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These antibiotics should continue to be first-line therapy for these infections [25�C27,31]. The most frequently encountered mechanism of macrolide resistance in pneumococci is target site modification mediated by the ermB-encoded methylase, conferring resistance to all macrolides, lincosamides, and streptogramin?B (MLSB?phenotype). The expression of this phenotype can be constitutive or inducible, becoming active only in the presence of inducing macrolides. The ermB gene is the major cause of macrolide resistance in most European countries, especially Belgium, France, Poland, Italy, and Spain [38]. The second most common mechanism is mediated by an efflux Hydroxychloroquine clinical trial pump codified by the mef genes (mefA, mefE). This mechanism confers the M?phenotype, with resistance to 14-membered and 15-membered ring macrolides, but not to lincosamides or streptogramins. The M?phenotype isolates predominate in the USA, Canada, the UK, Germany, and Norway. Less common macrolide resistance could be due to mutations in the 23S rRNA and/or alterations in ribosomal proteins (L4 and L22). Fasudil in vitro The prevalence of macrolide resistance mechanisms differs considerably among countries, as shown in Table?2 [44�C58]. The emergence of pneumococci that carry both ermB and mefE macrolide resistance genes is a cause for concern, especially in Asian countries, Russia, South Africa, and the USA [52,59]. Both genes (ermB and mefE), as well as the tetracycline resistance determinant (tetM), have been related to the composite element Tn2010, which is present in most multidrug-resistant isolates of serotype?19A of clonal complex?320 [18,60]. Macrolide-resistant pneumococci were first detected in 1967 in Canada, but rates of macrolide resistance among pneumococci remained low worldwide (Oxygenase Paris [61]. In Spain, resistance rates increased from 0% in 1979�C1980 to 9.4% in 1990 in a Barcelona hospital [9]. Thereafter, a rapid worldwide increase in the prevalence of macrolide resistance associated with an increase in macrolide consumption, especially of long-acting macrolides such as clarithromycin and azithromycin, was observed [38,62�C64]. Global surveillance studies have shown that macrolide resistance rates increased during the 1990s. The Alexander Project gave a global rate of macrolide resistance of 16.5�C21.9% in 1996�C1997, increasing up to 24.6% in 1998�C2000 [36].