Population-based analysis of invasive nontypeable pneumococci reveals that most have defective capsule synthesis genes.

Population-based analysis of invasive nontypeable pneumococci reveals that most have defective capsule synthesis genes.
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DOI:
10.1371/journal.pone.0097825
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Beall B
Beall B
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Park IH;Geno KA;Sherwood LK;Nahm MH;Beall B

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由于鼻咽部携带肺炎球菌先于侵袭性肺炎球菌疾病,因此携带分离株的特征可能被错误地认为反映了侵入性分离株的特征。虽然大多数肺炎球菌表达荚膜多糖,但有时会分离出不可分型的肺炎球菌。运输不可分型倾向于编码新的表面蛋白来代替荚膜多糖合成基因座,即 cps 基因座。相比之下,荚膜多糖被认为是侵袭性肺炎球菌疾病不可或缺的,并且基于人群的侵袭性肺炎球菌疾病监测中的不可分型尚未得到广泛表征。 2006 年至 2009 年期间,我们通过活性细菌核心监测计划收到了 14,328 株侵袭性肺炎球菌分离株。通过 PCR 血清分型、cps 位点序列分析和多位点序列分型对 Quellung 血清分型无法分型的分离株进行了表征。 88 个分离株是 Quellung 不可分型的 (0.61%)。其中,79 个(89.8%)包含 cps 位点。 22 个不可分型基因表现出存在缺陷的血清型 8 cps 位点,主要位于 wchA 内。其余九个分离株中的六个包含先前描述的 aliB 同源物来代替 cps 位点。多位点序列分型显示,大多数缺乏荚膜生物合成基因的不可分型基因与已建立的非荚膜谱系有关。因此,由不可分型肺炎球菌引起的侵袭性肺炎球菌疾病在美国仍然很少见,虽然缺乏cps位点的携带不可分型肺炎球菌经常被分离出来,但这种不可分型肺炎球菌在侵袭性肺炎球菌疾病中极为罕见。大多数侵袭性不可分型肺炎球菌具有缺陷的 cps 基因座基因,其中缺陷血清型 8 cps 变体的比例过高。
Since nasopharyngeal carriage of pneumococcus precedes invasive pneumococcal disease, characteristics of carriage isolates could be incorrectly assumed to reflect those of invasive isolates. While most pneumococci express a capsular polysaccharide, nontypeable pneumococci are sometimes isolated. Carriage nontypeables tend to encode novel surface proteins in place of a capsular polysaccharide synthetic locus, the cps locus. In contrast, capsular polysaccharide is believed to be indispensable for invasive pneumococcal disease, and nontypeables from population-based invasive pneumococcal disease surveillance have not been extensively characterized. We received 14,328 invasive pneumococcal isolates through the Active Bacterial Core surveillance program during 2006–2009. Isolates that were nontypeable by Quellung serotyping were characterized by PCR serotyping, sequence analyses of the cps locus, and multilocus sequence typing. Eighty-eight isolates were Quellung-nontypeable (0.61%). Of these, 79 (89.8%) contained cps loci. Twenty-two nontypeables exhibited serotype 8 cps loci with defects, primarily within wchA. Six of the remaining nine isolates contained previously-described aliB homologs in place of cps loci. Multilocus sequence typing revealed that most nontypeables that lacked capsular biosynthetic genes were related to established non-encapsulated lineages. Thus, invasive pneumococcal disease caused by nontypeable pneumococcus remains rare in the United States, and while carriage nontypeables lacking cps loci are frequently isolated, such nontypeable are extremely rare in invasive pneumococcal disease. Most invasive nontypeable pneumococci possess defective cps locus genes, with an over-representation of defective serotype 8 cps variants.
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