Oral Presentation International Pasteurellaceae Conference 2014

Antimicrobial resistance profiles and the genetic basis of resistance in Actinobacillus pleuropneumoniae isolates in the UKĀ  (#28)

Janine T. Bosse 1 , Yanwen Li 1 , Stephanie Walker 1 , Tom Atherton 1 , Susanna M. Williamson 2 , Jon Rogers 2 , Roy R. Chaudhuri 3 4 , Lucy A. Weinert 3 , Matt T. Holden 5 , Duncan J. Maskell 3 , Alexander W. Tucker 3 , Brendan W. Wren 6 , Andrew N. Rycroft 7 , Paul R. Langford 1 , on behalf of the BRaDP1T Consortium 1 3 6 7
  1. Department of Medicine, Imperial College London, London, UK
  2. Animal Health and Veterinary Laboratories Agency (AHVLA), Bury St Edmunds, UK
  3. Department of Veterinary Medicine, University of Cambridge, Cambridge, UK
  4. Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, UK
  5. The Pathogen Sequencing Unit, The Wellcome Trust Sanger Institute, Cambridge, UK
  6. Department of Pathogen Molecular Biology, London School of Hygiene & Tropical Medicine, London, UK
  7. Department of Pathology and Pathogen Biology, The Royal Veterinary College, Hatfield, UK

The aim of the present study was to evaluate the antimicrobial resistance (AMR) profiles of 107 clinical isolates of A. pleuropneumoniae (APP) collected in the UK from 1995 to 2011, and where possible, determine the genetic basis of the resistance. The isolates were tested for susceptibility to 9 antimicrobials (ampicillin, enrofloxacin, tetracycline, florfenicol, sulfonamide, trimethoprim, tilmycosin, tylosin, and erythromycin) by both disk diffusion and MIC. Shotgun genome sequence data (Illumina HiSeq 2000) was generated for the strains, and AMR genes were identified by BLAST. Specific genes were detected conferring resistance to ampicillin (blaRob1), enrofloxacin (gyrAS83F), tetracycline (tetBCDH), florfenicol (floR), sulfonamide (sulII), and trimethoprim (dfrA14). It was not possible to detect specific genes conferring resistance to tilmycosin, tylosin, or erythromycin. Only 33/107 isolates had none of the specific AMR genes, and many strains were resistant to multiple antimicrobials. Of the 107 strains tested, there were: 56% TetR, 43% SulR, 21% AmpR, 17% TriR, 7% EnR, and 1% FloR. The AMR genes detected were, in most cases, plasmid borne except the gyrAS83F mutation. However, in addition to presence on plasmid(s), the tetBCD genes were also found integrated into the chromosome as part of a 60 kb integrative conjugative element (ICE) in 33 strains. This is the first report of dfrA14, and also the first report of an ICE, in APP. Furthermore, this is the first report of FloR in APP in the UK.

Acknowledgements

This work was supported by a Longer and Larger (LoLa) grant from the Biotechnology and Biological Sciences Research Council (grant numbers BB/G020744/1, BB/G019177/1, BB/G019274/1 and BB/G003203/1), the UK Department for Environment, Food and Rural Affairs and Zoetis awarded to the Bacterial Respiratory Diseases of Pigs-1 Technology (BRaDP1T) consortium.