Objective: The most important virulence factor of Staphylococcus epidermidis is their capability to form a biofilm on the surfaces of implanted medical devices. The accumulative phase of biofilm formation is linked to the production of intercellular adhesin encoded by the icaADBC operon and accumulation-associated protein by the aap gene. The aim of the study was to investigate biofilm formation phenotypically and genetically in clinical strains of S. epidermidis in comparison with commensal strains.
Material and methods: The study was carried out in 4 hospitals in Riga, Latvia. In total, 105 clinical strains of Staphylococcus epidermidis isolated from patients' blood (n=67) and intravenous catheters (n=38) in a case of laboratory-confirmed bacteremia were studied. Moreover, 60 Staphylococcus epidermidis commensal strains isolated from nose epithelium of healthy people were included as a control group. Appearance of the icaA and aap genes was tested by polymerase chain reaction. The microtiter plate method was used.
Results: Biofilm formation was detected in 50 (47%) of Staphylococcus epidermidis isolates in the clinical group and 15 (25%) of isolates in the control group (P=0.0049). Among 50 biofilm-forming clinical isolates, 46 (92%) were positive for the icaA and/or aap genes. The icaA and aap genes were not found only in 4 strains.
Conclusions: The clinical isolates of Staphylococcus epidermidis were more likely to form biofilms than the commensal strains. The carriage of the icaA or aap gene alone, or their absence, is not applicable as a molecular marker for the discrimination invasive Staphylococcus epidermidis strains from contaminants.