Molecular Epidemiology of Hypervirulent Carbapenemase-Producing Klebsiella pneumoniae.
Molecular Epidemiology of Hypervirulent Carbapenemase-Producing Klebsiella pneumoniae.
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高毒力产碳青霉烯酶肺炎克雷伯菌的分子流行病学
DOI：
10.3389/fcimb.2021.661218
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发表时间：
2021
影响因子：
5.7
通讯作者：
Jiang X
中科院分区：
文献类型：
--
作者：
Hu D;Li Y;Ren P;Tian D;Chen W;Fu P;Wang W;Li X;Jiang X
目的研究肺炎克雷伯菌关键毒力基因的总体分布，特别是高毒力bla KPC阳性肺炎克雷伯菌（Hv-bla KPC(+)-KP）。从GenBank中收集521份肺炎克雷伯菌全基因组进行分析。研究了多位点序列分型、分子血清分型、抗生素耐药性、毒力基因和质粒复制子分型。毒力基因的阳性率差异很大，从2.9 （c-rmpA/A2）到99.6% （entB）不等。共有207株为fh、mrkD、entB和wzi阳性，190株为fh、mrkD、entB、irp2和wzi阳性，这是两种主要模式。高毒力肺炎克雷伯菌（HvKP）、bla KPC(+)-KP和Hv-bla KPC(+)-KP分别为94、165和29株。29株Hv-bla KPC(+)-KP中ST11株占17株；Hv-bla KPC(+)-KP菌株中iucA、p-rmpA2和p-rmpA基因分别阳性28、26和18株。29株Hv-bla KPC(+)-KP具有4个超级聚类，其中携带毒力基因的IncHI1B质粒和携带bla KPC的IncFII质粒分别为23株。肺炎克雷伯菌毒力基因阳性率差异显著。诱导Hv-bla KPC(+)-KP的主要基因为iucA、p-rmpA2和p-rmpA。携带毒力基因的IncHI1B质粒和携带bla KPC的IncFII质粒构成了负责Hv-bla KPC(+)-KP的主要组合。Hv-bla KPC(+)-KP的产生主要是通过bla KPC(+)-KP获取另一个携带毒力基因的质粒。
To investigate the overall distributions of key virulence genes in Klebsiella pneumoniae, especially the hypervirulent bla KPC-positive K. pneumoniae (Hv-bla KPC(+)-KP). A total of 521 complete genomes of K. pneumoniae from GenBank were collected and analyzed. Multilocus sequence typing, molecular serotyping, antibiotic-resistance, virulence genes and plasmid replicon typing were investigated. Positive rates of virulence genes highly varied, ranging from 2.9 (c-rmpA/A2) to 99.6% (entB). Totally 207 strains presented positive fimH, mrkD, entB and wzi and 190 showed positive fimH, mrkD, entB, irp2 and wzi, which were the two primary modes. A total of 94, 165 and 29 strains were denoted as hypervirulent K. pneumoniae (HvKP), bla KPC(+)-KP and Hv-bla KPC(+)-KP. ST11 accounted for 17 among the 29 Hv-bla KPC(+)-KP strains; Genes iucA, p-rmpA2 and p-rmpA were positive in 28, 26 and 18 Hv-bla KPC(+)-KP strains respectively. Among the 29 Hv-bla KPC(+)-KP strains exhibiting four super clusters from GenBank, IncHI1B plasmids carrying virulence genes and IncFII ones with bla KPC were responsible for both 23 strains respectively. Positive rates of virulence genes vary remarkably in K. pneumoniae. Genes iucA, p-rmpA2 and p-rmpA were primary ones inducing Hv-bla KPC(+)-KP. IncHI1B plasmids carrying virulence genes and IncFII ones with bla KPC constitute the primary combination responsible for Hv-bla KPC(+)-KP. The making of Hv-bla KPC(+)-KP is mostly via bla KPC(+)-KP acquiring another plasmid harboring virulence genes.