Evidence map›Paper›PMID 41714956›Full record

ArticleBMC genomics2026

Shifting of bla

Dakang Hu, Yuanxun Zhao, Shuli Mi, Shijie Wang, Jin Zhang, Xinhua Luo, Dan Li, Jin Chen, Guolin Hong

Abstract read
In one paragraph

Article in BMC genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Dakang Hu *Department of Laboratory Medicine, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University,, Taizhou, Zhejiang, 318000, China.
Yuanxun Zhao *Department of Clinical Laboratory, The First Affiliated Hospital of Xiamen University (Xiamen Key Laboratory of Genetic Testing), Xiamen, Fujian, 361003, China.
Shuli Mi *Cixi Biomedical Research Institute, Wenzhou Medical University, Ningbo, Zhejiang, 315300, China.
Shijie WangDepartment of Clinical Laboratory, Xiamen Humanity Hospital Fujian Medical University, Xiamen, Fujian, 361000, China.
Jin ZhangDepartment of Laboratory Medicine, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University,, Taizhou, Zhejiang, 318000, China.
Xinhua LuoDepartment of Laboratory Medicine, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University,, Taizhou, Zhejiang, 318000, China.
Dan LiInstitute of Antibiotics, Huashan Hospital, Fudan University, Shanghai, 200000, China.
Jin ChenDepartment of Pediatrics, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University, Taizhou, Zhejiang, 318000, China. 13738618227@163.com.
Guolin HongDepartment of Clinical Laboratory, The First Affiliated Hospital of Xiamen University (Xiamen Key Laboratory of Genetic Testing), Xiamen, Fujian, 361003, China. xmhgl9899@xmu.edu.cn.

Funding

National Natural Science Foundation of China 82371200Zhejiang Medical and Health Research Program 2023KY1326
6 · The paper itself

Abstract

backgroundKlebsiella pneumoniae continues to be a problem worldwide. This study aimed to elucidate the evolution of a K. pneumoniae strain from harbouring blaKPC−2 to blaKPC−90.

methodsThree K. pneumoniae strains (Kpn_XM11, Kpn_XM12, and Kpn_XM13) belonging to the same clone were isolated from a patient, followed by identification, antimicrobial susceptibility test, whole genome sequencing, and gene mutations.

resultsKpn_XM11 and Kpn_XM12 strains harbouring blaKPC−2 were resistant to carbapenems but susceptible to ceftazidime-avibactam (CZA) while Kpn_XM13 possessing blaKPC−90 was resistant to CZA but susceptible to imipenem. Compared to KPC-2, KPC-90 was a variant with an insertion of two amino acids (180 ins Tyr-Thr), which is structurally located between the α7 helix and α8 helix of KPC. The genetic structures of blaKPC in three strains were identified as IS26-ISKpn27-blaKPC-ISKpn6-IS26. Mutation of blaKPC−2 into blaKPC−90 in Kpn_XM11 conferred similar drug-resistance phenotype as that of Kpn_XM13. Deletion of blaKPC−2 in Kpn_XM11 and blaKPC−90 in Kpn_XM13 exerted susceptibility against CZA but retained carbapenem resistance. Kpn_XM11 to Kpn_XM13 possessed ompK35 but couldn’t yield OmpK35; in addition, they all presented R935H mutation in RecC. The plasmids carrying blaKPC−2 or blaKPC−90 could both be mated at ratios of a 10− 8 level.

conclusionsIt is of great concern that blaKPC−2 may evolve into other subtypes, conferring distinguished drug-resistance phenotype, even before the use of CZA, which may be associated with R935H mutation in RecC. Advanced methods are essential under such conditions so as to find out slight nucleotide differences and control infections efficiently.

Indexed as

Azabicyclo CompoundsBacterial Proteinsbeta-LactamasesCeftazidimeKlebsiella pneumoniaeAnti-Bacterial AgentsCarbapenemsDrug CombinationsHumansKlebsiella InfectionsMicrobial Sensitivity TestsMutationWhole Genome SequencingAnti-Bacterial Agentsavibactam, ceftazidime drug combinationAzabicyclo CompoundsBacterial Proteinsbeta-lactamase KPC-2, Klebsiella pneumoniaebeta-LactamasesCarbapenemsCeftazidimeDrug CombinationsCarbapenem resistanceKlebsiella pneumoniaeWithin-host adaptationβ-lactamase evolution

Identifiers

PMID41714956
PMCPMC13023152

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.