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

Publication ,  Journal Article
Berlon, NR; Qi, R; Sharma-Kuinkel, BK; Joo, H-S; Park, LP; George, D; Thaden, JT; Messina, JA; Maskarinec, SA; Mueller-Premru, M; Athan, E ...
Published in: J Infect
October 2015

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 PSMα1-4, PSMβ1, and δ-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.

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Published In

J Infect

DOI

EISSN

1532-2742

Publication Date

October 2015

Volume

71

Issue

4

Start / End Page

447 / 457

Location

England

Related Subject Headings

  • Staphylococcal Skin Infections
  • Soft Tissue Infections
  • Skin
  • Pneumonia, Ventilator-Associated
  • Phenotype
  • Phenols
  • Microbiology
  • Microbial Sensitivity Tests
  • Methicillin-Resistant Staphylococcus aureus
  • Humans
 

Citation

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ICMJE
MLA
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Berlon, N. R., Qi, R., Sharma-Kuinkel, B. K., Joo, H.-S., Park, L. P., George, D., … Fowler, V. G. (2015). Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins. J Infect, 71(4), 447–457. https://doi.org/10.1016/j.jinf.2015.06.005
Berlon, Nicholas R., Robert Qi, Batu K. Sharma-Kuinkel, Hwang-Soo Joo, Lawrence P. Park, Dennis George, Joshua T. Thaden, et al. “Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins.J Infect 71, no. 4 (October 2015): 447–57. https://doi.org/10.1016/j.jinf.2015.06.005.
Berlon NR, Qi R, Sharma-Kuinkel BK, Joo H-S, Park LP, George D, et al. Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins. J Infect. 2015 Oct;71(4):447–57.
Berlon, Nicholas R., et al. “Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins.J Infect, vol. 71, no. 4, Oct. 2015, pp. 447–57. Pubmed, doi:10.1016/j.jinf.2015.06.005.
Berlon NR, Qi R, Sharma-Kuinkel BK, Joo H-S, Park LP, George D, Thaden JT, Messina JA, Maskarinec SA, Mueller-Premru M, Athan E, Tattevin P, Pericas JM, Woods CW, Otto M, Fowler VG. Clinical MRSA isolates from skin and soft tissue infections show increased in vitro production of phenol soluble modulins. J Infect. 2015 Oct;71(4):447–457.
Journal cover image

Published In

J Infect

DOI

EISSN

1532-2742

Publication Date

October 2015

Volume

71

Issue

4

Start / End Page

447 / 457

Location

England

Related Subject Headings

  • Staphylococcal Skin Infections
  • Soft Tissue Infections
  • Skin
  • Pneumonia, Ventilator-Associated
  • Phenotype
  • Phenols
  • Microbiology
  • Microbial Sensitivity Tests
  • Methicillin-Resistant Staphylococcus aureus
  • Humans