Diversity and antifungal susceptibility of Norwegian Candida glabrata clinical isolates

Kari-Mette Andersen; Anne Karin Kristoffersen; André Ingebretsen; Katharina Johnsen Vikholt; Ulf Thore Örtengren; Ingar Olsen; Morten Enersen; Peter Gaustad

doi:10.3402/jom.v8.29849

Diversity and antifungal susceptibility of Norwegian Candida glabrata clinical isolates

J Oral Microbiol. 2016 Feb 8:8:29849. doi: 10.3402/jom.v8.29849. eCollection 2016.

Authors

Kari-Mette Andersen^{1

2}, Anne Karin Kristoffersen³, André Ingebretsen⁴, Katharina Johnsen Vikholt³, Ulf Thore Örtengren¹, Ingar Olsen³, Morten Enersen³, Peter Gaustad⁴

Affiliations

¹ Institute of Clinical Odontology, University of Tromsø, Tromsø, Norway.
² Department of Oral Biology (DOB), Faculty of Dentistry, University of Oslo, Oslo, Norway; andersen.karimette@gmail.com.
³ Department of Oral Biology (DOB), Faculty of Dentistry, University of Oslo, Oslo, Norway.
⁴ Department of Microbiology, Oslo University Hospital (OUS), Rikshospitalet, University of Oslo, Oslo, Norway.

Abstract

Background: Increasing numbers of immunocompromised patients have resulted in greater incidence of invasive fungal infections with high mortality. Candida albicans infections dominate, but during the last decade, Candida glabrata has become the second highest cause of candidemia in the United States and Northern Europe. Reliable and early diagnosis, together with appropriate choice of antifungal treatment, is needed to combat these challenging infections.

Objectives: To confirm the identity of 183 Candida glabrata isolates from different human body sites using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) and VITEK(®)2, and to analyze isolate protein profiles and antifungal susceptibility. The minimum inhibitory concentration (MIC) of seven antifungal drugs was determined for the isolates to elucidate susceptibility.

Design: A total of 183 C. glabrata isolates obtained between 2002 and 2012 from Norwegian health-care units were analyzed. For species verification and differentiation, biochemical characterization (VITEK(®)2) and mass spectrometry (MALDI-TOF) were used. MIC determination for seven antifungal drugs was undertaken using E-tests(®).

Results: Using VITEK(®)2, 92.9% of isolates were identified as C. glabrata, while all isolates (100%) were identified as C. glabrata using MALDI-TOF. Variation in protein spectra occurred for all identified C. glabrata isolates. The majority of isolates had low MICs to amphotericin B (≤1 mg/L for 99.5%) and anidulafungin (≤0.06 mg/L for 98.9%). For fluconazole, 18% of isolates had MICs >32 mg/L and 82% had MICs in the range ≥0.016 mg/L to ≤32 mg/L.

Conclusions: Protein profiles and antifungal susceptibility characteristics of the C. glabrata isolates were diverse. Clustering of protein profiles indicated that many azole resistant isolates were closely related. In most cases, isolates had highest susceptibility to amphotericin B and anidulafungin. The results confirmed previous observations of high MICs to fluconazole and flucytosine. MALDI-TOF was more definitive than VITEK(®)2 for C. glabrata identification.

Keywords: C. glabrata; MALDI-TOF; MICs; biochemical; identification.