of the hospital environment led to the recovery of A. fumigatus strains harboring the TR34/L98H and the G448S Cyp51A azole resistance mechanisms. Isolate genotyping showed that one strain from the environment was isogenic with the patient strains. These are the first environmental A. fumigatus azole resistant strains collected in a hospita

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Agnihotri, S., M. Li, M. R. Wilson, et al. "PS2 - 174 Hexokinase 2 Drives Radio-Resistance through ERK Signaling and Sensitizes Cells to Azole Compounds." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, S4 (2016): S14. http://dx.doi.org/10.1017/cjn.2016.368.

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Our ongoing work has demonstrated that hexokinase 2 (HK2) but not HK1 or HK3 is a critical mediator of tumour glycolysis and mitochondrial metabolism in Glioblastoma (GB). Furthermore, HK2 is highly expressed in GB but not in normal brain making it an attractive therapeutic target. Our current findings now support that loss of HK2 alters tumor vasculature, increases sensitivity to radiation, and confers a significant survival benefit in several GB xenograft-bearing mice. Using a genome wide transcript analysis, we identified that loss of HK2 attenuates several pro-growth signaling pathways in

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Aruanno, Marion, Samantha Gozel, Isabelle Mouyna, et al. "Insights in the molecular mechanisms of an azole stress adapted laboratory-generated Aspergillus fumigatus strain." Medical Mycology 59, no. 8 (2021): 763–72. http://dx.doi.org/10.1093/mmy/myaa118.

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Abstract Aspergillus fumigatus is the main cause of invasive aspergillosis, for which azole drugs are the first-line therapy. Emergence of pan-azole resistance among A. fumigatus is concerning and has been mainly attributed to mutations in the target gene (cyp51A). However, azole resistance may also result from other mutations (hmg1, hapE) or other adaptive mechanisms. We performed microevolution experiment exposing an A. fumigatus azole-susceptible strain (Ku80) to sub-minimal inhibitory concentration of voriconazole to analyze emergence of azole resistance. We obtained a strain with pan-azol

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Arendrup, Maiken Cavling, Rasmus Hare Jensen, and Manuel Cuenca-Estrella. "In VitroActivity of ASP2397 against Aspergillus Isolates with or without Acquired Azole Resistance Mechanisms." Antimicrobial Agents and Chemotherapy 60, no. 1 (2015): 532–36. http://dx.doi.org/10.1128/aac.02336-15.

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ABSTRACTASP2397 is a new compound with a novel and as-yet-unknown target different from that of licensed antifungal agents. It has activity againstAspergillusandCandida glabrata. We compared itsin vitroactivity against wild-type and azole-resistantA. fumigatusandA. terreusisolates with that of amphotericin B, itraconazole, posaconazole, and voriconazole. Thirty-four isolates, including 4 wild-typeA. fumigatusisolates, 24A. fumigatusisolates with alterations in CYP51A TR/L98H (5 isolates), M220 (9 isolates), G54 (9 isolates), and HapE (1 isolate), andA. terreusisolates (2 wild-type isolates and

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Kim, Sang Hu, Kali R. Iyer, Lakhansing Pardeshi, et al. "Genetic Analysis of Candida auris Implicates Hsp90 in Morphogenesis and Azole Tolerance and Cdr1 in Azole Resistance." mBio 10, no. 1 (2019): e02529-18. http://dx.doi.org/10.1128/mbio.02529-18.

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ABSTRACT Candida auris is an emerging fungal pathogen and a serious global health threat as the majority of clinical isolates display elevated resistance to currently available antifungal drugs. Despite the increased prevalence of C. auris infections, the mechanisms governing drug resistance remain largely elusive. In diverse fungi, the evolution of drug resistance is enabled by the essential molecular chaperone Hsp90, which stabilizes key regulators of cellular responses to drug-induced stress. Hsp90 also orchestrates temperature-dependent morphogenesis in Candida albicans, a key virulence tr

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Mosquera, J., and D. W. Denning. "Azole Cross-Resistance in Aspergillus fumigatus." Antimicrobial Agents and Chemotherapy 46, no. 2 (2002): 556–57. http://dx.doi.org/10.1128/aac.46.2.556-557.2002.

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ABSTRACT We susceptibility tested 17 clinical isolates of Aspergillus fumigatus, for most of which MICs of itraconazole were elevated (MIC at which 50% of the isolates tested are inhibited, 16 μg/ml), against itraconazole, posaconazole, ravuconazole, and voriconazole. Posaconazole was the most active against itraconazole-susceptible isolates. A complex pattern of cross-resistance and hypersusceptibility was seen with voriconazole and ravuconazole, suggesting marked differences in activity and mechanisms of resistance.

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Sun, Xianyun, Kangji Wang, Xinxu Yu, et al. "Transcription Factor CCG-8 as a New Regulator in the Adaptation to Antifungal Azole Stress." Antimicrobial Agents and Chemotherapy 58, no. 3 (2013): 1434–42. http://dx.doi.org/10.1128/aac.02244-13.

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ABSTRACTAntifungal azoles are widely used for controlling fungal infections. Fungi are able to change the expression of many genes when they adapt to azole stress, and increased expression of some of these genes can elevate resistance to azoles. However, the regulatory mechanisms behind transcriptional adaption to azoles in filamentous fungi are poorly understood. In this study, we found that deletion of the transcription factor geneccg-8, which is known to be a clock-controlled gene, madeNeurospora crassahypersensitive to azoles. A comparative genome-wide analysis of the responses to ketocona

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Kontoyiannis, D. P. "Genetic Analysis of Azole Resistance by Transposon Mutagenesis in Saccharomyces cerevisiae." Antimicrobial Agents and Chemotherapy 43, no. 11 (1999): 2731–35. http://dx.doi.org/10.1128/aac.43.11.2731.

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ABSTRACT The increasing resistance of Candida species to fluconazole is cause for concern. To determine the molecular mechanisms involved in resistance to fluconazole, I used a scheme of transposon mutagenesis in Saccharomyces cerevisiae, a genetically tractable yeast that is closely related to Candida albicans. This technique, which permits the generation and analysis of multiple random Tn3::LEU2::lacZfusions, can be used as a disruption mutagen (N. B. Burns et al., Genes Dev. 8:1087–1105, 1994). By using the Tn3::LEU2::lacZlibrary as a disruption mutagen, I found recessive mutations in genes

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Gonçalves, Paulo, Aryse Melo, Marta Dias, et al. "Azole-Resistant Aspergillus fumigatus Harboring the TR34/L98H Mutation: First Report in Portugal in Environmental Samples." Microorganisms 9, no. 1 (2020): 57. http://dx.doi.org/10.3390/microorganisms9010057.

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Introduction: The frequency in detection of azole-resistant Aspergillus fumigatus isolates has increased since 2010. In Portugal, the section Fumigati is one of the most frequent, and resistant strains to have been found in clinical and environmental contexts. Although several cryptic species within the Fumigati section show intrinsic resistance to azoles, one factor driving (acquired) resistance is selective pressure deriving from the extensive use of azoles. This is particularly problematic in occupational environments where high fungal loads are expected, and where there is an increased ris

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Price, Claire L., Josie E. Parker, Andrew GS Warrilow, Diane E. Kelly, and Steven L. Kelly. "Azole fungicides - understanding resistance mechanisms in agricultural fungal pathogens." Pest Management Science 71, no. 8 (2015): 1054–58. http://dx.doi.org/10.1002/ps.4029.

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Pérez-Cantero, Alba, Loida López-Fernández, Josep Guarro, and Javier Capilla. "Azole resistance mechanisms in Aspergillus: update and recent advances." International Journal of Antimicrobial Agents 55, no. 1 (2020): 105807. http://dx.doi.org/10.1016/j.ijantimicag.2019.09.011.

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White, Theodore C., Scott Holleman, Francis Dy, Laurence F. Mirels, and David A. Stevens. "Resistance Mechanisms in Clinical Isolates of Candida albicans." Antimicrobial Agents and Chemotherapy 46, no. 6 (2002): 1704–13. http://dx.doi.org/10.1128/aac.46.6.1704-1713.2002.

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ABSTRACT Resistance to azole antifungals continues to be a significant problem in the common fungal pathogen Candida albicans. Many of the molecular mechanisms of resistance have been defined with matched sets of susceptible and resistant clinical isolates from the same strain. Mechanisms that have been identified include alterations in the gene encoding the target enzyme ERG11 or overexpression of efflux pump genes including CDR1, CDR2, and MDR1. In the present study, a collection of unmatched clinical isolates of C. albicans was analyzed for the known molecular mechanisms of resistance by st

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Vandeputte, Patrick, Guy Tronchin, Françoise Rocher, et al. "Hypersusceptibility to Azole Antifungals in a Clinical Isolate of Candida glabrata with Reduced Aerobic Growth." Antimicrobial Agents and Chemotherapy 53, no. 7 (2009): 3034–41. http://dx.doi.org/10.1128/aac.01384-08.

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ABSTRACT Petite mutations have been described in Saccharomyces cerevisiae and pathogenic yeasts. However, previous studies of the phenotypic traits of these petite mutants reported that they express azole resistance. We describe a clinical isolate of Candida glabrata with a striking association between increased susceptibility to azoles and respiratory deficiency. This isolate was obtained from a urine sample together with a respiration-competent C. glabrata isolate which exhibited azole resistance. The respiratory status of the two isolates was confirmed by cultivation on glycerol-containing

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Pinjon, E., G. P. Moran, D. C. Coleman, and D. J. Sullivan. "Azole susceptibility and resistance in Candida dubliniensis." Biochemical Society Transactions 33, no. 5 (2005): 1210–14. http://dx.doi.org/10.1042/bst0331210.

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Candida dubliniensis is a recently described species of pathogenic yeast that shares many phenotypic features with Candida albicans. It is primarily associated with oral colonization and infection in HIV-infected individuals. Isolates of C. dubliniensis are generally susceptible to commonly used azole antifungal agents; however, resistance has been observed in clinical isolates and can be induced by in vitro exposure. Molecular mechanisms of azole resistance in C. dubliniensis include increased drug efflux, modifications of the target enzyme and alterations in the ergosterol biosynthetic pathw

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Chowdhary, Anuradha, Cheshta Sharma, Ferry Hagen, and Jacques F. Meis. "Exploring azole antifungal drug resistance inAspergillus fumigatuswith special reference to resistance mechanisms." Future Microbiology 9, no. 5 (2014): 697–711. http://dx.doi.org/10.2217/fmb.14.27.

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Liu, Musang, Rong Zeng, Lili Zhang, et al. "Multiplecyp51A-Based Mechanisms Identified in Azole-Resistant Isolates of Aspergillus fumigatus from China." Antimicrobial Agents and Chemotherapy 59, no. 7 (2015): 4321–25. http://dx.doi.org/10.1128/aac.00003-15.

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ABSTRACTSeventy-twoA. fumigatusclinical isolates from China were investigated for azole resistance based on mutations ofcyp51A. We identified four azole-resistant strains, among which we found three strains highly resistant to itraconazole, two of which exhibit the TR34/L98H/S297T/F495I mutation, while one carries only the TR34/L98H mutation. To our knowledge, the latter has not been found previously in China. The fourth multiazole-resistant isolate (with only moderate itraconazole resistance) carries a new G432A mutation.

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Brun, Sophie, Christophe Aubry, Osana Lima, et al. "Relationships between Respiration and Susceptibility to Azole Antifungals in Candida glabrata." Antimicrobial Agents and Chemotherapy 47, no. 3 (2003): 847–53. http://dx.doi.org/10.1128/aac.47.3.847-853.2003.

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ABSTRACT Over the past two decades, the incidence of infections due to Candida glabrata, a yeast with intrinsic low susceptibility to azole antifungals, has increased markedly. Respiratory deficiency due to mutations in mitochondrial DNA (mtDNA) associated with resistance to azoles frequently occurs in vitro in this species. In order to specify the relationships between respiration and azole susceptibility, the effects of respiratory chain inhibitors on a wild-type isolate of C. glabrata were evaluated. Respiration of blastoconidia was immediately blocked after extemporaneous addition of potas

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Chen, Yong, Zhongyi Lu, Jingjun Zhao, et al. "Epidemiology and Molecular Characterizations of Azole Resistance in Clinical and Environmental Aspergillus fumigatus Isolates from China." Antimicrobial Agents and Chemotherapy 60, no. 10 (2016): 5878–84. http://dx.doi.org/10.1128/aac.01005-16.

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ABSTRACTAzole resistance inAspergillus fumigatushas emerged as a worldwide public health problem. We sought here to demonstrate the occurrence and characteristics of azole resistance inA. fumigatusfrom different parts of China. A total of 317 clinical and 144 environmentalA. fumigatusisolates from 12 provinces were collected and subjected to screening for azole resistance. Antifungal susceptibility,cyp51Agene sequencing, and genotyping were carried out for all suspected azole-resistant isolates and a subset of azole-susceptible isolates. As a result, 8 (2.5%) clinical and 2 (1.4%) environmenta

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Rodriguez-Tudela, Juan Luis, Laura Alcazar-Fuoli, Emilia Mellado, Ana Alastruey-Izquierdo, Araceli Monzon, and Manuel Cuenca-Estrella. "Epidemiological Cutoffs and Cross-Resistance to Azole Drugs in Aspergillus fumigatus." Antimicrobial Agents and Chemotherapy 52, no. 7 (2008): 2468–72. http://dx.doi.org/10.1128/aac.00156-08.

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ABSTRACT Antifungal susceptibility testing of molds has been standardized in Europe and in the United States. Aspergillus fumigatus strains with resistance to azole drugs have recently been detected and the underlying molecular mechanisms of resistance characterized. Three hundred and ninety-three isolates, including 32 itraconazole-resistant strains, were used to define wild-type populations, epidemiological cutoffs, and cross-resistance between azole drugs. The epidemiological cutoff for itraconazole, voriconazole, and ravuconazole for the wild-type populations of A. fumigatus was ≤1 mg/lite

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Pinjon, Emmanuelle, Colin J. Jackson, Steven L. Kelly, et al. "Reduced Azole Susceptibility in Genotype 3 Candida dubliniensis Isolates Associated with Increased CdCDR1 and CdCDR2 Expression." Antimicrobial Agents and Chemotherapy 49, no. 4 (2005): 1312–18. http://dx.doi.org/10.1128/aac.49.4.1312-1318.2005.

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ABSTRACT Candida dubliniensis is a recently identified yeast species primarily associated with oral carriage and infection in individuals infected with the human immunodeficiency virus. The species can be divided into at least four genotypes on the basis of the nucleotide sequence of the internal transcribed spacer region of the rRNA operon. Previous studies have shown that a small number of clinical isolates belonging to genotype 1 are resistant to the commonly used antifungal drug fluconazole. The aim of the present study was to investigate the molecular mechanisms responsible for reduced su

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Mavridou, Eleftheria, Joseph Meletiadis, Antony Rijs, Johan W. Mouton, and Paul E. Verweij. "The Strength of Synergistic Interaction between Posaconazole and Caspofungin Depends on the Underlying Azole Resistance Mechanism of Aspergillus fumigatus." Antimicrobial Agents and Chemotherapy 59, no. 3 (2015): 1738–44. http://dx.doi.org/10.1128/aac.04469-14.

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ABSTRACTThe majority of azole resistance mechanisms inAspergillus fumigatuscorrespond to mutations in thecyp51Agene. As azoles are less effective against infections caused by multiply azole-resistantA. fumigatusisolates, new therapeutic options are warranted for treating these infections. We therefore investigated thein vitrocombination of posaconazole (POSA) and caspofungin (CAS) against 20 wild-type and resistantA. fumigatusisolates with 10 different resistance mechanisms. Fungal growth was assessed with the XTT [2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide inner

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Song, Jinxing, Jingwen Zhou, Lei Zhang, and Rongpeng Li. "Mitochondria-Mediated Azole Drug Resistance and Fungal Pathogenicity: Opportunities for Therapeutic Development." Microorganisms 8, no. 10 (2020): 1574. http://dx.doi.org/10.3390/microorganisms8101574.

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In recent years, the role of mitochondria in pathogenic fungi in terms of azole resistance and fungal pathogenicity has been a rapidly developing field. In this review, we describe the molecular mechanisms by which mitochondria are involved in regulating azole resistance and fungal pathogenicity. Mitochondrial function is involved in the regulation of drug efflux pumps at the transcriptional and posttranslational levels. On the one hand, defects in mitochondrial function can serve as the signal leading to activation of calcium signaling and the pleiotropic drug resistance pathway and, therefor

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Sanglard, Dominique, Françoise Ischer, David Calabrese, Michelle de Micheli, and Jacques Bille. "Multiple resistance mechanisms to azole antifungals in yeast clinical isolates." Drug Resistance Updates 1, no. 4 (1998): 255–65. http://dx.doi.org/10.1016/s1368-7646(98)80006-x.

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Rogers, P. David, and Katherine S. Barker. "Evaluation of Differential Gene Expression in Fluconazole-Susceptible and -Resistant Isolates of Candida albicans by cDNA Microarray Analysis." Antimicrobial Agents and Chemotherapy 46, no. 11 (2002): 3412–17. http://dx.doi.org/10.1128/aac.46.11.3412-3417.2002.

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ABSTRACT The opportunistic fungal pathogen Candida albicans is the major causative agent of oropharyngeal candidiasis (OPC) in AIDS. The development of azoles, such as fluconazole, for the treatment of OPC has proven effective except in cases where C. albicans develops resistance to fluconazole during the course of treatment. In the present study, we used microarray technology to examine differences in gene expression from a fluconazole-susceptible and a fluconazole-resistant well-characterized, clinically obtained matched set of C. albicans isolates to identify genes which are differentially

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Vasicek, Erin M., Elizabeth L. Berkow, Stephanie A. Flowers, Katherine S. Barker, and P. David Rogers. "UPC2Is Universally Essential for Azole Antifungal Resistance in Candida albicans." Eukaryotic Cell 13, no. 7 (2014): 933–46. http://dx.doi.org/10.1128/ec.00221-13.

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ABSTRACTInCandida albicans, the transcription factor Upc2 is central to the regulation of ergosterol biosynthesis.UPC2-activating mutations contribute to azole resistance, whereas disruption increases azole susceptibility. In the present study, we investigated the relationship ofUPC2to fluconazole susceptibility, particularly in azole-resistant strains. In addition to the reduced fluconazole MIC previously observed withUPC2disruption, we observed a lower minimum fungicidal concentration (MFC) for aupc2Δ/Δ mutant than for its azole-susceptible parent, SC5314. Moreover, theupc2Δ/Δ mutant was una

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Arastehfar, Amir, Farnaz Daneshnia, Ahmed Hafez, et al. "Antifungal susceptibility, genotyping, resistance mechanism, and clinical profile of Candida tropicalis blood isolates." Medical Mycology 58, no. 6 (2019): 766–73. http://dx.doi.org/10.1093/mmy/myz124.

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Abstract Candida tropicalis is one of the major candidaemia agents, associated with the highest mortality rates among Candida species, and developing resistance to azoles. Little is known about the molecular mechanisms of azole resistance, genotypic diversity, and the clinical background of C. tropicalis infections. Consequently, this study was designed to address those questions. Sixty-four C. tropicalis bloodstream isolates from 62 patients from three cities in Iran (2014–2019) were analyzed. Strain identification, antifungal susceptibility testing, and genotypic diversity analysis were perf

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