Foreign body infection and ‘wild type’Staphylococcus epidermidis– Potential of biofilm formation and antimicrobial resistance

Abstract number: 1134_03_411

Parschalk B., Grisold A., Yassin F., Adametz H., Graninger W., Presterl E.

Objectives:  

Foreign body infections (FBI) due to Staphylococcus epidermidis have become major clinical problems associated with considerable morbidity and costs. Biofilm formation and resistance to multiple antibiotics are the major obstacles for a successful treatment. The aim of the study was to test Staphylococcus epidermidis isolates from patients with verified foreign body infections i) for their ability to form biofims and ii) for their susceptibility to 12 standard antibiotics, and compare these to ‘wild type’Staphylococcus epidermidis isolated from the skin of healthy volunteers.

Methods:  

Sixty patients with verified FBI were evaluated. Hundred and twenty-nine blood culture isolates from 60 patients with FBI, and 52-skin isolates from healthy, not hospital-associated, volunteers were analysed. Identification of Staphylococcus epidermidis was done using routine methods. To exclude doubles FBI isolates were genotyped by PFGE. The susceptibility testing was done using disk diffusion method according to the NCCLS. Antimicrobial agents tested were penicillin, oxacillin, erythromycin, clindamycin, gentamicin, amikacin, vancomycin, fosfomycin, fusidic acid, rifampicin, ciprofloxacin, trimethoprim and linezolid. Biofilm formation was tested using a microtiter plate biofilm model.

Results:  

Among the 129 FBI isolates 86 strains with distinct PFGE profiles were identified. Biofilm formation was detected in 86.4% of FBI strains and in 76.9% of the ‘wild type’ isolates (not significant). More than 30% of all FBI strains were resistant to penicillin, oxacillin, erythromycin, clindamycin, ciprofloxacin and trimethoprim. The 52 ‘wild type’Staphylococcus epidermidis were generally more susceptible than the clinical isolates (p < 0.05): However, 46.2 % of these controls were resistant to penicillin and to erythromycin, 17.3% were resistant to clindamycin.

Conclusions:  

Biofilm formation is present to the same extent in both, FBI-associated and ‘wild type’Staphylococcus epidermidis strains demonstrating the potential of skin flora to cause FBIs. Although it is well known that nosocomial Staphylococcus epidermidis are resistant to multiple antibiotics, the ‘wild type’ isolates show alarming resistance to erythromycin and clindamycin possibly reflecting the abundant use of macrolides for minor infections in the population.