1567. Association between psm-mec on the Mobile Genetic Element and Clinical Manifestation of Methicillin-Resistant Staphylococcus aureus Infection
Session: Poster Abstract Session: Microbial and Host Genetic Factors in Disease
Saturday, October 5, 2013
Room: The Moscone Center: Poster Hall C
  • IDweek_2013_10_01.pdf (567.0 kB)
  • Background: Phenol-soluble modulines (PSMs) are staphylococcal cytolytic toxins that are crucial in immune evasion. PSM over-expression results in high virulence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and leads to more severe infection than hospital-associated MRSA (HA-MRSA). The psm-mec gene was identified in the staphylococcal cassette chromosome (SCC) element mec encoding methicillin resistance, which was significant in HA-MRSA with SCCmec type-II and -III. psm-mec transcription products suppressed PSM production, while some HA-MRSA strains showed a psm-mec promoter mutation that attenuated transcription. However, it was unclear whether the psm-mecpromoter mutation in HA-MRSA with SCCmec type-II affected virulence properties and clinical characteristics.

    Methods: Fifty-two patients over 18 years old who were positive blood culture for MRSA were enrolled in the study  between March 2009 and December 2011. Fifty-two MRSA were evaluated for the psm-mec promoter mutation and SCCmec typing. Next, we examined bacterial virulence properties and analyzed clinical characteristics and outcomes between bacteremia due to MRSA with and without the mutation.

    Results: Fifty-one (98%) MRSA were classified as SCCmec type-II and none had Panton Valentine Lukocidine. Ten (19.6%) had psm-mec promoter one point mutation (-7T>C) among SCCmec type-II MRSA. In these strains, production of PSMα3 was significantly increased compared with intact MRSA, but biofilm formation was suppressed. Mutant MRSA was observed more frequently within 48 h after admission compared to intact strains (4/10 vs 4/41, p = 0.038). Intact MRSA caused more catheter-related bloodstream infections compared to mutant strains (30/41 vs 3/10, p = 0.0028); mutant MRSA formed more deep abscesses compared to intact strains (4/10 vs 3/41, p = 0.035). However, 30-day mortality from MRSA bacteremia for mutant strains was lower compared to intact strains (1/10 vs 13/41, p = 0.25), but the difference was not significant.

    Conclusion: A mutation in the psm-mec promoter was associated with virulence of HA-MRSA with SCCmec type-II. Clinical characteristics caused by HA-MRSA with mutation were similar to those of CA-MRSA. psm-mec function may play a central role in determining MRSA virulence and clinical features.

    Tetsuji Aoyagi, MD, PhD1, Chikara Kaito, PhD2, Kazuhisa Sekimizu, PhD2, Yosuke Omae2, Yuki Saito2, Han Mao2, Shinya Inomata, MD1, Shiro Endo, MD, PhD1, Masumitsu Hatta, MD, PhD1, Yoshiaki Gu, MD, MPH3, Koichi Tokuda, MD, PhD, MPH1, Hisakazu Yano, MD, PhD1, Miho Kitagawa1 and Mitsuo Kaku, MD, PhD1, (1)Department of Infection Control and Laboratory Diagnostics, Tohoku University Graduate School of Medicine, Sendai, Japan, (2)Garduate School of Pharmaceutical Sciences, The University of Tokyo., Tokyo, Japan, (3)Department of Regional Cooperation for Infectious Diseases, Tohoku University Graduate School of Medicine, Sendai, Japan


    T. Aoyagi, None

    C. Kaito, None

    K. Sekimizu, None

    Y. Omae, None

    Y. Saito, None

    H. Mao, None

    S. Inomata, None

    S. Endo, None

    M. Hatta, None

    Y. Gu, None

    K. Tokuda, None

    H. Yano, None

    M. Kitagawa, None

    M. Kaku, None

    Findings in the abstracts are embargoed until 12:01 a.m. PST, Oct. 2nd with the exception of research findings presented at the IDWeek press conferences.