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Emergence of azole-resistant Candida blankii as a cause of bloodstream infection

ABSTRACT: Azole-resistant C. blankii as a cause of fungemia

PROVIDER: PRJEB25918 | ENA |

REPOSITORIES: ENA

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Azole-resistant Candida blankii as a newly recognized cause of bloodstream infection.

Project description:Candida blankii is a newly recognized human pathogen. Here we describe a case of bloodstream infection in a preterm neonate. The yeast was repeatedly isolated from blood, and its identity was confirmed by PCR sequencing of rDNA. Additionally, C. blankii DNA was detected directly in a blood sample. The isolates initially developed pink colonies on CHROMagar Candida which later turned into dark metallic blue similar to Candida tropicalis. Inaccurate identification by the VITEK 2 yeast identification system as Stephanoascus ciferrii and intrinsic resistance to fluconazole (MIC 12-16 ?g/mL) underscore the need for its accurate identification for appropriate therapeutic management.

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[Candida] blankii strain:ABL

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Azole Resistance Mechanism in Candida glabrata

Project description:Microarray was used to analyze azole resistance of Candida glabrata oropharyngeal isolates from 7 hematopoietic stem cell transplant recipients receiving fluconazole prophylaxis. Transcriptional profiling of the sequential-paired clinical isolates by microarray revealed 19 genes upregulated in the majority of resistant isolates compared to their paired-susceptible isolates. All seven resistant isolates had greater than two fold upregulation of CgPDR1, a master transcriptional regulator of PDR network, and all 7 resistant isolates showed upregulation of known CgPDR1-target genes. The altered transcriptome can be explained in part by the observation that all 7 resistant isolates had acquired a single nonsynonymous mutation in their CgPDR1 ORF. Four mutations occurred in the regulatory domain (L280P, L344S, G348A, S391L) and one in the activation domain (G943S) while two mutations (N764I, R772I) occurred in an undefined region. Association of azole resistance and the CgPDR1 mutations was investigated in the same genetic background by introducing the CgPDR1 sequences from one sensitive and five resistant isolates into a laboratory azole-sensitive strain (cgpdr1) via integrative transformation. The cgpdr1 strain was restored to wild-type fluconazole susceptibility when transformed with CgPDR1 from the susceptible isolate but became resistant when transformed with CgPDR1 from the resistant isolates. However, despite the identical genetic background, upregulation of CgPDR1 and CgPDR1-target genes varied between the 5 transformants, independent of the domain locations in which the mutations occurred. In sum, gain-of-function mutations in CgPDR1 not only contributed to the clinical azole resistance but different mutations had varying degrees of impact on the CgPDR1-target genes.

2010-07-07 | GSE21355 | GEO

[Candida] blankii strain:NG 19339

Project description:Candida blankii NG 19339 Raw sequence reads

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[Candida] blankii strain:FH20-21

Project description:Candida blankii FH20-21 Raw sequence reads

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[Candida] blankii strain:FH20-22

Project description:Candida blankii FH20-22 Raw sequence reads

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[Candida] blankii strain:FH20-20

Project description:Candida blankii FH20-20 Raw sequence reads