OBJECTIVES:Contact lens-acquired bacterial infections are a serious problem. Of the reported cases, inadequate cleaning of the lens case was the most common cause of lens contamination. Organoselenium has been shown to inhibit bacterial attachment to different polymer materials. This study evaluates the ability of an organoselenium monomer, incorporated into the polymer of a polypropylene contact lens case coupon, to block the formation of biofilms in a lens case.METHODS:The bacteria tested were Pseudomonas aeruginosa, Staphylococcus aureus, Stenotrophomonas maltophilia, and Serratia marcescens. For this study, the bacteria were allowed to grow overnight, in trypticase soy broth media, in the presence of the selenium-containing polymer or the same polymer without organoselenium. The material was studied by both colony-forming unit determination and by confocal laser scanning microscopy.RESULTS:The results showed that the organoselenium polymer versus the control polymer resulted in the following effect on biofilm formation: (1) a reduction in P. aeruginosa of 7.3 logs (100%); (2) a reduction in S. aureus of 7.3 logs (100%); (3) a reduction in S. maltophilia of 7.5 logs (100%); and (4) a reduction in S. marcescens reduction of 3.3 logs (99.9%). To test the stability of the organoselenium polypropylene contact lens coupon, the coupon was soaked in PBS for eight weeks at room temperature. It was found that when these soaked coupons were tested against S. aureus, complete inhibition (8.1 logs) was obtained. Because organoselenium cannot leach from the polymer, this would imply that the organoselenium polypropylene contact lens case coupon would be inhibitory toward bacterial biofilm for the life of the case.CONCLUSION:The organoselenium polypropylene contact lens case coupon shows the ability to inhibit biofilm formation. The use of organoselenium copolymer should play an important role in protecting against contact lens case-acquired infection.

Purpose Biofilm formation is a problem for solid and sponge-type scleral buckles. This can lead to complications that require removal of the buckle, and result in vision loss due to related ocular morbidity, primarily infection, or recurrent retinal detachment. We investigate the ability of a covalent organo-selenium coating to inhibit biofilm formation on a scleral buckle. Methods Sponge and solid Labtican brand scleral buckles were coated with organo-selenium coupled to a silyation reagent. Staphylococcus aureus biofilm formation was monitored by a standard colony-forming unit assay and the confocal laser scanning microscopy, while Pseudomonas aeruginosa biofilm formation was examined by scanning electron microscopy. Stability studies were done, by soaking in phosphate buffer saline (PBS) at room temperature for 2 months. Toxicity against human corneal epithelial cell was examined by growing the cells in the presence of organo-selenium–coated scleral buckles. Results The organo-selenium coating inhibited biofilm formation by gram-negative and gram-positive bacteria. The buckle coatings also were shown to be fully active after soaking in PBS for 2 months. The organo-selenium coatings had no effect on the viability of human corneal epithelial cells. Conclusions Organo-selenium can be used to covalently coat a scleral buckle, which is stable and inhibits biofilm formation for gram-negative and gram-positive bacteria. The organo-selenium buckle coating was stable and nontoxic to cell culture. Translational Relevance This technology provides a means to inhibit bacterial attachment to devices attached to the eye, without damage to ocular cells.

Biofilm formation in wounds is a serious problem which inhibits proper wound healing. One possible contributor to biofilm formation in a wound is the bacteria growing within the overlying bandage. To test this mechanism, we used bandages that contained a coating of organo-selenium that was covalently attached to the bandage. We tested the ability of this coating to kill bacteria on the bandage and in the underlying tissue. The bandage material was tested with both lab strains and clinical isolates of Staphylococcus aureus, Pseudomonas aeruginosa and Staphylococcus epidermidis. It was found that the organo-selenium coated bandage showed inhibition, of biofilm formation on the bandage in vitro (7–8 logs), with all the different bacteria tested, at selenium concentrations in the coating of less than 1.0%. These coatings were found to remain stable for over one month in aqueous solution, 15 min in boiling water, and over 6 years at room temperature. The bandages were also tested on a mouse wound model where the bacteria were injected between the bandage and the wound. Not only did the selenium bandage inhibit biofilm formation in the bandage, but it also inhibited biofilm formation in the wound tissue. Since selenium does not leave the bandage, this would appear to support the idea that a major player in wound biofilm formation is bacteria which grows in the overlying bandage.

Colonization of central venous catheters (CVCs) by pathogenic bacteria leads to catheter-related bloodstream infections (CRBSIs). These colonizing bacteria form highly antibiotic-resistant biofilms. Staphylococcus aureus is one of the most frequently isolated pathogens in CRBSIs. Impregnating CVC surfaces with antimicrobial agents has various degrees of effectiveness in reducing the incidence of CRBSIs. We recently showed that organoselenium covalently attached to disks as an antibiofilm agent inhibited the development of S. aureus biofilms. In this study, we investigated the ability of an organoselenium coating on hemodialysis catheters (HDCs) to inhibit S. aureus biofilms in vitro and in vivo. S. aureus failed to develop biofilms on HDCs coated with selenocyanatodiacetic acid (SCAA) in either static or flowthrough continuous-culture systems. The SCAA coating also inhibited the development of S. aureus biofilms on HDCs in vivo for 3 days. The SCAA coating was stable and nontoxic to cell culture or animals. This new method for coating the internal and external surfaces of HDCs with SCAA has the potential to prevent catheter-related infections due to S. aureus.

Previous experiments have shown that when selenium was attached to a surface, biofilm development on the surface was inhibited. Selenium is a catalytic producer of superoxide radicals via oxygen reduction. The superoxide radicals can cause damage to the outer membrane of bacterial cells that frequently results in cell death. Therefore, we propose selenium attachment to an RO membrane surface as a biofouling inhibition technique. Selenium was attached to the surface of RO membranes via monomer (selenocystamine) and polymer (aceto acetoxy ethyl methacrylate) attachment mechanisms. Using confocal microscopy and Staphylococcus aureus cell counting to evaluate S. aureus biofilm growth, the number of attached S. aureus cells was seen to be significantly reduced on RO membranes coated with selenium. While both selenium coatings had similar S. aureus inhibition, the selenium coatings had much different impacts on permeate flux. The selenocystamine attachment method maintained a higher permeate flux compared to the AAEMA attachment method due to AAEMA requiring a harsh attachment procedure. Ultimately, attached selenocystamine showed great potential to serve as a biofouling inhibitor by reducing attached S. aureus growth on RO membranes without excessive permeate flux loss.

The purpose of this study was to determine the inhibitory effect of selenocystamine coated intraocular lenses (IOLs) on the formation of posterior capsule opacification (PCO) in an ex vivo canine lens capsular bag assay. Selenocystamine was covalently bound to the surface of poly(2-hydroxyethyl methacrylate) (poly(HEMA)) discs. Three groups of canine lens capsules (6 coated IOLs (SeIOLs), 7 non-coated control IOLs and 8 empty capsules) were cultured for 10 days. During the culture period PCO was scored based on visual inspection of the capsules using phase contrast microscopy. On day 10 all the capsules were prepared for light microscopic examination and lens epithelial cells (LECs) were quantified. Proliferating cell nuclear antigen (PCNA), alpha-smooth muscle actin (alpha-SMA) and cleaved caspase-3 were examined by immunohistochemistry. Additionally, cell viability assays were performed on LECs cultured in tissue culture medium pre-incubated with either a SeIOL or control IOL. The viability assays demonstrated that no detectable cytotoxic leachables were associated with the functionalized IOLs. The central posterior capsule was free of cells underneath all SeIOLs, although large numbers of LECs populated the capsular periphery. Apoptotic cells were observed underneath the periphery of some SeIOLs. Both the PCO scores and LEC counts of SeIOL containing capsules were significantly lower than those of control group capsules (p < 0.01 and p = 0.0004, respectively). The use of selenium functionalized IOLs resulted in a significant reduction of PCO in this ex vivo model. Binding of selenocystamine to a foldable IOL may provide an effective method to prevent population of the central posterior capsule with LECs.

ABSTRACTAmong the most difficult bacterial infections encountered in treating patients are wound infections, which may occur in burn victims, patients with traumatic wounds, necrotic lesions in people with diabetes, and patients with surgical wounds. Within a wound, infecting bacteria frequently develop biofilms. Many current wound dressings are impregnated with antimicrobial agents, such as silver or antibiotics. Diffusion of the agent(s) from the dressing may damage or destroy nearby healthy tissue as well as compromise the effectiveness of the dressing. In contrast, the antimicrobial agent selenium can be covalently attached to the surfaces of a dressing, prolonging its effectiveness. We examined the effectiveness of an organoselenium coating on cellulose discs in inhibitingPseudomonas aeruginosaandStaphylococcus aureusbiofilm formation. Colony biofilm assays revealed that cellulose discs coated with organoselenium completely inhibitedP. aeruginosaandS. aureusbiofilm formation. Scanning electron microscopy of the cellulose discs confirmed these results. Additionally, the coating on the cellulose discs was stable and effective after a week of incubation in phosphate-buffered saline. These results demonstrate that 0.2% selenium in a coating on cellulose discs effectively inhibits bacterial attachment and biofilm formation and that, unlike other antimicrobial agents, longer periods of exposure to an aqueous environment do not compromise the effectiveness of the coating.