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.
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.
Department of Infection Control and Laboratory Diagnostics, Internal Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
T
T
Aoyagi
C
C
Kaito
K
K
Sekimizu
Y
Y
Omae
Y
Y
Saito
H
H
Mao
S
S
Inomata
M
M
Hatta
S
S
Endo
H
H
Kanamori
Y
Y
Gu
K
K
Tokuda
H
H
Yano
M
M
Kitagawa
M
M
Kaku
D000368:Aged; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D016470:Bacteremia / Q000382:microbiology / Q000401:mortality / Q000473:pathology; D005260:Female; D005798:Genes, Bacterial; D005838:Genotype; D006801:Humans; D020071:Interspersed Repetitive Sequences; D007564:Japan; D008297:Male; D055624:Methicillin-Resistant Staphylococcus aureus / Q000145:classification / Q000235:genetics* / Q000302:isolation & purification*; D008826:Microbial Sensitivity Tests; D008875:Middle Aged; D012189:Retrospective Studies; D013203:Staphylococcal Infections / Q000382:microbiology* / Q000401:mortality / Q000473:pathology*; D016019:Survival Analysis; D017334:Teicoplanin / Q000494:pharmacology; D016896:Treatment Outcome; D014640:Vancomycin / Q000494:pharmacology; D037521:Virulence Factors / Q000235:genetics*
D000900:Anti-Bacterial Agents; D037521:Virulence Factors; D017334:Teicoplanin; D014640:Vancomycin
MRSA; clinical characteristics; phenol-soluble modulins; psm-mec mutation; teicoplanin; vancomycin