JAC Advance Access published online on November 15, 2005
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dki385
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1 Department of Medical Microbiology, University Hospital of North Norway, Tromsø, Norway; Department of Microbiology and Virology, University of Tromsø, Tromsø, Norway
* To whom correspondence should be addressed. Objectives: To determine whether Staphylococcus aureus small colony variants (SCVs) are resistant to the antimicrobial peptide lactoferricin B. To assess if deficiency in transmembrane potential, a common characteristic of SCVs that are haemin- or menadione-auxotrophs, affects the uptake of the peptide into the bacterial cytoplasm. Methods: A broth microdilution technique was used for susceptibility testing to determine the MIC of lactoferricin B for SCVs with three different auxotrophisms (haemin, menadione or thymidine) and their isogenic parent strains. Both clinical isolates and genetically defined mutants were used. The internalization of lactoferricin B in a hemB mutant and the respective parent strain was studied using transmission electron microscopy and immunogold labelling. Results: All SCVs showed reduced susceptibility to lactoferricin B irrespective of their auxotrophy compared with their isogenic parent strains. The MIC for all SCVs was >256 mg/L, whereas the MICs for the parent strains ranged from 16-256 mg/L. Surprisingly, the hemB mutant contained significantly more lactoferricin B intracellularly than the respective parent strain. Conclusions: The resistance mechanism of SCVs towards the antimicrobial peptide lactoferricin B is presumably caused by the metabolic changes present in SCVs rather than by a changed transmembrane potential of SCVs or reduced uptake of the peptide.
Received August 4, 2005
Revised September 28, 2005
Accepted September 28, 2005
Brief report
Staphylococcus aureus small colony variants are resistant to the antimicrobial peptide lactoferricin B
rjan Samuelsen 1 *,
Hanne Husom Haukland 1,
Barbara C. Kahl 2,
Christof von Eiff 2,
Richard A. Proctor 3,
Hilde Ulvatne 4,
Kjersti Sandvik 4,
and
Lars H. Vorland 5
2 Institute of Medical Microbiology, University Hospital of Münster, Münster, Germany
3 Department of Medicine and Medical Microbiology/Immunology, University of Wisconsin Medical School, Madison, Wisconsin, USA
4 Department of Medical Microbiology, University Hospital of North Norway, Tromsø, Norway
5 Department of Microbiology and Virology, University of Tromsø, Tromsø, Norway; Northern Norway Regional Health Authority, Bodø, Norway
rjan Samuelsen, E-mail: orjan.samuelsen{at}unn.no
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