Staphylococcal Bacteremia and Endocarditis

Bayer, Arnold S.

doi:10.1001/archinte.1982.00340190125020

Cited by 35 publications

(8 citation statements)

References 43 publications

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“…Indeed, we found this to be true in both mgrA/sarA double mutants vs. their respective parental strains, utilizing the endocarditis model. In this model, clearance of the organism from infected heart valves is principally dependent on the bactericidal effects of the antibiotics, without substantial contributions from the adaptive immune system [35, 36]. Our studies emphasized the enhanced effect between autolysis regulatory mutants and oxacillin.…”

Section: Discussionmentioning

confidence: 99%

Role ofmgrAandsarAin Methicillin‐ResistantStaphylococcus aureusAutolysis and Resistance to Cell Wall–Active Antibiotics

et al. 2009

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Background We have previously shown the importance of mgrA and sarA in controlling autolysis of Staphylococcus aureus, with MgrA and SarA both being negative regulators of murein hydrolases. Methods In this study, we analyzed the effects of mgrA and sarA on antibiotic-mediated lysis in vitro, and on the responses to cell wall-active antibiotic therapy in an experimental endocarditis model using two representative MRSA strains: laboratory strain COL and community-acquired clinical isolate, MW2. Results We found that mgrA and sarA independently down-regulated sarV (a marker for autolysis), although the alteration in sarV expression did not correlate directly with the autolysis profiles of single mgrA and sarA mutants. Importantly, the mgrA/sarA double mutants of both strains were more autolytic in vitro as compared with the single mutants. In vivo, we demonstrated that, despite equivalent intrinsic virulence between the parents and their isogenic mgrA/sarA double mutants in the endocarditis model, oxacillin and vancomycin treatment of the mgrA/sarA double mutants of MRSA strains COL and MW2 yielded significant reductions in vegetation bacterial densities vs. their respective parents. Conclusions These results suggest that down-regulation of mgrA/sarA in combination with cell wall-active antibiotics may represent a novel approach to treat MRSA infections.

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Section: Discussionmentioning

confidence: 99%

Role ofmgrAandsarAin Methicillin‐ResistantStaphylococcus aureusAutolysis and Resistance to Cell Wall–Active Antibiotics

et al. 2009

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“…Hypergammaglobulinemia, high levels of circulating immune complexes, and reticuloendothelial irregularities, which can lead to false-positive syphilis, Coombs tests, or thrombotic thrombocytopenic purpura have all been described in this population [35,[68][69][70].…”

Section: Host Immune Status and Localization Of Valve Lesionmentioning

confidence: 98%

“…It has been suggested that left-side S. aureus endocarditis in IDUs evolves primarily in the setting of an appropriate background endocardial lesion, such as a congenital abnormality or a prosthetic valve [35]. However, in the study by Chambers [34] only 40% of nonaddicts had underlying valvular disease, leaving 34% of nonaddicts with unexplained left-side S. aureus endocarditis (the remaining 26% had right-side valvular involvement).…”

Section: Relationship Of Infecting Organism and Valvular Locationmentioning

confidence: 99%

Right-Side Endocarditis in Injection Drug Users: Review of Proposed Mechanisms of Pathogenesis

Frontera¹,

Gradon²

2000

Clinical Infectious Diseases

215

149

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Infective endocarditis of the right-side heart valves occurs commonly in injection drug users. Although a variety of hypotheses have been put forward to explain this clinical observation, no single hypothesis is adequate. In this article, basic scientific, clinical, and microbiological data on this topic are presented. It is apparent that no clear unifying mechanism emerges to explain the well-documented clinical predilection for the infection of the right-side heart valves in this population. Further investigation of this topic utilizing large international clinical registries may help to clarify matters further.

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“…Staphiylococclus aureus continues to be a major pathogen in both acute and subacute infective endocarditis (2,17). Despite the use of newer antimicrobial agents to treat these infections, the morbidity and mortality rates remain high (17).…”

mentioning

confidence: 99%

Role of the sar locus of Staphylococcus aureus in induction of endocarditis in rabbits

et al. 1994

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A regulatory locus on the Staphylococcus aureus chromosome, designated sar, is involved in the expression of cell wall proteins, some of which are potentially important in the pathogenesis of endocarditis. For instance, mutant 11D2 (sar::Tn917LTV1) was found to bind substantially less to matrix proteins (i.e., fibrinogen and fibronectin) than parent strain DB. Remarkably, these two strains did not differ in other phenotypes considered important in the initiation of endocarditis (e.g., binding to platelets and resistance to plateletderived microbicidal proteins). The isogenic pair were compared for pathogenicity in a rabbit endocarditis model. There were significant differences in infectivity rates between the two strains (71 and 88% for DB versus 17 and 42% for mutant 11D2 at inocula of 103 and 104 CFU, respectively). In early adherence studies, parent

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Staphylococcal Bacteremia and Endocarditis

Cited by 35 publications

References 43 publications

Role ofmgrAandsarAin Methicillin‐ResistantStaphylococcus aureusAutolysis and Resistance to Cell Wall–Active Antibiotics

Role ofmgrAandsarAin Methicillin‐ResistantStaphylococcus aureusAutolysis and Resistance to Cell Wall–Active Antibiotics

Right-Side Endocarditis in Injection Drug Users: Review of Proposed Mechanisms of Pathogenesis

Role of the sar locus of Staphylococcus aureus in induction of endocarditis in rabbits

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