Evolution of Acinetobacter baumannii In Vivo: International Clone II, More Resistance to Ceftazidime, Mutation in ptk.
Evolution of Acinetobacter baumannii In Vivo: International Clone II, More Resistance to Ceftazidime, Mutation in ptk.
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鲍曼不动杆菌体内进化：国际克隆 II、头孢他啶更强耐药性、ptk 突变
DOI：
10.3389/fmicb.2017.01256
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发表时间：
2017
影响因子：
5.2
通讯作者：
Yu Y
中科院分区：
文献类型：
--
作者：
Hua X;Zhou Z;Yang Q;Shi Q;Xu Q;Wang J;Shi K;Zhao F;Sun L;Ruan Z;Jiang Y;Yu Y
鲍曼不动杆菌是一种重要的医院感染病原菌。对A.鲍曼不动杆菌的基因突变为提高鲍曼不动杆菌的治疗水平提供了分子基础。鲍曼不动杆菌感染了解A.鲍曼不动杆菌在人体内存活，本文报道了鲍曼不动杆菌的基因组分析。从中国患者中分离的鲍曼不动杆菌。我们利用A.从同一患者分离鲍曼不动杆菌，以确定单核苷酸变异、插入序列作图和基因变化。测定了10种抗菌药物的MIC。对携带ptk突变的分离对进行运动性测定和显微镜检查。基因ptk编码一个假定的蛋白酪氨酸激酶参与生产荚膜多糖。从同一患者分离的菌株中约有一半（39/86）具有相同的MLST模式，并且在国际克隆谱系II（ICL-II）和非ICL-II菌株的替换过程中，大多数变化是非ICL-II菌株被ICL-II菌株替换（10/12）。A.鲍曼不动杆菌对主要抗菌药物耐药，而在宿主内进化后，菌株对头孢他啶、阿奇霉素和磺胺类药物更耐药。ICL-II谱系的分离株显示出比非ICL-II分离株更强的抗菌药物耐药性。ICL-II型菌株比非ICL-II型菌株具有更多的抗性基因和移动的元件。几个谱系进化出更粘液样的表型。基因组测序显示，表型是通过ptk基因的遗传变化实现的。ICL-II（尤其是ST 195和ST 208）是细菌在宿主内进化后的最终目的地。这些结果表明，ICL-II菌株的分子基础和治疗需要进一步研究。
Acinetobacter baumannii is an important nosocomial pathogen worldwide. A more comprehensive understanding of the within-host genomic evolution of A. baumannii would provide a molecule basis for improving treatment of A. baumannii infection. To understand the evolutionary mechanism facilitating A. baumannii survived in human body, we here reported the genomic analysis of A. baumannii isolated sampled from Chinese patients. We used whole-genome sequence of A. baumannii isolates from the same patient to determine single-nucleotide variants, insertion sequence mapping, and gene change. The MICs for 10 antimicrobial agents were determined. Motility assay and microscopy were performed on the isolated pairs harboring ptk mutations. The gene ptk encoded a putative protein tyrosine kinase involved in the production of capsular polysaccharide. Approximately half (39/86) of the strains isolated from the same patient harbored the same MLST patterns, and during the replacement of international clonal lineage II (ICL-II) and non-ICL-II strains, most of the alteration was that non-ICL-II strain was replaced by ICL-II strain (10/12). A. baumannii was resistant to major antimicrobial agents, whereas the strains were more resistant to ceftazidime, azithromycin, and sulfonamides after within-host evolution. Isolates from the ICL-II lineage displayed greater resistance to antimicrobial agents than non-ICL-II isolates. Isolates from ICL-II harbored more resistance genes and mobile elements than non-ICL-II strains. Several lineages evolved a more mucoid phenotype. Genome sequencing revealed that the phenotype was achieved by genetic changes in the ptk gene. ICL-II (especially ST195 and ST208) was the terminal destination for bacteria after within-host evolution. These results indicate that the molecular basis and the treatment for ICL-II strains needed further investigation.
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影响因子：
30.8
作者：
通讯作者：
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影响因子：
3.9
作者：
Adams MD;Bishop B;Wright MS
通讯作者：
Wright MS
影响因子：
16.8
作者：
Losey, HC;Ruthenburg, AJ;Verdine, GL
通讯作者：
Verdine, GL
影响因子：
5.8
作者：
Page, Andrew J.;Cummins, Carla A.;Parkhill, Julian
通讯作者：
Parkhill, Julian
DOI：
10.1038/nrmicro2259
发表时间：
2010-01
期刊：
Nature reviews. Microbiology
影响因子：
--
作者：
通讯作者：
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