First three reported cases of nosocomial fungemia caused by Candida auris

Abstract

Candida auris is a newly described species whose clinical significance is not clear. Here, we describe the first three cases of nosocomial fungemia caused by C. auris, which confirms that it is a causative agent of bloodstream infections. All three patients presented persistent fungemia for 10 to 31 days. The isolates obtained from the three patients were misidentified as Candida haemulonii and Rhodotorula glutinis by the Vitek 2 and the API 20C systems, respectively. C. auris was confirmed by sequence analysis of the internal transcribed spacer region and D1/D2 regions of the 26S ribosomal DNA of the rRNA gene. The MIC ranges of amphotericin B (AMB), fluconazole (FLU), itraconazole, and voriconazole were 0.5 to 1, 2 to 128, 0.125 to 2, and 0.06 to 1 μg/ml, respectively. All isolates were susceptible to caspofungin (MIC = 0.06 μg/ml) and micafungin (MIC = 0.03 μg/ml). One patient developed breakthrough fungemia while receiving FLU therapy, and two patients who received FLU therapy followed by AMB showed therapeutic failure and fatal outcomes. Our cases show that C. auris fungemia can be persistent, despite FLU or AMB therapy, which emphasizes the importance of accurately identifying this species.

Fig. 1.

Treatment regimens and outcomes for three patients with Candida auris fungemia. Therapeutic failure, which was defined as persistence of Candida in the bloodstream despite 3 days of antifungal therapy or development of breakthrough candidemia while receiving antifungal agents for 3 or more days, was observed in all three patients. Gray bars, period of hospital stay, with numbers denoting hospital days; black bars, period of blood culture positivity for C. auris; line with closed diamonds, period and dose (per day) of antifungal treatment; inverted closed triangles, time of removal of vascular catheter; arrows, dates of positive blood culture.