Genetic Analysis of a High-Level Vancomycin-Resistant Isolate of Staphylococcus aureus
By L. Weigel, D. Clewell, S. Gill, N. Clark, L. McDougal, S. Flannagan, J. Kolonay, Jyoti Shetty, G. Killgore, F. Tenover. Science, 2003
923 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Infectious Diseases, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6114f29f1d39e7bda29fb226878f8f72d8ab9940
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In Clinical Biochemistry
In Infectious Diseases
- T. Foster
- Kunyan Zhang
- Sahreena S. Lakhundi
- A. Peschel
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- David L. Paterson
- Hermínia de Lencastre
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In Molecular Biology
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- Kunyan Zhang
- T. Foster
- Sahreena S. Lakhundi
- A. Peschel
- Jacques Ravel
- Henry F. Chambers
Citations in the corpus
- Immune evasion by staphylococci (2005, background): “Furthermore, the isolation of MRSA strains that have also become resistant to vancomyci”
- Call of the wild: antibiotic resistance genes in natural environments (2010, background): “In particular, resistance determinants in pathogens are commonly encountered after the introduction of an antibiotic to clinical use, and treating human pathogens with antibiotics directly affects the frequency of resistance to those antibiotics in these pathogen”
- Vancomycin resistance in gram-positive cocci. (2006, background): “A vancomycin-resistant E. faecalis strain and a vancomycin-susceptible MRSA strain (MI-MRSA) were isolated from the same patient as MI-VRSA and are considered to be the Tn1546 donor and recipient, respectively [40].”
- Methicillin-Resistant Staphylococcus aureus: Molecular Characterization, Evolution, and Epidemiology (2018, background): “acquired vancomycin resistance genes from enterococci via horizontal transfer (394).”
- Intrinsic and acquired resistance mechanisms in enterococcus (2012, background): “faecalis.(72,73) Sequence homology has been observed between plasmids found in VRSA isolates and GRE isolates taken from VRSA infected patients, with the most overlap occurring with E.”
- Antibiotic Resistance Mechanisms in Bacteria: Relationships Between Resistance Determinants of Antibiotic Producers, Environmental Bacteria, and Clinical Pathogens (2018, background): “The known conditions for resistance gene transfer by conjugation include high density settings, such as the human or animal gut, biofilms, hospitals, and co-infection conditions (Weigel et al., 2003; Savage et al., 2013; Huddleston, 2014; Andersson and Hughes, 2017).”
- Antimicrobial Resistance in ESKAPE Pathogens (2020, background): “Classic examples of composite transposons associated with the carriage of AMR genes include Tn9 (IS1; chloramphenicol resistance), Tn10 (IS10; tetracycline resistance), Tn5 (IS50; aminoglycoside and bleomycin resistance) (262, 265), and, more recently, Tn6330 (ISApl1), which is responsible for mobil”
- Methicillin-resistant Staphylococcus aureus (2018, background): “been transferred from Enterococcus faecalis on the plasmid-borne transposon Tn1546 (REF.(221)).”
- Insights on Evolution of Virulence and Resistance from the Complete Genome Analysis of an Early Methicillin-Resistant Staphylococcus aureus Strain and a Biofilm-Producing Methicillin-Resistant Staphylococcus epidermidis Strain (2005, background): “The most recent example of such gene movement is the acquisition of the Enterococcus faecalis Tn1546 vancomycin resistance element by plasmid-mediated transfer into S. aureus ( 52 ).”
- CRISPR interference: RNA-directed adaptive immunity in bacteria and archaea (2010, background): “strains, the genesis of which is directly linked to the transfer of antibiotic resistance genes by plasmid conjugatio”
- Lipid II as a target for antibiotics (2006, neutral): “…had long been reliable in treating infections caused by bacteria resistant to several other antibiotics, such as the ‘super bug’ methicillin-resistant Staphylococcus aureus (MRSA), but even vancomycin resistance has now become quite common 1 , further underlining the need for new antibiotics.”
- Waves of resistance: Staphylococcus aureus in the antibiotic era (2009, background): “aureus (VRSA) strains, which are inhibited only at concentrations of 16 μg ml −1 or mor”