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Antimicrobial Agents and Chemotherapy, December 2005, p. 5007-5012, Vol. 49, No. 12
0066-4804/05/$08.00+0 doi:10.1128/AAC.49.12.5007-5012.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
ová,2
Aaron Wood,3 and
Rebecca Hutton-Thomas1
Medical and Research Services, Louis Stokes Cleveland VA Medical Center,1 Cleveland VA Research and Education Foundation,2 Department of Medicine, Case Medical School, Cleveland, Ohio3
Received 28 June 2005/ Returned for modification 8 August 2005/ Accepted 19 September 2005
Using 15 unrelated Enterococcus faecium isolates as donors, we demonstrated that ampicillin resistance was transferable to an E. faecium recipient containing a pbp5 deletion for all but four strains. The transfers occurred at low frequencies (generally ca. 109 transconjugants/recipient CFU), consistent with chromosome-to-chromosome transfer. pbp5 transfer occurred within large genetic regions, and insertion into the recipient genome occurred most commonly into the recipient SmaI restriction fragment that had been created by the previous pbp5 deletion. Restriction mapping of the region upstream of pbp5 revealed a commonality of fragment sizes among the clinical isolates from the United States which differed significantly from those of three strains that were isolated from turkey feces. These data prove conclusively that E. faecium pbp5 is a transferable determinant, even in the absence of a coresiding vancomycin resistance mobile element. They also suggest that the spread of high-level ampicillin resistance among U.S. E. faecium strains is due in part to the transfer of low-affinity pbp5 between clinical isolates.
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