Biofilms are complex bacterial communities that resist the action of antibiotics and the human immune system. Bacteria within biofilms are the cause of numerous, almost impossible to eradicate, persistent infections. Biofilms can form on many medical devices and implants, and so have an enormous impact on medicine. Due to the lack of effective anti-biofilm antibiotics, novel alternative compounds or strategies are urgently required. This review describes some of the latest approaches in the field of biofilm treatment. New anti-biofilm technologies target different stages in the biofilm formation process. Some act to modify the colonized biomaterials to make them resistant to biofilm formation. One potentially important candidate treatment uses silver nanoparticles that show anti-bacterial and anti-biofilm activity. The biological action of nano-silver is complex and seems to involve a number of pathways. However, there have been few reports on the anti-biofilm activity of silver nanoparticles and the precise mechanism underlying their action remains unresolved. Here, we describe some anti-biofilm approaches employing AgNPs and consider the challenges and problems that need to be addressed in order to make silver nanoparticles a part of an effective anti-biofilm strategy.

Nearly all bacterial species, including pathogens, have the ability to form biofilms. Biofilms are defined as structured ecosystems in which microbes are attached to surfaces and embedded in a matrix composed of polysaccharides, eDNA, and proteins, and their development is a multistep process. Bacterial biofilms constitute a large medical problem due to their extremely high resistance to various types of therapeutics, including conventional antibiotics. Several environmental and genetic signals control every step of biofilm development and dispersal. From among the latter, quorum sensing, cyclic diguanosine-5’-monophosphate, and small RNAs are considered as the main regulators. The present review describes the control role of these three regulators in the life cycles of biofilms built by Pseudomonas aeruginosa, Staphylococcus aureus, Salmonella enterica serovar Typhimurium, and Vibrio cholerae. The interconnections between their activities are shown. Compounds and strategies which target the activity of these regulators, mainly quorum sensing inhibitors, and their potential role in therapy are also assessed.

In this paper, we describe the facile synthesis and physicochemical characteristic of nitroxide-coated silver nanoparticles. The proposed procedure allows to obtain isolatable, devoid of Ag + impurities, longterm stable, spherical nanoparticles with an average diameter ca. 7 nm, which exhibit high antibacterial 10 activity towards both Gram-negative and Gram-positive strains. The determined Minimum Bactericidal Concentrations (MBCs) are significantly lower than the values reported for other thiolate-capped silver nanoparticles and range from 4 µg/ml (against Pseudomonas aeruginosa) to 12 µg/ml (against Staphylococcus aureus). Our studies proved that the nitroxide coverage favours antibacterial activity of silver nanoparticles, probably due to the ability of nitroxides to be oxidized by reactive oxygen species 15 (ROS) to positively charged oxoammonium ions which can interact strongly with bacterial membrane. Furthermore, the mechanism of chemisorption of disulphide bisnitroxide on silver surface has been discussed on the basis of XPS, FTIR and ESR results. 65 impurities from AgNPs suspensions on the accurate evaluation their toxicity. It is worth to point out that the comprehensive

The objective of this study was to characterize the effects of silver nanoparticles on Pseudomonas aeruginosa. Their interactions with several conventional antibiotics and ability to induce a stress response were examined. Interactions between silver nanoparticles (AgNPs) and antibiotics against free-living cells and biofilm of P. aeruginosa were studied using the chequerboard method and time-kill assays. The ability of AgNPs to induce a stress response was determined by evaluation of cellular levels of the DnaK and HtpG chaperones using SDS-PAGE and Western blot analysis. Synergistic activity against free-living P. aeruginosa between AgNPs and ampicillin, streptomycin, rifampicin and tetracycline, but not oxacillin, ciprofloxacin, meropenem or ceftazidime, was demonstrated by the chequerboard method. No such interactions were observed against P. aeruginosa biofilm. The results of time-kill assays confirmed synergy only for the AgNPs-streptomycin combination. AgNPs induced the expression of chaperone DnaK. No induction of the HtpG chaperone was detected. In conclusion, AgNPs not only display potent bactericidal activity against P. aeruginosa, but also act synergistically with several conventional antibiotics to enhance their effect against free-living bacteria as determined by the chequerboard method. The time-kill assay proved synergy between AgNPs and streptomycin only. The ability of AgNPs to induce the major chaperone protein DnaK may influence bacterial resistance to antimicrobials.

Vancomycin-resistant Enterococcus faecium represents a growing threat in hospital-acquired infections. Two outbreaks of this pathogen from neighboring Warsaw hospitals have been analyzed in this study. Pulsed-field gel electrophoresis (PFGE) of SmaI-digested DNA, multilocus VNTR analysis (MLVA), and multilocus sequence typing (MLST) revealed a clonal variability of isolates which belonged to three main lineages (17, 18, and 78) of nosocomial E. faecium. All isolates were multidrug resistant and carried several resistance, virulence, and plasmid-specific genes. Almost all isolates shared the same variant of Tn1546 transposon, characterized by the presence of insertion sequence ISEf1 and a point mutation in the vanA gene. In the majority of cases, this transposon was located on 50 kb or 100 kb pRUM-related plasmids, which lacked, however, the axe-txe toxin-antitoxin genes. 100 kb plasmid was easily transferred by conjugation and was found in various clonal backgrounds in both institutions, while 50 kb plasmid was not transferable and occurred solely in MT159/ST78 strains that disseminated clonally in one institution. Although molecular data indicated the spread of VRE between two institutions or a potential common source of this alert pathogen, epidemiological investigations did not reveal the possible route by which outbreak strains disseminated.