Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Stigbøjlen 4, 1870 Frederiksberg, Denmark.
Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Stigbøjlen 4, 1870 Frederiksberg, Denmark.
Vet Microbiol. 2014 Jan 10;168(1):141-7. doi: 10.1016/j.vetmic.2013.10.008. Epub 2013 Oct 24.
A collection of 46 avian pathogenic Escherichia coli (APEC) isolates was examined for the presence of mutators by determining the rate of mutation to rifampicin resistance. The collection included 34 E. coli isolates obtained in pure culture from chronic lesions of salpingitis and peritonitis in 34 broiler breeders, of which 12 were associated with the development of secondary septicemia. Twelve additional isolates were obtained from a clonal outbreak (ST95) of E. coli peritonitis syndrome (EPS), the lesions of which changed gradually over time into a subacute/chronic form. The hypothesis of the present study was that mutation rates would be higher for chronic infection isolates than for isolates from acute infections/exacerbations. The distribution of mutation rates followed a pattern similar to that found for other clinical isolates of E. coli, with a modal/median value of 1.47 × 10(-8). Of the 46 isolates, 24% (n=11) were weakly hypermutable (2.00 × 10(-8) ≤ μ<2.00 × 10(-7)), however, no strong mutators were detected (μ ≥ 2.00 × 10(-7)). Chronic salpingitis isolates had the highest proportion (45%, P=0.001) of weak mutators and also, significantly higher mutation rates (P=0.003) compared to isolates that caused septicemia (4%). In addition, mutation rates were significantly lower among ST95 isolates (P<0.0005), and among isolates from the same clonal group as ST95 (P=0.027), when compared to isolates from other groups. Although a clear association with the time phase of infection (as lesions of EPS became more chronic) could not be observed (ρ=0.523, P=0.081), a higher frequency of weak mutators among chronic infection isolates suggests that increased mutation rates play a role in adaptation of APEC to long-term persistence in an infected host environment.
对 46 株禽源致病性大肠杆菌(APEC)分离株进行了突变体的检测,方法是测定其对利福平耐药性的突变率。该分离株集包括 34 株大肠杆菌分离株,这些分离株均从 34 只种鸡输卵管炎和腹膜炎慢性病变中纯培养获得,其中 12 株与继发性败血病的发生有关。另外 12 株分离株来自大肠杆菌腹膜炎综合征(EPS)克隆性爆发(ST95),其病变随时间逐渐转变为亚急性/慢性形式。本研究的假设是,慢性感染分离株的突变率高于急性感染/加重分离株。突变率的分布模式与其他临床大肠杆菌分离株相似,模式/中位数值为 1.47×10^-8。在 46 株分离株中,24%(n=11)为弱突变体(2.00×10^-8≤μ<2.00×10^-7),但未检测到强突变体(μ≥2.00×10^-7)。慢性输卵管炎分离株中弱突变体的比例最高(45%,P=0.001),与引起败血症的分离株相比,突变率也显著更高(P=0.003)。此外,与其他组分离株相比,ST95 分离株的突变率显著更低(P<0.0005),与 ST95 同克隆群的分离株的突变率也显著更低(P=0.027)。尽管不能观察到与感染时间阶段的明显关联(随着 EPS 病变变得更加慢性)(ρ=0.523,P=0.081),但慢性感染分离株中弱突变体的频率更高表明,增加的突变率在 APEC 适应感染宿主环境的长期持续存在中发挥作用。