4.7 Article

Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins

Journal

JOURNAL OF INFECTION
Volume 71, Issue 4, Pages 447-457

Publisher

W B SAUNDERS CO LTD
DOI: 10.1016/j.jinf.2015.06.005

Keywords

Phenol soluble modulin; MRSA; Skin and soft infection; Pneumonia; Endocarditis

Funding

  1. Infectious Disease Society of America's Medical Scholars Program
  2. National Institute of Health [R01-AI068804, K24-AI093969]
  3. Intramural Research Program of the National Institute of Allergy and Infectious Diseases

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Background: Phenol-soluble modulins (PSMs) are amphipathic, pro-inflammatory proteins secreted by most Staphylococcus aureus isolates. This study tested the hypothesis that in vitro PSM production levels are associated with specific clinical phenotypes. Methods: 177 methicillin-resistant S. aureus (MRSA) isolates from infective endocarditis (IE), skin and soft tissue infection (SSTI), and hospital-acquired/ventilator-associated pneumonia (HAP) were matched by geographic origin, then genotyped using spa-typing. In vitro PSM production was measured by high performance liquid chromatography/mass spectrometry. Statistical analysis was performed using Chi-squared or Kruskal-Wallis tests as appropriate. Results: Spa type 1 was significantly more common in SSTI isolates (62.7% SSTI; 1.7% IE; 16.9% HAP; p < 0.0001) while HAP and IE isolates were more commonly spa type 2 (0% SSTI; 37.3% IE; 40.7% HAP; p < 0.0001). USA300 isolates produced the highest levels of PSMs in vitro. SSTI isolates produced significantly higher quantities of PSMa1-4, PSMb1, and d-toxin than other isolates (p < 0.001). These findings persisted when USA300 isolates were excluded from analysis. Conclusions: Increased in vitro production of PSMs is associated with an SSTI clinical source. This significant association persisted after exclusion of USA300 genotype isolates from analysis, suggesting that PSMs play a particularly important role in the pathogenesis of SSTI as compared to other infection types. (C) 2015 Published by Elsevier Ltd on behalf of The British Infection Association.

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