Antifungal Resistance in
antifungal resistance has made Candida infections a problematic clinical challenge, especially with populations of susceptible patients on the rise. Some Candida species are intrinsically more resistant to fluconazole treatment, e.g. C. glabrata. Others acquire resistance rapidly, especially in patients with recurrent infection that must be repeatedly treated. Resistance mechanisms include efflux pumps (e.g. MDR1), enzyme mutations that prevent drug binding (e.g. the FKS1 mutation negating echinocandin function), overexpression antifungal target genes (e.g. ERG11) to overcome antifungal activity, and the evolution of compensatory survival pathways
(e.g. Candida species that survive despite lower cell membrane ergosterol thereby reducing polyene susceptibility). The recent emergence of
C. auris, overwhelmingly resistant to fluconazole, and occasionally resistant to echinocandins and AmpB, has led to outbreaks in hospital ICUs that are surprisingly difficult to contain.