Genomic characterization of Staphylococcus aureus isolates causing osteoarticular infections in otherwise healthy

Walter Dehority1, Valerie J Morley2, Daryl B Domman2

  • 1Department of Pediatrics, The University of New Mexico School of Medicine, Albuquerque, New Mexico, United States of America.

Plos One
|August 29, 2022
PubMed

Insights

Staphylococcus aureus causing pediatric bone and joint infections show genetic diversity. These bacteria more often carry immune evasion genes, but mutations are rare, suggesting other regulatory mechanisms are key.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genomics

Background:

  • Pediatric osteoarticular infections are frequently caused by Staphylococcus aureus.
  • The role of Staphylococcus aureus genomic variability in the pathogenesis of these infections is not well understood.

Purpose of the Study:

  • To investigate the genomic variability of Staphylococcus aureus isolates from children with varying degrees of S. aureus infection.
  • To correlate genetic features with the clinical presentation and biofilm-forming capacity of S. aureus.

Main Methods:

  • Whole genome sequencing of S. aureus isolates from 47 children (skin colonization, skin abscesses, osteoarticular infections).
  • Assessment of 254 virulence genes, mutations, and phylogenetic analysis.
  • Comparison of biofilm formation capacity among isolates.

Main Results:

  • No specific sequence types predominated in osteoarticular infections.
  • Isolates from osteoarticular infections more frequently carried immune evasion genes (p = .02).
  • Limited mutations were found in virulence genes, and biofilm formation varied significantly, with control isolates showing more robust biofilm formation.

Conclusions:

  • Staphylococcus aureus causing pediatric osteoarticular infections are genetically diverse.
  • These isolates possess more immune evasion genes but similar overall virulence gene carriage compared to less invasive strains.
  • Pathogenesis may be primarily regulated at transcriptional and/or translational levels due to infrequent mutations.
Abstract