The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient

Hypervirulent Klebsiella pneumoniae (hvKp) is a major pathogen causing community-acquired infections, particularly severe diseases such as liver abscesses. Although extensive research has been conducted on the virulence mechanisms of hvKp and the genetic properties of resistance plasmids, studies on...

Full description

Saved in:
Bibliographic Details
Main Authors: Gaoqin Teng, Qiuying Qin, Shuo Ding, Yanchao Wu, Yingying Fu, Meng Zhang, Xiaoqiang Yang, Ye Jin, Zhijiang Xu, Man Huang
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-05-01
Series:Frontiers in Microbiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fmicb.2025.1577629/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850137425937956864
author Gaoqin Teng
Gaoqin Teng
Qiuying Qin
Qiuying Qin
Shuo Ding
Shuo Ding
Yanchao Wu
Yanchao Wu
Yingying Fu
Meng Zhang
Xiaoqiang Yang
Ye Jin
Ye Jin
Zhijiang Xu
Zhijiang Xu
Man Huang
Man Huang
author_facet Gaoqin Teng
Gaoqin Teng
Qiuying Qin
Qiuying Qin
Shuo Ding
Shuo Ding
Yanchao Wu
Yanchao Wu
Yingying Fu
Meng Zhang
Xiaoqiang Yang
Ye Jin
Ye Jin
Zhijiang Xu
Zhijiang Xu
Man Huang
Man Huang
author_sort Gaoqin Teng
collection DOAJ
description Hypervirulent Klebsiella pneumoniae (hvKp) is a major pathogen causing community-acquired infections, particularly severe diseases such as liver abscesses. Although extensive research has been conducted on the virulence mechanisms of hvKp and the genetic properties of resistance plasmids, studies on the adaptive evolution of clinical strains within the host are still limited. This study aimed to investigate the impact of genetic mutations on phenotypic changes in high-virulence K. pneumoniae within a host environment. We isolated three strains of K. pneumoniae from the same patient, two of which had identical genetic backgrounds but exhibited distinct phenotypic traits. Comparative genomic analysis was performed to identify genetic differences. A nucleotide mutation in the wzc gene was identified as a potential factor associated with changes in the mucoid phenotype. This mutation was verified using string tests and anti-centrifugal assays. Additionally, in vivo bioassays and animal infection models were conducted to further validate the findings. The comparative genomic analysis revealed a nucleotide mutation in the wzc gene, which was associated with changes in the mucoid phenotype of the strain. This was confirmed through string tests and anti-centrifugal assays. In vivo experiments and animal infection models suggested that hvKp adapts to the host by reducing capsular polysaccharide synthesis, thereby trading off some virulence for enhanced colonization capabilities. Our findings indicate that genetic mutations in hvKp can lead to significant phenotypic changes that facilitate adaptation within the host. The observed reduction in capsular polysaccharide synthesis appears to be a trade-off between virulence and colonization ability. This study provides insights into the adaptive evolution of hvKp and highlights the importance of considering intrahost genetic changes when studying the pathogenesis of hvKp. Future research should focus on further elucidating the mechanisms underlying these adaptations and their clinical implications.
format Article
id doaj-art-c626fd9336734b5587b8a55a97eebca0
institution OA Journals
issn 1664-302X
language English
publishDate 2025-05-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Microbiology
spelling doaj-art-c626fd9336734b5587b8a55a97eebca02025-08-20T02:30:50ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2025-05-011610.3389/fmicb.2025.15776291577629The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patientGaoqin Teng0Gaoqin Teng1Qiuying Qin2Qiuying Qin3Shuo Ding4Shuo Ding5Yanchao Wu6Yanchao Wu7Yingying Fu8Meng Zhang9Xiaoqiang Yang10Ye Jin11Ye Jin12Zhijiang Xu13Zhijiang Xu14Man Huang15Man Huang16Department of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaDepartment of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaDepartment of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, ChinaDepartment of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, ChinaDepartment of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, ChinaKey Laboratory of Multiple Organ Failure (Zhejiang University), Ministry of Education, Zhejiang, ChinaHypervirulent Klebsiella pneumoniae (hvKp) is a major pathogen causing community-acquired infections, particularly severe diseases such as liver abscesses. Although extensive research has been conducted on the virulence mechanisms of hvKp and the genetic properties of resistance plasmids, studies on the adaptive evolution of clinical strains within the host are still limited. This study aimed to investigate the impact of genetic mutations on phenotypic changes in high-virulence K. pneumoniae within a host environment. We isolated three strains of K. pneumoniae from the same patient, two of which had identical genetic backgrounds but exhibited distinct phenotypic traits. Comparative genomic analysis was performed to identify genetic differences. A nucleotide mutation in the wzc gene was identified as a potential factor associated with changes in the mucoid phenotype. This mutation was verified using string tests and anti-centrifugal assays. Additionally, in vivo bioassays and animal infection models were conducted to further validate the findings. The comparative genomic analysis revealed a nucleotide mutation in the wzc gene, which was associated with changes in the mucoid phenotype of the strain. This was confirmed through string tests and anti-centrifugal assays. In vivo experiments and animal infection models suggested that hvKp adapts to the host by reducing capsular polysaccharide synthesis, thereby trading off some virulence for enhanced colonization capabilities. Our findings indicate that genetic mutations in hvKp can lead to significant phenotypic changes that facilitate adaptation within the host. The observed reduction in capsular polysaccharide synthesis appears to be a trade-off between virulence and colonization ability. This study provides insights into the adaptive evolution of hvKp and highlights the importance of considering intrahost genetic changes when studying the pathogenesis of hvKp. Future research should focus on further elucidating the mechanisms underlying these adaptations and their clinical implications.https://www.frontiersin.org/articles/10.3389/fmicb.2025.1577629/fullhypervirulent Klebsiella pneumoniaevirulencewzccapsular polysaccharidemucoid
spellingShingle Gaoqin Teng
Gaoqin Teng
Qiuying Qin
Qiuying Qin
Shuo Ding
Shuo Ding
Yanchao Wu
Yanchao Wu
Yingying Fu
Meng Zhang
Xiaoqiang Yang
Ye Jin
Ye Jin
Zhijiang Xu
Zhijiang Xu
Man Huang
Man Huang
The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
Frontiers in Microbiology
hypervirulent Klebsiella pneumoniae
virulence
wzc
capsular polysaccharide
mucoid
title The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
title_full The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
title_fullStr The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
title_full_unstemmed The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
title_short The wzc mutation mediates virulence changes in K1-type Klebsiella pneumoniae within the same patient
title_sort wzc mutation mediates virulence changes in k1 type klebsiella pneumoniae within the same patient
topic hypervirulent Klebsiella pneumoniae
virulence
wzc
capsular polysaccharide
mucoid
url https://www.frontiersin.org/articles/10.3389/fmicb.2025.1577629/full
work_keys_str_mv AT gaoqinteng thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT gaoqinteng thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT qiuyingqin thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT qiuyingqin thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT shuoding thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT shuoding thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yanchaowu thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yanchaowu thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yingyingfu thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT mengzhang thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT xiaoqiangyang thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yejin thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yejin thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT zhijiangxu thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT zhijiangxu thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT manhuang thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT manhuang thewzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT gaoqinteng wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT gaoqinteng wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT qiuyingqin wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT qiuyingqin wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT shuoding wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT shuoding wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yanchaowu wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yanchaowu wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yingyingfu wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT mengzhang wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT xiaoqiangyang wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yejin wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT yejin wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT zhijiangxu wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT zhijiangxu wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT manhuang wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient
AT manhuang wzcmutationmediatesvirulencechangesink1typeklebsiellapneumoniaewithinthesamepatient