Variability in SCC<it>mec</it>_N1spreading among injection drug users in Zurich, Switzerland

• Main Authors: McCallum Nadine, Berger-Bächi Brigitte, Ender Miriam
• Format: Article
• Language: English
• Published: BMC 2007-07-01
• Series: BMC Microbiology
• Online Access: http://www.biomedcentral.com/1471-2180/7/62

<p>Abstract</p> <p>Background</p> <p>An extremely low level methicillin resistant <it>Staphylococcus aureus </it>(MRSA) belonging to ST45, circulates among intravenous drug users in the Zurich area. This clone can be misinterpreted as an MSSA by phenotypic oxacillin resistance tests, although it carries a staphylococcal cassette chromosome <it>mec </it>(SCC<it>mec</it>) element encoding a functional <it>mecA </it>gene and it produces PBP2a.</p> <p>Results</p> <p>This clone carried a new 45.7-kb element, termed SCC<it>mec</it>_N1, containing a class B <it>mec </it>complex (<it>mecA-</it>Δ<it>mecR1::IS1272</it>), a truncated Tn<it>4003 </it>harbouring the <it>dfrA </it>gene, and a <it>fusB1 </it>gene, conferring methicillin, trimethoprim and low level fusidic acid resistance, respectively. In addition to the two insertion site sequences (ISS) framing the SCC<it>mec</it>, a third ISS (ISS*) was identified within the element. SCC<it>mec</it>_N1also harboured two distinct <it>ccrAB </it>complexes belonging to the class 4 subtype, both of which were shown to be active and to be able to excise the SCC<it>mec</it>_N1or parts thereof. Slight variations in the SmaI-PFGE pattern of the clinical MRSA isolates belonging to this clone were traced back to differences in the sizes of the SCC<it>mec </it>J2 regions and/or to a 6.4-kb deletion extending from ISS* to the right end ISS. This latter deletion led to a variant right SCC<it>mec</it>-chromosomal junction site. MRSA clones carrying the shorter SCC<it>mec </it>with the 6.4-kb deletion were usually ciprofloxacin resistant, while strains with the complete SCC<it>mec</it>_N1were co-trimoxazole resistant or had no additional resistances. This suggested that the genetic backbone of the host <it>S. aureus</it>, although identical by PFGE pattern, had at some stage diverged with one branch acquiring a sulfonomide resistance mutation and the other ciprofloxacin resistance.</p> <p>Conclusion</p> <p>This description of the structure and variations of SCC<it>mec</it>_N1will allow for quicker and easier molecular detection of this clone and monitoring of its spread.</p>