The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Michael Otto - One of the best experts on this subject based on the ideXlab platform.
-
Immune Evasion Mechanisms of Staphylococcus Epidermidis Biofilm Infection
Frontiers in Microbiology, 2018Co-Authors: Katherine Y. Le, Matthew D. Park, Michael OttoAbstract:The primary virulence factor of the skin commensal and opportunistic pathogen, Staphylococcus Epidermidis, is the ability to form biofilms on surfaces of implanted materials. Much of this microorganism’s pathogenic success has been attributed to its ability to evade the innate immune system. The primary defense against Staphylococcus Epidermidis biofilm infection consists of complement activation, recruitment and subsequent killing of the pathogen by effector cells. Among pathogen-derived factors, the biofilm exopolysaccharide polysaccharide intercellular adhesion (PIA), as well as the accumulation-associated protein (Aap), and the extracellular matrix binding protein (Embp) have been shown to modulate effector cell-mediated killing of S. Epidermidis. Phenol-soluble modulins (PSMs) constitute the only class of secreted toxins by S. Epidermidis, at least one type of which (PSM) possesses strong cytolytic properties toward leukocytes. However, through selective production of non-cytolytic subtypes of PSMs, S. Epidermidis is able to maintain a low inflammatory infection profile and avoid eradication by the host immune system. Taken together, our emerging understanding of the mechanisms behind immune modulation by S. Epidermidis elucidates the microorganism’s success in the initial colonization of device surfaces as well as the maintenance of a chronic and indolent course of biofilm infection.
-
host response to staphylococcus Epidermidis colonization and infections
Frontiers in Cellular and Infection Microbiology, 2017Co-Authors: Thuan H Nguyen, Matthew D. Park, Michael OttoAbstract:The majority of research in the Staphylococcus field has been dedicated to the understanding of Staphylococcus aureus infections. In contrast, there is limited information on infections by coagulase-negative Staphylococci (CoNS) and how the host responds to them. S. Epidermidis, a member of the coagulase-negative Staphylococci, is an important commensal organism of the human skin and mucous membranes; and there is emerging evidence of its benefit for human health in fighting off harmful microorganisms. However, S. Epidermidis can cause opportunistic infections, which include particularly biofilm-associated infections on indwelling medical devices. These often can disseminate into the bloodstream; and in fact, S. Epidermidis is the most frequent causes of nosocomial sepsis. The increasing use of medical implants and the dramatic shift in the patient demographic population in recent years have contributed significantly to the rise of S. Epidermidis infections. Furthermore, treatment has been complicated by the emergence of antibiotic-resistant strains. Today, S. Epidermidis are major nosocomial pathogens posing significant medical and economic burdens. In this review, we present the current understanding of mechanisms of host defense against the prototypical CoNS species S. Epidermidis as commensals of the skin and mucous membranes, and during biofilm-associated infection and sepsis.
-
Staphylococcus Epidermidis Pathogenesis
Methods of Molecular Biology, 2013Co-Authors: Michael OttoAbstract:Abstract Staphylococcus Epidermidis is the most frequently encountered member of the coagulase-negative staphylococci on human epithelial surfaces. It has emerged as an important nosocomial pathogen, especially in infections of indwelling medical devices. The mechanisms that S. Epidermidis uses to survive during infection are in general of a passive nature, reflecting their possible origin in the commensal life of this bacterium. Most importantly, S. Epidermidis excels in forming biofilms, sticky agglomerations that inhibit major host defense mechanisms. Furthermore, S. Epidermidis produces a series of protective surface polymers and exoenzymes. Moreover, S. Epidermidis has the capacity to secrete strongly cytolytic members of the phenol-soluble modulin (PSM) family, but PSMs in S. Epidermidis overall appear to participate primarily in biofilm development. Finally, there is evidence for a virulence gene reservoir function of S. Epidermidis, as it appears to have transferred important immune evasion and antibiotic resistance factors to Staphylococcus aureus. Conversely, S. Epidermidis also has a beneficial role in balancing the microflora on human epithelial surfaces by controlling outgrowth of harmful bacteria such as in particular S. aureus. Recent research yielded detailed insight into key S. Epidermidis virulence determinants and their regulation, in particular as far as biofilm formation is concerned, but we still have a serious lack of understanding of the in vivo relevance of many pathogenesis mechanisms and the factors that govern the commensal life of S. Epidermidis.
-
staphylococcus Epidermidis strategies to avoid killing by human neutrophils
PLOS Pathogens, 2010Co-Authors: Gordon Y C Cheung, Kevin Rigby, Rong Wang, Shu Y Queck, Kevin R Braughton, Adeline R Whitney, Martin Teintze, Frank R Deleo, Michael OttoAbstract:Staphylococcus Epidermidis is a leading nosocomial pathogen. In contrast to its more aggressive relative S. aureus, it causes chronic rather than acute infections. In highly virulent S. aureus, phenol-soluble modulins (PSMs) contribute significantly to immune evasion and aggressive virulence by their strong ability to lyse human neutrophils. Members of the PSM family are also produced by S. Epidermidis, but their role in immune evasion is not known. Notably, strong cytolytic capacity of S. Epidermidis PSMs would be at odds with the notion that S. Epidermidis is a less aggressive pathogen than S. aureus, prompting us to examine the biological activities of S. Epidermidis PSMs. Surprisingly, we found that S. Epidermidis has the capacity to produce PSMδ, a potent leukocyte toxin, representing the first potent cytolysin to be identified in that pathogen. However, production of strongly cytolytic PSMs was low in S. Epidermidis, explaining its low cytolytic potency. Interestingly, the different approaches of S. Epidermidis and S. aureus to causing human disease are thus reflected by the adaptation of biological activities within one family of virulence determinants, the PSMs. Nevertheless, S. Epidermidis has the capacity to evade neutrophil killing, a phenomenon we found is partly mediated by resistance mechanisms to antimicrobial peptides (AMPs), including the protease SepA, which degrades AMPs, and the AMP sensor/resistance regulator, Aps (GraRS). These findings establish a significant function of SepA and Aps in S. Epidermidis immune evasion and explain in part why S. Epidermidis may evade elimination by innate host defense despite the lack of cytolytic toxin expression. Our study shows that the strategy of S. Epidermidis to evade elimination by human neutrophils is characterized by a passive defense approach and provides molecular evidence to support the notion that S. Epidermidis is a less aggressive pathogen than S. aureus.
-
Role of spx in biofilm formation of Staphylococcus Epidermidis.
Fems Immunology and Medical Microbiology, 2010Co-Authors: Chongzhen Wang, Amer E. Villaruz, Chuan Wang, Michael OttoAbstract:Infections caused by the leading nosocomial pathogen Staphylococcus Epidermidis are characterized by biofilm formation on implanted medical devices. In a previous study, we found that ClpP protease plays an essential role in biofilm formation of S. Epidermidis. However, the mechanism by which ClpP impacts S. Epidermidis biofilms has remained unknown. Here, we show that the Spx protein accumulates in the clpP mutant strain of S. Epidermidis and controls biofilm formation of S. Epidermidis via a pronounced effect on the transcription of the icaADBC operon coding for the production of the biofilm exopolysaccharide polysaccharide intercellular adhesion (PIA). Notably, in contrast to Staphylococcus aureus, Spx controls PIA expression via an icaR-independent mechanism. Furthermore, Spx affected primary surface attachment, although not by regulating the production of the autolysin AtlE. Our results indicate that ClpP enhances the formation of S. Epidermidis biofilms by degrading Spx, a negative regulator of biofilm formation.
Dietrich Mack - One of the best experts on this subject based on the ideXlab platform.
-
Staphylococcus Epidermidis in Biomaterial-Associated Infections
Biomaterials Associated Infection, 2012Co-Authors: Dietrich Mack, Holger Rohde, Llinos G Harris, Angharad P. Davies, Rose E. Jeeves, Ben Pascoe, Johannes K.-m. Knobloch, Thomas S. WilkinsonAbstract:Coagulase-negative staphylococci, mainly Staphylococcus Epidermidis, are currently the most frequent cause of hospital acquired infections in the USA. Mostly, but not exclusively, S. Epidermidis infections are linked to the use of implanted medical devices like central venous catheters, prosthetic joints and heart valves, pacemakers, cardiac assist devices, cerebrospinal fluid shunts, and intraocular lenses. As new molecular techniques reveal that S. Epidermidis are by no means the most prominent bacteria of the skin and mucous membrane flora, the implication is that S. Epidermidis has specific virulence factors, which transforms this commensal bacterial species into one of the most successful pathogens in modern medicine. A vast array of specific attachment factors for native and host protein-modified device surfaces and the ability to accumulate in adherent multilayered biofilms appear to be vital for the success of S. Epidermidis as a pathogen. Biofilm formation contributes to the ability of the organism to withstand the host’s innate and acquired immune defense mechanisms and to resist antimicrobial therapy, so that device removal is a regular feature for the treatment of S. Epidermidis biomaterial-associated infection. Recent developments in the understanding of S. Epidermidis virulence are reviewed in this chapter.
-
the giant extracellular matrix binding protein of staphylococcus Epidermidis mediates biofilm accumulation and attachment to fibronectin
Molecular Microbiology, 2010Co-Authors: Martin Christner, Nina N Schommer, Friedrich Buck, Gefion Franke, Ulrike Wendt, Kim Wegert, Philip Pehle, Gesche Kroll, Christian Schulze, Dietrich MackAbstract:Summary Virulence of nosocomial pathogen Staphylococcus Epidermidis is essentially related to formation of adherent biofilms, assembled by bacterial attachment to an artificial surface and subsequent production of a matrix that mediates interbacterial adhesion. Growing evidence supports the idea that proteins are functionally involved in S. Epidermidis biofilm accumulation. We found that in S. Epidermidis 1585v overexpression of a 460 kDa truncated isoform of the extracellular matrix-binding protein (Embp) is necessary for biofilm formation. Embp is a giant fibronectin-binding protein harbouring 59 Found In Various Architectures (FIVAR) and 38 protein G-related albumin-binding (GA) domains. Studies using defined Embp-positive and -negative S. Epidermidis strains proved that Embp is sufficient and necessary for biofilm formation. Further data showed that the FIVAR domains of Embp mediate binding of S. Epidermidis to solid-phase attached fibronectin, constituting the first step of biofilm formation on conditioned surfaces. The binding site in fibronectin was assigned to the fibronectin domain type III12. Embp-mediated biofilm formation also protected S. Epidermidis from phagocytosis by macrophages. Thus, Embp is a multifunctional cell surface protein that mediates attachment to host extracellular matrix, biofilm accumulation and escape from phagocytosis, and therefore is well suited for promoting implant-associated infections.
-
Biofilm Formation Induces C3a Release and Protects Staphylococcus Epidermidis from IgG and Complement Deposition and from Neutrophil‐Dependent Killing
The Journal of Infectious Diseases, 2008Co-Authors: Sascha a. Kristian, Timo a. Birkenstock, Ursula Sauder, Dietrich Mack, Friedrich Gotz, Regine LandmannAbstract:BACKGROUND: Biofilm formation is considered to be an important virulence factor of the opportunistic pathogen Staphylococcus Epidermidis. We hypothesized that biofilm formation could interfere with the deposition of immunoglobulins and complement on the bacterial surface, leading to diminished activation of the complement system and protection from killing by human phagocytes. METHODS: The killing of biofilm-encased and planktonically grown wild-type (wt) S. Epidermidis and the killing of an isogenic biofilm-negative ica mutant (ica(-)) by human polymorphonuclear neutrophils (PMNs) were compared. C3a induction and deposition of C3b and immunoglobulin G (IgG) on the bacteria after opsonization with human serum were assessed by enzyme-linked immunosorbent assay, flow cytometry, and electron microscopy. The virulence of the bacterial strains was compared in a mouse model of catheter-associated infection. RESULTS: Biofilm-embedded wt S. Epidermidis was killed less well by human PMNs and induced more C3a than planktonically grown wt and ica(-) S. Epidermidis. However, the deposition of C3b and IgG on the bacterial surface was diminished in biofilm-encased staphylococci. wt S. Epidermidis was more virulent in implant-associated infections and was killed more slowly than ica(-) in ex vivo assays of killing by PMNs. CONCLUSIONS: The results indicate that prevention of C3b and IgG deposition on the bacterial surface contributes to the biofilm-mediated protection of S. Epidermidis from killing by PMNs
-
induction of staphylococcus Epidermidis biofilm formation via proteolytic processing of the accumulation associated protein by staphylococcal and host proteases
Molecular Microbiology, 2005Co-Authors: Holger Rohde, Johannes K.-m. Knobloch, Christine Heilmann, Christoph Burdelski, Katrin Bartscht, Muzaffar Hussain, Friedrich Buck, Matthias A Horstkotte, Mathias Herrmann, Dietrich MackAbstract:Summary Because of its biofilm forming potential Staphylococcus Epidermidis has evolved as a leading cause of device-related infections. The polysaccharide intercellular adhesin (PIA) is significantly involved in biofilm accumulation. However, infections because of PIA-negative strains are not uncommon, suggesting the existence of PIA-independent biofilm accumulation mechanisms. Here we found that biofilm formation in the clinically significant S. Epidermidis 5179 depended on the expression of a truncated 140 kDa isoform of the 220 kDa accumulation-associated protein Aap. As expression of the truncated Aap isoform leads to biofilm formation in aap -negative S. Epidermidis 1585, this domain mediates intercellular adhesion in a polysaccharide-independent manner. In contrast, expression of full-length Aap did not lead to a biofilm-positive phenotype. Obviously, to gain adhesive function, full-length Aap has to be proteolytically processed through staphylococcal proteases as demonstrated by inhibition of biofilm formation by a a a 2 macroglobulin. Importantly, also exogenously added granulocyte proteases activated Aap, thereby inducing biofilm formation in S. Epidermidis 5179 and four additional, independent clinical S. Epidermidis strains. It is therefore reasonable to assume that in vivo effector mechanisms of the innate immunity can directly induce protein-dependent S. Epidermidis cell aggregation and biofilm formation, thereby enabling the pathogen to evade clearance by phagocytes.
Holger Rohde - One of the best experts on this subject based on the ideXlab platform.
-
Nasal commensal Staphylococcus Epidermidis counteracts influenza virus
Scientific Reports, 2016Co-Authors: Hui-wen Chen, Holger Rohde, Xing-quan Zhang, Robert T. Schooley, Richard L. Gallo, Chun-ming HuangAbstract:Several microbes, including Staphylococcus Epidermidis ( S. Epidermidis ), a Gram-positive bacterium, live inside the human nasal cavity as commensals. The role of these nasal commensals in host innate immunity is largely unknown, although bacterial interference in the nasal microbiome may promote ecological competition between commensal bacteria and pathogenic species. We demonstrate here that S. Epidermidis culture supernatants significantly suppressed the infectivity of various influenza viruses. Using high-performance liquid chromatography together with mass spectrometry, we identified a giant extracellular matrix-binding protein (Embp) as the major component involved in the anti-influenza effect of S. Epidermidis . This anti-influenza activity was abrogated when Embp was mutated, confirming that Embp is essential for S. Epidermidis activity against viral infection. We also showed that both S. Epidermidis bacterial particles and Embp can directly bind to influenza virus. Furthermore, the injection of a recombinant Embp fragment containing a fibronectin-binding domain into embryonated eggs increased the survival rate of virus-infected chicken embryos. For an in vivo challenge study, prior Embp intranasal inoculation in chickens suppressed the viral titres and induced the expression of antiviral cytokines in the nasal tissues. These results suggest that S. Epidermidis in the nasal cavity may serve as a defence mechanism against influenza virus infection.
-
Staphylococcus Epidermidis in Biomaterial-Associated Infections
Biomaterials Associated Infection, 2012Co-Authors: Dietrich Mack, Holger Rohde, Llinos G Harris, Angharad P. Davies, Rose E. Jeeves, Ben Pascoe, Johannes K.-m. Knobloch, Thomas S. WilkinsonAbstract:Coagulase-negative staphylococci, mainly Staphylococcus Epidermidis, are currently the most frequent cause of hospital acquired infections in the USA. Mostly, but not exclusively, S. Epidermidis infections are linked to the use of implanted medical devices like central venous catheters, prosthetic joints and heart valves, pacemakers, cardiac assist devices, cerebrospinal fluid shunts, and intraocular lenses. As new molecular techniques reveal that S. Epidermidis are by no means the most prominent bacteria of the skin and mucous membrane flora, the implication is that S. Epidermidis has specific virulence factors, which transforms this commensal bacterial species into one of the most successful pathogens in modern medicine. A vast array of specific attachment factors for native and host protein-modified device surfaces and the ability to accumulate in adherent multilayered biofilms appear to be vital for the success of S. Epidermidis as a pathogen. Biofilm formation contributes to the ability of the organism to withstand the host’s innate and acquired immune defense mechanisms and to resist antimicrobial therapy, so that device removal is a regular feature for the treatment of S. Epidermidis biomaterial-associated infection. Recent developments in the understanding of S. Epidermidis virulence are reviewed in this chapter.
-
staphylococcus Epidermidis uses distinct mechanisms of biofilm formation to interfere with phagocytosis and activation of mouse macrophage like cells 774a 1
Infection and Immunity, 2011Co-Authors: Nina N Schommer, Martin Christner, Moritz Hentschke, Klaus Ruckdeschel, Martin Aepfelbacher, Holger RohdeAbstract:Assembly of adherent biofilms is the key mechanism involved in Staphylococcus Epidermidis virulence during device-associated infections. Aside from polysaccharide intercellular adhesin (PIA), the accumulation-associated protein Aap and the extracellular matrix binding protein Embp act as intercellular adhesins, mediating S. Epidermidis cell aggregation and biofilm accumulation. The aim of this study was to investigate structural features of PIA-, Aap-, and Embp-mediated S. Epidermidis biofilms in more detail and to evaluate their specific contributions to biofilm-related S. Epidermidis immune escape. PIA-, Embp-, and Aap-mediated biofilms exhibited substantial morphological differences. Basically, PIA synthesis induced formation of macroscopically visible, rough cell clusters, whereas Aap- and Embp-dependent biofilms preferentially displayed a smooth layer of aggregated bacteria. On the microscopic level, PIA was found to form a string-like organized extracellular matrix connecting the bacteria, while Embp produced small deposits of intercellular matrix and Aap was strictly localized to the bacterial surface. Despite marked differences, S. Epidermidis strains using PIA, Aap, or Embp for biofilm formation were protected from uptake by J774A.1 macrophages, with similarly efficiencies. In addition, compared to biofilm-negative S. Epidermidis strains, isogenic biofilm-forming S. Epidermidis induced only a diminished inflammatory J774A.1 macrophage response, leading to significantly (88.2 to 88.7%) reduced NF-κB activation and 68.8 to 83% reduced interleukin-1β (IL-1β) production. Mechanical biofilm dispersal partially restored induction of NF-κB activation, although bacterial cell surfaces remained decorated with the respective intercellular adhesins. Our results demonstrate that distinct S. Epidermidis biofilm morphotypes are similarly effective at protecting S. Epidermidis from phagocytic uptake and at counteracting macrophage activation, providing novel insights into mechanisms that could contribute to the chronic and persistent course of biofilm-related S. Epidermidis foreign material infections.
-
induction of staphylococcus Epidermidis biofilm formation via proteolytic processing of the accumulation associated protein by staphylococcal and host proteases
Molecular Microbiology, 2005Co-Authors: Holger Rohde, Johannes K.-m. Knobloch, Christine Heilmann, Christoph Burdelski, Katrin Bartscht, Muzaffar Hussain, Friedrich Buck, Matthias A Horstkotte, Mathias Herrmann, Dietrich MackAbstract:Summary Because of its biofilm forming potential Staphylococcus Epidermidis has evolved as a leading cause of device-related infections. The polysaccharide intercellular adhesin (PIA) is significantly involved in biofilm accumulation. However, infections because of PIA-negative strains are not uncommon, suggesting the existence of PIA-independent biofilm accumulation mechanisms. Here we found that biofilm formation in the clinically significant S. Epidermidis 5179 depended on the expression of a truncated 140 kDa isoform of the 220 kDa accumulation-associated protein Aap. As expression of the truncated Aap isoform leads to biofilm formation in aap -negative S. Epidermidis 1585, this domain mediates intercellular adhesion in a polysaccharide-independent manner. In contrast, expression of full-length Aap did not lead to a biofilm-positive phenotype. Obviously, to gain adhesive function, full-length Aap has to be proteolytically processed through staphylococcal proteases as demonstrated by inhibition of biofilm formation by a a a 2 macroglobulin. Importantly, also exogenously added granulocyte proteases activated Aap, thereby inducing biofilm formation in S. Epidermidis 5179 and four additional, independent clinical S. Epidermidis strains. It is therefore reasonable to assume that in vivo effector mechanisms of the innate immunity can directly induce protein-dependent S. Epidermidis cell aggregation and biofilm formation, thereby enabling the pathogen to evade clearance by phagocytes.
Denise Kuhnert - One of the best experts on this subject based on the ideXlab platform.
-
in host evolution of staphylococcus Epidermidis in a pacemaker associated endocarditis resulting in increased antibiotic tolerance
Nature Communications, 2019Co-Authors: Vanina Dengler Haunreiter, Mathilde Boumasmoud, Nicola Haffner, Dennis Wipfli, Nadja Leimer, Carole Rachmuhl, Denise KuhnertAbstract:Treatment failure in biofilm-associated bacterial infections is an important healthcare issue. In vitro studies and mouse models suggest that bacteria enter a slow-growing/non-growing state that results in transient tolerance to antibiotics in the absence of a specific resistance mechanism. However, little clinical confirmation of antibiotic tolerant bacteria in patients exists. In this study we investigate a Staphylococcus Epidermidis pacemaker-associated endocarditis, in a patient who developed a break-through bacteremia despite taking antibiotics to which the S. Epidermidis isolate is fully susceptible in vitro. Characterization of the clinical S. Epidermidis isolates reveals in-host evolution over the 16-week infection period, resulting in increased antibiotic tolerance of the entire population due to a prolonged lag time until growth resumption and a reduced growth rate. Furthermore, we observe adaptation towards an increased biofilm formation capacity and genetic diversification of the S. Epidermidis isolates within the patient. Staphylococcus Epidermidis is a frequent cause of medical implant-associated biofilm infections. Here, studying a patient with pacemaker-associated endocarditis, the authors report in-host evolution of S. Epidermidis leading to phenotypes exhibiting increased biofilm formation and antibiotic tolerance.
Pilar García - One of the best experts on this subject based on the ideXlab platform.
-
genomic characterization of two staphylococcus Epidermidis bacteriophages with anti biofilm potential
BMC Genomics, 2012Co-Authors: Diana Gutierrez, Beatriz Martinez, Ana Rodriguez, Pilar GarcíaAbstract:Staphylococcus Epidermidis is a commensal bacterium but can colonize the hospital environment due to its ability to form biofilms favouring adhesion to host tissues, medical devices and increasing resistance to antibiotics. In this context, the use of phages to destroy biofilms is an interesting alternative. The complete genomes of two Staphylococcus Epidermidis bacteriophages, vB_SepiS-phiIPLA5 and vB_SepiS-phiIPLA7, have been analyzed. Their genomes are 43,581 bp and 42,123 bp, and contain 67 and 59 orf s. Bioinformatic analyses enabled the assignment of putative functions to 36 and 29 gene products, respectively, including DNA packaging and morphogenetic proteins, lysis components, and proteins necessary for DNA recombination, regulation, modification and replication. A point mutation in vB_SepiS-phiIPLA5 lysogeny control-associated genes explained its strictly lytic behaviour. Comparative analysis of phi-IPLA5 and phi-IPLA7 genome structure resembled those of S. Epidermidis ϕPH15 and ϕCNPH82 phages. A mosaic structure of S. Epidermidis prophage genomes was revealed by PCR analysis of three marker genes (integrase, major head protein and holin). Using these genes, high prevalence (73%) of phage DNA in a representative S. Epidermidis strain collection consisting of 60 isolates from women with mastitis and healthy women was determined. Putative pectin lyase-like domains detected in virion-associated proteins of both phages could be involved in exopolysaccharide (EPS) depolymerization, as evidenced by both the presence of a clear halo surrounding the phage lysis zone and the phage-mediated biofilm degradation. Staphylococcus Epidermidis bacteriophages, vB_SepiS-phiIPLA5 and vB_SepiS-phiIPLA7, have a mosaic structure similar to other widespread S. Epidermidis prophages. Virions of these phages are provided of pectin lyase-like domains, which may be regarded as promising anti-biofilm tools.
-
Genomic characterization of two Staphylococcus Epidermidis bacteriophages with anti-biofilm potential
BMC Genomics, 2012Co-Authors: Diana Gutierrez, Beatriz Martinez, Ana Rodriguez, Pilar GarcíaAbstract:Background Staphylococcus Epidermidis is a commensal bacterium but can colonize the hospital environment due to its ability to form biofilms favouring adhesion to host tissues, medical devices and increasing resistance to antibiotics. In this context, the use of phages to destroy biofilms is an interesting alternative. Results The complete genomes of two Staphylococcus Epidermidis bacteriophages, vB_SepiS-phiIPLA5 and vB_SepiS-phiIPLA7, have been analyzed. Their genomes are 43,581 bp and 42,123 bp, and contain 67 and 59 orf s. Bioinformatic analyses enabled the assignment of putative functions to 36 and 29 gene products, respectively, including DNA packaging and morphogenetic proteins, lysis components, and proteins necessary for DNA recombination, regulation, modification and replication. A point mutation in vB_SepiS-phiIPLA5 lysogeny control-associated genes explained its strictly lytic behaviour. Comparative analysis of phi-IPLA5 and phi-IPLA7 genome structure resembled those of S. Epidermidis ϕPH15 and ϕCNPH82 phages. A mosaic structure of S. Epidermidis prophage genomes was revealed by PCR analysis of three marker genes (integrase, major head protein and holin). Using these genes, high prevalence (73%) of phage DNA in a representative S. Epidermidis strain collection consisting of 60 isolates from women with mastitis and healthy women was determined. Putative pectin lyase-like domains detected in virion-associated proteins of both phages could be involved in exopolysaccharide (EPS) depolymerization, as evidenced by both the presence of a clear halo surrounding the phage lysis zone and the phage-mediated biofilm degradation. Conclusions Staphylococcus Epidermidis bacteriophages, vB_SepiS-phiIPLA5 and vB_SepiS-phiIPLA7, have a mosaic structure similar to other widespread S. Epidermidis prophages. Virions of these phages are provided of pectin lyase-like domains, which may be regarded as promising anti-biofilm tools.