Meyerozyma guilliermondii species complex: review of current epidemiology, antifungal resistance, and mechanisms

Ghasemi, Reza; Lotfali, Ensieh; Rezaei, Kamran; Madinehzad, Seyed Ataollah; Tafti, Mahdi Falah; Aliabadi, Nikta; Kouhsari, Ebrahim; Fattahi, Azam

doi:10.1007/s42770-022-00813-2

Cited by 5 publications

(2 citation statements)

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“…12,13 Moreover, some strains of M. guilliermondii show intrinsically less susceptibility to polyenes. 2,14 Barchiesi et al reported that several strains showed tolerance to amphotericin B (AmB) with fungistatic activity of AmB instead of classically fungicidal activity. 11 AmB is also difficult to use because of its potential toxicity.…”

Section: Introductionmentioning

confidence: 99%

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Pan‐azole‐resistant Meyerozyma guilliermondii clonal isolates harbouring a double F126L and L505F mutation in Erg11

Moreau,

Noël,

Point

et al. 2024

Mycoses

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BackgroundMeyerozyma guilliermondii is a yeast species responsible for invasive fungal infections. It has high minimum inhibitory concentrations (MICs) to echinocandins, the first‐line treatment of candidemia. In this context, azole antifungal agents are frequently used. However, in recent years, a number of azole‐resistant strains have been described. Their mechanisms of resistance are currently poorly studied.ObjectiveThe aim of this study was consequently to understand the mechanisms of azole resistance in several clinical isolates of M. guilliermondii.MethodsTen isolates of M. guilliermondii and the ATCC 6260 reference strain were studied. MICs of azoles were determined first. Whole genome sequencing of the isolates was then carried out and the mutations identified in ERG11 were expressed in a CTG clade yeast model (C. lusitaniae). RNA expression of ERG11, MDR1 and CDR1 was evaluated by quantitative PCR. A phylogenic analysis was developed and performed on M. guilliermondii isolates. Lastly, in vitro experiments on fitness cost and virulence were carried out.ResultsOf the ten isolates tested, three showed pan‐azole resistance. A combination of F126L and L505F mutations in Erg11 was highlighted in these three isolates. Interestingly, a combination of these two mutations was necessary to confer azole resistance. An overexpression of the Cdr1 efflux pump was also evidenced in one strain. Moreover, the three pan‐azole‐resistant isolates were shown to be genetically related and not associated with a fitness cost or a lower virulence, suggesting a possible clonal transmission.ConclusionIn conclusion, this study identified an original combination of ERG11 mutations responsible for pan‐azole‐resistance in M. guilliermondii. Moreover, we proposed a new MLST analysis for M. guilliermondii that identified possible clonal transmission of pan‐azole‐resistant strains. Future studies are needed to investigate the distribution of this clone in hospital environment and should lead to the reconsideration of the treatment for this species.

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Section: Introductionmentioning

confidence: 99%

“…There is no data about a higher failure of echinocandin therapy in infections due to M. guilliermondii , however, breakthrough infections during caspofungin and micafungin prophylaxis have been reported 12,13 . Moreover, some strains of M. guilliermondii show intrinsically less susceptibility to polyenes 2,14 . Barchiesi et al.…”

Section: Introductionmentioning

confidence: 99%