The Abilities of a<i>Staphylococcus epidermidis</i>Wild-Type Strain and Its Slime-Negative Mutant To Induce Endocarditis in Rabbits Are Comparable

Perdreau-Remington, Françoise; Sande, Merle A.; Peters, Georg; Chambers, Henry F.

doi:10.1128/iai.66.6.2778-2781.1998

Cited by 30 publications

(7 citation statements)

References 28 publications

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“…S. epidermidis is normally regarded as skin bacteria. However, under certain conditions they lead to persistent infections that are difficult to treat mainly due to the ability to form biofilm at higher rate and to internalize human osteoblasts (Perdreau-Remington et al, 1998;Götz and Peters, 2000;Valour et al, 2013;Post et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

The Genome of Staphylococcus epidermidis O47

et al. 2020

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The skin colonizing coagulase-negative Staphylococcus epidermidis causes nosocomial infections and is an important opportunistic and highly adaptable pathogen. To gain more insight into this species, we sequenced the genome of the biofilm positive, methicillin susceptible S. epidermidis O47 strain (hereafter O47). This strain belongs to the most frequently isolated sequence type 2. In comparison to the RP62A strain, O47 can be transformed, which makes it a preferred strain for molecular studies. S. epidermidis O47's genome has a single chromosome of about 2.5 million base pairs and no plasmid. Its oriC sequence has the same directionality as S. epidermidis RP62A, S. carnosus, S. haemolyticus, S. saprophyticus and is inverted in comparison to Staphylococcus aureus and S. epidermidis ATCC 12228. A phylogenetic analysis based on all S. epidermidis genomes currently available at GenBank revealed that O47 is closest related to DAR1907. The genome of O47 contains genes for the typical global regulatory systems known in staphylococci. In addition, it contains most of the genes encoding for the typical virulence factors for S. epidermidis but not for S. aureus with the exception of a putative hemolysin III. O47 has the typical S. epidermidis genetic islands and several mobile genetic elements, which include staphylococcal cassette chromosome (SCC) of about 54 kb length and two prophages ϕO47A and ϕO47B. However, its genome has no transposons and the smallest number of insertion sequence (IS) elements compared to the other known S. epidermidis genomes. By sequencing and analyzing the genome of O47, we provide the basis for its utilization in genetic and molecular studies of biofilm formation.

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Section: Discussionmentioning

confidence: 99%

The Genome of Staphylococcus epidermidis O47

et al. 2020

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“…Similar results have been obtained previously by another group working with the closely related oral species, S. gordonii [ 183 ]. Later studies employing isogenic mutants of Enterococcus faecalis [ 184 ] or analysis of biofilm formation in clinical strains isolated from patients with or without endocarditis also failed to uncover a correlation between biofilm-forming ability and endocarditis causation in E. faecalis [ 185 ], S. epidermidis [ 186 ] and S. aureus [ 187 ]. Finally, Ge et al .…”

Section: Role Of S Sanguinis Biofilm Formation Inmentioning

confidence: 99%

Streptococcus Sanguinis Biofilm Formation & Interaction with Oral Pathogens

et al. 2018

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Caries and periodontitis are the two most common human dental diseases and are caused by dysbiosis of oral flora. Although commensal microorganisms have been demonstrated to protect against pathogens and promote oral health, most previous studies have addressed pathogenesis rather than commensalism. Streptococcus sanguinis is a commensal bacterium that is abundant in the oral biofilm and whose presence is correlated with health. Here, we focus on the mechanism of biofilm formation in S. sanguinis and the interaction of S. sanguinis with caries- and periodontitis-associated pathogens. In addition, since S. sanguinis is well known as a cause of infective endocarditis, we discuss the relationship between S. sanguinis biofilm formation and its pathogenicity in endocarditis.

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“…In a comparison of S. epidermidis RP62A and its mitomycin‐induced M7 mutant in a rabbit aortic valve endocarditis model, no differences were observed, indicating that AAP might not be an important virulence determinant in vivo (Perdreau‐Remington et al , 1998). On the other hand, mutant M7 can be eradicated more easily in vitro and in animal models by amikacin, levofloxacin, rifampin or teicoplanin (Schwank et al , 1998).…”

Section: Decreased Virulence Of Biofilm‐negative Mutants In Animal Momentioning

confidence: 99%

Staphylococcus and biofilms

Götz

2002

Molecular Microbiology

1,066

776

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Summary The genetic and molecular basis of biofilm formation in staphylococci is multifaceted. The ability to form a biofilm affords at least two properties: the adherence of cells to a surface and accumulation to form multilayered cell clusters. A trademark is the production of the slime substance PIA, a polysaccharide composed of β‐1,6‐linked N‐acetylglucosamines with partly deacetylated residues, in which the cells are embedded and protected against the host’s immune defence and antibiotic treatment. Mutations in the corresponding biosynthesis genes (ica operon) lead to a pleiotropic phenotype; the cells are biofilm and haemagglutination negative, less virulent and less adhesive on hydrophilic surfaces. ica expression is modulated by various environmental conditions, appears to be controlled by SigB and can be turned on and off by insertion sequence (IS) elements. A number of biofilm‐negative mutants have been isolated in which polysaccharide intercellular adhesin (PIA) production appears to be unaffected. Two of the characterized mutants are affected in the major autolysin (atlE) and in D‐alanine esterification of teichoic acids (dltA). Proteins have been identified that are also involved in biofilm formation, such as the accumulation‐associated protein (AAP), the clumping factor A (ClfA), the staphylococcal surface protein (SSP1) and the biofilm‐associated protein (Bap). Concepts for the prevention of obstinate polymer‐associated infections include the search for new anti‐infectives active in biofilms and new biocompatible materials that complicate biofilm formation and the development of vaccines.

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The Abilities of aStaphylococcus epidermidisWild-Type Strain and Its Slime-Negative Mutant To Induce Endocarditis in Rabbits Are Comparable

Cited by 30 publications

References 28 publications

The Genome of Staphylococcus epidermidis O47

The Genome of Staphylococcus epidermidis O47

Streptococcus Sanguinis Biofilm Formation & Interaction with Oral Pathogens

Staphylococcus and biofilms

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