Determination of nasal carriage and skin colonization, antimicrobial susceptibility and genetic relatedness of Staphylococcus aureus isolated from patients with atopic dermatitis in Szczecin, Poland

BACKGROUND: Atopic dermatitis (AD) is one of the most frequent chronic and inflammatory skin condition. AD is characterized by damaged epidermal barrier, xerosis and pruritus of eczematous skin lesions which tend to flare. The duration and frequency of exacerbation of AD symptoms markedly affects the quality of patient life. AD results from the interplay between host genetics, immunity, and environmental factors, however the detailed pathogenesis of this disease is still not entirely cleared. Furthermore, disturbances of the skin microbiota and skin functional impairment predispose to secondary skin infections. Staphylococcus aureus colonizes skin and mucous membranes of 20 to 80% of healthy individuals and of 90% of patients with AD in whom this bacterium is accounted as an important AD exacerbating factor. It is also proven, that S. aureus nasal carriage significantly increases the risk for self-transmission and endogenous infection. In the current study the presence of S. aureus either in nasal vestibule and on lesioned skin of 64 patients with AD enrolled in 10-year autovaccination program was determined. The genetic relatedness of 86 S. aureus isolated from patients nose and skin using Pulsed Field Gel Electrophoresis (PFGE) and antimicrobial susceptibility of all strains to methicillin, erythromycin, clindamycin, mupirocin, gentamicin, amikacin, tetracycline, chloramphenicol and cotrimoxazole was also evaluated. RESULTS: In total 23 PFGE genotypes and 24 unique patterns were distinguished. 34 patients were S. aureus nasal carriers. Simultaneous presence of S. aureus in nose and on affected skin was found in 16 carriers colonized by indistinguishable or potentially related S. aureus vs 2 carriers colonized with non-related S. aureus in nasal vestibule and on skin. 4 isolates were methicillin resistant (MRSA) among which 3 showed constitutive MLSB resistance phenotype and remaining one was resistant to tetracycline and chloramphenicol. In 4 isolates inducible MLSB resistance phenotype was found, one of them was additionally resistant to tetracycline. 7 S. aureus were mupirocin resistant among them 3 - isolated from one patient, were resistant simultaneously to tetracyclines and chloramphenicol. 7 strains demonstrated resistance to chloramphenicol and susceptibility to all tested antimicrobial agents. The susceptibility to gentamicin, amikacin and cotrimoxazole among all examined S. aureus was confirmed. CONCLUSION: The obtained results indicated non-clonal structure of S. aureus circulating in AD patients. PFGE results showed the clonal-structure of vast majority of S. aureus isolated from nose and skin from nasal carriers what may prove the autoinfection in these patients. All examined patients the moderate or strong severity of AD was reported. Susceptibility to most antibiotics among isolated strains was also observed.