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Barbara E. Murray
Researcher at University of Texas at Austin
Publications - 235
Citations - 23158
Barbara E. Murray is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: Enterococcus faecalis & Enterococcus faecium. The author has an hindex of 73, co-authored 232 publications receiving 21704 citations. Previous affiliations of Barbara E. Murray include Emerging Pathogens Institute & University of Texas Health Science Center at Houston.
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Journal ArticleDOI
Evaluation of Standard- and High-Dose Daptomycin versus Linezolid against Vancomycin-Resistant Enterococcus Isolates in an In Vitro Pharmacokinetic/Pharmacodynamic Model with Simulated Endocardial Vegetations
Ashley D. Hall,Molly E. Steed,Cesar A. Arias,Barbara E. Murray,Michael J. Rybak,Michael J. Rybak +5 more
TL;DR: Daptomycin displayed a dose-dependent response against three VRE isolates, with high-dose daptomecin producing sustained bactericidal activity, and the E. faecium mutants with reduced susceptibility were recovered at any dosage regimen.
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Characterization of the ebpfm pilus-encoding operon of Enterococcus faecium and its role in biofilm formation and virulence in a murine model of urinary tract infection
Jouko Sillanpää,Sreedhar R. Nallapareddy,Kavindra V. Singh,Vittal P. Prakash,Timothy Fothergill,Hung Ton-That,Barbara E. Murray +6 more
TL;DR: It is shown that the ebpABCfm locus encodes pili on the E. faecium TX82 cell surface and provide the first evidence that pili of this emerging pathogen are important for its ability to form biofilm and to cause infection in an ascending UTI model.
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Disruption of an Enterococcus faecium species-specific gene, a homologue of acquired macrolide resistance genes of staphylococci, is associated with an increase in macrolide susceptibility.
TL;DR: Disruption of msrC was associated with a two- to eightfold decrease in MICs of erythromycin azithromycin, tylosin, and quinupristin, suggesting that it may explain in part the apparent greater intrinsic resistance to macrolides of isolates of E. faecium relative to many streptococci.
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What can we do about vancomycin-resistant enterococci?
TL;DR: The article by Edmond et al. in this issue illustrates many of the features common to infection or colonization by vancomycin-resistant enterococci (VRE), such as the more frequent occurrence of VRE in teaching hospitals.
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In vitro studies of plasmid-mediated penicillinase from Streptococcus faecalis suggest a staphylococcal origin.
TL;DR: Based upon hybridization under stringent conditions of plasmid DNA from the S. faecalis strain to cloned penicillinase genes from Staphylococcus aureus, it appears that these resistance determinants are highly homologous and suggests that this enzyme was introduced into streptococci from staphylitis.