ArticleAntimicrobial agents and chemotherapy2003
Molecular mechanisms of itraconazole resistance in Candida dubliniensis.
Article in Antimicrobial agents and chemotherapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 64 citations in OpenAlex.
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- Erg251 has complex and pleiotropic effects on sterol composition, azole susceptibility, filamentation, and stress response phenotypes.PLoS pathogens · 2024Article
- Identification of the ergC gene involved in polyene drug sensitivity in the Mucorales species Phycomyces blakesleeanus.Molecular biology reports · 2022Article
- Loss of C-5 Sterol Desaturase Activity inAntimicrobial agents and chemotherapy · 2019Article
- Loss of Upc2p-InduciblemBio · 2018Article
- Antifungal Therapy: New Advances in the Understanding and Treatment of Mycosis.Frontiers in microbiology · 2017Review
- Emerging Threats in Antifungal-Resistant Fungal Pathogens.Frontiers in medicine · 2016Review
- Evaluation of amphotericin B and chloramphenicol as alternative drugs for treatment of chytridiomycosis and their impacts on innate skin defenses.Applied and environmental microbiology · 2014Article
- Multilaboratory study of epidemiological cutoff values for detection of resistance in eight Candida species to fluconazole, posaconazole, and voriconazole.Antimicrobial agents and chemotherapy · 2014Article
- Candida tropicalis antifungal cross-resistance is related to different azole target (Erg11p) modifications.Antimicrobial agents and chemotherapy · 2013Article
- Antifungal resistance and new strategies to control fungal infections.International journal of microbiology · 2012Article
- Longitudinal genotyping of Candida dubliniensis isolates reveals strain maintenance, microevolution, and the emergence of itraconazole resistance.Journal of clinical microbiology · 2010Article
- Genetic dissection of azole resistance mechanisms in Candida albicans and their validation in a mouse model of disseminated infection.Antimicrobial agents and chemotherapy · 2010Article
- Upregulation of the ERG11 gene in Candida krusei by azoles.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2010Article
- Recent insights into the mechanisms of antifungal resistance.Current infectious disease reports · 2006Article
- Aspergillus fumigatus C-5 sterol desaturases Erg3A and Erg3B: role in sterol biosynthesis and antifungal drug susceptibility.Antimicrobial agents and chemotherapy · 2006Article
- Candida albicans zinc cluster protein Upc2p confers resistance to antifungal drugs and is an activator of ergosterol biosynthetic genes.Antimicrobial agents and chemotherapy · 2005Article
- Reduced azole susceptibility in genotype 3 Candida dubliniensis isolates associated with increased CdCDR1 and CdCDR2 expression.Antimicrobial agents and chemotherapy · 2005Article
- Rapamycin control of exocrine protein levels in saliva after adenoviral vector-mediated gene transfer.Gene therapy · 2004Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has previously been shown that overexpression of the CdMDR1 gene is a major contributor to resistance in fluconazole-resistant isolates of Candida dubliniensis. However, since CdMdr1p does not mediate transport of other azole drugs such as itraconazole, we investigated the molecular mechanisms of stable resistance to itraconazole obtained in three strains of C. dubliniensis (two with nonfunctional CdCDR1 genes and one with functional CdCDR1 genes) by serial exposure to this antifungal agent in vitro. Seven derivatives that were able to grow on agar medium containing 64 micro g of itraconazole per ml were selected for detailed analysis. These derivatives were resistant to itraconazole, fluconazole, and ketoconazole but were not cross resistant to inhibitors. CdMDR1 expression was unchanged in the seven resistant derivatives and their parental isolates; however, all seven derivatives exhibited increased levels of CdERG11 expression, and six of the seven derivatives exhibited increased levels of CdCDR1 expression compared to the levels of expression by their respective parental isolates. Except for one derivative, the level of rhodamine 6G efflux was decreased in the itraconazole-resistant derivatives compared to the level of efflux in their parental isolates, suggesting altered membrane properties in these derivatives. Analysis of their membrane sterol contents was consistent with a defective sterol C5,6-desaturase enzyme (CdErg3p), which was confirmed by the identification of mutations in the alleles (CdERG3) encoding this enzyme and their lack of functional complementation in a Saccharomyces cerevisiae erg3 mutant. The results of this study show that the loss of function of CdErg3p was the primary mechanism of in vitro-generated itraconazole resistance in six of the seven the C. dubliniensis derivatives. However, the mechanism(s) of itraconazole resistance in the remaining seventh derivative has yet to be determined.
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