RESUMO
Here we report the molecular epidemiology of macrolide-resistant Streptococcus pyogenes (group A streptococci, GAS) isolated from children with pharyngotonsillitis between 2011 and 2013 in Japan. In 299 isolates, 124 (41.5%) isolates were macrolide-resistant. We characterized the isolates by emm typing, multilocus sequence typing (MLST), and pulsed-field gel electrophoresis (PFGE). Of 299 isolates, 124 (41.5%) were macrolide-resistant isolates, 76 (61.3%) possessed mefA and 46 (37.1%) possessed ermB. All 76 isolates with mefA possessed msrD. There were no isolates possessed ermTR in this study. Eight emm/MLST types were observed. The predominant type was emm1/ST28 (57 isolates, 46.0%), which possessed the mefA/msrD complex, presenting as the M phenotype. The second most predominant type was emm12/ST467, which possessed ermB, presenting as the cMLSB phenotype. Of the cMLSB phenotype isolates, types emm28/ST52 and emm12/ST36 had multiple genetic backgrounds. We found high proportions of macrolide-resistant GAS in the southwestern areas of Japan.
Assuntos
Antibacterianos/uso terapêutico , Farmacorresistência Bacteriana/efeitos dos fármacos , Macrolídeos/uso terapêutico , Streptococcus pyogenes/efeitos dos fármacos , Streptococcus pyogenes/isolamento & purificação , Antígenos de Bactérias/metabolismo , Proteínas da Membrana Bacteriana Externa/metabolismo , Criança , Humanos , Japão , Testes de Sensibilidade Microbiana/métodos , Epidemiologia Molecular/métodos , Fenótipo , Infecções Respiratórias/microbiologia , Infecções Estreptocócicas/microbiologia , Streptococcus pyogenes/metabolismoRESUMO
Accumulated inflammatory cytokines are considered to be a cause of febrile nonhemolytic transfusion reactions (FNHTRs) of platelet transfusions. Inflammatory cytokines have been found in red cell components stored at 4 degrees C; however, their relationship to FNHTRs has not been clearly demonstrated following red cell transfusions. We measured cytokine levels in stored blood, and determined whether inflammatory marker concentrations were elevated in subjects infused with autologous blood stored for 5 weeks. In conclusion, cytokines accumulated in blood stored at 4 degrees C, but their increases were small. No changes were seen in recipients' inflammatory markers after blood transfusion. Our results indicate that cytokines in stored autologous blood are not responsible for FNHTRs.