Biofilms play a major role in delaying chronic wounds from healing. A wound infiltrated with biofilm, or “critically colonised” wound, may become clinically infected if the number of microbes exceeds a critical level. Chronic wound biofilms represent a significant treatment challenge by demonstrating recalcitrance towards antimicrobial agents. However, a “window of opportunity” may exist after wound debridement when biofilms are more susceptible to topical antiseptics. Here, we discuss the role of antiseptics in the management of chronic wounds and biofilm, focusing on povidone‐iodine (PVP‐I) in comparison with two commonly used antiseptics: polyhexanide (PHMB) and silver. This article is based on the literature reviewed during a focus group meeting on antiseptics in wound care and biofilm management, and on a PubMed search conducted in March 2020. Compared with PHMB and silver, PVP‐I has a broader spectrum of antimicrobial activity, potent antibiofilm efficacy, no acquired bacterial resistance or cross‐resistance, low cytotoxicity, good tolerability, and an ability to promote wound healing. PVP‐I represents a viable therapeutic option in wound care and biofilm management, with the potential to treat biofilm‐infiltrated, critically colonised wounds. We propose a practical algorithm to guide the management of chronic, non‐healing wounds due to critical colonisation or biofilm, using PVP‐I.
Biofilm in chronic wounds is associated with delayed healing and ineffective local treatment. The purpose of this study was to investigate the in vitro anti-biofilm activity of two commonly used antimicrobials, povidone-iodine (PVP-I) and polyhexamethylene biguanide (PHMB). The rate of anti-biofilm activity of PVP-I, PHMB, and phosphate-buffered saline (negative control) was assessed on monomicrobial biofilms of varying maturity and composition. Antimicrobial efficacy was determined by counting colony-forming units (CFU). Live/dead cell staining and time-lapse confocal microscopy were also performed. Both PVP-I and PHMB demonstrated robust in vitro anti-biofilm activity against all tested biofilms; however, PVP-I had a more rapid action versus PHMB against methicillin-resistant Staphylococcus aureus (MRSA) biofilms, as determined by both CFU counts and microscopy. PVP-I completely eradicated Pseudomonas aeruginosa biofilms of 3- and 5-day maturity (in ≤0.5 h) and 7-day maturity (in ≤3 h), while PHMB only partially depleted cell density, with no complete biofilm eradication even after 24 h. In conclusion, PVP-I had a similar in vitro anti-biofilm activity to PHMB against biofilms of varying microbial compositions and maturity, and in some cases demonstrated more potent and rapid activity versus PHMB. PVP-I may be particularly effective in treating MRSA biofilms. However, further high-quality clinical research on the efficacy of antimicrobials is required.
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