Introduction. There are several β-lactamase genes described for Bacteroide s strains, of which cepA and cfiA are specific for Bacteroides fragilis and define two genetic divisions. The expression and phenotypic effects of these genes are usually regulated by insertional activation. Hypotheses/Gap Statement. Information is lacking about how cepA is regulated for most of the B. fragilis strains and whether there could be a genetic element for it. Aim. We aimed to investigate the molecular background of ampicillin (and other β-lactam) resistance among Bacteroides strains as mediated mainly by cepA and also to find a genetic element for it as known for cfiA. Methodology. Various PCR methods were used for β-lactamase-resistance gene and insertion sequence (IS) element detection in 42 Bacteroides strains. β-Lactamase activity measurements and antimicrobial-susceptibility testing using agar dilution were also applied. Further molecular experiments involved sequencing, gene targeting, Southern blotting and bioinformatic analyses. Results. We found that high antibiotic resistance and β-lactamase levels are brought about by insertional activation of the cepA gene or by similar or dissimilar activation of cfxA or cfiA, or by the newly described pbbA genes. Non-activated cepA genes produced low levels of specific β-lactamase activities that did not correlate with ampicillin resistance. We found a genetic element for cepA and another region close to it that are characteristic for division I B. fragilis strains, which are replaced by other sequences in division II B. fragilis strains. Conclusion. cepA usually is not activated by IS elements and usually produces low β-lactamase activities that do not correlate with the ampicillin MICs; therefore, it probably involves some non-β-lactamase-mediated resistance mechanism(s). pbpA is a newly described, effective β-lactamase gene that is located on a plasmid, and cepA resides on a well-defined chromosomal segment that is mutually replaced in division II B. fragilis strains. This latter finding demonstrates the genetic dichotomy of cepA–cfiA in B. fragilis and requires further investigation.

中文翻译：

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拟杆菌属的氨苄青霉素抗性和β-内酰胺酶基因的更新。

介绍。有几个针对拟杆菌属菌株描述的 β-内酰胺酶基因，其中cepA和cfiA对脆弱拟杆菌具有特异性，并定义了两个遗传分裂。这些基因的表达和表型效应通常受插入激活的调节。假设/差距声明。缺乏关于大多数脆弱拟杆菌菌株如何调节cepA以及是否可能存在遗传因素的信息。目的。我们旨在研究拟杆菌中氨苄青霉素（和其他 β-内酰胺）耐药性的分子背景 主要由cepA介导的菌株，并为其找到已知的cfiA遗传元件。方法。采用多种PCR方法对42株拟杆菌进行β-内酰胺酶抗性基因和插入序列（IS）元件检测。还应用了使用琼脂稀释的 β-内酰胺酶活性测量和抗菌药物敏感性测试。进一步的分子实验涉及测序、基因打靶、Southern 印迹和生物信息学分析。结果。我们发现高抗生素耐药性和 β-内酰胺酶水平是由cepA基因的插入激活或cfxA或 cfiA，或由新描述的pbbA基因。未激活的cepA基因产生低水平的特异性 β-内酰胺酶活性，这与氨苄青霉素抗性无关。我们发现了cepA和靠近它的另一个区域的遗传元件，这些区域是 I 部脆弱 B.菌株的特征，它们被 II 部脆弱 B.菌株中的其他序列取代。结论。cepA通常不会被 IS 元件激活，并且通常会产生与氨苄青霉素 MIC 无关的低 β-内酰胺酶活性；因此，它可能涉及一些非β-内酰胺酶介导的耐药机制。苯丙胺 是一种新描述的有效 β-内酰胺酶基因，位于质粒上，并且cepA位于明确定义的染色体片段上，该片段在 II 类脆弱芽孢杆菌菌株中相互替换。后者的发现表明遗传二分法CEPA，加拿大食品检验局在对脆弱和需要进一步调查。