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

• Published in: Clinical microbiology and infection Vol. 20; no. 9; pp. 912 - 919
• Main 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.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.09.2014; Elsevier Limited
• Subjects: Aged; Anti-Bacterial Agents - pharmacology; Bacteremia - microbiology; Bacteremia - mortality; Bacteremia - pathology; clinical characteristics; Female; Genes; Genes, Bacterial; Genotype; Humans; Interspersed Repetitive Sequences; Japan; Male; Methicillin-Resistant Staphylococcus aureus - classification; Methicillin-Resistant Staphylococcus aureus - genetics; Methicillin-Resistant Staphylococcus aureus - isolation & purification; Microbial Sensitivity Tests; Middle Aged; Mortality; MRSA; Mutation; phenol-soluble modulins; psm-mec mutation; Retrospective Studies; Staphylococcal Infections - microbiology; Staphylococcal Infections - mortality; Staphylococcal Infections - pathology; Staphylococcus aureus; Staphylococcus infections; Survival Analysis; teicoplanin; Teicoplanin - pharmacology; Treatment Outcome; vancomycin; Vancomycin - pharmacology; Virulence Factors - genetics; Japan; phenol-soluble modulins; teicoplanin; vancomycin; psm-mec mutation; clinical characteristics; MRSA
• ISSN: 1198-743X; 1469-0691
• DOI: 10.1111/1469-0691.12575

Over-expression of alpha-phenol-soluble modulins (PSMs) results in high virulence of community-associated methicillin-resistant Staphylococcus aureus (MRSA). The psm-mec gene, located in the mobile genetic element SCCmec-II, suppresses PSMαs production. Fifty-two patients with MRSA bacteraemia were enrolled. MRSA isolates were evaluated with regard to the psm-mec gene sequence, bacterial virulence, and the minimum inhibitory concentration (MIC) of vancomycin and teicoplanin. Fifty-one MRSA isolates were classified as SCCmec-II, and 10 had one point mutation in the psm-mec promoter. We compared clinical characteristics and outcomes between mutant MRSA and wild-type MRSA. Production of PSMα3 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 0.0028), whereas mutant MRSA formed more deep abscesses (4/10 vs. 3/41, p 0.035). Bacteraemia caused by mutant MRSA was associated with reduced 30-day mortality (1/10 vs. 13/41, p 0.25), although this difference was not significant. The MIC90 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 0.017). Mutation of the psm-mec promoter contributes to virulence of SCCmec-II MRSA, and the product of psm-mec may determine the clinical characteristics of bacteraemia caused by SCCmec-II MRSA, but it does not affect mortality.