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JAC Advance Access published online on September 25, 2009
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkp350
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Diversity of antimicrobial resistance pheno- and genotypes of methicillin-resistant Staphylococcus aureus ST398 from diseased swine

Kristina Kadlec1, Ralf Ehricht2, Stefan Monecke3, Ulrike Steinacker4, Heike Kaspar4, Joachim Mankertz4 and Stefan Schwarz1,*

1 Institute of Farm Animal Genetics, Friedrich-Loeffler-Institute (FLI), Neustadt-Mariensee, Germany 2 CLONDIAG GmbH, Jena, Germany 3 Institute for Medical Microbiology and Hygiene, Dresden University of Technology, Dresden, Germany 4 Federal Office of Consumer Protection and Food Safety (BVL), Berlin, Germany

Received 19 August 2009; returned 28 August 2009; revised 31 August 2009; accepted 31 August 2009

* Corresponding author. Tel: +49-5034-871-241; Fax: +49-5034-871-246; E-mail: stefan.schwarz{at}fli.bund.de

Objectives: Fifty-four methicillin-resistant Staphylococcus aureus (MRSA) ST398 isolates from unrelated diseased swine collected all over Germany were comparatively investigated for their antimicrobial resistance and virulence properties, and for their genomic relatedness.

Methods: MICs of 30 antimicrobial agents were determined by broth microdilution. Resistance and virulence genes were detected via a diagnostic DNA microarray and specific PCRs. The genomic relationships were determined by ApaI-PFGE, spa typing and SCCmec typing.

Results: Twenty-two distinct resistance patterns were observed. All 54 isolates were tetracycline resistant, mediated by tet(M), tet(K) and/or tet(L), with 14 isolates being only resistant to β-lactam antibiotics and tetracyclines. Trimethoprim resistance, seen in 28 isolates, was mostly due to the gene dfrK or dfrG. Among the 24 macrolide/lincosamide-resistant isolates, the genes erm(A), erm(B) and/or erm(C) were detected. The two chloramphenicol/florfenicol-resistant isolates harboured the gene fexA. The eight gentamicin-resistant isolates carried the gene aacA/aphD. Fifty-three isolates harboured SCCmec type V elements while the remaining one carried mecA and ugpQ, but no recombinase genes. All isolates were PVL negative, but one and three isolates, respectively, were positive for the enterotoxin B and enterotoxin K and Q genes. Eight different spa types were identified with t011 being the most predominant. Six ApaI-PFGE clusters with up to nine individual patterns were detected.

Conclusions: MRSA ST398 isolates varied slightly in their virulence properties and spa types but differed distinctly in their antimicrobial resistance pheno- and genotypes as well as their ApaI-PFGE patterns. These data underline the ability of ST398 to acquire genetic material that might increase antimicrobial resistance and virulence.

Key Words: MRSA , SCCmec , zoonosis , genotyping


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