AI Article Synopsis
- Infections from azole-resistant Candida tropicalis are rising in healthcare settings, but the reasons and mechanisms behind this resistance remain unclear.
- This study analyzed 239 strains of C. tropicalis from both environmental and human sources, finding that most had a diploid genome and exhibited similar survival and enzyme production capabilities.
- Resistant strains were identified in nearly 20% of both groups, with certain genetic mutations linked to azole resistance, suggesting a close genetic relationship between environmental and human isolates.
Article Abstract
Objectives: Infections caused by azole-resistant Candida tropicalis strains are increasing in clinical settings. The reason for this epidemical change and the mechanisms of C. tropicalis azole resistance are not fully understood.
Methods: In this study, we performed biological and genomic analyses of 239 C. tropicalis strains, including 115 environmental and 124 human commensal isolates.
Results: Most (99.2%) of the isolates had a baseline diploid genome. The strains from both environmental and human niches exhibit similar abilities to survive under stressful conditions and produce secreted aspartic proteases. However, the human commensal isolates exhibited a stronger ability to filament than the environmental strains. We found that 19 environmental isolates (16.5%) and 24 human commensal isolates (19.4%) were resistant to fluconazole. Of the fluconazole-resistant strains, 37 isolates (86.0%) also exhibited cross-resistance to voriconazole. Whole-genome sequencing and phylogenetic analyses revealed that both environmental and commensal isolates were widely distributed in a number of genetic clusters, but the two populations exhibited a close genetic association. The majority of fluconazole-resistant isolates were clustered within a single clade (X).
Conclusions: The combination of hotspot mutations (Y132F and S154F) and genomic expansion of ERG11, which encodes the azole target lanosterol 14-α-demethylase and represents a major target of azole drugs, was a major mechanism for the development of azole resistance. The isolates carrying both hotspot mutations and genomic expansion of ERG11 exhibited cross-resistance to fluconazole and voriconazole. Moreover, the azole-resistant isolates from both the environmental and human commensal niches showed similar genotypes.
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| http://dx.doi.org/10.1016/j.ijantimicag.2023.107010 | DOI Listing |
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