S. aureus endocarditis: Clinical aspects and experimental approaches

Hoerr, Verena; Franz, Marcus; Pletz, Mathias W.; Diab, Mahmoud; Niemann, Silke; Faber, Cornelius; Doenst, Torsten; Schulze, P. Christian; Deinhardt‐Emmer, Stefanie; Löffler, Bettina

doi:10.1016/j.ijmm.2018.02.004

Cited by 31 publications

(24 citation statements)

References 158 publications

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“…The only situation in which TTE is equal to TOE with respect to sensitivity of IE detection is right heart IE in patients with a good acoustic window [4]. Additionally novel imaging technologies such as white blood cell (WBC) single-photon emission CT (SPECT)/CT and 18 F-FDG positron emission tomography (PET)/CT are generally recommended for complex clinical situations [4] [13], but are not widely used for variety of reasons including cost, availability, and the experience of interpreting cardiologists.…”

Section: Recent Evidence Related To Diagnosis Of Staphylococcus Aureumentioning

confidence: 99%

An update on Staphylococcus aureus infective endocarditis from the International Society of Antimicrobial Chemotherapy (ISAC)

Saeed

Bal

Gould

et al. 2019

International Journal of Antimicrobial Agents

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Section: Recent Evidence Related To Diagnosis Of Staphylococcus Aureumentioning

confidence: 99%

An update on Staphylococcus aureus infective endocarditis from the International Society of Antimicrobial Chemotherapy (ISAC)

Saeed

Bal

Gould

et al. 2019

International Journal of Antimicrobial Agents

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“…Over the last years the incidence of Staphylococcus aureus (S. aureus) infective endocarditis (IE) has continuously increased (Bussani et al, 2019). Along with medical progress, intensive treatment conditions such as renal hemodialysis, immunosuppression, and long term indwelling central venous catheters, but also the application of modern cardiac device implants and valve prostheses constitute increasing sources of infection (Hoerr et al, 2018). S. aureus is one of the leading pathogens, as it adheres easily through its plethora of adhesins on the surface of implants and is able to form thick multilayered biofilms (Manandhar et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Isolating Crucial Steps in Induction of Infective Endocarditis With Preclinical Modeling of Host Pathogen Interaction

et al. 2020

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Animal models of Staphylococcus aureus infective endocarditis (IE), especially in rodents, are commonly used to investigate the underlying pathogenesis, disease progression, potential diagnostic approaches, and therapeutic treatment. All these models are based on surgical interventions, and imply valve trauma by placing a polyurethane catheter at the aortic root. While the influence of endothelial damage and inflammation on the induction of IE has been studied intensively, the role of the catheter, as permanent source of bacteremia, and the interplay with bacterial virulence factors during the formation of IE is poorly understood. In our study, we aimed at identifying which set of preconditions is required for induction and formation of IE: (1) tissue injury, (2) permanent presence of bacteria, and (3) presence of the full bacterial repertoire of adhesion proteins. We investigated the manifestation of the disease in different modifications of the animal model, considering different degrees of endothelial damage and the presence or absence of the catheter. In four infection models the induction of IE was assessed by using two bacterial strains with different expression patterns of virulence factors-S. aureus 6850 and Newman. In vivo magnetic resonance imaging showed conspicuous morphological structures on the aortic valves, when an endothelial damage and a continuous bacterial source were present simultaneously. Cellular and inflammatory pathophysiology were characterized additionally by histology, real-time quantitative polymerase chain reaction analysis, and bacterial counts, revealing strain-specific pathogenesis and manifestation of IE, crucially influenced by bacterial adherence and toxicity. The severity of IE was dependent on the degree of endothelial irritation. However, even severe endothelial damage in the absence of a permanent bacterial source resulted in reduced valve infection. The spread of bacteria to other organs was also dependent on the pathogenic profile of the infectious agent.

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“…The resulting uncontrolled fibrin formation is thought to play a role in abscess development and bacterial attachment to cardiac valves in acute endocarditis or vascular implants (6)(7)(8). In endocarditis bacteria colonize the endocardium-either following endothelial layer injury or endothelial cell activation-and the bacterial products, as well as the inflammatory process can destroy the heart valve tissue (9). A common complication is the occurrence of septic embolisms (10), but in the absence of data on the characteristics of the fibrin matrix formed by SCG-PT the exact contribution of this fibrin to the fragmentation and embolization of the bacterial vegetations is not clear (11).…”

Section: Introductionmentioning

confidence: 99%

Structure, Mechanical, and Lytic Stability of Fibrin and Plasma Coagulum Generated by Staphylocoagulase From Staphylococcus aureus

Farkas

Szabó

et al. 2019

Front. Immunol.

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Staphylococcus aureus causes localized infections or invasive diseases (abscesses or endocarditis). One of its virulence factors is staphylocoagulase (SCG), which binds prothrombin to form a complex with thrombin-like proteolytic activity and leads to uncontrolled fibrin generation at sites of bacterial inoculation. The aim of this study was to characterize the formation, structure, mechanical properties and lysis of SCG-generated clots. Recombinant SCG was expressed in Escherichia coli, purified and the amidolytic activity of its complexes with human prothrombin (SCG-PT) and thrombin (SCG-T) was determined using human thrombin as a reference. Fibrin clots were prepared from purified fibrinogen and human plasma using thrombin, SCG-PT or SCG-T as a coagulase. The kinetics of clot formation and lysis by tissue-type plasminogen activator (tPA) were monitored with turbidimetric assays. Fibrin ultrastructure was examined with scanning electron microscopy and small-angle X-ray scattering (SAXS). Fibrin clot porosity was characterized with fluid permeation assays, whereas the viscoelastic properties and mechanical stability were evaluated with oscillation rheometry. Compared to thrombin, the amidolytic and clotting activity of SCG-PT was 1.6-to 2.5-fold lower on a molar basis. SCG-T had equivalent amidolytic, but reduced clotting activity both on pure fibrinogen (1.6-fold), and in plasma (1.3-fold). The SCG-PT and SCG-T generated fibrin with thicker fibers (10-60% increase in median diameter) than thrombin due to increased number of fibrin protofibrils per fiber cross-section. According to the fluid permeability of the clots SCG-PT and SCG-T promoted the formation of more porous structures. The shear stress resistance in the pure fibrin and plasma clots generated by SCG-PT was significantly lower than in the thrombin clots (243.8 ± 22.0 Pa shear stress was sufficient for disassembly of SCG-PT fibrin vs. 937.3 ± 65.6 Pa in thrombin clots). The tPA-mediated lysis of both pure fibrin and plasma clots produced by SCG-PT or SCG-T was accelerated compared to thrombin, resulting in up to a 2.1-fold increase in tPA Farkas et al. Staphylocoagulase-Generated Fibrin potency. Our results indicate that SCG generates a thrombus scaffold with a structure characterized by impaired mechanical stability and increased lytic susceptibility. This proneness to clot disintegration could have implications in the septic embolism from endocardial bacterial vegetation.

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S. aureus endocarditis: Clinical aspects and experimental approaches

Cited by 31 publications

References 158 publications

An update on Staphylococcus aureus infective endocarditis from the International Society of Antimicrobial Chemotherapy (ISAC)

An update on Staphylococcus aureus infective endocarditis from the International Society of Antimicrobial Chemotherapy (ISAC)

Isolating Crucial Steps in Induction of Infective Endocarditis With Preclinical Modeling of Host Pathogen Interaction

Structure, Mechanical, and Lytic Stability of Fibrin and Plasma Coagulum Generated by Staphylocoagulase From Staphylococcus aureus

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