scholarly journals Non-Beta-Lactamase-Producing Penicillin-ResistantEnterococcus faeciumin a Clinical Setting

1990 ◽  
Vol 1 (3) ◽  
pp. 73-76 ◽  
Author(s):  
Daniel Eymard ◽  
Andre Dascal ◽  
John Hiscott ◽  
Sonia Gioseffini ◽  
Janet Stevenson ◽  
...  
Keyword(s):  
Clinical Setting ◽  
Plasmid Dna ◽  
Enterococcus Faecium ◽  
Binding Proteins ◽  
Clinical Isolates ◽  
Beta Lactamase ◽  
Penicillin Binding Proteins ◽  
Mechanism Of Resistance

Six clinical isolates ofEnterococcus faeciumhighly resistant to penicillin are reported. These strains did not produce beta-lactamase and no plasmid DNA could be detected. It is postulated that the mechanism of resistance is one or more chromosomally mediated alterations of penicillin-binding proteins.

scholarly journals Genomic Analyses of DNA Transformation and Penicillin Resistance in Streptococcus pneumoniae Clinical Isolates

2013 ◽  
Vol 58 (3) ◽  
pp. 1397-1403 ◽  
Author(s):  
Fereshteh Fani ◽  
Philippe Leprohon ◽  
George G. Zhanel ◽  
Michel G. Bergeron ◽  
Marc Ouellette
Keyword(s):  
Streptococcus Pneumoniae ◽  
Binding Proteins ◽  
Resistance Mechanisms ◽  
Clinical Isolates ◽  
Penicillin Resistance ◽  
Dna Transformation ◽  
Content Type ◽  
Penicillin Binding Proteins ◽  
Genomic Analyses ◽  
Genome Scale

ABSTRACTAlterations in penicillin-binding proteins, the target enzymes for β-lactam antibiotics, are recognized as primary penicillin resistance mechanisms inStreptococcus pneumoniae. Few studies have analyzed penicillin resistance at the genome scale, however, and we report the sequencing ofS. pneumoniaeR6 transformants generated while reconstructing the penicillin resistance phenotypes from three penicillin-resistant clinical isolates by serial genome transformation. The genome sequences of the three last-level transformants T2-18209, T5-1983, and T3-55938 revealed that 16.2 kb, 82.7kb, and 137.2 kb of their genomes had been replaced with 5, 20, and 37 recombinant sequence segments derived from their respective parental clinical isolates, documenting the extent of DNA transformation between strains. A role in penicillin resistance was confirmed for some of the mutations identified in the transformants. Several multiple recombination events were also found to have happened at single loci coding for penicillin-binding proteins (PBPs) that increase resistance. Sequencing of the transformants with MICs for penicillin similar to those of the parent clinical strains confirmed the importance of mosaic PBP2x, -2b, and -1a as a driving force in penicillin resistance. A role in resistance for mosaic PBP2a was also observed for two of the resistant clinical isolates.

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