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ABSTRACT: mcr-1 in multidrug-resistant blaKPC-2 clinical Enterobacteriaceae isolates in Singapore

PROVIDER: PRJEB14213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1432660_1.fastq.gz	Fastqsanger.gz
	ERR1432660_2.fastq.gz	Fastqsanger.gz
	ERR1432659_1.fastq.gz	Fastqsanger.gz
	ERR1432659_2.fastq.gz	Fastqsanger.gz
	ERR1544012_1.fastq.gz	Fastqsanger.gz

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Project description:Candida tropicalis is a leading cause of invasive candidiasis in the Asia-Pacific region, with mortality rates exceeding 50%. The rising prevalence of azole resistant clinical strains, particularly in this region, presents a significant clinical challenge. In this study, we analyzed 1,032 C. tropicalis isolates, including 1,016 clinical isolates collected over nine years from 27 hospitals across India, as well as 16 environmental isolates. Fluconazole resistance was detected in 5.1% of clinical isolates, with more than half also exhibiting cross-resistance to voriconazole and itraconazole. Multilocus sequence typing (MLST) and phylogenomic analysis of 1,571 global isolates, confirmed the clonal emergence and persistence of azole- resistant MLST clade 4 strains in Indian hospitals. Genomic analysis revealed that Indian isolates cluster closely with azole resistant strains from China, Singapore, and Taiwan. Azole resistance was found to be multifactorial, involving well-characterized hotspot mutations in the ERG11 gene (Y132F, S154F), ERG11 gene amplification (2–7.5 copies), and significant overexpression of ERG11. Transcriptomic profiling showed significant up regulation of virulence-associated genes in the fluconazole-resistant isolate. Notably, ALS7, a member of the agglutinin-like sequence (ALS) family involved in cell adhesion along with Secreted Aspartyl Proteinases (SAP) genes SAP7 and SAP9, were significantly upregulated in fluconazole-resistant isolates. Additionally, fluconazole-resistant isolates exhibited significantly enhanced biofilm formation compared to fluconazole-susceptible strains, indicating a higher virulence potential. Furthermore, fluconazole-resistant isolates exhibited reduced β-glucan exposure, a trait linked to immune evasion, and showed greater survival in both neutrophil and macrophage killing assays. Together, our findings provide comprehensive genomic and phenotypic evidence supporting the emergence, persistence, and increased pathogenic potential of azole-resistant C. tropicalis clade 4 in Indian hospitals. A deeper understanding of the epidemiological trends and molecular mechanisms driving drug resistance in C. tropicalis is essential for improving diagnostic accuracy, optimising antifungal susceptibility testing, and informing effective clinical management strategies.

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