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Journal of Clinical Microbiology, February 2008, p. 546-550, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01925-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Differences in Potential for Selection of Clindamycin-Resistant Mutants Between Inducible erm(A) and erm(C) Staphylococcus aureus Genes{triangledown}

Claire Daurel,1,2 Corinne Huet,2,3 Anne Dhalluin,2,4 Michèle Bes,5 Jerome Etienne,5 and Roland Leclercq1,2*

Service de Microbiologie, CHU Côte de Nacre,1 EA 2128 Interactions hôte et microorganismes des épithéliums,2 UFR Sciences Pharmaceutiques, Université de Caen Basse-Normandie, 14033 Caen cedex,4 CH Louis Pasteur, Cherbourg, 50100,3 INSERM U851, Centre National de Référence des Staphylocoques, Faculté Laennec, Université Lyon 1, 69008 Lyon, France5

Received 28 September 2007/ Returned for modification 17 November 2007/ Accepted 2 December 2007

In staphylococci, inducible macrolide-lincosamide-streptogramin B (MLSB) resistance is conferred by the erm(C) or erm(A) gene. This phenotype is characterized by the erythromycin-clindamycin "D-zone" test. Although clindamycin appears active in vitro, exposure of MLSB-inducible Staphylococcus aureus to this antibiotic may result in the selection of clindamycin-resistant mutants, either in vitro or in vivo. We have compared the frequencies of mutation to clindamycin resistance for 28 isolates of S. aureus inducibly resistant to erythromycin and bearing the erm(C) (n = 18) or erm(A) (n = 10) gene. Seven isolates susceptible to erythromycin or bearing the msr(A) gene (efflux) were used as controls. The frequencies of mutation to clindamycin resistance for the erm(A) isolates (mean ± standard deviation, 3.4 x 10–8 ± 2.4 x 10–8) were only slightly higher than those for the controls (1.1 x 10–8 ± 6.4 x 10–9). By contrast, erm(C) isolates displayed a mean frequency of mutation to clindamycin resistance (4.7 x 10–7 ± 5.5 x 10–7) 14-fold higher than that of the S. aureus isolates with erm(A). The difference was also observed, although to a lower extent, when erm(C) and erm(A) were cloned into S. aureus RN4220. We conclude that erm(C) and erm(A) have different genetic potentials for selection of clindamycin-resistant mutants. By the disk diffusion method, erm(C) and erm(A) isolates could be distinguished on the basis of high- and low-level resistance to oleandomycin, respectively.

* Corresponding author. Mailing address: CHU de Caen, Service de Microbiologie, Avenue Côte de Nacre, 14033 Caen Cedex, France. Phone: (33) 02 31 06 45 72. Fax: (33) 02 31 06 45 73. E-mail: leclercq-r{at}chu-caen.fr

{triangledown} Published ahead of print on 12 December 2007.

Journal of Clinical Microbiology, February 2008, p. 546-550, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01925-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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