Molecular Genetics of Staphylococcus Epidermidis Biofilms on Indwelling Medical Devices

Vadyvaloo, Viveka; Otto, Michael

doi:10.1177/039139880502801104

Cited by 57 publications

(34 citation statements)

References 92 publications

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“…epidermidis is known as an opportunistic pathogen because it predominantly causes infection in immuno-compromised individuals such as intravenous drug abusers, AIDS patients, patients receiving immuno-suppressive therapy and premature newborns (Vadyvaloo and Otto 2005). In otherwise healthy patients, S. epidermidis causes infection only after penetration of the skin or mucous membranes, which can occur by trauma, inoculation, or implantation of medical devices.…”

Section: S Epidermidis Infections On Indwelling Medical Devicesmentioning

confidence: 99%

Staphylococcal Biofilms

Otto

2008

Current Topics in Microbiology and Immunology

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Staphylococcus epidermidis and S. aureus are the most frequent causes of nosocomial infections and infections on indwelling medical devices, which characteristically involve biofilms. Recent advances in staphylococcal molecular biology have provided more detailed insight into the basis of biofilm formation in these opportunistic pathogens. A series of surface proteins mediate initial attachment to host matrix proteins, which is followed by the expression of a cationic glucosamine-based exopolysaccharide that aggregates the bacterial cells. In some cases, proteins may function as alternative aggregating substances. Furthermore, surfactant peptides have now been recognized as key factors involved in generating the 3-dimensional structure of a staphylococcal biofilm by cellcell disruptive forces, which eventually may lead to the detachment of entire cell clusters. Transcriptional profiling experiments have defined the specific physiology of staphylococcal biofilms and demonstrated that biofilm resistance to antimicrobials is due to gene-regulated processes. Finally, novel animal models of staphylococcal biofilm-associated infection have given us important information on which factors define biofilm formation in vivo. These recent advances constitute an important basis for the development of anti-staphylococcal drugs and vaccines.

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Section: S Epidermidis Infections On Indwelling Medical Devicesmentioning

confidence: 99%

Staphylococcal Biofilms

Otto

2008

Current Topics in Microbiology and Immunology

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665

686

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“…The ECM of S. epidermidis and Staphylococcus aureus, called PIA (polysaccharide intercellular adhesin), enables biofilm formation on catheters and other indwelling medical devices, making these bacteria one of the most common causes of nosocomial infections (Vadyvaloo and Otto 2005). A model for PIA biosynthesis by the ica (intercellular adhesin) gene products has been developed, based on several genetic and biochemical studies (reviewed in Götz 2002).…”

Section: The Y Pestis Pigmentation Phenotype Hms Locus and Biofilmmentioning

confidence: 99%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y. pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-β-1,6-N-acetyl-dglucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food-and water-borne enteric pathogen from which Y. pestis evolved recently, possesses identical hms genes and can form biofilm in vitro but not in the flea. The genetic changes in Y. pestis that resulted in adapting biofilm-forming capability to the flea gut environment, a critical step in the evolution of vector-borne transmission, have yet to be identified. During a flea bite, Y. pestis is regurgitated into the dermis in a unique biofilm phenotype, and this has implications for the initial interaction with the mammalian innate immune response.

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“…Certain S. epidermidis strains are able to form on polymer surfaces a multicellular agglomeration with a characteristic threedimensional structure and physiology called biofilm (3). Compared to the planktonic state, biofilm confers to S. epidermidis increased mechanical, metabolic, immune, and antibiotic resistance and its production is essentially mediated by the production of a polysaccharide intercellular adhesin (PIA) encoded by the accessory intercellular adhesion (ica) operon (4).…”

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confidence: 99%

Comparative Epidemiology of Staphylococcus epidermidis Isolates from Patients with Catheter-Related Bacteremia and from Healthy Volunteers

et al. 2013

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Staphylococcus epidermidis is a major cause of catheter-related bloodstream infections (CRBSIs). Recent studies suggested the existence of well-adapted, highly resistant, hospital-associated S. epidermidis clones. The molecular epidemiology of S. epidermidis in Belgian hospitals and the Belgian community has not been explored yet. We compared a set of 33 S. epidermidis isolates causing CRBSI in hospitalized patients with a set of 33 commensal S. epidermidis isolates. The factors analyzed included resistance to antibiotics and genetic diversity as determined by pulsed-field gel electrophoresis (PFGE), multilocus sequence typing (MLST), and SCCmec typing. Additionally, the presence of virulence-associated mobile genetic elements, the ica operon and the arginine catabolic mobile element (ACME), was assessed and compared against clinical data. CRBSI S. epidermidis isolates were significantly resistant to more antibiotics than commensal S. epidermidis isolates. The two populations studied were very diverse and genetically distinct as only 23% of the 37 PFGE types observed were harbored by both CRBSI and commensal isolates. ACME was found in 76% of S. epidermidis strains, regardless of their origin, while the ica operon was significantly more prevalent in CRBSI isolates than in commensal isolates (P < 0.05). Nine patients presented a clinically severe CRBSI, eight cases of which were due to an ica-positive multiresistant isolate belonging to sequence type 2 (ST2) or ST54. S. epidermidis isolates causing CRBSI were more resistant and more often ica positive than commensal S. epidermidis isolates, which were genetically heterogeneous and susceptible to the majority of antibiotics tested. Clinically severe CRBSIs were due to isolates belonging to two closely related MLST types, ST2 and ST54.

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Molecular Genetics of Staphylococcus Epidermidis Biofilms on Indwelling Medical Devices

Cited by 57 publications

References 92 publications

Staphylococcal Biofilms

Staphylococcal Biofilms

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Comparative Epidemiology of Staphylococcus epidermidis Isolates from Patients with Catheter-Related Bacteremia and from Healthy Volunteers

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