{"title":"First report of bla<sub>VEB-3</sub> and bla<sub>KPC-2</sub> coexistence with a novel bla<sub>KPC-2</sub> transposon in Klebsiella michiganensis.","authors":"Yuxia Zhong, Peibo Yuan, Liting Dai, Ling Yang, Zhenbo Xu, Dingqiang Chen","doi":"10.1016/j.meegid.2025.105740","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Klebsiella michiganensis, an emerging opportunistic pathogen, poses public health risks due to its increasing multidrug resistance (MDR), especially to carbapenems.</p><p><strong>Case and method: </strong>A 46-year-old man with pulmonary fibrosis was hospitalized in Guangzhou, China, for worsening pneumonia. A multidrug-resistant K. michiganensis strain (YK6) was isolated from his sputum before treatment. The strain was characterized using MALDI-TOF mass spectrometry, antimicrobial susceptibility testing (AST), and whole genome sequencing (WGS). Targeted therapy guided by AST successfully resolved the infection.</p><p><strong>Results: </strong>The YK6 strain exhibited resistance to carbapenems, β-lactam/β-lactamase inhibitors, cephalosporins, aminoglycosides, and quinolones, except colistin and tigecycline. Genomic analysis revealed a 41.9-kb MDR island and an intact I-E CRISPR-Cas system on the chromosome, along with two plasmids: IncFIA/IncFII plasmid pYK6-1 carrying bla<sub>KPC-2</sub> and IncC plasmid pYK6-2 harboring bla<sub>VEB-3</sub>. A novel bla<sub>KPC-2</sub>-transposon in pYK6-1 was identified, consisting of a non-Tn4401 element (NTE)-like structure (Tn3-ISKpn27-bla<sub>KPC-2</sub>-ΔISKpn6-korC) flanked by inversely oriented ISKpn19-tnpM-tnpR elements and 31-bp inverted repeats never reported, a configuration did not reported previously. Furthermore, the bla<sub>VEB-3</sub> genetic environment in pYK6-2 featured a unique cassette: IS26-IS6100-bla<sub>VEB-3</sub>-tnp-ISAs1-qacEΔ1-sul1-ISCR1. An additional ISAs1 insertion between the tnpF-like integrase and qacEΔ1 distinguishes it from similar bla<sub>VEB-3</sub>-harboring cassettes. The bla<sub>VEB-3</sub> resistance region in pYK6-2 likely originated from homologous recombination mediated by IS26 and Tn5403, which flank the gene cassette.</p><p><strong>Conclusions: </strong>To our knowledge, this is the first report of concurrent bla<sub>VEB-3</sub> and bla<sub>KPC-2</sub> in K. michiganensis, along with a novel bla<sub>KPC-2</sub> transposon structure. These findings highlight the urgent need for enhanced surveillance of MDR K. michiganensis to prevent treatment failures.</p>","PeriodicalId":54986,"journal":{"name":"Infection Genetics and Evolution","volume":" ","pages":"105740"},"PeriodicalIF":2.6000,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection Genetics and Evolution","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.meegid.2025.105740","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Klebsiella michiganensis, an emerging opportunistic pathogen, poses public health risks due to its increasing multidrug resistance (MDR), especially to carbapenems.
Case and method: A 46-year-old man with pulmonary fibrosis was hospitalized in Guangzhou, China, for worsening pneumonia. A multidrug-resistant K. michiganensis strain (YK6) was isolated from his sputum before treatment. The strain was characterized using MALDI-TOF mass spectrometry, antimicrobial susceptibility testing (AST), and whole genome sequencing (WGS). Targeted therapy guided by AST successfully resolved the infection.
Results: The YK6 strain exhibited resistance to carbapenems, β-lactam/β-lactamase inhibitors, cephalosporins, aminoglycosides, and quinolones, except colistin and tigecycline. Genomic analysis revealed a 41.9-kb MDR island and an intact I-E CRISPR-Cas system on the chromosome, along with two plasmids: IncFIA/IncFII plasmid pYK6-1 carrying blaKPC-2 and IncC plasmid pYK6-2 harboring blaVEB-3. A novel blaKPC-2-transposon in pYK6-1 was identified, consisting of a non-Tn4401 element (NTE)-like structure (Tn3-ISKpn27-blaKPC-2-ΔISKpn6-korC) flanked by inversely oriented ISKpn19-tnpM-tnpR elements and 31-bp inverted repeats never reported, a configuration did not reported previously. Furthermore, the blaVEB-3 genetic environment in pYK6-2 featured a unique cassette: IS26-IS6100-blaVEB-3-tnp-ISAs1-qacEΔ1-sul1-ISCR1. An additional ISAs1 insertion between the tnpF-like integrase and qacEΔ1 distinguishes it from similar blaVEB-3-harboring cassettes. The blaVEB-3 resistance region in pYK6-2 likely originated from homologous recombination mediated by IS26 and Tn5403, which flank the gene cassette.
Conclusions: To our knowledge, this is the first report of concurrent blaVEB-3 and blaKPC-2 in K. michiganensis, along with a novel blaKPC-2 transposon structure. These findings highlight the urgent need for enhanced surveillance of MDR K. michiganensis to prevent treatment failures.
期刊介绍：
(aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID)
Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance.
However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors.
Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases.
Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .
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