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J. Bacteriol. doi:10.1128/JB.00160-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Augmented expression of polysaccharide intercellular adhesin in a defined Staphylococcus epidermidis mutant with small colony variant phenotype

Institute of Medical Microbiology, University of Münster, Münster, Germany; Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany; Medical Microbiology and Infectious Diseases, The School of Medicine, University of Wales Swansea, Swansea, U.K.; Departments of Medical Microbiology/Immunology and Medicine, University of Wisconsin Medical School, Madison, Wisconsin, USA

^* To whom correspondence should be addressed. Email: eiffc{at}uni-muenster.de.

	Abstract

While coagulase-negative staphylococci (CoNS) with their ability to form a thick, multilayered biofilm on foreign bodies have been identified as the major cause of implant-associated infections, no data are available for biofilm formation of staphylococcal small-colony variants (SCVs). In the past years, a number of device-associated infections due to staphylococcal SCVs were described, among them several pacemaker infections due to SCVs of CoNS auxotrophic to hemin. To test the characteristics of SCVs of CoNS, in particular to study the ability of SCVs to form a biofilm on foreign bodies, we generated a stable mutant in electron transport by interrupting one of the hemin biosynthetic genes, hemB, in Staphylococcus epidermidis. In fact, this mutant displayed a stable SCV phenotype with tiny colonies showing strong adhesion to the agar surface. When extending the incubation time up to 48 h or using a higher inoculum, the mutant produced similar amounts of biofilm on polystyrene as the parent strain. When grown under planktonic conditions, the mutant formed markedly larger cell clusters than the parental strain which were completely disintegrated by the specific beta-1,6-hexosaminidase dispersin B, but were resistant to trypsin treatment. In a dot blot assay, the mutant expressed larger amounts of polysaccharide intercellular adhesin (PIA) than the parent strain. In conclusion, interrupting a hemin biosynthetic gene in S. epidermidis resulted in a SCV phenotype. Markedly larger cell clusters and the ability of the hemB mutant to form a biofilm are related to the augmented expression of PIA.

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