Emerg Infect Dis. 2018 Feb;24(2):242-248. doi: 10.3201/eid2402.171074.
During cefoxitin-based nasal screening, phenotypically categorized methicillin-resistant Staphylococcus aureus (MRSA) was isolated and tested negative for the presence of the mecA and mecC genes as well as for the SCCmec-orfX junction region. The isolate was found to carry a mecB gene previously described for Macrococcus caseolyticus but not for staphylococcal species. The gene is flanked by β-lactam regulatory genes similar to mecR, mecI, and blaZ and is part of an 84.6-kb multidrug-resistance plasmid that harbors genes encoding additional resistances to aminoglycosides (aacA-aphD, aphA, and aadK) as well as macrolides (ermB) and tetracyclines (tetS). This further plasmidborne β-lactam resistance mechanism harbors the putative risk of acceleration or reacceleration of MRSA spread, resulting in broad ineffectiveness of β-lactams as a main therapeutic application against staphylococcal infections.
在头孢西丁为基础的鼻腔筛查期间，分离出表型上分类为耐甲氧西林金黄色葡萄球菌 (MRSA) 的菌株，并对 mecA 和 mecC 基因以及 SCCmec-orfX 连接区进行了检测，结果均为阴性。该分离株携带 mecB 基因，该基因先前在巨球菌属（Macrococcus caseolyticus）中已有描述，但在葡萄球菌属中尚未发现。该基因被类似于 mecR、mecI 和 blaZ 的β-内酰胺调控基因所包围，是一个 84.6kb 的多药耐药质粒的一部分，该质粒还携带编码对氨基糖苷类（aacA-aphD、aphA 和 aadK）以及大环内酯类（ermB）和四环素类（tetS）抗生素耐药的基因。这种进一步的质粒介导的β-内酰胺耐药机制存在加速或重新加速 MRSA 传播的风险，导致β-内酰胺类药物作为治疗葡萄球菌感染的主要应用药物的广泛失效。
