Abstract
Purpose: Biomaterial-related infections continue to hamper the success of reconstructive and arthroplasty procedures in orthopaedic surgery. Staphylococci are the most common etiologic agents, with biofilm formation representing a major virulence factor. Environmental stress factors and sub-inhibitory concentration of some antibiotics have been identified to trigger staphylococcal biofilm formation through increased icaADBC expression. In staphylococci, production of polysaccharide intercellular adhesin (PIA) by the enzyme products of the icaADBC operon is the best understood mechanism of biofilm development, making the ica genes a potential target for biofilm inhibitors. Aims of the current study were
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Determine the minimum inhibitory concentration (MIC) of Povidone-iodine.
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Investigate the effect of Povidone-iodine on icaADBC operon encoded staphylococcal biofilm formation.
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Investigate wether any observed changes on biofilm by Povidone-iodine is mediated through a change in icaADBC operon.
Method: MIC of povidone – iodine for both reference strains and strains isolated from infected orthopaedic implants was determined. Biofilm assay was performed at different Povidone-iodine concentrations using 96-well polystyrene plates. Total RNA for cDNA synthesis was isolated from bacteria at different twofold dilutions of Povidone-iodine concentrations. Real time polymerase chain reaction was used to quantify effects of Povidone-iodine on gene expression pattern of the icaADBC operon using the constitutively expressed gyrB gene as internal control
Results: The MIC of povidone-iodine was 1.4% for all bacterial strains. Clinical in-use doses of povidone-iodine prevented biofilm formation.
A step-wise reduction of biofilm was observed at increasing sub-inhibitory doses of povidone-iodine (p< 0.0001).
IcaA expression correlated with biofilm formation in staphylococcal organisms. Decrease in icaA expression was strongly associated with an increase in expression in the biofilm repressor gene, icaR.
The repressive effect of povidone-iodine on biofilm formation by Staphylococcal bacteria is by a separate mechanism from its bacteriostatic mechanism of action.
Conclusion: This study shows that icaR is a potential therapeutic target through which the ability of Staphylococcal bacterial to form biofilm may be reduced. These data reveal an additional therapeutic benefit of povidone-iodine and suggest that studies to evaluate the suitability of povidone-iodine as biomaterial coating agent to reduce device-related infection rates are merited.
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