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成人中耐大环内酯类侵袭性肺炎球菌的血清型和基因型替换:耐药机制及与不同转座子的关联。

Serotype and genotype replacement among macrolide-resistant invasive Pneumococci in adults: mechanisms of resistance and association with different transposons.

机构信息

Microbiology Department, Institut d'Investigació Biomèdica de Bellvitge, University of Barcelona, Barcelona, Spain.

出版信息

J Clin Microbiol. 2010 Apr;48(4):1310-6. doi: 10.1128/JCM.01868-09. Epub 2010 Feb 10.

DOI:10.1128/JCM.01868-09
PMID:20147647
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2849543/
Abstract

The aim of this study was to analyze trends in adult invasive pneumococcal disease (IPD) due to macrolide-resistant strains and to study the evolution of serotypes, genotypes, and macrolide-resistant determinants of strains collected in a prospective study between 1999 and 2007 in Barcelona, Spain. IPD due to macrolide-resistant strains of serotypes included in the 7-valent conjugate vaccine (PCV7) decreased from 2.16/100,000 (pre-PCV7 period, 1999 to 2001) to 0.80/100,000 (late-PCV7 period, 2005 to 2007) (P = 0.001), whereas IPD due to macrolide-resistant strains of non-PCV7 serotypes increased from 1.08/100,000 to 2.83/100,000 (P < 0.001). These changes were related to a fall of clones of PCV7 serotypes (ST81 [P < 0.05], ST90, ST315, and ST17) and an increase in new clones of serotypes 19A and 24F (ST230) and 33F (ST717) in the late-PCV7 period. The most common phenotype was MLS(B) (90.9%), related to the erm(B) gene. The frequent association between MLS(B) phenotype and tetracycline resistance [tet(M) gene], was related to transposons of the Tn916-family such as Tn6002 or Tn3872. In conclusion, overall adult IPD rates due to macrolide-resistant pneumococci stabilized between 1999 and 2007 in Barcelona. The decrease in macrolide-resistant PCV7 pneumococci was balanced by the increase in macrolide-resistant non-PCV7 pneumococci.

摘要

本研究旨在分析西班牙巴塞罗那地区 1999 年至 2007 年前瞻性研究中分离的耐大环内酯类肺炎链球菌引起的成人侵袭性肺炎链球菌病(IPD)的趋势,并研究血清型、基因型和耐药决定因素的演变。含 7 价结合疫苗(PCV7)血清型的耐大环内酯类肺炎链球菌引起的 IPD 从每 10 万人 2.16 例(PCV7 前时期,1999 至 2001 年)降至每 10 万人 0.80 例(PCV7 后期,2005 至 2007 年)(P = 0.001),而非 PCV7 血清型的耐大环内酯类肺炎链球菌引起的 IPD 从每 10 万人 1.08 例增至每 10 万人 2.83 例(P < 0.001)。这些变化与 PCV7 血清型(ST81[P < 0.05]、ST90、ST315 和 ST17)克隆的减少和新的血清型 19A 和 24F(ST230)和 33F(ST717)克隆的增加有关,这些变化发生在 PCV7 后期。最常见的表型是 MLS(B)(90.9%),与 erm(B)基因有关。MLS(B)表型与四环素耐药性(tet(M)基因)的频繁关联与 Tn916 家族的转座子如 Tn6002 或 Tn3872 有关。总之,1999 年至 2007 年期间,巴塞罗那成人耐大环内酯类肺炎链球菌引起的 IPD 总发病率保持稳定。耐大环内酯类 PCV7 肺炎链球菌的减少与耐大环内酯类非 PCV7 肺炎链球菌的增加相平衡。

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