Abstract

Background: Candida species are opportunistic pathogenic fungi that colonize in the human body. They may cause diseases ranging from non-life-threatening mucosal Candida infections to life-threatening invasive candidiasis among people with the aggressive use of immunosuppressive agents, cytotoxic therapies, treatment with broad-spectrum antifungal agents, prolonged central venous catheterization, total parenteral nutrition, AIDS, diabetes, and drug abuse. Objectives: The aim of this study was to describe the distribution and antifungal susceptibility of clinical Candida isolates obtained from sterile fluids of patients who suffered from candidiasis from 2008 to 2010. Methods: Vitek2 YST, CHROMagar Candida medium, and multiple PCR were used to identify the Candida species. The susceptibility testing to seven common antifungal agents, including amphotericin B, flucytosine, fluconazole, itraconazole, ketoconazole, clotrimazole, and nystatin, was performed using the methodology recommended in the M27-A3 document of the clinical and laboratory standards institute (CLSI). Results: A total of 149 clinical Candida isolates were obtained from sterile fluids at a hospital in China. Within these isolates, Candida albicans was the most predominant species (47.7%), followed by C. glabrata (26.8%) and C. tropicalis (13.4%). The sources of fungal isolates were urine (75.8%), blood (16.8%), drainage liquid (4%), hydrothorax and ascites (2%), cerebrospinal fluid (0.7%), and succus prostaticus (0.7%). All of the Candida isolates were susceptible to amphotericin B. In addition, 27.5% of the isolates were resistant to ketoconazole, 22.1% to itraconazole, and 17.4% to fluconazole. Furthermore, 16.8% (25/149) of the isolates exhibited a cross-resistance to azoles. Interestingly, we found one flucytosine-resistant C. albicans isolated from urine. Conclusions: Our findings indicate that a better preventive management and limited use of azole drugs are needed for Candida infections and further research is indispensable to identify cross-resistance mechanisms of azoles.

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