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The skin and mucous membranes serve as the primary line of defense against pathogens by providing both physical and chemical protection. These barriers are essential in preventing the entry and establishment of microbes, thereby maintaining the integrity of the host.
The outer layer of the skin, the epidermis, is a robust barrier comprising layers of closely packed keratinized cells. This dense arrangement prevents microbes from penetrating the body. The periodic shedding of epidermal cells...
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Biofilms: A developmental niche for vancomycin-intermediate Staphylococcus aureus.

Jenelle E Chapman1, Shilpa E George2, Christiane Wolz2

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Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases
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This summary is machine-generated.

Staphylococcus aureus biofilms promote vancomycin intermediate resistance through the RecA/SOS response. This adaptation in biofilms, unlike planktonic cultures, enhances bacterial survival against antibiotics.

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Area of Science:

  • Microbiology
  • Antibiotic Resistance
  • Bacterial Pathogenesis

Background:

  • Staphylococcus aureus causes diverse infections, with MRSA strains often treated by vancomycin.
  • Emerging vancomycin-intermediate S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA) threaten vancomycin's efficacy.
  • VISA is linked to mutations in cell wall synthesis genes (e.g., rpoB, graS, yycG).

Purpose of the Study:

  • To investigate if vancomycin-intermediate resistance in S. aureus arises from stress within biofilms.
  • To determine if the RecA/SOS response mediates VISA development in S. aureus biofilms.

Main Methods:

  • S. aureus biofilms and planktonic cultures were exposed to sub-inhibitory vancomycin concentrations.
  • Wildtype, recA null mutant, and lexA mutant strains were utilized.
  • Efficiency of plating quantified vancomycin-intermediate resistant subpopulations.

Main Results:

  • Wildtype biofilms showed significantly higher vancomycin-intermediate resistance (4.16 × 10^2 CFUs) than planktonic cultures (1.53 × 10^1 CFUs).
  • Biofilms exhibited greater resistance compared to recA null mutant (8.15 × 10^1 CFUs) and lexA mutant (8.00 × 10^1 CFUs) strains.
  • The RecA/SOS pathway appears crucial for mediating this resistance.

Conclusions:

  • Biofilm environments facilitate the emergence of vancomycin-intermediate resistance in S. aureus.
  • The RecA/SOS response plays a key role in S. aureus adaptation to vancomycin stress within biofilms.
  • This adaptive mechanism highlights how biofilms contribute to antibiotic resistance and bacterial survival.