We investigated the molecular mechanisms underlying azole resistance in seven Candida tropicalis isolates that caused candidemia and candiduria in Paraná, Brazil (2016–2022). Biofilm production, antifungal susceptibility testing, multilocus sequence typing, amplification and sequencing of ERG11, and quantification of ERG11, MDR1, and CDR1 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 ERG11; Y132F and Y257N were predominant (71.4%), followed by Y132F and S154F (14.3%) and Y257H (14.3%). No differences in ERG11 expression were found between the susceptible and resistant groups, but MDR1 and CDR1 were more highly expressed in the susceptible isolates. All the isolates contained previously unassigned diploid sequence types. The emergence of C. tropicalis 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 ERG11 were the main resistance mechanism identified in C. tropicalis.

Invasive candidiasis (IC) contributes to the morbidity and mortality of hospitalized patients and represents a significant burden to the healthcare system. Previous Brazilian studies have reported the presence of endemic Candida parapsilosis sensu stricto genotypes causing candidemia and clonal transmission involving fluconazole-resistant isolates. We performed a 5-year retrospective analysis of IC cases in a Brazilian tertiary pediatric hospital and conducted a molecular investigation of C. parapsilosis sensu stricto. Non-duplicate C. parapsilosis sensu stricto genotyping was performed by microsatellite analysis. Antifungal susceptibility and biofilm formation were also evaluated. A total of 123 IC episodes were identified, with an IC incidence of 1.24 cases per 1000 hospital admissions and an overall mortality of 34%. The main species were the C. parapsilosis complex (35.8%), Candida albicans (29.2%), and Candida tropicalis (21.9%). All C. parapsilosis sensu stricto were recovered from blood cultures, and 97.5% were biofilm producers. Microsatellite typing identified high genotypic diversity among the isolates. We observed that all isolates were sensitive to amphotericin B, and although one isolate was non-sensitive to fluconazole, only a silent mutation on ERG11 gene was identified. No clear evidence of clonal outbreak or emergence of fluconazole-resistant isolates was found, suggesting that multiple sources may be involved in the epidemiology of IC in children.