J Med Microbiol International Journal of Systematic and Evolutionary Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Puopolo, K. M.
Right arrow Articles by Cieslewicz, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Puopolo, K. M.
Right arrow Articles by Cieslewicz, M. J.
Agricola
Right arrow Articles by Puopolo, K. M.
Right arrow Articles by Cieslewicz, M. J.
J Med Microbiol 56 (2007), 947-955; DOI: 10.1099/jmm.0.47131-0
© 2007 Society for General Microbiology
ISSN 1473-5644

A composite transposon associated with erythromycin and clindamycin resistance in group B Streptococcus

Karen M. Puopolo1,2,3, David C. Klinzing1,3, Michelle P. Lin1,{dagger}, Derek L. Yesucevitz1 and Michael J. Cieslewicz3,4

1 Channing Laboratory, Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA

2 Department of Newborn Medicine, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA

3 Harvard Medical School, Boston, MA 02115, USA

4 Division of Infectious Diseases, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA

Correspondence
Karen M. Puopolo
kpuopolo{at}partners.org

Received 19 December 2006
Accepted 1 March 2007

Group B Streptococcus (GBS) resistant to erythromycin and clindamycin has been isolated with increasing frequency since the mid-1990s. This work studied GBS isolates from three US cities to determine the genetic basis of the macrolide resistance phenotype. ermB genes were amplified from five isolates collected in Boston, Pittsburgh and Seattle from infant and adult sources. Gene-walking methods were used to determine the chromosomal location of ermB and to identify associated genes. Southern mapping and random amplified polymorphic DNA (RAPD) analyses were used to distinguish the isolates. The ermB gene was present on the chromosome within a composite Tn917/Tn916-like transposon similar to one identified in Streptococcus pneumoniae. Four strains from Boston and Pittsburgh were serotype V and identical by Southern hybridization and RAPD analysis. The Seattle isolate was serotype Ib, with different patterns on RAPD analysis and Southern mapping. The composite transposon was integrated at an identical chromosomal site in all five isolates. The presence of this composite transposon in both GBS and pneumococci suggests that ermB-mediated macrolide resistance in streptococci may be due to the horizontal transfer of a mobile transposable element, and raises concern for further dissemination of high-grade erythromycin and clindamycin resistance among streptococcal species.

Abbreviations: GBS, group B Streptococcus; RAPD, random amplified polymorphic DNA.

{dagger}Present address: University of Washington Medical School, Seattle, WA, USA.

The GenBank/EMBL/DDBJ accession number for the sequence reported in this paper is DQ355148.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL J MED MICROBIOL MICROBIOLOGY J GEN VIROL ALL SGM JOURNALS
Copyright © 2007 Society for General Microbiology.