Impact of psm‐mec in the mobile genetic element on the clinical characteristics and outcome of SCCmec‐II methicillin‐resistant Staphylococcus aureus bacteraemia in Japan. (6th March 2014)

• Record Type: Journal Article
• Authors: Aoyagi, T.; Kaito, C.; Sekimizu, K.; Omae, Y.; Saito, Y.; Mao, H.; Inomata, S.; Hatta, M.; Endo, S.; Kanamori, H.; Gu, Y.; Tokuda, K.; Yano, H.; Kitagawa, M.; Kaku, M.; Lina, G.
• Is Part Of: Clinical microbiology and infection. Volume 20:Number 9(2014:Sep.)
• Page Start: 912
• Page End: 919
• Publication Date: 2014-03-06
• Subjects: Medical microbiology -- Periodicals; Diagnostic microbiology -- Periodicals; Communicable diseases -- Periodicals; Infection -- Periodicals; 616.01
• DOI: 10.1111/1469-0691.12575
• Languages: English
• ISSNs: 1198-743X

Abstract

<abstract abstract-type="main" id="clm12575-abs-0001"> <title>Abstract</title> <sec id="clm12575-sec-0001" sec-type="section"> <p>Over‐expression of alpha‐phenol‐soluble modulins (PSMs) results in high virulence of community‐associated methicillin‐resistant <italic>Staphylococcus aureus</italic> (MRSA). The <italic>psm‐mec</italic> gene, located in the mobile genetic element SCC<italic>mec</italic>‐II, suppresses PSMαs production. Fifty‐two patients with MRSA bacteraemia were enrolled. MRSA isolates were evaluated with regard to the <italic>psm‐mec</italic> gene sequence, bacterial virulence, and the minimum inhibitory concentration (MIC) of vancomycin and teicoplanin. Fifty‐one MRSA isolates were classified as SCC<italic>mec</italic>‐II, and 10 had one point mutation in the <italic>psm‐mec</italic> promoter. We compared clinical characteristics and outcomes between mutant MRSA and wild‐type MRSA. Production of PSM<italic>α</italic>3 in mutant MRSA was significantly increased, but biofilm formation was suppressed. Wild‐type MRSA caused more catheter‐related bloodstream infections (30/41 vs. 3/10, p<italic> </italic>0.0028), whereas mutant MRSA formed more deep abscesses (4/10 vs. 3/41, p<italic> </italic>0.035). Bacteraemia caused by mutant MRSA was associated with reduced 30‐day mortality (1/10 vs. 13/41, p<italic> </italic>0.25), although this difference was not significant. The MIC<sub>90</sub> of teicoplanin was higher for wild‐type MRSA (1.5 mg/L vs. 1 mg/L), but the MIC of vancomycin was not different between the two groups. The 30‐day mortality of MRSA with a high MIC of teicoplanin (≥1.5 mg/L) was higher than that of strains with a lower MIC (≤0.75 mg/L) (6/10 vs. 6/33, p<italic> </italic>0.017). Mutation of the <italic>psm‐mec</italic> promoter contributes to virulence of SCC<italic>mec</italic>‐II MRSA, and the product of <italic>psm‐mec</italic> may determine the clinical characteristics of bacteraemia caused by SCC<italic>mec</italic>‐II MRSA, but it does not affect mortality.</p> </sec> </abstract>