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

Abstract

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-kbmultidrug-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.S taphylococcal cassette chromosome mec (SCCmec)- mediated β-lactam resistance resulting from production of an additional penicillin-binding protein (PBP) 2a drastically limits the treatment options in cases of hospital-and community-related infections by staphylococci, leading to increased illness, death, and socioeconomic costs (1,2).Besides methicillin-resistant coagulase-negative staphylococci, notorious for foreign body-associated infections, methicillin-resistant Staphylococcus aureus (MRSA) strains are a global public health priority, despite some countries in Europe reporting stabilizing or decreasing MRSA rates (3-5).Since the initial reports of MRSA in 1961, several epidemic waves have resulted in threats of healthcare-, community-, and livestock-associated MRSA (6-9).For staphylococci, 2 PBP 2a-encoding genes, mecA and mecC, including several allotypes, have been described as chromosomally located genetic bases for phenotypic methicillin resistance (10-14).In contrast, mecB,