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介导抗菌药物耐药性的移动遗传元件推动了艰难梭菌ST37/RT017的进化过程。

Mobile genetic elements mediating antimicrobial resistance drive the evolutionary process of Clostridioides difficile ST37/RT017.

作者信息

Lv Tao, Bi Xiajing, Zheng Lisi, Zhao Yuhong, Zhou Yizheng, Wu Tao, Shen Ping, Zhu Danhua, Chen Shiyao, Chen Yunbo

机构信息

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Department of nursing, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

出版信息

BMC Genomics. 2025 Jul 12;26(1):659. doi: 10.1186/s12864-025-11822-4.

DOI:10.1186/s12864-025-11822-4
PMID:40652164
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12255112/
Abstract

BACKGROUND

() ST37/RT017 is one of the most prevalent genotypes, exhibiting resistance to multiple antimicrobial agents and widespread dissemination, particularly in East Asia. However, its evolutionary history and genetic adaptation remains limited. Here, we aimed to systematically assess the genetic diversity, key evolutionary events, and potential driving forces of ST37/RT017.

RESULTS

To explored dynamic trends in the genomic characterization, diversity and changes, both phylogenetic and Bayesian evolutionary analyses revealed that the ST37/RT017 strains were clustered into three variant lineages as a directed bus-like topology, from VL I, to VL II, and VL III. An incremental increase in the median number of resistance genes was observed, with one in VL I, five in VL II, and six in VL III. Distinguishing features included variations in resistance genes or fluoroquinolone resistance mutation, such as (B), (M), , and (T82I). Further analysis of evolutionary mechanisms revealed that Tn, carrying (M), was present in 87.9% (160/182) of VL III and 92.6% (163/176) of VL II, but only 4.1% (5/122) of VL I. The Tn-like element, carrying (B), was found in 25.3% (46/182) of VL II and 84.7% (149/176) of VL III, with none detected in VL I. Furthermore, other functional genes, especially , were notable in ST37/RT017, which gradually acquired resistance genes from VL I to VL II and VL III.

CONCLUSIONS

The systematically analysis in this study suggests that the acquisition of antibiotic resistance genes was the primary driver of adaptive evolution in ST37/RT017. Horizontal gene transfer, particularly through mobile genetic elements is a key genetic mechanism in the adaptive evolution of ST37/RT017. Based on these genetic profiles, the active establishment and optimization of a rational system for antibiotic use will be crucial to prevent the emergence of a ST37/RT017 variant.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1186/s12864-025-11822-4.

摘要

背景

ST37/RT017是最常见的基因型之一,对多种抗菌药物具有抗性且广泛传播,尤其是在东亚地区。然而,其进化历史和遗传适应性仍不明确。在此,我们旨在系统评估ST37/RT017的遗传多样性、关键进化事件和潜在驱动力。

结果

为探究基因组特征、多样性和变化的动态趋势,系统发育分析和贝叶斯进化分析均显示,ST37/RT017菌株聚为三个变异谱系,呈类似公共汽车的定向拓扑结构,从VL I到VL II,再到VL III。观察到抗性基因中位数呈递增趋势,VL I中有1个,VL II中有5个,VL III中有6个。显著特征包括抗性基因或氟喹诺酮抗性突变的差异,如(B)、(M)、 、 和 (T82I)。对进化机制的进一步分析表明,携带(M)的Tn存在于87.9%(160/182)的VL III和92.6%(163/176)的VL II中,但仅存在于4.1%(5/122)的VL I中。携带(B)的类Tn元件在25.3%(46/182)的VL II和84.7%(149/176)的VL III中被发现,VL I中未检测到。此外,其他功能基因,尤其是 ,在ST37/RT017中很显著,其从VL I到VL II再到VL III逐渐获得抗性基因。

结论

本研究中的系统分析表明,抗生素抗性基因的获得是ST37/RT017适应性进化的主要驱动力。水平基因转移,特别是通过移动遗传元件的转移,是ST37/RT017适应性进化的关键遗传机制。基于这些遗传特征,积极建立和优化合理的抗生素使用系统对于预防ST37/RT017变异体的出现至关重要。

补充信息

在线版本包含可在10.1186/s12864 - 025 - 11822 - 4获取的补充材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/269b05195942/12864_2025_11822_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/5cb531b42b15/12864_2025_11822_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/25c9ddd25b33/12864_2025_11822_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/fa0f3d511110/12864_2025_11822_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/6191245ab6be/12864_2025_11822_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/f3450e9aeaa3/12864_2025_11822_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/269b05195942/12864_2025_11822_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/5cb531b42b15/12864_2025_11822_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/25c9ddd25b33/12864_2025_11822_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/fa0f3d511110/12864_2025_11822_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/6191245ab6be/12864_2025_11822_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/f3450e9aeaa3/12864_2025_11822_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ee6/12255112/269b05195942/12864_2025_11822_Fig6_HTML.jpg

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