Evolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus

Li, Min; Diep, Binh An; Villaruz, Amer E.; Braughton, Kevin R.; Jiang, Xiaofei; DeLeo, Frank R.; Chambers, Henry F.; Lu, Yuan; Otto, Michael

doi:10.1073/pnas.0900743106

Cited by 394Antimicrobial Resistance in StaphylococcusStreptococcal Infections and TreatmentsEscherichia coli research studies

Evolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus

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Li, Min, Diep, Binh An, Villaruz, Amer E., Braughton, Kevin R., Jiang, Xiaofei, DeLeo, Frank R., Chambers, Henry F., Lu, Yuan +1 more·2009·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0900743106PMC PMC2667066

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Abstract

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) has recently emerged worldwide. The United States, in particular, is experiencing a serious epidemic of CA-MRSA that is almost entirely caused by an extraordinarily infectious strain named USA300. However, the molecular determinants underlying the pathogenic success of CA-MRSA are mostly unknown. To gain insight into the evolution of the exceptional potential of USA300 to cause disease, we compared the phylogeny and virulence of USA300 with that of closely related MRSA clones. We discovered that the sublineage from which USA300 evolved is characterized by a phenotype of high virulence that is clearly distinct from other MRSA strains. Namely, USA300 and its progenitor, USA500, had high virulence in animal infection models and the capacity to evade innate host defense mechanisms. Furthermore, our results indicate that increased virulence in the USA300/USA500 sublineage is attributable to differential expression of core genome-encoded virulence determinants, such as phenol-soluble modulins and α-toxin. Notably, the fact that the virulence phenotype of USA300 was already established in its progenitor indicates that acquisition of mobile genetic elements has played a limited role in the evolution of USA300 virulence and points to a possibly different role of those elements. Thus, our results highlight the importance of differential gene expression in the evolution of USA300 virulence. This finding calls for a profound revision of our notion about CA-MRSA pathogenesis at the molecular level and has important implications for design of therapeutics directed against CA-MRSA.

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USA300 appears to have enhanced virulence as compared to the traditional hospital-associated MRSA strains.
“which appears to have enhanced virulence as compared to the traditional hospital-associated MRSA strains [26], [27], [28].”
From Interactions of Methicillin Resistant Staphylococcus aureus USA300 and Pseudomonas aeruginosa in Polymicrobial Wound Infection (2013) · cites this paper as [26]

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[19]Diep BA, Otto M. The role of virulence determinants in community-associated MRSA pathogenesis. Trends Microbiol. 2008;16:361–369. doi: 10.1016/j.tim.2008.05.002. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI

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Authors: Li, M., Diep, B. A., Villaruz, A. E., Braughton, K. R., Jiang, X., DeLeo, F. R., Chambers, H. F., Lu, Y., & Otto, M.
Affiliations: National Institutes of Health (US)
University of California, San Francisco (US)
Shanghai Medical College of Fudan University (CN)
ORCID: Li, Min
Diep, Binh An
Jiang, Xiaofei
DeLeo, Frank R.
Chambers, Henry F.
Lu, Yuan
Otto, Michael
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2009-04-07
Volume: 106
Issue: 14
Pages: 5883-5888
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0900743106
PMC: PMC2667066
OpenAlex: W2005636153
Cited by: 394
References: 43
Citations by year: 2026: 5 · 2025: 8 · 2024: 5 · 2023: 13 · 2022: 8 · 2021: 10 · 2020: 19 · 2019: 19 · 2018: 17 · 2017: 15 · 2016: 29 · 2015: 31 · 2014: 31 · 2013: 50 · 2012: 34
FWCI: 30.72
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Allergy and Infectious Diseases (R01AI070289, T32AI060537)
Topics: Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Streptococcal Infections and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Escherichia coli research studies
Keywords: community-associated methicillin-resistant Staphylococcus aureus, USA300, virulence evolution, phenol-soluble modulins, alpha-toxin, differential gene expression, mobile genetic elements, animal models of infection
MeSH terms: Animals, Disease Outbreaks, Humans, Phylogeny, United States, Virulence, Gene Expression Regulation, Bacterial, Evolution, Molecular, Methicillin-Resistant Staphylococcus aureus

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Evolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus

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