ABSTRACT
Candida albicans and related species pathogenic for man become resistent to antifungal agents, in particular triazole compounds, by expression of efflux pumps that reduce drug accumulation, alteration of the structure or concentration of antifungal target proteins, and alteration of membrane sterol composition. The clinical consequences of antifungal resistence can be seen in treatment failures in patients and in changes in the prevalence of Candida species causing disease. These effects were seen unequivocally in HIV-infected patients with oropharyngel candida infections, but their incidence has decreased dramatically with the introduction of highly active antiretroviral therapy. The evidence for similar emergence of antifungal-resistant yeast strains and species in other types of candida infections is confounded by non-standardised susceptibillity testing methods and definitions of a resistent fungal isolate. Recent large-scale surveys of yeasts isolated from blood cultures, based on standardised methodology and resistence definitions, do not support the view that antifungal resistance in pathogenic yeasts contitutes a significant or growing therapeutic problem