Conjugation of Virulence Plasmid in Clinical <i>Klebsiella pneumoniae</i> Strains through Formation of a Fusion Plasmid

Xie, Miaomiao; Chen, Kaichao; Ye, Lianwei; Yang, Xuemei; Xu, Qi; Yang, Chen; Dong, Ning; Chan, Edward Wai-Chi; Sun, Qiaoling; Shu, Lingbin; Gu, Danxia; Lin, Xiaodong; Zhang, Rong; Chen, Sheng

doi:10.1002/adbi.201900239

Cited by 55 publications

(40 citation statements)

References 33 publications

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“…The larger plasmid, pMS3802-CTXM-vir, belonged to the incompatibility group IncHI1B, and it is an example of hybrid resistance/virulence plasmid. Hybrid plasmids containing both drug-resistance and virulence-related genes have been recently described [ 23 , 32 , 33 , 34 , 35 ]. pMS3802-CTXM-vir carried a second copy of the bla CTX-M-15 gene within the same gene arrangement as the one located in the chromosome IS 26 -Tn 3 - wbuC - bla CTX-M-15 -IS Ec9 ( Figure 2 A), indicating that bla CTX-M-15 was acquired as a result of activities of these mobile genetic elements (MGEs).…”

Section: Resultsmentioning

confidence: 99%

First Report of an Extensively Drug-Resistant ST23 Klebsiella pneumoniae of Capsular Serotype K1 Co-Producing CTX-M-15, OXA-48 and ArmA in Spain

et al. 2021

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An extensively drug-resistant (XDR) Klebsiella pneumoniae isolate MS3802 from a tracheostomy exudate was whole-genome sequenced using MiSeq and Oxford Nanopore MinION platforms in order to identify the antimicrobial resistance and virulence determinates and their genomic context. Isolate MS3802 belonged to the clone ST23 and presented a capsular serotype K1, associated with hypervirulent K. pneumoniae (hvKp) isolates. The isolate harboured a chromosomally encoded blaCTX-M-15 gene and contained a large IncHI1B hybrid virulence/resistance plasmid carrying another copy of the blaCTX-M-15 and the virulence factors iucABCD-iutA, iroBCDN, rmpA and rmpA2. The carbapenemase gene blaOXA-48 was found in a Tn1999-like transposon and the 16S rRNA methylase armA gen located in the vicinity of other antibiotic-resistant genes on an IncM2 plasmid. This study represents, to the best of our knowledge, the first description of a blaCTX-M-15-, blaOXA-48- and armA-harbouring K. pneumoniae of ST23 and capsular serotype K1 in Spain. Our report emphasizes the importance of implementing new surveillance strategies to monitor the risk of emergence and spread of such XDR and hypervirulent K. pneumoniae isolates.

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Section: Resultsmentioning

confidence: 99%

First Report of an Extensively Drug-Resistant ST23 Klebsiella pneumoniae of Capsular Serotype K1 Co-Producing CTX-M-15, OXA-48 and ArmA in Spain

et al. 2021

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“…discovered such a hybrid plasmid in a clinical Klebsiella variicola strain and confirmed its self-transferable ability [ 15 ]. Another study observed homologous recombination between a virulence plasmid and an IncF1A plasmid in a clinical K. pneumoniae strain, which yielded a conjugative hybrid plasmid [ 16 ]. Li et al .…”

Section: Introductionmentioning

confidence: 99%

Mobilization of the nonconjugative virulence plasmid from hypervirulent Klebsiella pneumoniae

Zhang

Wang

et al. 2021

Genome Med

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Background Klebsiella pneumoniae, as a global priority pathogen, is well known for its capability of acquiring mobile genetic elements that carry resistance and/or virulence genes. Its virulence plasmid, previously deemed nonconjugative and restricted within hypervirulent K. pneumoniae (hvKP), has disseminated into classic K. pneumoniae (cKP), particularly carbapenem-resistant K. pneumoniae (CRKP), which poses alarming challenges to public health. However, the mechanism underlying its transfer from hvKP to CRKP is unclear. Methods A total of 28 sequence type (ST) 11 bloodstream infection-causing CRKP strains were collected from Ruijin Hospital in Shanghai, China, and used as recipients in conjugation assays. Transconjugants obtained from conjugation assays were confirmed by XbaI and S1 nuclease pulsed-field gel electrophoresis, PCR detection and/or whole-genome sequencing. The plasmid stability of the transconjugants was evaluated by serial culture. Genetically modified strains and constructed mimic virulence plasmids were employed to investigate the mechanisms underlying mobilization. The level of extracellular polysaccharides was measured by mucoviscosity assays and uronic acid quantification. An in silico analysis of 2608 plasmids derived from 814 completely sequenced K. pneumoniae strains available in GenBank was performed to investigate the distribution of putative helper plasmids and mobilizable virulence plasmids. Results A nonconjugative virulence plasmid was mobilized by the conjugative plasmid belonging to incompatibility group F (IncF) from the hvKP strain into ST11 CRKP strains under low extracellular polysaccharide-producing conditions or by employing intermediate E. coli strains. The virulence plasmid was mobilized via four modes: transfer alone, cotransfer with the conjugative IncF plasmid, hybrid plasmid formation due to two rounds of single-strand exchanges at specific 28-bp fusion sites or homologous recombination. According to the in silico analysis, 31.8% (242) of the putative helper plasmids and 98.8% (84/85) of the virulence plasmids carry the 28-bp fusion site. All virulence plasmids carry the origin of the transfer site. Conclusions The nonconjugative virulence plasmid in ST11 CRKP strains is putatively mobilized from hvKP or E. coli intermediates with the help of conjugative IncF plasmids. Our findings emphasize the importance of raising public awareness of the rapid dissemination of virulence plasmids and the consistent emergence of hypervirulent carbapenem-resistant K. pneumoniae (hv-CRKP) strains.

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“…Most importantly, these non-K1/K2 CR-HvKP strains, in particular the ST11 type of CR-HvKP, have quickly spread throughout China and severely undermined infection control effort. Recent studies reported the transmission of non-conjugative virulence plasmid through forming a conjugative fusion plasmid with a conjugative helper plasmid, while there is still lack of direct evidence of transmission of virulence from K1/K2 K. pneumoniae strains 31 , 32 . Our study revealed the process of transmission of the virulence plasmid from K2 HvKP to non-K1/K2 K. pneumoniae , generating non-K1/K2 CR-HvKP.…”

Section: Discussionmentioning

confidence: 99%

Clinical evolution of ST11 carbapenem resistant and hypervirulent Klebsiella pneumoniae

Xie

Yang

et al. 2021

Commun Biol

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Carbapenem-resistant and hypervirulent K. pneumoniae (CR-HvKP) strains that have emerged recently have caused infections of extremely high mortality in various countries. In this study, we discovered a conjugative plasmid that encodes carbapenem resistance and hypervirulence in a clinical ST86 K2 CR-HvKP, namely 17ZR-91. The conjugative plasmid (p17ZR-91-Vir-KPC) was formed by fusion of a non-conjugative pLVPK-like plasmid and a conjugative blaKPC-2-bearing plasmid and is present dynamically with two other non-fusion plasmids. Conjugation of p17ZR-91-Vir-KPC to other K. pneumoniae enabled them to rapidly express the carbapenem resistance and hypervirulence phenotypes. More importantly, genome analysis provided direct evidence that p17ZR-91-Vir-KPC could be directly transmitted from K2 CR-HvKP strain, 17ZR-91, to ST11 clinical K. pneumoniae strains to convert them into ST11 CR-HvKP strains, which explains the evolutionary mechanisms of recently emerged ST11 CR-HvKP strains.

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Conjugation of Virulence Plasmid in Clinical Klebsiella pneumoniae Strains through Formation of a Fusion Plasmid

Cited by 55 publications

References 33 publications

First Report of an Extensively Drug-Resistant ST23 Klebsiella pneumoniae of Capsular Serotype K1 Co-Producing CTX-M-15, OXA-48 and ArmA in Spain

First Report of an Extensively Drug-Resistant ST23 Klebsiella pneumoniae of Capsular Serotype K1 Co-Producing CTX-M-15, OXA-48 and ArmA in Spain

Mobilization of the nonconjugative virulence plasmid from hypervirulent Klebsiella pneumoniae

Clinical evolution of ST11 carbapenem resistant and hypervirulent Klebsiella pneumoniae

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