Staphylococcus aureus is a potentially pathogenic bacterium that causes a broad spectrum of diseases. S. aureus can adapt rapidly to the selective pressure of antibiotics, and this has resulted in the emergence and spread of methicillin-resistant S. aureus (MRSA). Resistance to methicillin and other beta-lactam antibiotics is caused by the mecA gene, which is situated on a mobile genetic element, the Staphylococcal Cassette Chromosome mec (SCCmec). To date, five SCCmec types (I-V) have been distinguished, and several variants of these SCCmec types have been described. All SCCmec elements carry genes for resistance to beta-lactam antibiotics, as well as genes for the regulation of expression of mecA. Additionally, SCCmec types II and III carry non-beta-lactam antibiotic resistance genes on integrated plasmids and a transposon. The epidemiology of MRSA has been investigated by pulsed-field gel electrophoresis (PFGE), multilocus sequence typing (MLST), spa typing and SCCmec typing. Numerous MRSA clones have emerged and disseminated worldwide. SCCmec has been acquired on at least 20 occasions by different lineages of methicillin-sensitive S. aureus. Although most MRSA strains are hospital-acquired (HA-MRSA), community-acquired MRSA (CA-MRSA) strains have now been recognised. CA-MRSA is both phenotypically and genotypically different from HA-MRSA. CA-MRSA harbours SCCmec types IV or V, and is associated with the genes encoding Panton-Valentine leukocidin. The prevalence of MRSA ranges from 0.6% in The Netherlands to 66.8% in Japan. This review describes the latest developments in knowledge concerning the structure of SCCmec, the molecular evolution of MRSA, the methods used to investigate the epidemiology of MRSA, and the risk-factors associated with CA-MRSA and HA-MRSA.

European Commission, 7th Framework Programme(grant agreement 223083).

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Background— Abdominal aortic aneurysms (AAA) are characterized by extensive transmural inflammation and C-reactive protein (CRP) has emerged as an independent risk factor for the development of cardiovascular disease. Therefore, we evaluated a possible association between serum CRP and aneurysm dimension in patients with asymptomatic AAA. Furthermore, the possibility of CRP production by aneurysmal tissue has been examined. Methods and Results— Serum CRP was determined highly sensitive ( hs CRP) and aneurysmal size was measured in 39 patients with AAA. The presence of CRP mRNA was assessed in the aneurysmal tissue of 16 patients. Mean (SD) hs CRP was 3.23 (2.96) mg/L. After log-transformation, hs CRP correlated significantly with aneurysmal size ( r =0.477, P =0.002). When the patients were divided into 3 equally sized groups according to hs CRP level, aortic diameter increased from lowest to upper hs CRP-tertile (49 mm, 61 mm, and 67 mm, respectively; P <0.05 for 3rd versus 1st tertile). This association persisted after correction for risk factors. CRP mRNA was found in 25% of aneurysmal aortic tissues. Conclusions— This is the first report showing that serum hs CRP is associated with aneurysmal size and that—in at least some patients—CRP may be produced by aneurysmal tissue. These data underscore the inflammatory nature of AAA formation, suggesting that serum hs CRP may serve as a marker of AAA disease and that CRP produced in vascular tissue might contribute to aneurysm formation.

The findings indicate that the mental state of angioplasty patients is positively associated with serological markers of inflammation. It remains to be seen whether the inflammation causes feelings of exhaustion, whether exhaustion and depression set the stage for inflammation, or whether existing feelings of exhaustion are amplified by the inflammation.