Corvec Stéphane, Prodhomme Adèle, Giraudeau Cécile, Dauvergne Sandie, Reynaud Alain, Caroff Nathalie
Laboratoire de Bactériologie-Hygiène, CHU, Nantes, France.
J Antimicrob Chemother. 2007 Oct;60(4):872-6. doi: 10.1093/jac/dkm284. Epub 2007 Jul 27.
To determine the phylogenetic group and the production of different virulence factors (VFs) of a collection of Escherichia coli strains overproducing their chromosomal AmpC cephalosporinase.
Fifty-five E. coli strains, isolated over a 12 year period, and previously identified as AmpC overproducers by increased MICs of third-generation cephalosporins without extended-spectrum beta-lactamase production (negative double-disc synergy test), were phylogrouped by multiplex PCR. As a comparison, 100 E. coli clinical isolates, susceptible to all beta-lactams, were also tested by the same method. The ampC promoter sequence was determined for all these isolates. ERIC-2 PCR (where ERIC stands for enterobacterial repetitive intergenic consensus) was used to compare the isolates. Search for virulence-associated genes (papG alleles, sfa/foc, hly and iucC) was performed by multiplex PCR for the 55 AmpC overproducers.
Most of the AmpC overproducers (47/55) belonged to phylogenetic group A, correlated with a low prevalence of the main VFs in these strains. The - 32, -42 and - 11 mutations, responsible for AmpC overproduction, were usually associated with DNA polymorphisms at positions - 88, - 82, -18, +1 and + 58 in the ampC promoter. In the control susceptible isolates, these polymorphisms were detected in 13 ampC promoters (9 group B1 and 4 group A). These polymorphisms were never associated with the main phylogenetic group B2, representing 66% of the susceptible isolates.
AmpC overproduction was clearly correlated with non-virulent commensal phylogenetic groups A and B1, and absence of the main E. coli VFs. Susceptible isolates harbouring the same sequence polymorphisms as AmpC overproducers also belonged to commensal phylogenetic groups.
确定一组过量产生染色体AmpC头孢菌素酶的大肠杆菌菌株的系统发育群及不同毒力因子(VF)的产生情况。
对在12年期间分离出的55株大肠杆菌菌株进行研究,这些菌株先前通过第三代头孢菌素的最低抑菌浓度升高且无超广谱β-内酰胺酶产生(双纸片协同试验阴性)被鉴定为AmpC过量产生菌,通过多重PCR对其进行系统发育分组。作为对照,还采用相同方法检测了100株对所有β-内酰胺类药物敏感的大肠杆菌临床分离株。测定所有这些分离株的ampC启动子序列。采用ERIC-2 PCR(其中ERIC代表肠杆菌重复基因间共有序列)对分离株进行比较。通过多重PCR对55株AmpC过量产生菌进行毒力相关基因(papG等位基因、sfa/foc、hly和iucC)的检测。
大多数AmpC过量产生菌(47/55)属于系统发育群A,这与这些菌株中主要VF的低流行率相关。导致AmpC过量产生的-32、-42和-11突变通常与ampC启动子中-88、-82、-18、+1和+58位的DNA多态性相关。在对照敏感分离株中,在13个ampC启动子中检测到这些多态性(9个为B1群,4个为A群)。这些多态性从未与占敏感分离株66%的主要系统发育群B2相关。
AmpC过量产生与无毒共生系统发育群A和B1以及缺乏主要大肠杆菌VF明显相关。携带与AmpC过量产生菌相同序列多态性的敏感分离株也属于共生系统发育群。