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Staphylococcus aureus prosthetic joint infections (PJI) can persist or relapse due to bacterial adaptation. Recurrent strains show increased adhesion and invasion, with genetic changes in virulence factors like adhesins.

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genomics

Background:

  • Prosthetic joint infections (PJI) caused by Staphylococcus aureus are challenging due to persistence and relapse.
  • Understanding bacterial adaptation is crucial for managing recurrent PJI.

Purpose of the Study:

  • To describe phenotypic and genomic changes in Staphylococcus aureus associated with PJI persistence and relapse.
  • To identify bacterial adaptation mechanisms contributing to treatment failure.

Main Methods:

  • Phenotypic and genotypic analysis of Staphylococcus aureus isolates from PJI cases.
  • Comparison of initial and recurrent isolates from persistent/relapsing PJI.
  • Analysis of isolates from PJI cases with favorable outcomes.

Main Results:

  • Recurrent S. aureus isolates showed increased adhesion, invasion, and persistence compared to resolved isolates.
  • No specific genes were consistently associated with PJI persistence or relapse.
  • Sequential isolates maintained the same sequence type (ST), but exhibited loss of resistance genes and variations in virulence genes, particularly adhesins (e.g., fnbA).

Conclusions:

  • Staphylococcus aureus adaptation, including phenotypic and genotypic changes, drives PJI relapse and persistence.
  • Key adaptation strategies involve intracellular persistence, loss of antibiotic resistance genes, and acquisition of variants in virulence genes, especially adhesins.