Prevalence and Mechanisms of Erythromycin Resistance in Group A and Group B Streptococcus : Implications for Reporting Susceptibility Results

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Abstract
Increased rates of erythromycin resistance among group B Streptococcus (GBS) and group A Streptococcus (GAS) have been reported. Cross-resistance to clindamycin may be present, depending on the mechanism of resistance. We determined the prevalence of macrolide-resistant determinants in GBS and GAS isolates to guide the laboratory reporting of erythromycin and clindamycin susceptibility. Susceptibilities were determined by the disk diffusion and broth microdilution methods. Inducible and constitutive resistance to clindamycin was determined by the double-disk diffusion method. The presence of the ermTR , ermB , and mefA genes was confirmed by PCR. Of the 338 GBS isolates, 55 (17%) were resistant to erythromycin, whereas 26 (8%) were resistant to clindamycin. The erm methylase gene was identified in 48 isolates, 22 of which had inducible resistance to clindamycin and 26 of which had constitutive resistance to clindamycin. The remaining seven resistant isolates had mefA . Of the 593 GAS isolates, 49 (8%) and 6 (1%) isolates were resistant to erythromycin and clindamycin, respectively. Erythromycin resistance was due to mefA in 33 isolates, whereas 14 isolates had erm -mediated resistance (9 isolates had inducible resistance and 5 isolates had constitutive resistance). In our population, erythromycin resistance in GAS was predominantly mediated by mefA and erythromycin resistance in GBS was predominantly mediated by erm . Regional differences in mechanisms of resistance need to be taken into consideration when deciding whether to report clindamycin susceptibility results on the basis of in vitro test results. Testing by the double-disk diffusion method would be an approach that could be used to address this issue, especially for GAS.

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