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首页> 外文期刊>Journal of Clinical Microbiology >Genomic Epidemiology of Penicillin-Nonsusceptible Pneumococci with Nonvaccine Serotypes Causing Invasive Disease in the United States
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Genomic Epidemiology of Penicillin-Nonsusceptible Pneumococci with Nonvaccine Serotypes Causing Invasive Disease in the United States

机译：美国青霉素-不敏感肺炎链球菌与非疫苗血清型引起侵袭性疾病的基因组流行病学

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Conjugate vaccination against seven pneumococcal serotypes (PCV7) reduced disease prevalence due to antibiotic-resistant strains throughout the 2000s. However, diseases caused by resistant nonvaccine type (NVT) strains increased. Some of these emerging strains were derived from vaccine types (VT) that had changed their capsule by recombination. The introduction of a vaccine targeting 13 serotypes (PCV13) in 2010 has led to concern that this scenario will repeat itself. We generated high-quality draft genomes from 265 isolates of NVT pneumococci not susceptible to penicillin (PNSP) in 2009 and compared them with the genomes of 581 isolates from 2012 to 2013 collected by the Active Bacterial Core surveillance (ABCs) of the Centers for Disease Control and Prevention (CDC). Of the seven sequence clusters (SCs) identified, three SCs fell into a single lineage associated with serogroup 23, which had an origin in 1908 as dated by coalescent analysis and included isolates with a divergent 23B capsule locus. Three other SCs represented relatively deep-branching lineages associated with serotypes 35B, 15A, and 15BC. In all cases, the resistant clones originated prior to 2010, indicating that PNSP are at present dominated by descendants of NVT clones present before vaccination. With one exception (15BC/ST3280), these SCs were related to clones identified by the Pneumococcal Molecular Epidemiology Network (PMEN). We conclude that postvaccine diversity in NVT PNSP between 2009 and 2013 was driven mainly by the persistence of preexisting strains rather than through de novo adaptation, with few cases of serotype switching. Future surveillance is essential for documenting the long-term dynamics and resistance of NVT PNSP.
机译：在整个2000年代，针对7种肺炎球菌血清型（PCV7）的联合疫苗接种降低了疾病流行率，原因是抗生素耐药株。但是，由耐药性非疫苗型（NVT）株引起的疾病增加。这些新兴菌株中的一些来源于疫苗类型（VT），这些疫苗通过重组改变了它们的胶囊。 2010年针对13种血清型（PCV13）的疫苗的引入导致人们担心这种情况会重演。我们在2009年从265株对青霉素（PNSP）不敏感的NVT肺炎球菌分离株中生成了高质量的基因组草图，并将其与疾病中心的主动细菌核心监测（ABCs）收集的2012年至2013年的581株分离株的基因组进行了比较。控制与预防（CDC）。在确定的七个序列簇（SC）中，三个SC落入了与血清群23相关的单一谱系，血清群的起源于1908年（通过聚结分析），并包括具有不同23B胶囊基因座的分离株。其他三个SC代表与血清型35B，15A和15BC相关的相对较深的分支谱系。在所有情况下，抗性克隆均始于2010年之前，表明PNSP目前被疫苗接种前存在的NVT克隆的后代所支配。除了一个例外（15BC / ST3280），这些SC与肺炎球菌分子流行病学网络（PMEN）鉴定的克隆有关。我们得出的结论是，2009年至2013年之间NVT PNSP的疫苗接种后多样性主要是由先前存在的毒株的持久性驱动的，而不是由 de novo 适应性驱动的，很少发生血清型转换。未来的监视对于记录NVT PNSP的长期动态和抵抗力至关重要。

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