Azole Resistance and Mutation in Clinical Isolates of .

We investigated the molecular mechanisms underlying azole resistance in seven isolates that caused candidemia and candiduria in Paraná, Brazil (2016-2022). Biofilm production, antifungal susceptibility testing, multilocus sequence typing, amplification and sequencing of , and quantification of , , and expression levels were performed. Notably, five isolates (71.4%) were from urine samples and two (28.6%) were from blood samples. All strains were biofilm producers, with levels ranging from moderate to strong. The minimum inhibitory concentration (MIC) values ranged from 8->64 mg/L for fluconazole and 0.25-1 mg/L for voriconazole. All isolates had mutations in ; Y132F and Y257N were predominant (71.4%), followed by Y132F and S154F (14.3%) and Y257H (14.3%). No differences in expression were found between the susceptible and resistant groups, but and were more highly expressed in the susceptible isolates. All the isolates contained previously unassigned diploid sequence types. The emergence of azole resistance has been previously described in Brazil; however, the presence of resistant isolates in urine highlights the need for surveillance resistant strains in both urinary and invasive contexts. In our study mutations in were the main resistance mechanism identified in .