Persistence of a Staphylococcus aureus small-colony variant under antibiotic pressure in vivo

Eric Brouillette1, Alejandro Martinez, Bobbi J Boyll

  • 1Centre d'Etude et de Valorisation de la Diversité Microbienne (CEVDM), Département de biologie, Université de Sherbrooke, Sherbrooke, Que., Canada J1K 2R1.

Insights

Staphylococcus aureus small-colony variants (SCVs) show reduced colonization but increased persistence in mouse mammary glands during antibiotic treatment. The SCV phenotype may explain persistent S. aureus infections despite antimicrobial therapy.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Bacterial Pathogenesis

Background:

  • Staphylococcus aureus small-colony variants (SCVs) are linked to persistent infections.
  • Bovine mastitis caused by S. aureus is challenging to treat with standard antibiotics.

Purpose of the Study:

  • To evaluate the colonization and persistence of S. aureus Newbould and its hemB mutant (SCV phenotype) in mouse mammary glands under antibiotic pressure.
  • To understand the role of the SCV phenotype in S. aureus persistence during antimicrobial therapy.

Main Methods:

  • Comparison of S. aureus Newbould and an isogenic hemB mutant (SCV) in a mouse mammary gland colonization model.
  • Assessment of bacterial persistence following administration of cephapirin at 1 or 2 mg kg(-1).
  • In vitro susceptibility testing of both strains to cephapirin.

Main Results:

  • The hemB mutant exhibited significantly reduced tissue colonization compared to the parental strain.
  • In vitro, the hemB mutant showed similar susceptibility to cephapirin as S. aureus Newbould.
  • Despite reduced colonization, the hemB mutant was over 100 times more persistent in mammary glands than the parental strain under antibiotic treatment.

Conclusions:

  • The SCV phenotype in S. aureus, while impairing initial colonization, enhances bacterial persistence in mammary glands during antibiotic treatment.
  • The SCV phenotype may be a key factor in the in vivo persistence of S. aureus under antimicrobial pressure.
  • These findings offer insights into the mechanisms behind chronic and difficult-to-eradicate S. aureus infections.

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