Brief reportMolecular and phenotypic characterization of methicillin-resistant Staphylococcus aureus isolates causing bacteremia at a major hospital in southern Mississippi
Section snippets
Methods
The Institutional Review Board of The University of Southern Mississippi and the Forrest General Hospital approved this study. Between March 2013 and February 2014, 322 MRSA isolates were collected from a large hospital in southern Mississippi. From these, 30 blood isolates were randomly selected for this study.
The presence of mecA, Panton-Valentine leukocidin genes (PVL) and hemolysin gamma were tested by polymerase chain reaction using chromosomal DNA prepared from the isolates. Pulsed-field
Results
The MRSA isolates belonged to 2 major clusters in pulsed-field gel electrophoresis, designated A and B (Fig 1). Cluster A was composed of isolates with USA100 and USA800 types, whereas cluster B was composed of USA300 and USA700 type isolates. USA300 was found to be the most common (40%). USA100, -700, and -800 accounted for 23.3%, 20%, and 13.3% of the isolates, respectively. Forty percent of the isolates belonged to ST5, constituting the largest group. ST8, ST72, and ST100 were found in 37%,
Discussion
Our analysis showed that the majority of bacteremia were caused by USA300-ST8-SCCmecIV isolates. This predominance of USA300 was observed in studies done in other regions of the United States as well. The predominance of community-associated (CA-MRSA) over HA-MRSA in hospital settings has been mathematically modeled by D'Agata et al.10 They predicted that CA-MRSA would eventually become dominant in hospitals. Our observation of hospitalized patients confirms the predominance of USA300 isolates
Conclusions
To the best of our knowledge, this is the first report of systematic analysis of MRSA isolates in Mississippi. Collectively our data show the presence of both CA-MRSA and HA-MRSA isolates among bacteremia-causing MRSA in this region and that USA300 is dominant in hospital settings, which is also an extension of a nationwide observation and mathematical prediction; however, the association of PVL genes as a risk for vancomycin MIC warrants more detailed investigation.
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This work was funded by a National Institutes of Health grant (No. 1R15AI099922) to MOE and by the Mississippi IDeA Networks of Biomedical Research Excellence, with an Institutional Development Award of the National Institute of General Medical Sciences (grant No. P20GM103476).
Conflicts of interest: None to report.