Epidermidis Biofilm Formation Research Articles

Enzymatic detachment of Staphylococcus epidermidis biofilms.

The gram-positive bacterium Staphylococcus epidermidis is the most common cause of infections associated with catheters and other indwelling medical devices. S. epidermidis produces an extracellular slime that enables it to form adherent biofilms on plastic surfaces. We found that a biofilm-releasing enzyme produced by the gram-negative periodontal pathogen Actinobacillus actinomycetemcomitans rapidly and efficiently removed S. epidermidis biofilms from plastic surfaces. The enzyme worked by releasing extracellular slime from S. epidermidis cells. Precoating surfaces with the enzyme prevented S. epidermidis biofilm formation. Our findings demonstrate that biofilm-releasing enzymes can exhibit broad-spectrum activity and that these enzymes may be useful as antibiofilm agents.

MP055 Host cell proteases induce S. epidermidis biofilm formation via proteolytic processing of the accumulation associated protein

Infektiologie hat sich in Deutschland als klinische Disziplin nur langsam entwickelt. Die Infektiologendichte und die Zahl der Fachabteilungen in Kliniken hier ist im europäischen Vergleich aber immer noch gering. Zugleich ist aber auch die Zahl anderer Fachärzte im Bereich Infektionsmedizin wie Medizinische Mikrobiologie und Krankenhaushygiene gering. Die Ursachen sind vielfältig, teilweise werden die Rolle und Leistungen des klinischen Infektiologen und auch der Unterschied zur Medizinischen Mikrobiologie gar nicht verstanden. Ein Blick in andere Länder zeigt die enorme Bedeutung besonders der Infektiologie für die klinische Versorgung von komplexen Infektionspatienten, für Behandlungsqualität und Patientensicherheit sowie für strategische Aufgaben im Bereich Sicherstellung rationaler Antibiotikaverordnung (antibiotic stewardship, ABS) und Resistenzminimierung. Der Blick in andere Länder zeigt auch, dass Infektiologen vielerorts Krankenhaushygiene-Funktionen übernehmen können, die Nutzwert moderner mikrobiologischer Diagnostik verbessern und für die translationale Infektionsforschung von außerordentlicher Bedeutung sind. Hochrechnungen ergeben, dass in Deutschland mehr als 1000 zusätzliche Infektiologen gebraucht werden, um eine adäquate Qualität sicherzustellen. Dabei können insbesondere in kleineren Krankenhäusern einige der Funktionen von geschulten ABS-Experten übernommen werden. Mehr Weiterbildungskapazität und Flexibilität für das Training von Infektiologen und von Experten im Bereich ABS und Krankenhaushygiene in Deutschland sind eine dringliche Angelegenheit vor dem Hintergrund der Probleme mit Antibiotikaresistenz.(Wie vom Gastherausgeber eingereicht)Clinical infectious diseases have only slowly been established as a medical specialty in Germany. The density of infectious diseases (ID) specialists and the number of ID divisions in general hospitals is still limited when compared with the situation in many other European countries, and there is also a lack of hospital-based medical microbiologists and infection control doctors for many reasons. Often, there is a lack of understanding of the roles and the performance of ID specialists versus microbiologists. Experience in other countries shows that ID specialists are important as clinical experts at the bedside, can help ascertain healthcare quality and patient safety, and are perfectly suited for undertaking strategic tasks in the field of cost-effective antimicrobial therapy algorithms and antibiotic stewardship (ABS) in hospitals. ID specialists are responsible for infection control in several countries, can improve the utility of diagnostic microbiology and are key partners in translational research. We estimate that more than 1,000 additional ID specialists are needed in this country, and believe that specially trained ABS experts can take over parts of their responsibilities and tasks in smaller hospitals. More capacity and flexibility in postgraduate training in infectious diseases, antibiotic stewardship and infection control in Germany will be critical to address the problem of antimicrobial resistance.(As supplied by publisher)

Use of the quorum-sensing inhibitor RNAIII-inhibiting peptide to prevent biofilm formation in vivo by drug-resistant Staphylococcus epidermidis.

Staphylococcus epidermidis is a frequent cause of infections associated with foreign bodies and indwelling medical devices. The bacteria are capable of surviving antibiotic treatment through encapsulation into biofilms. RNAIII-inhibiting peptide (RIP) is a heptapeptide that inhibits S. aureus pathogenesis by disrupting quorum-sensing mechanisms. In this study, RIP inhibited drug-resistant S. epidermidis biofilm formation through a mechanism similar to that evidenced for S. aureus. RIP is synergistic with antibiotics in eliminating 100% of graft-associated in vivo S. epidermidis infections, which suggests that RIP may be used to coat medical devices to prevent staphylococcal infections. Disruption of cell-cell communication can prevent infections associated with antibiotic-resistant strains.

Effect of subinhibitory antibiotic concentrations on polysaccharide intercellular adhesin expression in biofilm-forming Staphylococcus epidermidis.

Biofilm production is an important step in the pathogenesis of Staphylococcus epidermidis polymer-associated infections and depends on the expression of the icaADBC operon leading to the synthesis of a polysaccharide intercellular adhesin. A chromosomally encoded reporter gene fusion between the ica promoter and the beta-galactosidase gene lacZ from Escherichia coli was constructed and used to investigate the influence of both environmental factors and subinhibitory concentrations of different antibiotics on ica expression in S. epidermidis. It was shown that S. epidermidis biofilm formation is induced by external stress (i.e., high temperature and osmolarity). Subinhibitory concentrations of tetracycline and the semisynthetic streptogramin antibiotic quinupristin-dalfopristin were found to enhance ica expression 9- to 11-fold, whereas penicillin, oxacillin, chloramphenicol, clindamycin, gentamicin, ofloxacin, vancomycin, and teicoplanin had no effect on ica expression. A weak (i.e., 2.5-fold) induction of ica expression was observed for subinhibitory concentrations of erythromycin. The results were confirmed by Northern blot analyses of ica transcription and quantitative analyses of biofilm formation in a colorimetric assay.

Molecular mechanisms of Staphylococcus epidermidis biofilm formation

Coagulase-negative staphylococci, mainly Staphylococcus epidermidis, are the predominant cause of implanted medical-device related infections. The formation of adherent multilayered biofilms embedded into a glycocalyx composed of exopolysaccharides on implanted devices is believed to be essential for the pathogenesis of S. epidermidis infections. Biofilm formation may be separated into primary attachment of bacteria to native or modified polymer surfaces followed by proliferation of attached bacterial cells leading to accumulation of multi-layered cell-clusters and glycocalyx formation. Recent progress in the understanding of the molecular mechanisms cooperating in S. epidermidis biofilm formation is reviewed and current thinking on the relevance of these mechanisms for S. epidermidis device-related infections is discussed.

Antifrïction ball or roller units offer many material advantages in obtaining truck driveline slip: Young, J. R. SAE Journal, Vol 76, No 1 (January 1968) p68

Infections, especially those involving drivelines, are among the most serious complications that follow ventricular assist device implantation. Staphylococci are the most common causes of these infections. Once driveline infections are established, they can remain localized or progress as an ascending infection to cause metastatic seeding of other tissue sites. Although elaboration of biofilm appears to be critical in prosthetic device infections, its role as a facilitator of staphylococcal infection and migration along the driveline and other prosthetic devices is unclear.A murine model of driveline infection was used to investigate staphylococcal migration along the driveline. A biofilm-producing strain of Staphylococcus epidermidis and a Staphylococcus aureus strain and its intercellular adhesion gene cluster (ica)–negative (biofilm-deficient) isogenic mutant were used in these studies. Bacterial density on the driveline and the underlying tissue was measured over time. Scanning electron microscopy was used to examine the morphology of S epidermidis biofilm formation as the infection progressed.The biofilm-deficient S aureus mutant was less effective at infecting and migrating along the driveline than the wild-type strain over time. However, the ica mutation had no effect on the ability of the strain to infect underlying tissue. S aureus exhibited more rapid migration than S epidermidis. Scanning electron microscopy revealed the deposition of host matrix on the Dacron material after implantation. This was followed by elaboration of a bacterial biofilm that correlated with more rapid migration along the driveline.Biofilm formation is a critical virulence determinant that facilitates the progression of drivelines infections.