Klebsiella pneumoniae
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ABSTRACT:
PROVIDER: PRJNA999179 | ENA |
REPOSITORIES: ENA
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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:Klebsiella pneumoniae is a prominent human pathogen that has developed resistance to multiple antibiotics. While the roles of capsules and siderophores are well established, the identification of additional virulence determinants remains limited. In this study, we hypothesize that the two-component system response regulator CpxR is integral to the regulation of K. pneumoniae virulence via control of specific virulence-associated genes. Deletion of the cpxR gene resulted in reduced serum resistance and attenuated virulence in both Galleria mellonella larvae and murine infection models compared to the wild-type strain. To elucidate the repertoire of virulence-associated genes regulated by CpxR, a multidisciplinary workflow was employed, integrating RNA sequencing, Real-Time quantitative PCR, gene knockout strategies, serum resistance assays, and infection experiments utilizing Galleria mellonella. Among the genes identified with significantly diminished expression following cpxR deletion, KPHS_28080 emerged as a novel candidate virulence-associated gene. Deletion of KPHS_28080 impaired serum survival in both the carbapenem-resistant CRKp HS11286 and the hypervirulent hvKp ATCC43816 strains. Furthermore, deletion of KPHS_28080 in hvKp ATCC43816 led to significantly decreased colonization and impaired dissemination to multiple organs in murine models, corresponding with an overall reduction in virulence. The promoter region of KPHS_28080 harbors a conserved CpxR binding motif, which enhances promoter activity and gene transcription upon CpxR binding. Sequence alignment revealed that KPHS_28080 encodes a member of the short-chain dehydrogenase family, and this gene is highly conserved among K. pneumoniae strains. These results elucidate the pivotal role of CpxR in mediating virulence in K. pneumoniae and clarify its regulatory impact on virulence-associated gene expression.
2025-07-10 | GSE300466 | GEO
Project description:Klebsiella pneumoniae poses a significant global health threat primarily attributable to its pronounced resistance. Here, we report an in vitro acquired resistance analyses of K. pneumoniae to the combination of amikacin and polymyxin B. We found some differentially expressed genes associated with the resistome of K. pneumoniae. The main differences were found in the genes aphA, asmA, phoP, and in the arn operon. Once these genes are related to modification in lipopolysaccharides, aminoglycosides and in the membrane structure, the mechanisms associated with them can justify the resistance acquisition to amikacin and polymyxin b.
2024-04-26 | GSE264574 | GEO
Project description:K. pneumoniae, a Gram-negative bacterium, is normally associated with pneumonia in patients with weakened immune systems. However, it is also a prevalent nosocomial infectious agent that can be found in infected surgical sites and combat wounds. Many of these clinical strains display multi-drug resistance. We have worked with a clinical strain of K. pneumoniae that was initially isolated from a wound of an injured soldier. This strain demonstrated resistance to many commonly used antibiotics, but sensitivity to carbapenems. This isolate was capable of forming biofilms in vitro, contributing to its increased antibiotic resistance and impaired clearance. We were interested in determining how sublethal concentrations of carbapenem treatment specifically affect K. pneumoniae biofilms both in morphology and genomic expression. Scanning electron microscopy showed striking morphological differences between untreated and treated biofilms, including rounding, blebbing, and dimpling of treated cells. Comparative transcriptome analysis using RNA sequencing technology identified a large number of open reading frames (ORFs) differentially regulated in response to carbapenem treatment at 2 and 24 hours. ORFs upregulated with carbapenem treatment included genes involved in resistance, antiporters, and autoinducers. ORFs downregulated included metal transporters, membrane biosynthesis proteins, and motility proteins. Quantitative real time PCR validated the general trend of some of these differentially regulated ORFs. Treating K. pneumoniae biofilms with sublethal concentrations of carbapenems induced a wide-range of phenotypic and gene expression changes. This study reveals some of the mechanisms underlying how sublethal amounts of carbapenems could affect the overall fitness and pathogenic potential of K. pneumoniae biofilm cells.
2015-01-01 | GSE62045 | GEO
Project description:Carbapenem-resistant Klebsiella pneumoniae classified as multilocus sequence type 258 (ST258)are a problem in healthcare settings in many countries globally. ST258 isolates are resistant tomultiple classes of antibiotics and can cause life-threatening infections, such as pneumonia andsepsis, in susceptible individuals. Treatment strategies for such infections are limited. Hence,understanding the response of K. pneumoniae to host factors in the presence of antibiotics couldreveal mechanisms employed by the pathogen to evade killing in the susceptible host, as well asinform treatment of infections. Here, we investigated the ability of subinhibitory concentrationsof antibiotics to alter K. pneumoniae capsule polysaccharide (CPS) production and survival innormal human serum. Several antibiotics tested enhanced ST258 survival in normal humanserum. Unexpectedly, subinhibitory concentrations of mupirocin increased survival in 7 of 10clinical isolates tested, and caused up-regulated expression of CPS biosynthesis genes and CPSproduction in a selected ST258 clinical isolate (34446) compared with untreated controls.Additionally, mupirocin treatment caused a reduction in the deposition of the serum complementproteins C3b and C5b-9 on the surface of ST258. Transcriptome analyses with isolate 34446indicated that genes implicated in serum resistance, such as aroE, csrD, pyrB, pyrC and traT,were up-regulated following mupirocin treatment. In conclusion, mupirocin causes changes inthe K. pneumoniae transcriptome that likely contribute to the observed decrease in serumsusceptibility via a multifactorial process. Whether these responses are triggered by othercomponents of host defense or therapeutics that were not tested here merits further investigation.
2022-10-12 | GSE201383 | GEO
Project description:Bacteria can circumvent the effect of antibiotics by transitioning to a poorly understood physiological state that does not involve conventional genetic elements of resistance. Here we examine antibiotic susceptibility with a Class A β-lactamase+ invasive strain of Klebsiella pneumoniae that was isolated from a lethal outbreak within laboratory colonies of Chlorocebus aethiops sabaeus monkeys. Bacterial responses to the ribosomal synthesis inhibitors streptomycin and doxycycline resulted in distinct proteomic adjustments that facilitated decreased susceptibility to each antibiotic.
2019-03-14 | PXD009175 | Pride
Project description:Bacteria can circumvent the effect of antibiotics by transitioning to a poorly understood physiological state that does not involve conventional genetic elements of resistance. Here we examine antibiotic susceptibility with a Class A β-lactamase+ invasive strain of Klebsiella pneumoniae that was isolated from a lethal outbreak within laboratory colonies of Chlorocebus aethiops sabaeus monkeys. Bacterial responses to the ribosomal synthesis inhibitors streptomycin and doxycycline resulted in distinct proteomic adjustments that facilitated decreased susceptibility to each antibiotic. Drug-specific changes to proteomes included proteins for receptor-mediated membrane transport and sugar utilization, central metabolism, and capsule production, while mechanisms common to both antibiotics included elevated scavenging of reactive oxygen species and turnover of misfolded proteins. Resistance to combined antibiotics presented integrated adjustments to protein levels as well as unique drug-specific proteomic features. Our results demonstrate that dampening of Klebsiella pneumoniae susceptibility involves global remodeling of the bacterial proteome to counter the effects of antibiotics and stabilize growth.
2019-03-14 | PXD010244 | Pride
Project description:Klebsiella pneumoniae is a leading cause of global deaths due to antibiotic resistance. Of particular concern, is the rapid expansion within K. pneumoniae lineages of resistance to beta-lactams, the most prescribed class of antibiotics. Additionally, the environmental factors that influence pathogen physiology and, subsequently, antibiotic resistance remain poorly understood. Here we demonstrate that physiologically-relevant drops in culture medium pH result in increased antibiotic resistance particularly towards beta-lactams that inhibit cell division. We identified two genes that contribute to acid-dependent beta-lactam resistance, the class A PBP, PBP1b, and the paralogous class B PBP, PBP3PARA. Loss of either gene increases K. pneumoniae susceptibility to beta-lactams at low pH. Our data suggests that functional redundancy among cell wall synthesis enzymes allows for specialization and ensures that cell wall synthesis occurs robustly across a range of pH conditions.
2025-03-17 | GSE291667 | GEO
Project description:The inappropriate use of antibiotics is a severe public health problem worldwide, contributing to the emergence of multidrug-resistant (MDR) bacteria. To explore the possible impacts of the inappropriate use of antibiotics on the immune system, we use Klebsiella pneumoniae (K. pneumoniae) infection as an example and show that imipenem increases the mortality of mice infected by MDR K. pneumoniae. Further studies demonstrate that imipenem enhances the secretion of outer membrane vesicles (OMVs) with significantly elevated presentation of GroEL, which promotes the phagocytosis of OMVs by macrophages that depends on the interaction between GroEL and its receptor LOX-1. OMVs cause the pyroptosis of macrophages and the release of proinflammatory cytokines, which contribute to exacerbated inflammatory responses. We propose that the inappropriate use of antibiotics in the cases of infection by MDR bacteria such as K. pneumoniae might cause damaging inflammatory responses, which underlines the pernicious effects of inappropriate use of antibiotic.
2021-08-28 | GSE182766 | GEO
Project description:MDR Klebsiella pneumoniae subsp. pneumoniae ST14 and ST15
| PRJNA408270 | ENA