Aim <p>This study aimed to characterize the prevalence of fosfomycin resistance in clinical carbapenem-resistant hypervirulent <i>Klebsiella pneumoniae</i> (CR-hvKP) isolates.</p> Methods <p>Common drug resistance genes and virulence genes were amplified by polymerase chain reaction (PCR) and verified by whole-genome sequencing. The potential virulence of all the clinical CRKP strains was tested in a <i>Galleria mellonella</i> infection model.</p> Results <p>A total of 171 CR-hvKP isolates collected from a Chinese tertiary hospital were analyzed for fosfomycin resistance. 71 strains (41.5%) were sensitive to fosfomycin, and 100 strains (58.5%) were resistant to fosfomycin. All the clinical isolates were found to carry fosfomycin genes <i>fosA</i> and <i>fosA6</i>. Only one fosfomycin-resistant isolate was found to carry the gene <i>fosA3</i>. In addition to the modification of target enzyme murA, the mechanisms of fosfomycin resistance also involve the dysfunction of the transport system including <i>glpt</i>, <i>uhpT</i>, and their regulatory gene <i>CyaA</i> mutation deletion. The <i>Galleria mellonella</i> infection assays confirmed that all the CRKP strains exhibited hypervirulence.</p> Conclusion <p>Cumulatively, fosfomycin resistance in CR-hvKP is mediated by diverse mechanisms and is highly prevalent in a tertiary hospital from Jiangxi Province, South China. It is therefore critical to continuously monitor the epidemiology of these fosfomycin-resistant CR-hvKP while simultaneously minimizing potential risks from fosfomycin-resistant CR-hvKP.</p>

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High prevalence of fosfomycin resistance among ST11 carbapenem-resistant hypervirulent Klebsiella pneumoniae isolates in a tertiary hospital from Jiangxi Province, South China

  • Min Li,
  • Ping Li,
  • Jian Cui,
  • Peng Zhu,
  • Hui Guo,
  • Wei Zuo,
  • Wenjian Liao

摘要

Aim

This study aimed to characterize the prevalence of fosfomycin resistance in clinical carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP) isolates.

Methods

Common drug resistance genes and virulence genes were amplified by polymerase chain reaction (PCR) and verified by whole-genome sequencing. The potential virulence of all the clinical CRKP strains was tested in a Galleria mellonella infection model.

Results

A total of 171 CR-hvKP isolates collected from a Chinese tertiary hospital were analyzed for fosfomycin resistance. 71 strains (41.5%) were sensitive to fosfomycin, and 100 strains (58.5%) were resistant to fosfomycin. All the clinical isolates were found to carry fosfomycin genes fosA and fosA6. Only one fosfomycin-resistant isolate was found to carry the gene fosA3. In addition to the modification of target enzyme murA, the mechanisms of fosfomycin resistance also involve the dysfunction of the transport system including glpt, uhpT, and their regulatory gene CyaA mutation deletion. The Galleria mellonella infection assays confirmed that all the CRKP strains exhibited hypervirulence.

Conclusion

Cumulatively, fosfomycin resistance in CR-hvKP is mediated by diverse mechanisms and is highly prevalent in a tertiary hospital from Jiangxi Province, South China. It is therefore critical to continuously monitor the epidemiology of these fosfomycin-resistant CR-hvKP while simultaneously minimizing potential risks from fosfomycin-resistant CR-hvKP.