Persistent macrolide resistance among group A streptococci: the lack of accomplishment after 4 decades.

After isolation of erythromycin from a culture of Streptomyces erythreus in 1952 and the soon-to-follow introduction of erythromycin to clinical practice, eryth-romycin resistance required !2 decades to become apparent among clinical isolates of group A streptococci (GAS; Streptococ-cus pyogenes). A 1968 report in 1968 by Sanders et al. [1] about an erythromycin-resistant GAS (M type 12) isolate recovered from a patient's upper respiratory tract concluded with the admonition, " Therefore, determination of the in-vitro susceptibility of group A streptococci to these drugs appears advisable whenever their use is contemplated, and imperative when either the infection threatens life or there is an increased risk that late sequelae of such infections will develop. " Now, decades later, Richter et al. [2] similarly admonish physicians in their survey of mac-rolide resistance in the United States: " In vitro testing of S. pyogenes for macrolide susceptibility is warranted for patients who are allergic to b-lactams " (p. 606). Unfortunately, during this 37-year interval , there has been little change in the need to caution practitioners about the potential for macrolide resistance. There continue to be numerous reports that address clinical, epidemiological, and microbiological aspects of macrolide resistance for S. pyogenes. A review of PubMed citations revealed 240 studies related to macrolide resistance in GAS from the beginning of 2000 to April 2005. Recently published macrolide resistance rates range from ∼3%–4% in most areas of continental North America (e.g., [3]; new data indicate a similar figure for the Hawaiian Islands [4]) to more than 10 times that prevalence for several European countries. Many studies include emphasis on the molecular mechanisms responsible for macrolide resistance in GAS and the relationship of these mechanisms to clon-ality, as does the report by Richter et al. [2]. This is undoubtedly an important area for scientific investigation, but there remain inadequately addressed questions about how resistance affects clinical effectiveness for both the individual patient and for the public health and about what action can be effective in controlling resistance. All too often, authors only state, as the Richter and colleagues do in their conclusion, that there are " several large clones with potential for expansion " [2, p. 606]. The paramount issue is not adequately addressed. The practitioner is left wondering whether there is a role for surveillance and, if so, why does the problem persist, and what can be done to rectify the current situation? After reading their analysis …