Background: Staphylococcus epidermidis is a common inhabitant of the human skin and mucous membranes and frequently causes nosocomial infections associated with implanted foreign bodies. Its ability to form a biofilm on the surfaces of the medical devices is considered its major pathogenicity factor. Following the formation and maturation of the biofilm, bacterial cells can detach from the biofilm and seed to different sites – a process that is thought to play a major role in the development of sepsis.
Material and Methods: To identify and characterize the molecular mechanisms involved in S. epidermidis biofilm detachment, we performed transposon (Tn917) mutagenesis of the clinical isolate S. epidermidis O-47. Subsequently, we screened 4250 Tn917 insertion mutants for altered detachment behaviour by using a semi-quantitative biofilm formation assay.
Results: We identified three mutants with a different detachment behaviour that could be divided into two classes. The biofilms formed by class1 mutants (mut1 and mut2) persisted longer than the biofilms produced by the wild type. In contrast, biofilms produced by class2 mutants (mut3) detached significantly earlier than those of the wild type.
Conclusion: Our results suggest that we identified at least two different genetic loci involved in S. epidermidis biofilm detachment or its regulation. Analysis of the genetic loci inactivated in the mutants will identify the factors involved in these processes and leading the characterization of underlying mechanisms.