Abstract

As a clinical mycologist, one of the most frequent questions I get asked by clinical technicians is, “Do we still need to distinguish Candida dubliniensis from Candida albicans?” When I ask the questioner why they separate them, the usual response is that C. dubliniensis is often resistant to fluconazole. When C. dubliniensis was first described in 1995 (11), AIDS was epidemic and highly active antiretroviral therapy (HAART) was just becoming available. Because of these factors, mucocutaneous candidasis was commonly seen and fluconazole prophylaxis was often prescribed. Many of the first strains of C. dubliniensis from HIV-positive patients exhibited elevated fluconazole MIC values or the ability to develop fluconazole resistance under drug pressure in vitro (5, 6). Despite this, the original discoverers of C. dubliniensis reported that it remained fairly susceptible to fluconazole (9). To try to put this question to rest, we tested 42 isolates of C. dubliniensis for susceptibility to fluconazole. Isolates were collected as part of a population-based candidemia surveillance conducted by the CDC in Atlanta and Baltimore. Isolates were identified as C. dubliniensis by a Luminex-based assay (4) or by sequencing of the D1/D2 region of the ribosomal DNA (rDNA). Isolates were tested by broth microdilution using the methodology of Clinical and Laboratory Standards Institute standard M27-A3 (3). The MIC 50 of these 42 isolates was 0.25 g/ml, and the MIC 90 was 0.5 g/ml, with only two isolates (4.8%) having a MIC value above 0.5 g/ml, both of which had a MIC value of 16 g/ml. The two isolates with elevated MIC

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