Plasmid-Encoded Transferable mecB-Mediated Methicillin Resistance in Staphylococcus aureus

被引:146
|
作者
Becker, Karsten [1 ]
van Alen, Sarah [2 ]
Idelevich, Evgeny A. [2 ]
Schleimer, Nina [2 ]
Seggewiss, Jochen [2 ]
Mellmann, Alexander [2 ]
Kaspar, Ursula [2 ]
Peters, Georg [2 ,3 ]
机构
[1] Univ Hosp Munster, Inst Med Microbiol, Med Microbiol, Munster, Germany
[2] Univ Hosp Munster, Munster, Germany
[3] Cells Mot, Munster, Germany
关键词
CASSETTE CHROMOSOME MEC; IN-VITRO ACTIVITY; COAGULASE-NEGATIVE STAPHYLOCOCCI; GERMAN GENERAL-POPULATION; CLONAL COMPLEX 398; MACROCOCCUS-CASEOLYTICUS; ANTIMICROBIAL RESISTANCE; BACTERIOPHAGE ENDOLYSIN; MRSA; CEFTAROLINE;
D O I
10.3201/eid2402.171074
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 beta-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 plasmid-borne beta-lactam resistance mechanism harbors the putative risk of acceleration or reacceleration of MRSA spread, resulting in broad ineffectiveness of beta-lactams as a main therapeutic application against staphylococcal infections.
引用
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页码:242 / 248
页数:7
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