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Luis Ostrosky-Zeichner, Editorial Commentary: Candida glabrata and FKS Mutations: Witnessing the Emergence of the True Multidrug-Resistant Candida, Clinical Infectious Diseases, Volume 56, Issue 12, 15 June 2013, Pages 1733–1734, https://doi.org/10.1093/cid/cit140
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(See the Major Article by Alexander et al on pages 1724–32.)
The term “multidrug-resistant Candida” has been used loosely in the mycology literature since the early 2000s [1–4]. In 2009, the Clinical and Laboratory Standards Institute subcommittee on antifungal susceptibility testing formally adopted the term, defining multidrug resistance in Candida as resistance or lack of susceptibility to at least 1 drug in 2 or more antifungal classes (unpublished data). Up until recently, this was little more than an academic exercise, as these isolates were usually found buried within very large epidemiologic surveys or in case reports [1, 5, 6]. Case in point: In a recent population-based study of candidemia in the United States, Cleveland et al [7] reported a 7% incidence of fluconazole resistance, 1% incidence of echinocandin resistance, and 0.4% incidence of both echinocandin and fluconazole resistance (8 of 9 isolates were Candida glabrata).
The molecular mechanisms of echinocandin resistance were described in parallel to the development of the first echinocandins [8]. Early descriptions were focused on the FKS1/ETG1 mutations [9, 10] and over the years clinicians were reassured because these mutations were, for the most part, created in the laboratory to study resistance and mechanisms of action and because when sporadically found in clinical isolates, correlation with both minimum inhibitory concentrations (MICs) and clinical outcomes was poor [11].
