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918 Genetic and Phylogenetic Characterization of Staphylococcus Aureus Strains Isolated from Atopic Dermatitis Pediatric Patients and Their Cohabitants
  1. S Pecetta1,
  2. C Pascolini2,
  3. G Prignano2,
  4. F Ensoli2,
  5. B Capitanio2,
  6. C Passariello1
  1. 1Department of Public Health and Infectious Diseases, University ‘La Sapienza’
  2. 2Clinical Pathology and Microbiology Laboratory and Pediatric Dermatology Division, IFO-IRCCS San Gallicano, Rome, Italy


Atopic dermatitis (AD) is characterized by dysfunctional skin susceptible to Staphylococcus aureus colonization, which can exacerbate the symptoms. Recent studies indicate that the S. aureus’s great versatility is direct consequence of its genome’s plasticity and adaptability.

The present study evaluated the prevalence of S. aureus in 175 pediatric AD patients and their 195 cohabitants in relation with the severity of the disease. Moreover, isolated strains were characterized for pathogenic and virulence factors (PCR analysis), for genome structure (PFGE analysis) and for phylogenetic relations (MLST analysis) to investigate the possible correlation between genetic characteristics and the different stages of disease and the effects of atopic environment on the genome structure of these strains.

Our data showed that both patients and their cohabitants had high prevalence of S. aureus, that was proportional to the severity of the disease. PFGE analysis showed the existence of clonal identity among isolates from different sites of the same patient and between isolates from patients and their cohabitants. MLST data showed that there was a significant phylogenetic distance among strains with identical PFGE profile.

Our results demonstrate that the family is a source of infection/reinfection for patients and a source of risk for cohabitants. Moreover, our data suggests that although bacterial strains from atopic skin show conserved genomic structures (identical PFGE profiles), they came from very different genetic backgrounds (different MLST profiles). We assume that the peculiar atopic tissue environment may induce the evolution of these strains, with changes in genomic structure and regulation of virulence factors.

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