Antimicrobial, antibiofilm, and microbial barrier properties of poly (ε-caprolactone)/cloisite 30B thin films
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Development of antibacterial and antibiofilm surfaces is in high demand. In this study, nanocomposite of Poly (ε-caprolactone)/Cloisite 30B was prepared by the solvent casting method. The membranes were characterised by SEM, AFM, and FTIR. Evaluation of water uptake, antimicrobial, antibiofilm, and microbial barrier properties demonstrated a significant antimicrobial and antibiofilm activity against MTCC strain of Staphylococcus haemolyticus and strong biofilm positive Staphylococcus epidermidis of clinical origin at low clay concentrations. These membranes acted as an excellent barrier to the penetration of microorganism. These nanocomposites can have promising applications in various fields including packaging.Keywords:
Caprolactone
This paper presented the influence of Al(III) on biodegradability, micromorphology, composition and functional groups characteristics of the biofilm extracellular polymeric substances (EPS) during different growth phases. The sequencing batch biofilm reactors were developed to cultivate biofilms under different Al(III) dosages. The results elucidated that Al(III) affected biofilm development adversely at the beginning of biofilm growth, but promoted the biofilm mass and improved the biofilm activity with the growth of the biofilm. The micromorphological observation indicated that Al(III) led to a reduction of the filaments and promotion of the EPS secretion in growth phases of the biofilm, also Al(III) could promote microorganisms to form larger colonies for mature biofilm. Then, the analysis of EPS contents and components suggested that Al(III) could increase the protein (PN) of tightly bound EPS (TB-EPS) which alleviated the metal toxicity inhibition on the biofilm during the initial phases of biofilm growth. The biofilm could gradually adapt to the inhibition caused by Al(III) at the biofilm maturation moment. Finally, through the Fourier transform infrared spectroscopy, it was found that Al(III) was beneficial for the proliferation and secretion of TB-EPS functional groups, especially the functional groups of protein and polysaccharides.
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The current study has been designed to delineate the efficacy of geraniol (GE) on biofilm formation in Staphylococcus epidermidis as well as the effect of subinhibitory concentrations of GE on the development of adaptive resistance.Biofilm biomass quantification assay was performed to evaluate the antibiofilm activity of GE against S. epidermidis. Microscopic observation of biofilms and extracellular polymeric substance (EPS), slime and cell surface hydrophobicity (CSH) production were also studied to support the antibiofilm potential of GE. In addition, S. epidermidis was examined for its adaptive resistance development upon continuous exposure of GE at its subinhibitory concentrations.Results/Key findings. The MIC of GE against S. epidermidis was 512 µg ml-1. Without hampering the growth of the pathogen, GE at its sub-MICs (50, 100, 150 and 200 µg ml-1) exhibited a dose-dependent increase in antibiofilm activity. The minimal biofilm inhibitory concentration (MBIC) of GE was found to be 200 µg ml-1 with a maximum biofilm inhibition of 85 %. Disintegrated biofilm architecture, reduced EPS, slime and CSH production validated the antibiofilm efficacy of GE. Although the action of GE on preformed biofilm is limited, a 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) reduction assay and live/dead cell staining method revealed reduction in the viability (47 %) of biofilm inhabitants at 2×MIC concentration. Sequential exposure of S. epidermidis to the sub-MICs of GE resulted in poor development of adaptive resistance with diminished biofilm formation.The present study highlights the potential of GE as a suitable candidate for the control of biofilm-mediated S. epidermidis infections.
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Staphylococcus epidermidis is recognized as cause of biofilm-associated infections and interest in the development of new approaches for S. epidermidis biofilm treatment has increased. In a previous paper we reported that the supernatant of Antarctic bacterium Pseudoalteromonas haloplanktis TAC125 presents an anti-biofilm activity against S. epidermidis and preliminary physico-chemical characterization of the supernatant suggested that this activity is due to a polysaccharide. In this work we further investigated the chemical nature of the anti-biofilm P. haloplanktis TAC125 molecule. The production of the molecule was evaluated in different conditions, and reported data demonstrated that it is produced in all P. haloplanktis TAC125 biofilm growth stages, also in minimal medium and at different temperatures. By using a surface coating assay, the surfactant nature of the anti-biofilm compound was excluded. Moreover, a purification procedure was set up and the analysis of an enriched fraction demonstrated that the anti-biofilm activity is not due to a polysaccharide molecule but that it is due to small hydrophobic molecules that likely work as signal. The enriched fraction was also used to evaluate the effect on S. epidermidis biofilm formation in dynamic condition by BioFlux system.
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Staphylococcus epidermidis is a significant nosocomial pathogen in predisposed hosts because of its capability of forming a biofilm on indwelling medical devices. The initial stage of biofilm formation has a key role in S. epidermidis abiotic surface colonization. Recently, many strategies have been developed to create new anti-biofilm surfaces able to control bacterial adhesion mechanisms. In this work, the self-assembled amphiphilic layers formed by two fungal hydrophobins (Vmh2 and Pac3) have proven to be able to reduce the biofilm formed by different strains of S. epidermidis on polystyrene surfaces. The reduction in the biofilm thickness on the coated surfaces and the preservation of cell vitality have been demonstrated through confocal laser scanning microscope analysis. Moreover, the anti-biofilm efficiency of the self-assembled layers on different medically relevant materials has also been demonstrated using a CDC biofilm reactor.
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Development of biofilm is a key mechanism involved in Staphylococcus epidermidis virulence during device-associated infections. We aimed to investigate antibiofilm formation and mature biofilm eradication ability of ethanol and water extracts of Thai traditional herbal recipes including THR-SK004, THR-SK010, and THR-SK011 against S. epidermidis . A biofilm forming reference strain, S. epidermidis ATCC 35984 was employed as a model for searching anti-biofilm agents by MTT reduction assay. The results revealed that the ethanol extract of THR-SK004 (THR-SK004E) could inhibit the formation of S. epidermidis biofilm on polystyrene surfaces. Furthermore, treatments with the extract efficiently inhibit the biofilm formation of the pathogen on glass surfaces determined by scanning electron microscopy and crystal violet staining. In addition, THR-SK010 ethanol extract (THR-SK010E; 0.63–5 μ g/mL) could decrease 30 to 40% of the biofilm development. Almost 90% of a 7-day-old staphylococcal biofilm was destroyed after treatment with THR-SK004E (250 and 500 μ g/mL) and THR-SK010E (10 and 20 μ g/mL) for 24 h. Therefore, our results clearly demonstrated THR-SK004E could prevent the staphylococcal biofilm development, whereas both THR-SK004E and THR-SK010E possessed remarkable eradication ability on the mature staphylococcal biofilm.
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The majority of staphylococci produce biofilm on medical devices, which is the main mechanism to infect humans. Staphylococcal biofilms attach to abiotic or biotic surfaces, forming aggregates and protecting themselves against the immune system and the antimicrobial compounds of the host. Few studies on biofilm formation mechanism in Staphylococcus epidermidis and other coagulase-negative staphylococci (CNS) have been performed; however, there is a great interest in studying and controlling biofilm formation of this genus. This chapter exhibits the state of the art on biofilm formation in S. epidermidis and other staphylococcal species. The main goal of this chapter is to recognize the importance of biofilm formation in Staphylococcus. The participating molecules in staphylococcal biofilm formation are described. Currently, biofilm producer strains of Staphylococcus and mainly CNS have been frequently isolated at hospitals, causing significant economic losses. This chapter includes promising solutions in order to prevent medical device-associated infections, as the development of medical devices possessing anti-biofilm materials or surfaces that act against the adhesion or viability of the microorganisms.
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This study sought to identify novel and nontoxic biofilm inhibitors from the Actinomycete library for attenuating biofilm formation by Staphylococcus epidermidis. After investigating the antibiofilm activities of spent media from 185 Actinomycete strains using two S. epidermidis strains (ATCC 35984 and a clinical strain 5‐121‐2) as target bacteria, three strains of tested Actinomycete (TRM 46200, TRM 41337, and TRM 46814) showed a significant inhibition against S. epidermidis biofilm formation without affecting the growth of planktonic cells. The characteristics of three strains of supernatants suggested that hydrophilic compound possibly extracellular peptides or proteins from these three strains, confer the biofilm reduction in S. epidermidis. An attempt was made to assess their effects on biofilm components and cell surface hydrophobicities in order to disclose acting mechanisms. The crude proteins from spent media of three strains degraded not only exopolysaccharides but also extracellular DNA in S. epidermidis biofilm. The active substances in crude proteins caused S. epidermidis cells to become less hydrophobic. Given these results, the metabolites from Actinomycete strains should keep further attention as potential antibiofilm agents against biofilm formation of S. epidermidis, even biofilm infections of the other bacteria. Staphylococcus epidermidis infections are frequently associated with biofilms that are difficult to eradicate with conventional antibiotics. The new biofilm inhibitors from Actinomycete will have a great value in the prevention and treatment of dairy cow mastitis and other biofilm‐related infections.
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Staphylococcus epidermidis is a clinically important opportunistic pathogen that forms biofilm infections on nearly all types of indwelling medical devices. The biofilm forming capability of S. epidermidis has been linked to the presence of the ica operon in the genome, and the amount of biofilm formation measured by the crystal violet (CV) adherence assay. Six S. epidermidis strains were characterized for their ica status using PCR, and their biofilm forming ability over 6 days, using the CV assay and a flow cell system. Ica-negative strains characterized as 'negative for biofilm formation' based on the CV assay were demonstrated to form strongly attached biofilms after 6 days. However, the biofilms were not as extensive as the ica-positive strains. It was concluded that ica is not required for biofilm formation, nor is the 24-h CV assay generalizable for predicting the 6-day biofilm-forming ability for all S. epidermidis strains.
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