No abstract

Overall, 25% and 13% of isolates were MDR and multi-azole resistant, respectively. The most common resistance combination was azoles and 5-flucytosine in 14% followed by azoles and amphotericin B in 7% and azoles and echinocandins in 2% of isolates.

dCandida auris is a multidrug-resistant yeast that causes a wide spectrum of infections, especially in intensive care settings. We investigated C. auris prevalence among 102 clinical isolates previously identified as Candida haemulonii or Candida famata by the Vitek 2 system. Internal transcribed spacer region (ITS) sequencing confirmed 88.2% of the isolates as C. auris, and matrixassisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) easily separated all related species, viz., C. auris (n ‫؍‬ 90), C. haemulonii (n ‫؍‬ 6), C. haemulonii var. vulnera (n ‫؍‬ 1), and Candida duobushaemulonii (n ‫؍‬ 5). The in vitro antifungal susceptibility was determined using CLSI broth microdilution (CLSI-BMD), the Vitek 2 antifungal susceptibility test, and the Etest method. C. auris isolates revealed uniformly elevated fluconazole MICs (MIC 50 , 64 g/ml), and an alarming percentage of isolates (37%) exhibited elevated caspofungin MICs by CLSI-BMD. Notably, 34% of C. auris isolates had coexisting elevated MICs (>2 g/ml) for both fluconazole and voriconazole, and 10% of the isolates had elevated coexisting MICs (>2 g/ml) to two additional azoles, i.e., posaconazole and isavuconazole. In contrast to reduced amphotericin B MICs by CLSI-BMD (MIC 50 , 1 g/ml) for C. auris, elevated MICs were noted by Vitek 2 (MIC 50 , 8 g/ml), which were statistically significant. Candida auris remains an unnoticed pathogen in routine microbiology laboratories, as 90% of the isolates characterized by commercial identification systems are misidentified as C. haemulonii. MALDI-TOF MS proved to be a more robust diagnostic technique for rapid identification of C. auris. Considering that misleading elevated MICs of amphotericin B by the Vitek AST-YS07 card may lead to the selection of inappropriate therapy, a cautionary approach is recommended for laboratories relying on commercial systems for identification and antifungal susceptibility testing of rare yeasts. In recent years, two species, namely, Candida pseudohaemulonii and Candida auris, which are phylogenetically closely related to Candida haemulonii in the Metschnikowiaceae clade, have been described (1). The yeast C. auris, isolated from the external ear canal of a Japanese patient, was described as a new species in 2009 (2). This pathogen was recently recognized as an emerging multidrug-resistant (MDR) yeast that can cause a wide spectrum of infections, ranging from fungemia to deep-seated infections, especially in intensive care settings (3-8). Candida auris is reported to be misidentified as C. haemulonii, Candida famata, and Rhodotorula glutinis by commercial identification systems, such as Vitek 2 and API20C-AUX, and exhibits a unique susceptibility profile (5-8). Notably, the potential of clonal transmission of C. auris, highly elevated MICs to fluconazole, and reduced susceptibility to voriconazole, caspofungin, and flucytosine are matters of serious concern (7-9). Therefore, accurate identification is important, because treatment strategies are often directed ...

Candida auris is a recently described rare agent of fungemia. It is notable for its antifungal resistance. A total of 15 C. auris isolates, originating from seven cases of fungemia, three cases of diabetic gangrenous foot, and one case of bronchopneumonia from a tertiary care hospital in south India, were investigated. All of the 15 isolates were identified by sequencing and 14 of these along with 12 C. auris isolates previously reported from two hospitals in Delhi, north India, two each from Japan and Korea were genotyped by amplified fragment length polymorphism (AFLP). In vitro antifungal susceptibility testing (AFST) was done by the Clinical and Laboratory Standards Institute (CLSI) broth microdilution method. Candida auris isolates were misidentified as Candida haemulonii by VITEK. All were resistant to fluconazole [geometric mean minimum inhibitory concentration (MIC) 64 μg/ml] and 11 isolates were resistant to voriconazole (MIC ≥1 μg/ml). Forty-seven percent of the C. auris isolates were resistant to flucytosine (MIC ≥64 μg/ml) and 40% had high MIC (≥1 μg/ml) of caspofungin. Breakthrough fungemia developed in 28.6% of patients and therapeutic failure in 4 (66.7%) patients. Interestingly, the 26 Indian C. auris isolates from north and south India were clonal and phenotypically and genotypically distinct from Korean and Japanese isolates. The present study demonstrates that C. auris is a potential emerging pathogen that can cause a wide spectrum of human mycotic infections. The prevalence of a C. auris endemic clonal strain resistant to azoles and other antifungals in Indian hospitals with high rates of therapeutic failure in cases of fungemia is worrisome.

A new clonal strain of Candida auris is an emerging etiologic agent of fungemia in Delhi, India. In 12 patients in 2 hospitals, it was resistant to fluconazole and genotypically distinct from isolates from South Korea and Japan, as revealed by M13 and amplified fragment length polymorphism typing.