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JAC Advance Access originally published online on July 8, 2005
Journal of Antimicrobial Chemotherapy 2005 56(3):447-450; doi:10.1093/jac/dki249
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Leading article

Mechanisms of resistance to telithromycin in Streptococcus pneumoniae

Tamiko Hisanaga1,*, Daryl J. Hoban1,2 and George G. Zhanel1,2,3

1 Department of Medical Microbiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; 2 Department of Clinical Microbiology, Health Sciences Centre, MS673-820 Sherbrook Street, Winnipeg, Manitoba, R3A 1R9, Canada; 3 Department of Medicine, Health Sciences Centre, MS673-820 Sherbrook Street, Winnipeg, Manitoba, R3A 1R9, Canada

* Corresponding author. Tel: +1-204-787-4684; Fax: +1-204-787-4699; E-mail: thisanaga{at}shaw.ca

Reports of ketolide resistance remain scarce, however, a few laboratory-derived and clinical isolates of resistant Streptococcus pneumoniae have been documented. Mutations in key telithromycin-binding sites such as domains II and V of the 23S rRNA and ribosomal proteins L4 and L22, as well as mutations of the resistance determinant erm(B) are associated with elevated telithromycin MICs. Mutations in the secondary binding site of domain II coupled with ribosomal methylation may have serious resistance consequences should the domain II binding site be lost. Although ketolides are purported to maintain excellent activity against efflux-positive isolates, laboratory-derived telithromycin-resistant strains have been generated. As telithromycin usage increases, ketolide-resistant isolates of S. pneumoniae may well increase.

Keywords: mutations , 23S rRNA , mef(A) , erm(B)


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