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Candida glabrata, an Emerging Oral Opportunistic Pathogen

¹ Department of Oral Health and Diagnostic Sciences, School of Dental Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1710, USA; and
² Department of General Dentistry, School of Dentistry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900, USA

View larger version (19K): [in this window] [in a new window]   Figure 1. Comparison of cytotoxic potential of C. glabrata and C. albicans. OKF6-TERT2 cells were co-cultured with C. glabrata GDH2269, 94-11, MRL2302, and MRL7525, as well as with C. albicans SC5314 at 0.1:1, 1:1, or 10:1 fungal cell to epithelial cell ratio. Cell supernatants were analyzed for LDH presence 36 hrs post-infection. Values were obtained by analysis of two separate experiments with conditions set up in duplicate. The bars represent SEM.

View larger version (67K): [in this window] [in a new window]   Figure 2. Comparison of tissue-damaging and invasive potential of oral C. glabrata and oral C. albicans in an in vitro 3-D model of the oral mucosa. (A) Infection with oral C. glabrata strain GDH2269 caused minimal loss of the normal mucosal architecture, with only a mild edema in the uppermost keratinocyte layers 48 hrs post-infection. C. glabrata formed a thin biofilm and invaded only the superficial epithelial layers. (B) Oral C. albicans strain ATCC28366 formed a thicker soft-tissue biofilm and invaded both the mucosal and submucosal layers. Extensive cellular necrosis and loss of cellular junctions in the stratum basale were evident 48 hrs post-infection. Bars = 60 µm.