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dc.contributor.author김경효*
dc.date.accessioned2018-12-14T16:30:56Z-
dc.date.available2018-12-14T16:30:56Z-
dc.date.issued2018*
dc.identifier.issn1471-2334*
dc.identifier.otherOAK-22591*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/247753-
dc.description.abstractBackground: Understanding the population genetics of pneumococci will allow detection of changes in the prevalence of circulating genotypes and evidence for capsular switching. We aimed to analyze the genetic structure of invasive pneumococcal isolates obtained from children before and after the use of pneumococcal conjugate vaccines (PCVs) in Korea. Methods: A total of 285 invasive pneumococcal isolates were analyzed using serotyping, multilocus sequence typing, and antimicrobial susceptibility testing. We classified the isolation year to pre-PCV7 (1995-2003; n = 70), post-PCV7 (2004-2010; n = 142), and post-PCV13 (2011-2013; n = 73) periods. Results: Of the 10 clonal complexes (CCs), antibiotic-resistant international clones, CC320 (31.6%), CC81 (14.7%), and CC166 (6.7%) were the main complexes. Serotype 19A was the main serotype of CC320 throughout the periods. Serotypes of CC81 mainly comprised of 23F (53.3%) in pre-PCV7 period and replaced by non-vaccine types (NVTs; 6C [10%], 13 [30%], 15A [40%], and 15B/C [20%]) in post-PCV13 period. The main serotype responsible for CC166 also changed from 9 V (80%) in pre-PCV7 to NVT 11A (50%) in post-PCV13 periods. Non-susceptibility to penicillin (42.3%) was the highest in CC320, increasing from 0 to 76%. Conclusion: The genetic structures of invasive pneumococcal isolates in Korean children have changed concomitantly with serotype after the implementation of PCVs. © 2018 The Author(s).*
dc.languageEnglish*
dc.publisherBioMed Central Ltd.*
dc.subjectChildren*
dc.subjectInvasive pneumococcal diseases*
dc.subjectMultilocus sequence typing*
dc.subjectPneumococcal conjugate vaccine*
dc.titleGenetic structures of invasive Streptococcus pneumoniae isolates from Korean children obtained between 1995 and 2013*
dc.typeArticle*
dc.relation.issue1*
dc.relation.volume18*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.journaltitleBMC Infectious Diseases*
dc.identifier.doi10.1186/s12879-018-3177-7*
dc.identifier.wosidWOS:000434995400003*
dc.identifier.scopusid2-s2.0-85048261616*
dc.author.googleYun K.W.*
dc.author.googleChoi E.H.*
dc.author.googleLee H.J.*
dc.author.googleKang J.H.*
dc.author.googleKim K.-H.*
dc.author.googleKim D.S.*
dc.author.googleKim Y.-J.*
dc.author.googleEun B.W.*
dc.author.googleOh S.H.*
dc.author.googleCho H.-K.*
dc.author.googleHong Y.J.*
dc.author.googleKim K.N.*
dc.author.googleKim N.H.*
dc.author.googleKim Y.-K.*
dc.author.googleLee H.*
dc.author.googleLee T.*
dc.author.googleKim H.M.*
dc.author.googleCho E.Y.*
dc.author.googleKim C.S.*
dc.author.googlePark S.E.*
dc.author.googleOh C.E.*
dc.author.googleJo D.S.*
dc.author.googleChoi Y.Y.*
dc.author.googleLee J.*
dc.contributor.scopusid김경효(35448653000)*
dc.date.modifydate20240301081003*


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