Abstract
Candida glabrata is the second leading cause of candidemia in North America and reports of treatment failure attributed to echinocandin-resistant C. glabrata are increasing. This report describes a case of clinical failure of C. glabrata treatment associated with de novo resistance to micafungin (MICA) after prolonged MICA therapy in a patient with multiple intra-abdominal abscesses. The decreased susceptibility to MICA was associated with acquired mutations in Fks1p and Fks2p subunits of the 1,3-β-D-glucan synthase complex.
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