Zhou Zhemin, McCann Angela, Litrup Eva, Murphy Ronan, Cormican Martin, Fanning Seamus, Brown Derek, Guttman David S, Brisse Sylvain, Achtman Mark
Environmental Research Institute, University College Cork, Cork, Ireland.
PLoS Genet. 2013 Apr;9(4):e1003471. doi: 10.1371/journal.pgen.1003471. Epub 2013 Apr 18.
Salmonella enterica serovar Agona has caused multiple food-borne outbreaks of gastroenteritis since it was first isolated in 1952. We analyzed the genomes of 73 isolates from global sources, comparing five distinct outbreaks with sporadic infections as well as food contamination and the environment. Agona consists of three lineages with minimal mutational diversity: only 846 single nucleotide polymorphisms (SNPs) have accumulated in the non-repetitive, core genome since Agona evolved in 1932 and subsequently underwent a major population expansion in the 1960s. Homologous recombination with other serovars of S. enterica imported 42 recombinational tracts (360 kb) in 5/143 nodes within the genealogy, which resulted in 3,164 additional SNPs. In contrast to this paucity of genetic diversity, Agona is highly diverse according to pulsed-field gel electrophoresis (PFGE), which is used to assign isolates to outbreaks. PFGE diversity reflects a highly dynamic accessory genome associated with the gain or loss (indels) of 51 bacteriophages, 10 plasmids, and 6 integrative conjugational elements (ICE/IMEs), but did not correlate uniquely with outbreaks. Unlike the core genome, indels occurred repeatedly in independent nodes (homoplasies), resulting in inaccurate PFGE genealogies. The accessory genome contained only few cargo genes relevant to infection, other than antibiotic resistance. Thus, most of the genetic diversity within this recently emerged pathogen reflects changes in the accessory genome, or is due to recombination, but these changes seemed to reflect neutral processes rather than Darwinian selection. Each outbreak was caused by an independent clade, without universal, outbreak-associated genomic features, and none of the variable genes in the pan-genome seemed to be associated with an ability to cause outbreaks.
肠炎沙门氏菌阿贡纳血清型自1952年首次分离以来,已引发多起食源性肠胃炎暴发。我们分析了来自全球各地的73株菌株的基因组,将五次不同的暴发与散发性感染以及食品污染和环境进行了比较。阿贡纳由三个谱系组成,突变多样性极小:自1932年阿贡纳进化并随后在20世纪60年代经历一次主要的种群扩张以来,非重复的核心基因组中仅积累了846个单核苷酸多态性(SNP)。与肠炎沙门氏菌的其他血清型的同源重组在谱系中的5/143个节点中导入了42个重组片段(360 kb),这导致了另外3164个SNP。与这种遗传多样性的匮乏形成对比的是,根据脉冲场凝胶电泳(PFGE),阿贡纳具有高度的多样性,PFGE用于将分离株归类到暴发事件中。PFGE多样性反映了一个高度动态的辅助基因组,该基因组与51个噬菌体、10个质粒和6个整合接合元件(ICE/IME)的获得或丢失(插入缺失)相关,但与暴发并没有唯一的相关性。与核心基因组不同,插入缺失在独立节点中反复出现(同源性),导致PFGE谱系不准确。除了抗生素抗性外,辅助基因组中仅包含很少与感染相关的货物基因。因此,这种最近出现的病原体中的大多数遗传多样性反映了辅助基因组的变化,或者是由于重组,但这些变化似乎反映的是中性过程而非达尔文选择。每次暴发都是由一个独立的进化枝引起的,没有普遍的、与暴发相关的基因组特征,并且泛基因组中的可变基因似乎都与引起暴发的能力无关。