A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China

Zhou, Kai1; Xue, Chun-Xu L.1; Xu, Tingting1; Shen, Ping2; Wei, Sha1; Wyres, Kelly3; Lam, Margaret M. C. E.3; Liu, Jinquan1; Lin, Haoyun4; Chen, Yunbo2,6; Holt, Kathryn3,5; Ding, Hui7; Liu, Yongyun8; Mao, Haifeng9; Huang, Ying10; Yang, Zhenghai; Dai, Yuanyuan; Liao, Guolin; Zhu, Lisha; Zhang, Liping; Li, Yanhong; Xu, Hongyun; Cao, Junmin; Zhang, Baohua; Guo, Liang; Dong, Haixin; Hu, Shuyan; Man, Sijin; Wang, Lu; Liao, Zhixiang; Xu, Rong; Liu, Dan; Jin, Yan; Zhou, Yizheng; Liao, Yiqun; Chen, Fenghong; Gu, Beiqing; Wang, Jiliang; Liang, Jinhua; Zheng, Lin; Li, Aiyun; Shen, Jilu; Dong, Yinqiao; Zhang, Lixia; Hu, Hongxia; Quan, Bo; Zhu, Wencheng; Liang, Kunpeng; Liu, Qiang; Wang, Shifu; Yan, Xiaoping; Kang, Jiangbang; Xia, Xiusan; Ma, Lan; Sun, Li; Luan, Liang; Wang, Jianzhong; Li, Zhuo; Qiao, Dengyan; Zhang, Lin; Wan, Chuandan; Qi, Xiaoyan; Du, Fei; Xiao, Yonghong2

2023-04-28

10.1038/s41467-023-38061-z

NATURE COMMUNICATIONS   Impact Factor & Quartile

2041-1723

["Adaptation to selective pressures is crucial for clinically important pathogens to establish epidemics, but the underlying evolutionary drivers remain poorly understood. The current epidemic of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a significant threat to public health. In this study we analyzed the genome sequences of 794 CRKP bloodstream isolates collected in 40 hospitals in China between 2014 and 2019. We uncovered a subclonal replacement in the predominant clone ST11, where the previously prevalent subclone OL101:KL47 was replaced by O2v1:KL64 over time in a stepwise manner. O2v1:KL64 carried a higher load of mobile genetic elements, and a point mutation exclusively detected in the recC of O2v1:KL64 significantly promotes recombination proficiency. The epidemic success of O2v1:KL64 was further associated with a hypervirulent sublineage with enhanced resistance to phagocytosis, sulfamethoxazole-trimethoprim, and tetracycline. The phenotypic alterations were linked to the overrepresentation of hypervirulence determinants and antibiotic genes conferred by the acquisition of an rmpA-positive pLVPK-like virulence plasmid and an IncFII-type multidrug-resistant plasmid, respectively. The dissemination of the sublineage was further promoted by more frequent inter-hospital transmission. The results collectively demonstrate that the expansion of O2v1:KL64 is correlated to a repertoire of genomic alterations convergent in a subpopulation with evolutionary advantages.","Authors carry out a genomic analysis of carbapenem-resistant Klebsiella pneumoniae bloodstream isolates, noting subclonal expansion, associated with the emergence of a hypervirulent subpopulation."]

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First ; Corresponding

National Key R&D Program of China["2021YFC2300300","2022YFE0103200"] ; National Natural Science Foundation of China["81902030","81971984","82172330"] ; China Postdoctoral Science Foundation[2022M712187] ; Shenzhen Basic Research Key projects[JCYJ20200109144220704] ; Shenzhen Basic Research projects[JCYJ20190807144409307] ; Fundamental Research Funds for the Central Universities[2022ZFJH003] ; Research Project of Jinan Microecological Biomedicine Shandong Laboratory[JNL-2022027C]

Science & Technology - Other Topics

Multidisciplinary Sciences

WOS:000983415900001

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42.Luan Civily Hosp, Luan, Peoples R China
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44.Henan Univ, Huaihe Hosp, Kaifeng, Peoples R China
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Zhou, Kai,Xue, Chun-Xu L.,Xu, Tingting,et al. A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China[J]. NATURE COMMUNICATIONS,2023,14(1).

Zhou, Kai.,Xue, Chun-Xu L..,Xu, Tingting.,Shen, Ping.,Wei, Sha.,...&Xiao, Yonghong.(2023).A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China.NATURE COMMUNICATIONS,14(1).

Zhou, Kai,et al."A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China".NATURE COMMUNICATIONS 14.1(2023).