In-vivo selection of an azole-resistant petite mutant of Candida glabrata

Bouchara, Jean‐Philippe; Zouhair, Rachid; Boudouil, Sandrine Le; Rénier, Gilles; Filmon, R.; Chabasse, Dominique; Hallet, J. N.; Defontaine, Alain

doi:10.1099/0022-1317-49-11-977

Cited by 86 publications

(75 citation statements)

References 25 publications

(38 reference statements)

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“…Resistance in this case was explained by elevated expression of genes coding for drug efflux pumps in response to the loss of a functional mitochondrion (Sanglard et al 2001). While the respiratory-deficient mutant isolated here demonstrated elevated tolerance to amphotericin B, those isolated by Defontaine et al (1999) and Bouchara et al (2000) did not. This may be attributable to the fact that ethidium bromide mutagenesis can yield a range of different respiratory-deficient mutants in yeast and that, while the majority of the genome may be destroyed, small fragments can be retained and amplified to give a mitochondrial DNA content equivalent in size to that of the wild type (Whittaker and Danks 1978).…”

Section: Discussionmentioning

confidence: 86%

“…Respiratory-deficient mutants of C. glabrata have been isolated clinically and implicated in the failure of anti-fungal therapy due to elevated resistance to azole anti-fungal drugs (Defontaine et al 1999;Bouchara et al 2000). Resistance in this case was explained by elevated expression of genes coding for drug efflux pumps in response to the loss of a functional mitochondrion (Sanglard et al 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Respiratory-deficient cells of C. glabrata have previously been shown to manifest an increased tolerance to azole anti-fungal drugs (Defontaine et al 1999;Bouchara et al 2000), and respiratory-deficient mutants of C. albicans show enhanced tolerance to the anti-microbial peptide histatin 5 297 Fig. 1 Cytochrome profiles of Candida albicans strains.…”

Section: Amphotericin B Susceptibility Of C Albicans Strainsmentioning

confidence: 99%

“…incapable of aerobic respiration (Defontaine et al 1999). Respiratory-deficient isolates of Candida glabrata demonstrate tolerance to polyene (Geber et al 1995) and azole anti-fungal drugs (Bouchara et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Disruption of mitochondrial function in Candida albicans leads to reduced cellular ergosterol levels and elevated growth in the presence of amphotericin B

Geraghty

Kavanagh

2003

Arch Microbiol

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A respiratory-deficient mutant of Candida albicans MEN was generated by culturing cells in medium supplemented with ethidium bromide at 37°C for 5 days. The respiratory-deficient mutant (C. albicans MMU11) was incapable of growth on glycerol, had a reduced oxygen uptake rate and demonstrated an altered mitochondrial cytochrome profile. Respiratory-competent cybrids were formed by mitochondrial transfer following fusion of protoplasts with those of C. albicans ATCC 44990. Mutant MMU11 possessed lower levels of ergosterol than the parental isolates and the cybrids, and demonstrated a small but statistically significant increase in tolerance to amphotericin B. The results demonstrated that disruption of mitochondrial function in C. albicans increases the tolerance to amphotericin B, possibly mediated by a reduction in cellular ergosterol content.

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Amphotericin B Susceptibility Of C Albicans Strainsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Disruption of mitochondrial function in Candida albicans leads to reduced cellular ergosterol levels and elevated growth in the presence of amphotericin B

Geraghty

Kavanagh

2003

Arch Microbiol

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“…For C. glabrata, in vitro exposure to fluconazole can give rise to mitochondrial mutants at high frequency Brun et al 2003Brun et al , 2004. Selection of these mutants in the clinical context is much less frequent (Bouchara et al 2000;Ferrari et al 2011a). Although some C. glabrata clinical isolates with mitochondrial dysfunction do not show fitness defects compared with wild-type parents in a mouse infection model (Ferrari et al 2011a), other C. glabrata petite mutants are avirulent Singh-Babak et al 2012).…”

Section: Mitochondrial Defectsmentioning

confidence: 99%

Mechanisms of Antifungal Drug Resistance

Cowen

Sanglard

Howard

et al. 2014

Cold Spring Harb Perspect Med

479

399

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Antifungal therapy is a central component of patient management for acute and chronic mycoses. Yet, treatment choices are restricted because of the sparse number of antifungal drug classes. Clinical management of fungal diseases is further compromised by the emergence of antifungal drug resistance, which eliminates available drug classes as treatment options. Once considered a rare occurrence, antifungal drug resistance is on the rise in many high-risk medical centers. Most concerning is the evolution of multidrug-resistant organisms refractory to several different classes of antifungal agents, especially among common Candida species. The mechanisms responsible are mostly shared by both resistant strains displaying inherently reduced susceptibility and those acquiring resistance during therapy. The molecular mechanisms include altered drug affinity and target abundance, reduced intracellular drug levels caused by efflux pumps, and formation of biofilms. New insights into genetic factors regulating these mechanisms, as well as cellular factors important for stress adaptation, provide a foundation to better understand the emergence of antifungal drug resistance.

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In vitro antimycotic activity of some plant extracts towards yeast and yeast‐like strains

Turchetti

Pinelli

Buzzini

et al. 2005

Phytotherapy Research

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As part of screening aimed at the selection of novel antimycotic compounds of vegetable origin, leaf extracts of Camellia sinensis L., Cupressus sempervirens L. and Pistacia lentiscus L. and the seed extract of Glycine soja Sieb. et Zucc. were tested against yeast and yeast-like species implicated in human mycoses. Of the extracts only those of C. sinensis (obtained from a commercial preparation of green tea) exhibited broad activity towards Candida glabrata, Clavispora lusitatiae, Cryptococcus laurentii, Filobasidiella neoformans, Issatchenkia orientalis, Saccharomyces cerevisiae and Prototheca wickerhamii strains. MICs ranging from 300 to 4800 µ µ µ µ µg extract/mL (corresponding to 130-2010 µ µ µ µ µg/mL total polyphenols) were observed. Concentrations of the C. sinensis extract over 25 000 µ µ µ µ µg/mL caused a rapid decrease of viable cells of Fil. neoformans and its activity was dose-dependent. Tests carried out using the pure polyphenols present in C. sinensis extract composition, showed that only epicatechin-3-O-gallate (ECG) and epigallocatechin-3-O-gallate (EGCG) possess antimycotic activity.

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In-vivo selection of an azole-resistant petite mutant of Candida glabrata

Cited by 86 publications

References 25 publications

Disruption of mitochondrial function in Candida albicans leads to reduced cellular ergosterol levels and elevated growth in the presence of amphotericin B

Disruption of mitochondrial function in Candida albicans leads to reduced cellular ergosterol levels and elevated growth in the presence of amphotericin B

Mechanisms of Antifungal Drug Resistance

In vitro antimycotic activity of some plant extracts towards yeast and yeast‐like strains

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