Project description:The study aimed to characterize plasmids mediating carbepenem resistance in Klebsiella pneumoniae in Pretoria, South Africa. We analysed 56 K. pneumoniae isolates collected from academic hospital around Pretoria. Based on phenotypic and molecular results of these isolates, 6 representative isolates were chosen for further analysis using long reads sequencing platform. We observed multidrug resistant phenotype in all these isolates, including resistance to aminoglycosides, tetracycline, phenicol, fosfomycin, floroquinolones, and beta-lactams antibiotics. The blaOXA-48/181 and blaNDM-1/7 were manily the plasmid-mediated carbapenemases responsible for carbapenem resistance in the K. pneumoniae isolates in these academic hospitals. These carbapenemase genes were mainly associated with plasmid replicon groups IncF, IncL/M, IncA/C, and IncX3. This study showed plasmid-mediated carbapenemase spread of blaOXA and blaNDM genes mediated by conjugative plasmids in Pretoria hospitals.
2019-10-17 | GSE138949 | GEO
Project description:carbapenemase encoding plasmids from multiple species Genome sequencing and assembly
Project description:This experiment aimed to characterise transcriptomes of plasmid-based mouse models of liver cancer, hepatotoxin-induced chronic liver injury and the combination thereof. In detail, C57BL/6JAusb mice received hydrodynamic tail vein injection (HTVI) of plasmids encoding Sleeping Beauty transposase (SB), alone or in combination with transposon plasmids encoding myristylated AKT1 (AKT), c-Met and NRasV12 (NRas), previously characterised by Ho et al. (2012) (Hepatology 55(3):833-45) and Hu et al. (2016) (Sci Rep 6:20484). 8-10 days post-HTVI, mice began biweekly intraperitoneal (i.p.) injections of saline or the hepatotoxin thioacetamide (TAA), 10-11 doses.
Project description:Plasmid fitness is directed by two orthogonal processes—vertical transfer through cell division and horizontal transfer through conjugation. When considered individually, improvements in either mode of transfer can promote how well a plasmid spreads and persists. Together, however, the metabolic cost of conjugation could create a tradeoff that constrains plasmid evolution. Here we present evidence for the presence, consequences, and molecular basis of a conjugation-growth tradeoff across 40 plasmids derived from clinical E. coli pathogens. We discover that most plasmids operate below a conjugation efficiency threshold for major growth effects, indicating strong natural selection for vertical transfer. Below this threshold, E. coli demonstrates a remarkable growth tolerance to over four orders of magnitude change in conjugation efficiency. This tolerance fades as nutrients become scarce and horizontal transfer attracts a greater share of host resources. Our results provide insight into evolutionary constraints directing plasmid fitness and strategies to combat the spread of antibiotic resistance.
Project description:An incompatibility P-7 plasmid pCAR1 can be efficiently transferred among artificial microcosms in the presence of divalent cations Ca2+ and Mg2+. One on one mating assays between Pseudomonas strains with different plasmids showed that the promotion of transfer efficiency by divalent cations was also found in other plasmids including pB10 and NAH7, whereas the impacts were larger in IncP-7 plasmids. The impact on pCAR1 transfer altered by different pairs of donor and recipient strains, and the promotion of transfer efficiency was clearly detected between donors P. resinovorans CA10dm4 and P. fluorescens Pf0-1 to the recipients P. putida KT2440 and CA10dm4. Transcriptome analyses showed that genes on the pCAR1 did not respond to the presence of cations, including the tra/trh genes involved in its transfer. Notably, transcriptions of oprH genes, encoding a putative outer membrane proteins, in both of donor and recipient were commonly upregulated under the cation-limited condition. Transfer frequency of the pCAR1 to the transposon mutant of oprH in KT2440 was not promoted by the cations. This effect was partially recovered by the complementation with oprH gene, suggesting that OprH is involved in the promotion the pCAR1 transfer by divalent cations.