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Updated: Apr 26, 2026

Targeting Biofilm Associated Staphylococcus aureus Using Resazurin Based Drug-susceptibility Assay
Published on: May 5, 2016
Comparison of biofilm formation between major clonal lineages of methicillin resistant Staphylococcus aureus
Evelyn Vanhommerig1, Pieter Moons1, Daniel Pirici2
1Department of Medical Microbiology, University of Antwerp, Antwerp, Belgium; Vaccine & Infectious Disease Institute, University of Antwerp, Antwerp, Belgium.
Objectives:
Epidemic methicillin-resistant S. aureus (MRSA) clones cause infections in both hospital and community settings. As a biofilm phenotype further facilitates evasion of the host immune system and antibiotics, we compared the biofilm-forming capacities of various MRSA clones.
Methods:
Seventy-six MRSA classified into 13 clones (USA300, EMRSA-15, Hungarian/Brazilian etc.), and isolated from infections or from carriers were studied for biofilm formation under static and dynamic conditions. Static biofilms in microtitre plates were quantified colorimetrically. Dynamic biofilms (Bioflux 200, Fluxion, USA) were studied by confocal laser-scanning and time-lapse microscopy, and the total volume occupied by live/dead bacteria quantified by Volocity 5.4.1 (Improvision, UK).
Results:
MRSA harbouring SCCmec IV produced significantly more biomass under static conditions than SCCmec I-III (P = 0.003), and those harbouring SCCmec II significantly less than those harbouring SCCmec I or III (P<0.001). In the dynamic model, SCCmec I-III harbouring MRSA were significantly better biofilm formers than SCCmec IV (P = 0.036). Only 16 strains successfully formed biofilms under both conditions, of which 13 harboured SCCmec IV and included all tested USA300 strains (n = 3). However, USA300 demonstrated remarkably lower percentages of cell-occupied space (6.6%) compared to the other clones (EMRSA-15 = 19.0%) under dynamic conditions. Time-lapse microscopy of dynamic biofilms demonstrated that USA300 formed long viscoelastic tethers that stretched far from the point of attachment, while EMRSA-15 consisted of micro-colonies attached densely to the surface.
Conclusions:
MRSA harbouring SCCmec types IV and I-III demonstrate distinct biofilm forming capacities, possibly owing to their adaptation to the community and hospital settings, respectively. USA300 demonstrated abundant biofilm formation under both conditions, which probably confers a competitive advantage, contributing to its remarkable success as a pathogen.
Insights
Methicillin-resistant Staphylococcus aureus (MRSA) clones exhibit varied biofilm formation. USA300 MRSA, a successful pathogen, forms abundant biofilms under diverse conditions, potentially conferring a competitive advantage.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Epidemic methicillin-resistant Staphylococcus aureus (MRSA) clones are significant causes of hospital and community infections.
- Biofilm formation by MRSA enhances immune evasion and antibiotic resistance, posing a therapeutic challenge.
Purpose of the Study:
- To compare the biofilm-forming capacities of various MRSA clones.
- To investigate the influence of SCCmec types on MRSA biofilm formation.
Main Methods:
- Seventy-six MRSA strains from 13 clones were analyzed for biofilm formation under static and dynamic conditions.
- Static biofilms were quantified colorimetrically; dynamic biofilms were assessed using confocal laser-scanning and time-lapse microscopy.
Main Results:
- MRSA strains with SCCmec IV showed greater biomass in static biofilms compared to SCCmec I-III (P = 0.003).
- SCCmec I-III strains were superior biofilm formers under dynamic conditions compared to SCCmec IV (P = 0.036).
- USA300 MRSA demonstrated robust biofilm formation in both models, forming distinct viscoelastic tethers.
Conclusions:
- Distinct SCCmec types in MRSA correlate with differing biofilm-forming capacities, potentially reflecting adaptations to community versus hospital environments.
- The abundant biofilm formation by USA300 MRSA likely contributes to its success as a pathogen.
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