title: Decrease in macrolide resistance and clonal instability among Streptococcus pyogenes in Portugal.
abstract: Macrolide resistance among Streptococcus pyogenes (group A streptococci) in Portugal was stable during 1998-2003, but a rapid inversion in the dominant phenotypes was noted in the same period, with a sharp decrease in the proportion of isolates presenting the MLS(B) phenotype and a concomitant increase in isolates presenting the M phenotype. The characterization of group A streptococci recovered during 2004-2006, which is reported here, revealed that resistance was not stable during this period and that the decline in erythromycin resistance observed during 2004-2006 was due to a decrease in the prevalence of isolates presenting the M phenotype, while the proportion of isolates expressing the MLS(B) phenotype remained stable. Characterization by emm typing, T serotyping, pulsed-field gel electrophoresis (PFGE) profiling and multilocus sequence typing revealed a very diverse population. Several of the major PFGE clusters identified had already been found in the 1998-2003 study period, but others were found for the first time, e.g. T11/emm11/ST403, carrying the erm(B) gene, and T3/13/emm3/ST315, carrying the mef(A) gene. The clone defined as T12/emm12/ST36, previously found to be associated with mef(A), was now found to be predominantly associated with erm(B). The clonal dynamics of macrolide-resistant group A streptococci emphasizes the importance of considering factors other than antibiotic consumption in explaining the prevalence of resistant isolates.
authors.affiliation: Institute of Microbiology/Molecular Medicine, Faculty of Medicine, Lisbon University, Lisbon, Portugal.
authors.forename: C
authors.initials: C
authors.lastname: Silva-Costa
authors.forename: F R
authors.initials: FR
authors.lastname: Pinto
authors.forename: M
authors.initials: M
authors.lastname: Ramirez
authors.forename: J
authors.initials: J
authors.lastname: Melo-Cristino
mesh_terms: D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D015373:Bacterial Typing Techniques; D016000:Cluster Analysis; D016172:DNA Fingerprinting; D004269:DNA, Bacterial / Q000235:genetics; D024881:Drug Resistance, Bacterial; D016521:Electrophoresis, Gel, Pulsed-Field; D005838:Genotype; D006801:Humans; D055231:Lincosamides / Q000494:pharmacology; D018942:Macrolides / Q000494:pharmacology*; D008826:Microbial Sensitivity Tests; D011174:Portugal; D017422:Sequence Analysis, DNA; D012703:Serotyping; D013290:Streptococcal Infections / Q000382:microbiology*; D013297:Streptococcus pyogenes / Q000145:classification* / Q000187:drug effects* / Q000235:genetics / Q000302:isolation & purification; D025381:Streptogramin B / Q000494:pharmacology
chemical_list: D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D055231:Lincosamides; D018942:Macrolides; D025381:Streptogramin B