Part 2: Effectiveness of a novel gentamicinpalmitate coating on biofilm formation of Staphylococcus aureus and Staphylococcus epidermidis

2010 ◽  
Vol 3 (1) ◽  
pp. 107 ◽  
Author(s):  
Klaus Dieter Kuhn ◽  
Jorg Brunke
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation

scholarly journals Anaerobic Conditions Induce Expression of Polysaccharide Intercellular Adhesin in Staphylococcus aureus and Staphylococcus epidermidis

2001 ◽  
Vol 69 (6) ◽  
pp. 4079-4085 ◽  
Author(s):  
Sarah E. Cramton ◽  
Martina Ulrich ◽  
Friedrich Götz ◽  
Gerd Döring
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Extracellular Polysaccharide ◽  
Growth Conditions ◽  
Anaerobic Conditions ◽  
Anaerobic Environment ◽  
Specific Mrna

ABSTRACT Products of the intercellular adhesion (ica) operon in Staphylococcus aureus and Staphylococcus epidermidis synthesize a linear β-1,6-linked glucosaminylglycan. This extracellular polysaccharide mediates bacterial cell-cell adhesion and is required for biofilm formation, which is thought to increase the virulence of both pathogens in association with prosthetic biomedical implants. The environmental signal(s) that triggers ica gene product and polysaccharide expression is unknown. Here we demonstrate that anaerobic in vitro growth conditions lead to increased polysaccharide expression in both S. aureus and S. epidermidis, although the regulation is less stringent inS. epidermidis. Anaerobiosis also dramatically stimulates ica-specific mRNA expression inica- and polysaccharide-positive strains of both S. aureus and S. epidermidis.These data suggest a mechanism whereby ica gene expression and polysaccharide production may act as a virulence factor in an anaerobic environment in vivo.

scholarly journals Effects of oregano, carvacrol and thymol on Staphylococcus aureus and Staphylococcus epidermidis biofilms

2007 ◽  
Vol 56 (4) ◽  
pp. 519-523 ◽  
Author(s):  
Antonia Nostro ◽  
Andrea Sudano Roccaro ◽  
Giuseppe Bisignano ◽  
Andreana Marino ◽  
Maria A. Cannatelli ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Essential Oil ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Inhibitory Concentration ◽  
Oregano Essential Oil ◽  
Planktonic Growth ◽  
Subinhibitory Concentrations

The aim of this study was to evaluate the effect of oregano essential oil, carvacrol and thymol on biofilm-grown Staphylococcus aureus and Staphylococcus epidermidis strains, as well as the effects of the oils on biofilm formation. For most of the S. aureus (n=6) and S. epidermidis (n=6) strains tested, the biofilm inhibitory concentration (0.125–0.500 %, v/v, for oregano, and 0.031–0.125 %, v/v, for carvacrol and thymol) and biofilm eradication concentration (0.25–1.0 %, v/v, for oregano and 0.125–0.500 %, v/v, for carvacrol and thymol) values were twofold or fourfold greater than the concentration required to inhibit planktonic growth. Subinhibitory concentrations of the oils attenuated biofilm formation of S. aureus and S. epidermidis strains on polystyrene microtitre plates.

scholarly journals Oral Administration of the Broad-Spectrum Antibiofilm Compound Toremifene Inhibits Candida albicans and Staphylococcus aureus Biofilm FormationIn Vivo

2014 ◽  
Vol 58 (12) ◽  
pp. 7606-7610 ◽  
Author(s):  
Kaat De Cremer ◽  
Nicolas Delattin ◽  
Katrijn De Brucker ◽  
Annelies Peeters ◽  
Soña Kucharíková ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Candida Albicans ◽  
Broad Spectrum ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Candida Krusei ◽  
Content Type ◽  
And Staphylococcus Aureus

ABSTRACTWe here report on thein vitroactivity of toremifene to inhibit biofilm formation of different fungal and bacterial pathogens, includingCandida albicans,Candida glabrata,Candida dubliniensis,Candida krusei,Pseudomonas aeruginosa,Staphylococcus aureus, andStaphylococcus epidermidis. We validated thein vivoefficacy of orally administered toremifene againstC. albicans and S. aureusbiofilm formation in a rat subcutaneous catheter model. Combined, our results demonstrate the potential of toremifene as a broad-spectrum oral antibiofilm compound.

scholarly journals The Teicoplanin-Associated Locus Regulator (TcaR) and the Intercellular Adhesin Locus Regulator (IcaR) Are Transcriptional Inhibitors of the ica Locus in Staphylococcus aureus

2004 ◽  
Vol 186 (8) ◽  
pp. 2449-2456 ◽  
Author(s):  
Kimberly K. Jefferson ◽  
Danielle B. Pier ◽  
Donald A. Goldmann ◽  
Gerald B. Pier
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Negative Regulator ◽  
Regulatory Proteins ◽  
Polysaccharide Intercellular Adhesin ◽  
Topoisomerase Iv ◽  
Exogenous Factors ◽  
Dna Affinity Chromatography

ABSTRACT Infections involving Staphylococcus aureus are often more severe and difficult to treat when the organism assumes a biofilm mode of growth. The polysaccharide poly-N-acetylglucosamine (PNAG), also known as polysaccharide intercellular adhesin, is synthesized by the products of the intercellular adhesin (ica) locus and plays a key role in biofilm formation. Numerous conditions and exogenous factors influence ica transcription and PNAG synthesis, but the regulatory factors and pathways through which these environmental stimuli act have been only partially characterized. We developed a DNA affinity chromatography system to purify potential regulatory proteins that bind to the ica promoter region. Using this technique, we isolated four proteins, including the staphylococcal gene regulator SarA, a MarR family transcriptional regulator of the teicoplanin-associated locus TcaR, DNA-binding protein II, and topoisomerase IV, that bound to the ica promoter. Site-directed deletion mutagenesis of tcaR indicated that TcaR was a negative regulator of ica transcription, but deletion of tcaR alone did not induce any changes in PNAG production or in adherence to polystyrene. We also investigated the role of IcaR, encoded within the ica locus but divergently transcribed from the biosynthetic genes. As has been shown previously in Staphylococcus epidermidis, we found that IcaR was also a negative regulator of ica transcription in S. aureus. We also demonstrate that mutation of icaR augmented PNAG production and adherence to polystyrene. Transcription of the ica locus, PNAG production, and adherence to polystyrene were further increased in a tcaR icaR double mutant. In summary, TcaR appeared to be a weak negative regulator of transcription of the ica locus, whereas IcaR was a strong negative regulator, and in their absence PNAG production and biofilm formation were enhanced.

scholarly journals Antibacterial Effects of Phage Lysin LysGH15 on Planktonic Cells and Biofilms of Diverse Staphylococci

2018 ◽  
Vol 84 (15) ◽  
Author(s):  
Yufeng Zhang ◽  
Mengjun Cheng ◽  
Hao Zhang ◽  
Jiaxin Dai ◽  
Zhimin Guo ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Multidrug Resistant ◽  
Planktonic Cells ◽  
Content Type ◽  
Resistant Strains ◽  
Staphylococcus Hominis ◽  
Phage Lysin

ABSTRACT Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we observed the ability of the phage lysin LysGH15 to eliminate staphylococcal planktonic cells and biofilms formed by Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus, and Staphylococcus hominis. All these strains were sensitive to LysGH15, showing reductions in bacterial counts of approximately 4 log units within 30 min after treatment with 20 μg/ml of LysGH15, and the MICs ranged from 8 μg/ml to 32 μg/ml. LysGH15 efficiently prevented biofilm formation by the four staphylococcal species at a dose of 50 μg/ml. At a higher dose (100 μg/ml), LysGH15 also showed notable disrupting activity against 24-h and 72-h biofilms formed by S. aureus and coagulase-negative species. In the in vivo experiments, a single intraperitoneal injection of LysGH15 (20 μg/mouse) administered 1 h after the injection of S. epidermidis at double the minimum lethal dose was sufficient to protect the mice. The S. epidermidis cell counts were 4 log units lower in the blood and 3 log units lower in the organs of mice 24 h after treatment with LysGH15 than in the untreated control mice. LysGH15 reduced cytokine levels in the blood and improved pathological changes in the organs. The broad antistaphylococcal activity exerted by LysGH15 on planktonic cells and biofilms makes LysGH15 a valuable treatment option for biofilm-related or non-biofilm-related staphylococcal infections. IMPORTANCE Most staphylococcal species are major causes of health care- and community-associated infections. In particular, Staphylococcus aureus is a common and dangerous pathogen, and Staphylococcus epidermidis is a ubiquitous skin commensal and opportunistic pathogen. Treatment of infections caused by staphylococci has become more difficult because of the emergence of multidrug-resistant strains as well as biofilm formation. In this study, we found that all tested S. aureus, S. epidermidis, Staphylococcus haemolyticus, and Staphylococcus hominis strains were sensitive to the phage lysin LysGH15 (MICs ranging from 8 to 32 μg/ml). More importantly, LysGH15 not only prevented biofilm formation by these staphylococci but also disrupted 24-h and 72-h biofilms. Furthermore, the in vivo efficacy of LysGH15 was demonstrated in a mouse model of S. epidermidis bacteremia. Thus, LysGH15 exhibits therapeutic potential for treating biofilm-related or non-biofilm-related infections caused by diverse staphylococci.

scholarly journals The Glycosyltransferases sdgA and sdgB Expression in Staphylococcus Epidermidis Depends On The Conditions of Biofilm Formation.

2021 ◽  
Author(s):  
Itzia S. Gómez-Alonso ◽  
Ilse D. Estrada-Alemán ◽  
Sergio Martínez-García ◽  
Humberto Peralta ◽  
Erika T. Quintana ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Cathepsin G ◽  
Dynamic Conditions ◽  
Static Conditions ◽  
Sessile Cells ◽  
In Cells

Abstract The Staphylococcus aureus’ SdrG protein is glycosylated by SdgA and SdgB for their protection against its degradation by the neutrophil’s cathepsin G. So far, there is not information about the role of Staphylococcus epidermidis’ SdgA nor SdgB in the production of biofilm, therefore the main of this work was to determine the distribution and expression of sdrG, sdgA and sdgB genes in S. epidermidis in conditions of biofilm. The frequency of the genes sdrG, sdgA and sdgB were evaluated by PCR in a collection of 75 isolates. The isolates were grown in dynamic conditions (in agitation) or static conditions (biofilm productor: planktonic or sessile cells). The expression of sdrG, sdgA and sdgB were determined by RT-qPCR in cells grown under dynamic conditions (CGDC), as well as planktonic and sessile cells, and in cells adhered to a catheter (in vivo). The genes sdrG and sdgB were detected in 100% of isolates, meanwhile the gene sdgA was detected in 71% of the samples (p<0.001). The CGDC did not expressed the sdrG, sdgA and sdgB mRNAs. The planktonic and sessile cells expressed sdrG and sdgB, and the same was seen in cells adhered to the catheter. In particular, one isolate, able to induce biofilm under cathepsin G treatment, expressed sdrG and sdgB in planktonic, sessile and in cells adhered to the catheter. This suggests that the state of cells adherence is an important factor for the transcription of sdgA, sdgB and sdrG.

scholarly journals Vitamin E for prevention of biofilm-caused Healthcare-associated infections

Open Medicine ◽  
2019 ◽  
Vol 15 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Franca Vergalito ◽  
Laura Pietrangelo ◽  
Giulio Petronio Petronio ◽  
Federica Colitto ◽  
Marco Alfio Cutuli ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Vitamin E ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Bacterial Biofilm ◽  
Tocopheryl Acetate ◽  
Healthcare Associated Infections ◽  
Biofilm Development ◽  
Healthcare Associated

AbstractThe healthcare-associated infections (HCAIs) occur in patients both in nosocomial environments and in community. More often HCAIs are associated to the use of medical devices and bacterial biofilm development on these equipments. Due to the clinical and economic relevance of this topic, new strategies for the treatment of infections caused by biofilm proliferation are unceasingly searched by scientists.The present study investigated the role of vitamin E to reduce the biofilm formation for a larger panel of human pathogens, including strains of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Acinetobacter baumannii, Pseudomonas aeruginosa and Pseudomonas putida.This potential activity was tested by placing a preparation of vitamin E (α-Tocopheryl acetate) as interface between the bacterial culture and the polystyrene walls of a 96 well plate at different concentrations of glucose, used as a biofilm enhancer.The Staphylococcus genus was further investigated by spreading the vitamin E on a silicone catheter lumen and evaluating its influence on the bacterial colonization.From our results, vitamin E has been able to interfere with bacterial biofilm and prevent in vitro biofilm formation. Furthermore, the ability of Staphylococcus aureus and Staphylococcus epidermidis to colonize the catheter surface decreased as a result of vitamin E application.

scholarly journals Small Molecules Produced by Commensal Staphylococcus epidermidis Disrupt Formation of Biofilms by Staphylococcus aureus

2019 ◽  
Vol 86 (5) ◽  
Author(s):  
Thaís Glatthardt ◽  
Juliana Curityba de Mello Campos ◽  
Raiane Cardoso Chamon ◽  
Thiago Freitas de Sá Coimbra ◽  
Giulia de Almeida Rocha ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Bloodstream Infections ◽  
Proteinase K ◽  
Antibiofilm Activity ◽  
Skin Microbiome ◽  
Chronic Infections ◽  
Content Type ◽  
Treatment And Prevention

ABSTRACT The microbiota influences host health through several mechanisms, including protecting it from pathogen colonization. Staphylococcus epidermidis is one of the most frequently found species in the skin microbiota, and its presence can limit the development of pathogens such as Staphylococcus aureus. S. aureus causes diverse types of infections ranging from skin abscesses to bloodstream infections. Given the increasing prevalence of S. aureus drug-resistant strains, it is imperative to search for new strategies for treatment and prevention. Thus, we investigated the activity of molecules produced by a commensal S. epidermidis isolate against S. aureus biofilms. We showed that molecules present in S. epidermidis cell-free conditioned media (CFCM) caused a significant reduction in biofilm formation in most S. aureus clinical isolates, including all 4 agr types and agr-defective strains, without any impact on growth. S. epidermidis molecules also disrupted established S. aureus biofilms and reduced the antibiotic concentration required to eliminate them. Preliminary characterization of the active compound showed that its activity is resistant to heat, protease inhibitors, trypsin, proteinase K, and sodium periodate treatments, suggesting that it is not proteinaceous. RNA sequencing revealed that S. epidermidis-secreted molecules modulate the expression of hundreds of S. aureus genes, some of which are associated with biofilm production. Biofilm formation is one of the main virulence factors of S. aureus and has been associated with chronic infections and antimicrobial resistance. Therefore, molecules that can counteract this virulence factor may be promising alternatives as novel therapeutic agents to control S. aureus infections. IMPORTANCE S. aureus is a leading agent of infections worldwide, and its main virulence characteristic is the ability to produce biofilms on surfaces such as medical devices. Biofilms are known to confer increased resistance to antimicrobials and to the host immune responses, requiring aggressive antibiotic treatment and removal of the infected surface. Here, we investigated a new source of antibiofilm compounds, the skin microbiome. Specifically, we found that a commensal strain of S. epidermidis produces molecules with antibiofilm activity, leading to a significant decrease of S. aureus biofilm formation and to a reduction of previously established biofilms. The molecules potentiated the activity of antibiotics and affected the expression of hundreds of S. aureus genes, including those associated with biofilm formation. Our research highlights the search for compounds that can aid us in the fight against S. aureus infections.

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