TO THE EDITOR—We thank Gandra et al for their analysis of clindamycin/erythromycin-resistant methicillin-susceptible Staphylococcus aureus (MSSA) across the United States between 1999 and 2011 [1]. The authors observed a steady increase in this resistance profile nationwide, with a particularly steep jump in New York state between 2002 and 2004 and subsequently in the Northeast region around 2007–2008. Based on our study and others [2–4], Gandra et al suggest that this pattern of resistance to erythromycin and clindamycin with preserved susceptibility to tetracycline might serve as a surrogate marker for the emergence and spread of ST398 MSSA in the United States. In support of this observation, we note that the projected timeline coincides with the detection of ST398 in our studies in northern Manhattan [5, 6] and adjacent regions [7]. In addition, 25% (n = 48/196) of non-ST398 MSSA strains harbored clindamycin/erythromycin resistance in our study, of which 23% (n = 11/48) were also resistant to other antibiotics, in particular levofloxacin and tetracycline. In contrast, we only observed resistance to levofloxacin in 1 ST398 isolate [2]. Although the data provided by Gandra et al provide a comprehensive summary of drug resistance in MSSA across the United States, studies on the molecular epidemiology of MSSA in the United

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be further evaluated in targeted molecular surveillance studies, increasing our ability to recognize emerging pathogenic clones in real time.

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Notes Financial support. We report research support from the National Institutes of Health (grant numbers K08 AI090013 to A. C. U. and R01 AI077690 and R01 AI077690-S1 to F. D. L.) and by the Paul A. Marks Scholarship (to A. C. U.). Potential conflicts of interest. Both authors: No reported conflicts. Both authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Anne-Catrin Uhlemann1 and Franklin D. Lowy1,2 1 Division of Infectious Diseases, Department of Medicine, and 2Department of Pathology, Columbia University College of Physicians and Surgeons, New York, New York

References 1. Gandra S, Braykov N, Laxminarayan R. Is methicillin-susceptible Staphylococcus aureus (MSSA) sequence type 398 confined to northern Manhattan? Rising prevalence of erythromycinand clindamycin-resistant MSSA clinical isolates in the United States. Clin Infect Dis 2014; 58: 306–7. 2. Uhlemann AC, Hafer C, Miko BA, et al. Emergence of sequence type 398 as a community- and healthcare-associated methicillinsusceptible Staphylococcus aureus in northern Manhattan. Clin Infect Dis 2013; 57:700–3. 3. Vandendriessche S, Kadlec K, Schwarz S, Denis O. Methicillin-susceptible Staphylococcus

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aureus ST398-t571 harbouring the macrolidelincosamide-streptogramin B resistance gene erm(T) in Belgian hospitals. J Antimicrob Chemother 2011; 66:2455–9. Verkade E, Bergmans AM, Budding AE, et al. Recent emergence of Staphylococcus aureus clonal complex 398 in human blood cultures. PLoS One 2012; 7:e41855. Bhat M, Dumortier C, Taylor BS, et al. Staphylococcus aureus ST398, New York City and Dominican Republic. Emerg Infect Dis 2009; 15:285–7. Uhlemann AC, Porcella SF, Trivedi S, et al. Identification of a highly transmissible animal-independent Staphylococcus aureus ST398 clone with distinct genomic and cell adhesion properties. MBio 2012; 3. pii: e00027-12. Mediavilla JR, Chen L, Uhlemann AC, et al. Methicillin-susceptible Staphylococcus aureus ST398, New York and New Jersey, USA. Emerg Infect Dis 2012; 18:700–2. Miko BA, Hafer CA, Lee CJ, et al. Molecular characterization of methicillin-susceptible Staphylococcus aureus clinical isolates in the United States, 2004 to 2010. J Clin Microbiol 2013; 51:874–9. Goering RV, Shawar RM, Scangarella NE, et al. Molecular epidemiology of methicillin-resistant and methicillin-susceptible Staphylococcus aureus isolates from global clinical trials. J Clin Microbiol 2008; 46:2842–7.

Correspondence: Anne-Catrin Uhlemann, MD, PhD, Department of Medicine, Division of Infectious Diseases, Columbia University Medical Center, 630 W 168th St, New York, NY 10032 ([email protected]). Clinical Infectious Diseases 2014;58(2):307–8 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/cid/cit685

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States have so far failed to detect ST398 in sizable numbers across the country [8, 9]. The authors acknowledge that other clones are likely to contribute to the proportion of MSSA that are resistant only to erythromycin and clindamycin. Extrapolating from our studies in northern Manhattan, isolates with a diverse genetic background, including of the CC30 and CC8 lineages, accounted for this susceptibility pattern among the non-ST398 isolates [2]. It would have been interesting to correlate the resistance data presented by Gandra et al with the nationwide usage of macrolides and clindamycin. This could help delineate whether the observed evolving resistance in MSSA is a direct consequence of increased drug pressure, or rather a fingerprint of a clone harboring the erythromycin/clindamycin resistance genotype. Interestingly, in ST398 MSSA, ermT is integrated into the core chromosome rather than carried on a plasmid, providing a potential mechanism for a preferential clonal spread of erythromycin- and clindamycin-resistant ST398 MSSA [3, 6]. Nationwide databases on resistance and drug usage, as accessed by Gandra et al in their study, have the potential to rapidly provide profiles of shifting patterns in drug resistance. These can then

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