Occurrence of resistance to chloramphenicol and resistance genes in members of the Staphylococcus sciuri group

  • Tomasz Hauschild, Department of Microbiology, Institute of Biology, University of Bialystok, Bialystok, Poland
  • Ivana Dakic, Department of Bacteriology, Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Belgrade, Yugoslavia
  • Srdjan Stepanovic, Department of Bacteriology, Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Belgrade, Yugoslavia
  • Dragana Vukovic, Department of Bacteriology, Institute of Microbiology and Immunology, School of Medicine, University of Belgrade, Belgrade, Yugoslavia
  • Stefan Schwarz, Institute of Farm Animal Genetics, Friedrich-Loeffler Institute (FLI), Neustadt-Mariensee, Germany

    • Objectives: Data on chloramphenicol resistance in members of the S. sciuri group are scarce and mainly limited to single isolates of animal origin. The aim of this study was to provide insight into the occurrence of resistance as well as into the mechanisms conferring resistance to chloramphenicol among members of the S. sciuri group obtained from human, animal, hospital and non-hospital environments.
    Methods: The susceptibilities to chloramphenicol of the 317 S. sciuri group isolates were tested by disk diffusion and agar dilution methods, and MICs of chloramphenicol and clindamycin were determined. Presence of the major cat genes encoding chloramphenicol acetyltransferases, as well as the genes fexA and cfr was tested by PCR
    Results: Only four (1.3%) isolates, one S. lentus isolate of human origin, and 3 S. sciuri isolates of animal origin were chloramphenicol resistant. The presence of catpC221 and catpC194 genes were detected in 3 and 1 isolates, respectively. Since the catpC194 has not yet been detected in staphylococci of animal origin, the 2.9-kb plasmid pSCS34, which carried this gene, was sequenced completely. Sequence analysis revealed a high degree of homology in the regions coding chloramphenicol resistance and replication function to staphylococcal plasmids of the pC194 family, but also to a chloramphenicol resistance plasmid integrated in the chromosomal DNA of Streptocococcus pneumoniae.
    Conclusions: A low selective pressure as imposed by the restricted use of chloramphenicol may in part explain the low frequency of chloramphenicol resistance in members of the S. sciuri group observed in this study.