Scholarlink

<p><i>Pseudomonas aeruginosa</i> is an important nosocomial pathogen which can cause serious infections across diverse anatomic locations. Infections can spread within an individual to different body sites, but the rate and directionality of this process is unknown. Here, we explore within-host diversity as well as the body site translocation dynamics using de-convoluted metagenomic <i>P. aeruginosa</i> reads from 256 hospital patients sampled at both respiratory and gut sites. Of the 84 patients where <i>P. aeruginosa</i> genomes could be recovered, there were 27 cases where the same <i>P. aeruginosa</i> clone was detected across multiple body sites. Using a simulation approach, we find that the majority of body site sharing is likely due to within-patient translocation of clones rather than independent acquisition from the hospital environment. Using ancestral reconstruction, we predict that most clones likely occupied a respiratory niche, and that the probable direction of clone transmission is lung-to-gut. Analysis of within-patient variation highlights strong enrichment of mutations in genes associated with antimicrobial resistance, irrespective of sample type. We report significantly more translocation than has been previously reported and highlight that lower respiratory tract infections can result in persistent gut colonisation of <i>P. aeruginosa</i>, a major risk factor for sepsis in vulnerable patients.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

High frequency body site translocation of nosocomial Pseudomonas aeruginosa

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月25日

查看全文
  • Lewis W. S. Fisher,
  • Harry A. Thorpe,
  • Davide Sassera,
  • Jukka Corander,
  • Josephine M. Bryant

摘要

Pseudomonas aeruginosa is an important nosocomial pathogen which can cause serious infections across diverse anatomic locations. Infections can spread within an individual to different body sites, but the rate and directionality of this process is unknown. Here, we explore within-host diversity as well as the body site translocation dynamics using de-convoluted metagenomic P. aeruginosa reads from 256 hospital patients sampled at both respiratory and gut sites. Of the 84 patients where P. aeruginosa genomes could be recovered, there were 27 cases where the same P. aeruginosa clone was detected across multiple body sites. Using a simulation approach, we find that the majority of body site sharing is likely due to within-patient translocation of clones rather than independent acquisition from the hospital environment. Using ancestral reconstruction, we predict that most clones likely occupied a respiratory niche, and that the probable direction of clone transmission is lung-to-gut. Analysis of within-patient variation highlights strong enrichment of mutations in genes associated with antimicrobial resistance, irrespective of sample type. We report significantly more translocation than has been previously reported and highlight that lower respiratory tract infections can result in persistent gut colonisation of P. aeruginosa, a major risk factor for sepsis in vulnerable patients.