Abstract
Methicillin-resistant Staphylococcus aureus (MRSA), the most commonly detected drug-resistant microbe in hospitals, adheres to substrates and forms biofilms that are resistant to immunological responses and antimicrobial drugs. Currently, there is a need to develop alternative approaches for treating infections caused by biofilms to prevent delays in wound healing. Silver has long been used as a disinfectant, which is non-specific and has relatively low cytotoxicity. Silver sulfadiazine (SSD) is a chemical complex clinically used for the prevention of wound infections after injury. However, its effects on biofilms are still unclear. In this study, we aimed to analyze the mechanisms underlying SSD action on biofilms formed by MRSA. The antibacterial effects of SSD were a result of silver ions and not sulfadiazine. Ionized silver from SSD in culture media was lower than that from silver nitrate; however, SSD, rather than silver nitrate, eradicated mature biofilms by bacterial killing. In SSD, sulfadiazine selectively bound to biofilms, and silver ions were then liberated. Consequently, the addition of an ion-chelator reduced the bactericidal effects of SSD on biofilms. These results indicate that SSD is an effective compound for the eradication of biofilms; thus, SSD should be used for the removal of biofilms formed on wounds.
Highlights
Biofilms (BFs) are a cause of chronic infections
We investigated the essential mechanisms underlying the antibacterial action of Silver sulfadiazine (SSD), especially against BFs, using SSD elements, silver and SD, and analyzed the effects of the compounds on a clinical strain of BF-forming Methicillin-resistant S. aureus (MRSA)
One colony grown on tryptic soy agar (TSA) was inoculated in tryptic soy broth (TSB) and grown at 37 ◦C until the optical density (OD) = 0.57 (λ = 578 nm)
Summary
Biofilms (BFs) are a cause of chronic infections. Several types of symbiotic bacteria, such as Staphylococcus aureus and Pseudomonas aeruginosa, colonize our body and form BFs [1,2,3]. Methicillin-resistant S. aureus (MRSA) causes soft-tissue infections, indwelling catheter-associated infections, bacteremia, endocarditis, and osteomyelitis. 80% of chronic wound infections are attributed to bacteria or BFs [1]. BFs produce a subpopulation of drug-resistant cells called persister cells [4,5,6,7]. Specific molecules targeting BFs and effective drugs for BF eradication have not been identified yet. The BF itself becomes a serious exacerbation factor in antimicrobial resistance
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