scholarly journals Viscoelasticity of Staphylococcus aureus Biofilms in Response to Fluid Shear Allows Resistance to Detachment and Facilitates Rolling Migration

2005 ◽  
Vol 71 (4) ◽  
pp. 2175-2178 ◽  
Author(s):  
Cory J. Rupp ◽  
Christoph A. Fux ◽  
Paul Stoodley

ABSTRACT Staphylococcus aureus is a leading cause of catheter-related bloodstream infections and endocarditis. Both involve (i) biofilm formation, (ii) exposure to fluid shear, and (iii) high rates of dissemination. We found that viscoelasticity allowed S. aureus biofilms to resist detachment due to increased fluid shear by deformation, while remaining attached to a surface. Further, we report that S. aureus microcolonies moved downstream by rolling along the lumen walls of a glass flow cell, driven by the flow of the overlying fluid. The rolling appeared to be controlled by viscoelastic tethers. This tethered rolling may be important for the surface colonization of medical devices by nonmotile bacteria.

2020 ◽  
Vol 21 (4) ◽  
pp. 304-310
Author(s):  
I. Kara Terki ◽  
H. Hassaine ◽  
A. Kara Terki ◽  
B. Nadira ◽  
N. Kara Terki ◽  
...  

Background: Staphylococcus aureus is one of the species of bacteria most frequently isolated from medical devices. The ability to produce biofilm is an important step in the pathogenesis of these staphylococci infection, and biofilm formation is strongly dependent on environmental conditions as well as antibiotics and disinfectants used in the treatment and prevention of infections.Methodology: In this study, 28 S. aureus isolated from medical devices at the University Hospital Center of Sidi Bel Abbes in Northwestern Algeria were tested for biofilm formation by culture on Red Congo Agar (RCA). The tube method (TM) and tissue culture plate (TCP) techniques were also used to investigate the effect of penicillin, ethanol and betadine on pre-formed biofilm.Results: Nineteen S. aureus isolates produced biofilm on the RCA and 7 produced biofilms by the tube method, 2 of which were high producer. In addition, 9 S. aureus isolates produced biofilm on polystyrene micro-plates, and in the presence of penicillin and ethanol, this number increased to 19 and 11 biofilm producing S. aureus isolates respectively. On the other hand, no biofilm was formed in the presence of betadine.Conclusion: It is important to test for biofilm formation following an imposed external constraint such as disinfectants and antibiotics in order to develop new strategies to combat bacterial biofilms but also to better control their formation. Keywords : Staphylococcus aureus, biofilm, medical device, disinfectant, antibiotic French Title: Effets de certains désinfectants et antibiotiques sur la formation de biofilms par Staphylococcus aureus isolé à partir de dispositifs médicaux au Centre Hospitalier Universitaire de Sidi Bel Abbès, Algérie Contexte: Staphylococcus aureus est l'une des espèces de bactéries les plus fréquemment isolées des dispositifs médicaux. La capacité de produire du biofilm est une étape importante dans la pathogenèse de ces infections à staphylocoques, et la formation de biofilm dépend fortement des conditions environnementales ainsi que des antibiotiques et des désinfectants utilisés dans le traitement et la prévention des infections. Méthodologie: Dans cette étude, 28 S. aureus isolés à partir de dispositifs médicaux au Centre hospitalier universitaire de Sidi Bel Abbès dans le nord-ouest de l'Algérie ont été testés pour la formation de biofilm par culture sur gélose rouge du Congo (RCA). La méthode des tubes (TM) et les techniques de plaques de culture tissulaire (TCP) ont également été utilisées pour étudier l'effet de la pénicilline, de l'éthanol et de la bétadine sur le biofilm préformé. Résultats: Dix-neuf isolats de S. aureus ont produit un biofilm sur le RCA et 7 ont produit des biofilms par la méthode des tubes, dont 2 étaient très productifs. De plus, 9 isolats de S. aureus ont produit du biofilm sur des microplaques en polystyrène, et en présence de pénicilline et d'éthanol, ce nombre est passé à 19 et 11 isolats de S. aureus producteurs de biofilm respectivement. En revanche, aucun biofilm ne s'est formé en présence de bétadine. Conclusion: Il est important de tester la formation de biofilm suite à une contrainte externe imposée comme les désinfectants et les antibiotiques afin de développer de nouvelles stratégies pour lutter contre les biofilms bactériens mais aussi pour mieux contrôler leur formation. Mots-clés: Staphylococcus aureus, biofilm, dispositif médical, désinfectant, antibiotique  


2012 ◽  
Vol 1415 ◽  
Author(s):  
Qi Wang ◽  
Thomas J. Webster

ABSTRACTBiofilms are a common cause of persistent infections on medical devices as they are easy to form and hard to treat. Selenium and its compounds are considered to be a novel material for a wide range of applications including anticancer applications and antibacterial applications. The objective of this study was to coat selenium nanoparticles on the surface of polycarbonate medical devices and examine their effectiveness at preventing biofilm formation. The results of this in vitro study showed that the selenium coating significantly inhibited Staphylococcus aureus growth on the surface of polycarbonate after 24 hours. Thus, this study suggests that coating polymers with nanostructured selenium is a fast and effective way to reduce bacteria functions leading to medical device infections.


2015 ◽  
Vol 82 (1) ◽  
pp. 394-401 ◽  
Author(s):  
Jakub Kwiecinski ◽  
Manli Na ◽  
Anders Jarneborn ◽  
Gunnar Jacobsson ◽  
Marijke Peetermans ◽  
...  

ABSTRACTStaphylococcus aureusbiofilm infections of indwelling medical devices are a major medical challenge because of their high prevalence and antibiotic resistance. As fibrin plays an important role inS. aureusbiofilm formation, we hypothesize that coating of the implant surface with fibrinolytic agents can be used as a new method of antibiofilm prophylaxis. The effect of tissue plasminogen activator (tPA) coating onS. aureusbiofilm formation was tested within vitromicroplate biofilm assays and anin vivomouse model of biofilm infection. tPA coating efficiently inhibited biofilm formation by variousS. aureusstrains. The effect was dependent on plasminogen activation by tPA, leading to subsequent local fibrin cleavage. A tPA coating on implant surfaces prevented both early adhesion and later biomass accumulation. Furthermore, tPA coating increased the susceptibility of biofilm infections to antibiotics.In vivo, significantly fewer bacteria were detected on the surfaces of implants coated with tPA than on control implants from mice treated with cloxacillin. Fibrinolytic coatings (e.g., with tPA) reduceS. aureusbiofilm formation bothin vitroandin vivo, suggesting a novel way to prevent bacterial biofilm infections of indwelling medical devices.


2003 ◽  
Vol 47 (6) ◽  
pp. 1979-1983 ◽  
Author(s):  
Andrea Giacometti ◽  
Oscar Cirioni ◽  
Yael Gov ◽  
Roberto Ghiselli ◽  
Maria Simona Del Prete ◽  
...  

ABSTRACT Staphylococcus aureus is a prevalent cause of bacterial infections associated with indwelling medical devices. RNA III inhibiting peptide (RIP) is known to inhibit S. aureus pathogenesis by disrupting quorum-sensing mechanisms. RIP was tested in the present study for its ability to inhibit S. aureus biofilm formation in a rat Dacron graft model. The activity of RIP was synergistic with those of antibiotics for the complete prevention of drug-resistant S. aureus infections.


2012 ◽  
Vol 81 (2) ◽  
pp. 496-504 ◽  
Author(s):  
David E. Payne ◽  
Nicholas R. Martin ◽  
Katherine R. Parzych ◽  
Alex H. Rickard ◽  
Adam Underwood ◽  
...  

ABSTRACTStaphylococcus aureusis a human commensal and pathogen that is capable of forming biofilms on a variety of host tissues and implanted medical devices. Biofilm-associated infections resist antimicrobial chemotherapy and attack from the host immune system, making these infections particularly difficult to treat. In order to gain insight into environmental conditions that influenceS. aureusbiofilm development, we screened a library of small molecules for the ability to inhibitS. aureusbiofilm formation. This led to the finding that the polyphenolic compound tannic acid inhibitsS. aureusbiofilm formation in multiple biofilm models without inhibiting bacterial growth. We present evidence that tannic acid inhibitsS. aureusbiofilm formation via a mechanism dependent upon the putative transglycosylase IsaA. Tannic acid did not inhibit biofilm formation of anisaAmutant. Overexpression of wild-type IsaA inhibited biofilm formation, whereas overexpression of a catalytically dead IsaA had no effect. Tannin-containing drinks like tea have been found to reduce methicillin-resistantS. aureusnasal colonization. We found that black tea inhibitedS. aureusbiofilm development and that anisaAmutant resisted this inhibition. Antibiofilm activity was eliminated from tea when milk was added to precipitate the tannic acid. Finally, we developed a rodent model forS. aureusthroat colonization and found that tea consumption reducedS. aureusthroat colonization via anisaA-dependent mechanism. These findings provide insight into a molecular mechanism by which commonly consumed polyphenolic compounds, such as tannins, influenceS. aureussurface colonization.


2005 ◽  
Vol 73 (8) ◽  
pp. 4596-4606 ◽  
Author(s):  
Robert M. Q. Shanks ◽  
Niles P. Donegan ◽  
Martha L. Graber ◽  
Sarah E. Buckingham ◽  
Michael E. Zegans ◽  
...  

ABSTRACT Heparin, known for its anticoagulant activity, is commonly used in catheter locks. Staphylococcus aureus, a versatile human and animal pathogen, is commonly associated with catheter-related bloodstream infections and has evolved a number of mechanisms through which it adheres to biotic and abiotic surfaces. We demonstrate that heparin increased biofilm formation by several S. aureus strains. Surface coverage and the kinetics of biofilm formation were stimulated, but primary attachment to the surface was not affected. Heparin increased S. aureus cell-cell interactions in a protein synthesis-dependent manner. The addition of heparin rescued biofilm formation of hla, ica, and sarA mutants. Our data further suggest that heparin stimulation of biofilm formation occurs neither through an increase in sigB activity nor through an increase in polysaccharide intracellular adhesin levels. These finding suggests that heparin stimulates S. aureus biofilm formation via a novel pathway.


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 ◽  
...  

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.


2009 ◽  
Vol 53 (9) ◽  
pp. 3914-3922 ◽  
Author(s):  
Melphine M. Harriott ◽  
Mairi C. Noverr

ABSTRACT 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.


2006 ◽  
Vol 50 (4) ◽  
pp. 1463-1469 ◽  
Author(s):  
M. A. Jabra-Rizk ◽  
T. F. Meiller ◽  
C. E. James ◽  
M. E. Shirtliff

ABSTRACT Staphylococcus aureus is among the leading pathogens causing bloodstream infections able to form biofilms on host tissue and indwelling medical devices and to persist and cause disease. Infections caused by S. aureus are becoming more difficult to treat because of increasing resistance to antibiotics. In a biofilm environment particularly, microbes exhibit enhanced resistance to antimicrobial agents. Recently, farnesol was described as a quorum-sensing molecule with possible antimicrobial properties. In this study, the effect of farnesol on methicillin-resistant and -susceptible strains of S. aureus was investigated. With viability assays, biofilm formation assessment, and ethidium bromide uptake testing, farnesol was shown to inhibit biofilm formation and compromise cell membrane integrity. The ability of farnesol to sensitize S. aureus to antimicrobials was assessed by agar disk diffusion and broth microdilution methods. For both strains of staphylococci, farnesol was only able to reverse resistance at a high concentration (150 μM). However, it was very successful at enhancing the antimicrobial efficacy of all of the antibiotics to which the strains were somewhat susceptible. Therefore, synergy testing of farnesol and gentamicin was performed with static biofilms exposed to various concentrations of both agents. Plate counts of harvested biofilm cells at 0, 4, and 24 h posttreatment indicated that the combined effect of gentamicin at 2.5 times the MIC and farnesol at 100 μM (22 μg/ml) was able to reduce bacterial populations by more than 2 log units, demonstrating synergy between the two antimicrobial agents. This observed sensitization of resistant strains to antimicrobials and the observed synergistic effect with gentamicin indicate a potential application for farnesol as an adjuvant therapeutic agent for the prevention of biofilm-related infections and promotion of drug resistance reversal.


2016 ◽  
Vol 61 (1) ◽  
Author(s):  
Mircea Radu Mihu ◽  
Vitor Cabral ◽  
Rodney Pattabhi ◽  
Moses T. Tar ◽  
Kelvin P. Davies ◽  
...  

ABSTRACT Staphylococcus aureus is frequently isolated in the setting of infections of indwelling medical devices, which are mediated by the microbe's ability to form biofilms on a variety of surfaces. Biofilm-embedded bacteria are more resistant to antimicrobial agents than their planktonic counterparts and often cause chronic infections and sepsis, particularly in patients with prolonged hospitalizations. In this study, we demonstrate that sustained nitric oxide-releasing nanoparticles (NO-np) interfere with S. aureus adhesion and prevent biofilm formation on a rat central venous catheter (CVC) model of infection. Confocal and scanning electron microscopy showed that NO-np-treated staphylococcal biofilms displayed considerably reduced thicknesses and bacterial numbers compared to those of control biofilms in vitro and in vivo, respectively. Although both phenotypes, planktonic and biofilm-associated staphylococci, of multiple clinical strains were susceptible to NO-np, bacteria within biofilms were more resistant to killing than their planktonic counterparts. Furthermore, chitosan, a biopolymer found in the exoskeleton of crustaceans and structurally integrated into the nanoparticles, seems to add considerable antimicrobial activity to the technology. Our findings suggest promising development and translational potential of NO-np for use as a prophylactic or therapeutic against bacterial biofilms on CVCs and other medical devices.


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