Echinocandin-resistant Candida: Molecular methods and phenotypes

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations

Abstract

We now have a decade of experience with echinocandin drugs. Large-scale epidemiologic antifungal surveillance studies have demonstrated that caspofungin, micafungin, and anidulafungin retain high potency on clinical isolates of Candida, and resistance remains relatively low. Yet reports of breakthrough infections involving strains with a high minimum inhibitory concentration (MIC) are mounting. Mechanism-specific resistance involving amino acid substitutions in the Fks subunit(s) of the drug target glucan synthase results in reduced enzyme sensitivity to drug and high MICs. The mechanism affects all three drugs and is encountered in all Candida species, as well as in Aspergillus. An initial susceptibility testing breakpoint failed to adequately distinguish wild-type susceptible isolates from fks mutant resistant strains. Considering data from epidemiologic, microbiologic, pharmacokinetic/ pharmacodynamic, biochemical, and genetic studies that better capture resistant isolates with fks genotypes has resulted in a proposed new breakpoint which provides a more reliable measure of probable therapeutic success.

Original languageEnglish (US)
Pages (from-to)113-119
Number of pages7
JournalCurrent Fungal Infection Reports
Volume5
Issue number3
DOIs
StatePublished - Sep 2011

All Science Journal Classification (ASJC) codes

  • Infectious Diseases

Keywords

  • Anidulafungin
  • Candida albicans
  • Candida glabrata
  • Caspofungin
  • Clinical breakpoint
  • Echinocandins
  • Epidemiologic cutoff value
  • FKS
  • Glucan synthase
  • Micafungin
  • Resistance

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