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BACKGROUND: Biofilms represent a complex milieu of matrix-enclosed microorganisms, which can significantly contribute to the pathology of chronic wounds. In this study, we compare the activity of three commercial antimicrobial wound-care solutions, Vashe® (HOCl-based), PhaseOne® (HOCl-based), and Sulfamylon® (mafenide acetate), for their in vitro activity against bacterial and fungal biofilms. METHODS: Reference and clinical isolates of 6 Gram-negative bacterial species (36 total strains), 3 Gram-positive bacteria (21 strains), and 3 Candida species (9 strains) were used to create biofilms. Various working concentrations of the 3 antiseptic agents were incubated with the biofilms in microwell plates; they were monitored from 1 minute to 24 hours to compare bacterial and fungal viability through colony forming unit (CFU) analysis. RESULTS: Vashe® and PhaseOne® displayed excellent bactericidal and fungicidal activity, whereas Sulfamylon® demonstrated minimal activity against the biofilms tested. With the exception of C. albicans, all biofilms were eliminated at either 1 or 10 minutes using Vashe® and PhaseOne® solutions. In most cases, mafenide was unable to eliminate both bacterial and fungal biofilms, even with 24 hours of treatment. CONCLUSIONS: Biofilms represent a major clinical challenge, with no clear consensus for treatment of chronic wounds or prosthetic devices. Our results suggest that hypochlorous acid-based wound solutions such as Vashe® and PhaseOne® are more efficacious than mafenide in eliminating bacterial and fungal biofilms. Further studies are necessary to investigate and compare the in vivo efficacy of these products in clinical care.

A 40-year-old woman with a history of recurrent medulloblastoma presented for outpatient evaluation of a postoperative wound of the posterior scalp. The patient was diagnosed with medulloblastoma 9 years prior and was initially managed with surgical resection and craniospinal radiotherapy. She had

A significant proportion of human infections involve biofilms, which are more resistant to antimicrobial agents than their planktonic counterparts. It is well established that C. albicans readily forms polymicrobial biofilms with S. aureus. We hypothesized that the addition of an antifungal to an antibacterial, or combination therapy would be more effective in reducing the microbial load, most notably in polymicrobial biofilms, and possibly impact overall management of infection. In vitro results demonstrate that clinical strains of both methicillin-susceptible and methicillin-resistant S. aureus are less susceptible to vancomycin in polymicrobial biofilms with C. albicans when compared to S. aureus monomicrobial biofilms. Treatment of biofilms with either amphotericin B or caspofungin in combination with vancomycin resulted in greater inhibition and even elimination of methicillin-susceptible and methicillin-resistant S. aureus in C. albicans polymicrobial biofilms. The results of this study indicate that combination therapy should be a consideration in the management of polymicrobial biofilms, specifically C. albicans-S. aureus biofilm infections.

Candida albicans is the most prevalent human fungal pathogen, with an ability to inhabit diverse host niches and cause disease in both immunocompetent and immunocompromised individuals. C. albicans also readily forms biofilms on indwelling medical devices and mucosal tissues, which serve as an infectious reservoir that is difficult to eradicate, and can lead to lethal systemic infections. Biofilm formation occurs within a complex milieu of host factors and other members of the human microbiota. Polymicrobial interactions will probably dictate the cellular and biochemical composition of the biofilm, as well as influence clinically relevant outcomes, such as drug and host resistance and virulence. In this manuscript, we review C. albicans infections in the context of in vivo polymicrobial biofilms and implications for pathogenesis.

Current understanding of resistance and susceptibility to vulvovaginal candidiasis challenges existing paradigms of host defence against fungal infection. While abiotic biofilm formation has a clearly established role during systemic Candida infections, it is not known whether C. albicans forms biofilms on the vaginal mucosa and the possible role of biofilms in disease. In vivo and ex vivo murine vaginitis models were employed to examine biofilm formation by scanning electron and confocal microscopy. C. albicans strains included 3153A (lab strain), DAY185 (parental control strain), and mutants defective in morphogenesis and/or biofilm formation in vitro (efg1/efg1 and bcr1/bcr1). Both 3153A and DAY815 formed biofilms on the vaginal mucosa in vivo and ex vivo as indicated by high fungal burden and microscopic analysis demonstrating typical biofilm architecture and presence of extracellular matrix (ECM) co-localized with the presence of fungi. In contrast, efg1/efg1 and bcr1/bcr1 mutant strains exhibited weak or no biofilm formation/ECM production in both models compared to wild-type strains and complemented mutants despite comparable colonization levels. These data show for the first time that C. albicans forms biofilms in vivo on vaginal epithelium, and that in vivo biotic biofilm formation requires regulators of biofilm formation (BCR1) and morphogenesis (EFG1).

Candida albicans and Staphylococcus aureus form vigorous polymicrobial biofilms in serum, which may serve as the source of coinfection in patients. More importantly, S. aureus is highly resistant to vancomycin during polymicrobial biofilm formation, with no decreases in bacterial viability observed with up to 1,600 μg/ml drug. In these mixed-species biofilms, S. aureus preferentially associates with C. albicans hyphae, which express a variety of unique adhesins. We tested C. albicans mutants deficient in transcriptional regulators of morphogenesis ( CPH1 and EFG1 ) and biofilm formation ( BCR1 ) to investigate the role of hyphae in mediating polymicrobial biofilm formation. These mutants also have reduced expression of hypha-specific adhesins. The ability to form polymicrobial biofilms correlated with the ability to form hyphae in these mutants. However, only mutants that could adhere to the abiotic surface could induce S. aureus vancomycin resistance, regardless of the presence of hyphae. In examining factors that may mediate interspecies adhesion, we found that the C. albicans ALS family of adhesins (Als1 to Als7 and Als9) was not involved, and neither was the hypha-specific adhesin Hwp1. Therefore, polymicrobial biofilm formation and subsequent antibiotic resistance is a multifactorial process that may require a unique combination of fungal and/or bacterial adhesins.

Candida albicans readily forms biofilms on the surface on indwelling medical devices, and these biofilms serve as a source of local and systemic infections. It is estimated that 27% of nosocomial C. albicans bloodstream infections are polymicrobial, with Staphylococcus aureus as the third most common organism isolated in conjunction with C. albicans . We tested whether S. aureus and C. albicans are able to form a polymicrobial biofilm. Although S. aureus formed poor monoculture biofilms in serum, it formed a substantial polymicrobial biofilm in the presence of C. albicans . In terms of architecture, S. aureus formed microcolonies on the surface of the biofilm, with C. albicans serving as the underlying scaffolding. In addition, S. aureus matrix staining revealed a different phenotype in polymicrobial versus monomicrobial biofilms, suggesting that S. aureus may become coated in the matrix secreted by C. albicans. S. aureus resistance to vancomycin was enhanced within the polymicrobial biofilm, required viable C. albicans , and was in part mediated by C. albicans matrix. However, the growth or sensitivity to amphotericin B of C. albicans is not altered in the polymicrobial biofilm.