First report of blaVEB-3 and blaKPC-2 coexistence with a novel blaKPC-2 transposon in Klebsiella michiganensis

IF 2.6 4区 医学 Q3 INFECTIOUS DISEASES
Yuxia Zhong , Peibo Yuan , Liting Dai , Ling Yang , Zhenbo Xu , Dingqiang Chen
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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.
blaVEB-3和blaKPC-2与一个新的blaKPC-2转座子共存的首次报道。
背景:密歇根克雷伯菌(Klebsiella michiganensis)是一种新兴的机会致病菌,由于其对碳青霉烯类多药耐药性(MDR)的增加,对公共卫生构成了威胁。病例与方法:一名46岁男性肺纤维化患者因肺炎恶化在中国广州住院。治疗前痰中分离出一株耐多药的密歇根乳杆菌(YK6)。采用MALDI-TOF质谱法、抗菌药敏试验(AST)和全基因组测序(WGS)对菌株进行鉴定。AST引导下的靶向治疗成功解决了感染。结果:除粘菌素和替加环素外,YK6菌株对碳青霉烯类、β-内酰胺/β-内酰胺酶抑制剂、头孢菌素、氨基糖苷类和喹诺酮类药物均有耐药性。基因组分析显示染色体上有41.9 kb的MDR岛和完整的I-E CRISPR-Cas系统,以及两个质粒:IncFIA/IncFII质粒pYK6-1携带blaKPC-2, IncC质粒pYK6-2携带blaVEB-3。在pYK6-1中发现了一个新的blakpc -2转座子,由一个非tn4401元件(NTE)样结构(Tn3-ISKpn27-blaKPC-2-ΔISKpn6-korC)组成,两侧是一个反向定向的ISKpn19-tnpM-tnpR元件和31 bp的倒置重复序列,这是一个以前没有报道过的配置。此外,pYK6-2中的blaVEB-3遗传环境具有独特的卡带:IS26-IS6100-blaVEB-3-tnp-ISAs1-qacEΔ1-sul1-ISCR1。在tnpf样整合酶和qacEΔ1之间额外的ISAs1插入将其与类似的blaveb -3- harbase区分开来。pYK6-2的blaVEB-3抗性区可能源于基因盒两侧的IS26和Tn5403介导的同源重组。结论:据我们所知,这是首次报道在k.m akanensis中同时存在blaVEB-3和blaKPC-2,以及一个新的blaKPC-2转座子结构。这些发现强调迫切需要加强对耐多药密歇根乳杆菌的监测,以防止治疗失败。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Infection Genetics and Evolution
Infection Genetics and Evolution 医学-传染病学
CiteScore
8.40
自引率
0.00%
发文量
215
审稿时长
82 days
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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