ArticleAntimicrobial agents and chemotherapy2014
In vivo and in vitro acquisition of resistance to voriconazole by Candida krusei.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
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- Prevalence of Antifungal Resistance, Genetic Basis of Acquired Azole and Echinocandin Resistance, and Genotyping of Candida krusei Recovered from an International Collection.Antimicrobial agents and chemotherapy · 2022Article
- Experimental and in-host evolution of triazole resistance in human pathogenic fungi.Frontiers in fungal biology · 2022Review
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- Identification of novel antifungal agents: antimicrobial evaluation, SAR, ADME-Tox and molecular docking studies of a series of imidazole derivatives.BMC chemistry · 2019Article
- Resistance Mechanism in a Terbinafine-Resistant Strain of Microsporum canis.Mycopathologia · 2018Article
- Strong Synergism of Palmatine and Fluconazole/Itraconazole Against Planktonic and Biofilm Cells ofFrontiers in microbiology · 2018Article
- Genetic Differentiation, Diversity, and Drug Susceptibility ofFrontiers in microbiology · 2018Article
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- Whole Genome Sequence of the Heterozygous Clinical IsolateG3 (Bethesda, Md.) · 2017Article
- Molecular epidemiology and azole resistance mechanism study of Candida guilliermondii from a Chinese surveillance system.Scientific reports · 2017Article
- Fluconazole resistance inInfection and drug resistance · 2017Review
- Antifungal Therapy: New Advances in the Understanding and Treatment of Mycosis.Frontiers in microbiology · 2017Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida krusei is an important agent of opportunistic infections that often displays resistance to several antifungals. We describe here the in vivo acquisition of resistance to voriconazole (VRC) by C. krusei isolates recovered from a leukemia patient during a long period of VRC therapy. In order to mimic the in vivo development of VRC resistance, a susceptible C. krusei isolate was exposed daily to 1 μg/ml of VRC in vitro. Interestingly, after 5 days of exposure to VRC, a MIC of 4 μg/ml was achieved; this value remained constant after 25 additional days of treatment with VRC and also after 30 consecutive days of incubation in VRC-free medium. Our objective was to determine the associated molecular resistance mechanisms, such as expression of efflux pump genes and ERG11 gene mutations, among the resistant strains. Synergistic effects between the efflux blocker tacrolimus (FK506) and VRC were found in all of the resistant strains. Moreover, ABC1 gene expression increased over time in both the in vivo- and in vitro-induced resistant strains, in contrast to the ABC2 and ERG11 genes, whose expression was invariably lower and constant. ERG11 gene sequencing showed two different types of mutations, i.e., heterozygosity at T1389T/C, corresponding to synonymous mutations, in C. krusei strains and a missense mutation at position T418C, resulting in a change from Tyr to His, among resistant C. krusei clinical isolates. This study highlights the relevance of ATP-dependent efflux pump (namely, Abc1p) activity in VRC resistance and describes new mutations in the ERG11 gene among resistant C. krusei clinical isolates.
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