Effects of a topical essential oil-containing formulation on biofilm-forming coagulase-negative staphylococci

J Al-Shuneigat1, S D Cox, J L Markham

  • 1Centre for Horticulture and Plant Sciences, University of Western Sydney, NSW, Australia.

Abstract

Insights

Polytoxinol (PT), an essential oil formulation, effectively inhibits coagulase-negative staphylococci biofilm formation. It prevents bacterial adherence, suggesting topical efficacy for essential oils.

Area of Science:

  • Microbiology
  • Dermatology
  • Natural Products

Background:

  • Coagulase-negative staphylococci (CoNS) are significant pathogens, often forming biofilms.
  • Biofilm formation by CoNS contributes to persistent infections and antibiotic resistance.
  • Topical treatments are crucial for managing CoNS-related skin and soft tissue infections.

Purpose of the Study:

  • To assess the antimicrobial activity of Polytoxinol (PT), an essential oil-based topical formulation.
  • To evaluate PT's efficacy against biofilm-producing strains of coagulase-negative staphylococci.
  • To investigate PT's impact on bacterial adherence and biofilm development.

Main Methods:

  • A microtitre plate assay was employed to measure PT's inhibitory effects.
  • Susceptibility testing was performed on clinical isolates of biofilm-forming CoNS.
  • Minimum Inhibitory Concentration (MIC) was determined for PT.

Main Results:

  • PT demonstrated antimicrobial effects against CoNS, with variable susceptibility (MIC = 0.6-20,000 ppm).
  • For Staphylococcus warneri, PT inhibited biofilm growth at concentrations 32-fold lower than those inhibiting planktonic growth.
  • PT inhibited the initial adherence of S. warneri to polystyrene, preventing biofilm development.

Conclusions:

  • Polytoxinol exhibits antimicrobial efficacy against clinical isolates of CoNS in vitro.
  • PT can inhibit biofilm formation in tolerant CoNS isolates at sub-inhibitory concentrations.
  • Essential oils may exert topical efficacy by preventing biofilm formation independently of direct cell killing.

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