The Fibrinogen- and Fibronectin-Binding Domains of
            <i>Staphylococcus aureus</i>
            Fibronectin-Binding Protein A Synergistically Promote Endothelial Invasion and Experimental Endocarditis

Piroth, Lionel; Que, Yok-Ai; Widmer, Eleonora; Panchaud, Alexandre; Piu, Stéphane; Entenza, José M.; Moreillon, Philippe

doi:10.1128/iai.00405-08

Cited by 90 publications

(94 citation statements)

References 28 publications

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“…tst was almost exclusively associated with the CC30 MSSA isolates, and this was also noted by Blomfeldt et al (36). Although clfA has been shown to be important in nasal colonization (37) and endocarditis (38), the S. aureus isolates in our cohort containing this gene all belonged to CC8; it is therefore uncertain whether elevated vancomycin MIC is due to clfA itself or other features of this clonal complex. The high frequency of ACME carriage in CC8 ST239-MRSA-III (39) may also explain the association between the ACME locus and elevated vancomycin MIC in our cohort.…”

Section: Discussionmentioning

confidence: 87%

Genetic and Molecular Predictors of High Vancomycin MIC in Staphylococcus aureus Bacteremia Isolates

et al. 2014

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Section: Discussionmentioning

confidence: 87%

Genetic and Molecular Predictors of High Vancomycin MIC in Staphylococcus aureus Bacteremia Isolates

et al. 2014

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“…In particular, clumping factors A and B (ClfA and ClfB, respectively; also known as fibrinogen-binding proteins) are key for attachment to and colonization of the valvular tissue. Fibronectin-binding protein A (FnBPA) and FnBPB facilitate binding to both fibrinogen and fibronectin and also play a role in subsequent endothelial cell invasion and inflammation (157,158). In addition, Clf, FnBP, and the serine-aspartate repeat protein SdrE induce platelet aggregation and activation (159,160).…”

Section: Pathophysiologymentioning

confidence: 99%

Staphylococcus aureus Infections: Epidemiology, Pathophysiology, Clinical Manifestations, and Management

et al. 2015

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SUMMARY Staphylococcus aureus is a major human pathogen that causes a wide range of clinical infections. It is a leading cause of bacteremia and infective endocarditis as well as osteoarticular, skin and soft tissue, pleuropulmonary, and device-related infections. This review comprehensively covers the epidemiology, pathophysiology, clinical manifestations, and management of each of these clinical entities. The past 2 decades have witnessed two clear shifts in the epidemiology of S. aureus infections: first, a growing number of health care-associated infections, particularly seen in infective endocarditis and prosthetic device infections, and second, an epidemic of community-associated skin and soft tissue infections driven by strains with certain virulence factors and resistance to β-lactam antibiotics. In reviewing the literature to support management strategies for these clinical manifestations, we also highlight the paucity of high-quality evidence for many key clinical questions.

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“…The present study addressed primarily induction of infection (with relatively early sacrifice 24 h after inoculation), because this is the unavoidable primum movens for further invasion. Moreover, it attempted to correlate adherence to fibrinogen and fibronectin with the capacity to promote experimental endocarditis, because the adhesins mediating these phenotypes were specifically associated with valve infection in previous studies (26,32,35), whereas other adhesins were not (46). Therefore, the system model is pertinent to the questions asked.…”

Section: Fig 3 Adherence Of S Aureus Carriage and Infection Isolatmentioning

confidence: 99%

Natural Variability of In Vitro Adherence to Fibrinogen and Fibronectin Does Not Correlate with In Vivo Infectivity of Staphylococcus aureus

et al. 2010

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Adherence to fibrinogen and fibronectin plays a crucial role in Staphylococcus aureus experimental endocarditis. Previous genetic studies have shown that infection and carriage isolates do not systematically differ in their virulence-related genes, including genes conferring adherence, such as clfA and fnbA. We set out to determine the range of adherence phenotypes in carriage isolates of S. aureus, to compare the adherence of these isolates to the adherence of infection isolates, and to determine the relationship between adherence and infectivity in a rat model of experimental endocarditis. A total of 133 healthy carriage isolates were screened for in vitro adherence to fibrinogen and fibronectin, and 30 isolates were randomly chosen for further investigation. These 30 isolates were compared to 30 infective endocarditis isolates and 30 blood culture isolates. The infectivities of the carriage isolates, which displayed either extremely low or high adherence to fibrinogen and fibronectin, were tested using a rat model of experimental endocarditis. The levels of adherence to both fibrinogen and fibronectin were very similar for isolates from healthy carriers and members of the two groups of infection isolates. All three groups of isolates showed a wide range of adherence to fibrinogen and fibronectin. Moreover, the carriage isolates that showed minimal adherence and the carriage isolates that showed strong adherence had the same infectivity in experimental endocarditis. Adherence was proven to be important for pathogenesis in experimental endocarditis, but even the least adherent carriage strains had the ability to induce infection. We discuss the roles of differential gene expression, human host factors, and gene redundancy in resolving this apparent paradox.

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The Fibrinogen- and Fibronectin-Binding Domains of Staphylococcus aureus Fibronectin-Binding Protein A Synergistically Promote Endothelial Invasion and Experimental Endocarditis

Cited by 90 publications

References 28 publications

Genetic and Molecular Predictors of High Vancomycin MIC in Staphylococcus aureus Bacteremia Isolates

Genetic and Molecular Predictors of High Vancomycin MIC in Staphylococcus aureus Bacteremia Isolates

Staphylococcus aureus Infections: Epidemiology, Pathophysiology, Clinical Manifestations, and Management

Natural Variability of In Vitro Adherence to Fibrinogen and Fibronectin Does Not Correlate with In Vivo Infectivity of Staphylococcus aureus

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