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Whole-genome sequencing investigation of a large nosocomial outbreak caused by ST131 H30Rx KPC-producing Escherichia coli in Italy

ABSTRACT: Whole-genome sequencing investigation of a large nosocomial outbreak caused by ST131 H30Rx KPC-producing Escherichia coli in Italy

PROVIDER: PRJEB40388 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4596830_1.fastq.gz	Fastqsanger.gz
	ERR4596830_2.fastq.gz	Fastqsanger.gz
	ERR4596840_1.fastq.gz	Fastqsanger.gz
	ERR4596840_2.fastq.gz	Fastqsanger.gz
	ERR4596850_1.fastq.gz	Fastqsanger.gz

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Whole-Genome Sequencing Investigation of a Large Nosocomial Outbreak Caused by ST131 H30Rx KPC-Producing Escherichia coli in Italy.

Project description:KPC-producing Escherichia coli (KPC-Ec) remains uncommon, being mainly reported as the cause of sporadic episodes of infection rather than outbreak events. Here we retrospectively describe the dynamics of a large hospital outbreak sustained by KPC-Ec, involving 106 patients and 25 hospital wards, during a six-month period. Twenty-nine representative KPC-Ec isolates (8/29 from rectal swabs; 21/29 from other clinical specimens) have been investigated by Whole-Genome Sequencing (WGS). Outbreak isolates showed a multidrug-resistant profile and harbored several resistance determinants, including blaCTX-M-27, aadA5, dfrA17, sulI, gyrA1AB and parC1aAB. Phylogenomic analysis identified the ST131 cluster 1 (23/29 isolates), H30Rx clade C, as responsible for the epidemic event. A further two KPC-Ec ST131 clusters were identified: cluster 2 (n = 2/29) and cluster 3 (n = 1/29). The remaining KPC-Ec resulted in ST978 (n = 2/29) and ST1193 (n = 1/29), and were blaKPC-3 associated. The KPC-Ec ST131 cluster 1, originated in a previous KPC-Kp endemic context probably by plasmid transfer, and showed a clonal dissemination strategy. Transmission of the blaKPC gene to the globally disseminated high-risk ST131 clone represents a serious cause of concern. Application of WGS in outbreak investigations could be useful to better understand the evolution of epidemic events in order to address infection control and contrast interventions, especially when high-risk epidemic clones are involved.

| S-EPMC8232337 | biostudies-literature

Comprehensive Assessment of Initial Adaptation of ESBL Positive ST131 E. coli to Carbapenem Exposure

Project description:Background: It remains unclear how high-risk Escherichia coli lineages, like sequence type (ST) 131, initially adapt to carbapenem exposure in its progression to becoming carbapenem resistant. Methods: Carbapenem mutation frequency was measured in multiple subclades of extended-spectrum β-lactamase (ESBL) positive ST131 clinical isolates using a fluctuation assay followed by whole genome sequencing (WGS) characterization. Genomic, transcriptomic, and porin analyses of ST131 C2/H30Rx isolate, MB1860, under prolonged, increasing carbapenem exposure was performed using two distinct experimental evolutionary platforms to measure fast vs. slow adaptation. Results: All thirteen ESBL positive ST131 strains selected from a diverse (n=184) ST131 bacteremia cohort had detectable ertapenem (ETP) mutational frequencies with a statistically positive correlation between initial ESBL gene copy number and mutation frequency (r = 0.87, P<1e-5). WGS analysis of mutants showed initial response to ETP exposure resulted in significant increases in ESBL gene copy numbers or mutations in outer membrane porin (Omp) encoding genes in the absence of ESBL gene amplification with subclade specific adaptations. In both experimental evolutionary platforms, MB1860 responded to initial ETP exposure by increasing blaCTX-M-15 copy numbers via modular, insertion sequence 26 (IS26) mediated pseudocompound transposons (PCTns). Transposase activity driven by PCTn upregulation was a conserved expression signal in both experimental evolutionary platforms. Stable mutations in Omp encoding genes were detected only after prolonged increasing carbapenem exposure consistent with clinical observations. Conclusions: ESBL gene amplification is a conserved response to initial carbapenem exposure, especially within the high-risk ST131 C2 subclade. Targeting such amplification could assist with mitigating carbapenem resistance development.

2024-08-04 | GSE273456 | GEO

Escherichia coli strain:ST131 C2/H30Rx

Project description:Escherichia coli strain:ST131 C2/H30Rx Genome sequencing and assembly

| PRJNA1141466 | ENA

Agrobacterium (Rhizobium) spp. nosocomial outbreak

Project description:Agrobacterium spp. nosocomial outbreak assessment using rapid MALDI-TOF MS based typing, confirmed by whole genome sequencing

| PRJEB34002 | ENA

A Nosocomial Respiratory Infection Outbreak of Carbapenem-Resistant Escherichia coli ST131 With Multiple Transmissible bla KPC-2 Carrying Plasmids.

Project description:Escherichia coli sequence type 131 (ST131) is well known for its multidrug resistance profile. Carbapenems have been considered the treatment of choice for E. coli ST131 infections, and resistance to carbapenems is emerging due to the acquisition of carbapenemase-encoding genes. In this study, 45 carbapenem-resistant E. coli strains were collected in a hospital. The resistance mechanisms, plasmid profiles, and genetic relatedness of these strains were determined. Phylogenetic relationships between these strains were assessed by molecular profiling and aligned with patient clinical details. The genetic context of bla KPC-2 was analyzed to trace the potential dissemination of bla KPC-2. The 45 carbapenem-resistant E. coli ST131 strains were closely related. Initially prevalent only in a single ward, ST131 subsequently spread to other ward, resulting in a respiratory infection outbreak of carbapenem-resistant E. coli ST131. Eight of the 30 patients died within 28 days of the first isolation of E. coli ST131. The bla KPC-2-positive plasmid profiles suggest that the carbapenem resistance was due to the acquisition by E. coli ST131 of transmissible plasmids pE0272_KPC and pE0171_KPC carrying bla KPC-2. Additionally, diverse multidrug resistance elements were transferred and rearranged between these plasmids mediated by IS26. Our research indicates that clinical attention should be paid to the importance of E. coli ST131 in respiratory infections and the spread of bla KPC -carrying E. coli ST131.

| S-EPMC7516988 | biostudies-literature

Differentially expressed genes in KPC Cxcr2 KO vs KPC mouse PDAC

Project description:Recently, Bailey et al (2016, Nature) defined four subtypes of pancreatic cancer that are associated with distinct histopathological characteristics and differential survival, namely, Squamous, Pancreatic Progenitor, Immunogenic, and ADEX (Aberrantly Differentiated Endocrine eXocrine). We set out to assess by RNASeq whether loss of CXCR2 was significantly associated with a specific PDAC subtype. Pancreatic tumors were harvested from KPC or KPC Cxcr2-/- mice at endpoint (n=5 v 5), RNA prepared, and RNASeq analysis carried out. Reads were analysed using the bcbio-nextgen framework (https://bcbio-nextgen.readthedocs.org/en/latest/). After quality control and adaptor trimming, reads were aligned to the mouse genome build (UCSC mouse mm10) using STAR. Counts for known genes were generated using the function featureCounts in the R/Bioconductor package \Rsubread\. The R/Bioconductor package edgeR was used to identify differentially expressed genes.

2018-03-31 | E-MTAB-4659 | biostudies-arrayexpress

antigenic KPC model_bulk pancreas RNASeq

Project description:We report the application of bulk RNAseq of live cells from pancreas of KPC or KPC-OG genetic mice at 6 weeks of age. These sponteneous tumors were unperturbed otherwise until timepoint.

2020-01-01 | GSE131602 | GEO

Mouse KPC cell secreted extracellular vesicle LC-MSMS

Project description:For Mouse KPC cell secreted extracellular vesicle LC-MSMS, extracellular vesicles in Alkbh5-WT or Alkbh5-KO KPC cell culture medium were isolated by ultracentrifugation. The protein and its levels in extracellular vesicle were determined through LC-MSMS.

2025-03-26 | PXD061967 | Pride

Project description:Escherichia coli ST131 H30Rx of diverse origin

| PRJNA748602 | ENA

RNA seq of C57B6 mice KPC tumor treated with IKE and 10A3

Project description:Test the efficacy of IKE (imidazole ketone) and 10A3 (5-Ethyl-3-(4-methoxybenzyl)-1,3,5-thiadiazinane-2-thione) on KPC tumors from C57B6 mice. Tumors generated by subcutaneous injection of KPC cells were allowed to reach a size of 80-100 mm3. Mice were randomly assigned to four groups and administered 10A3 (20 mg/kg, intraperitoneal, on days 4, 6, 8, 10, 12, 14, and 16) either alone or in combination with IKE (40 mg/kg, intraperitoneal, on days 4, 8, 12, and 16).

2025-01-03 | E-MTAB-13371 | biostudies-arrayexpress

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