solates within CC5 and CC30. The results of Fowler et al are in accordance with our results for CC5 but not for CC30. However, in their study it was the MRSA isolates within CC30 that were significantly associated with invasiveness. Our study only involved MSSA isolates, and CC30-MRSA are rare to virtually non-existent in Sweden. Thus epidemiological differences between the places where the studies were performed may explain this apparent discrepancy. Of isolates assigned to CC5, the majority originated from patients with IE. Although the total number of isolates within CC5 was limited, this result may suggest an association between CC5 and serious invasive S. aureus disease. Due to polymorphisms in the gene encoding an autoinducing peptide in the agr locus, the S. aureus isolates are assigned to agr groups I to IV. As described in previous studies, the agr groups are strongly linked to bacterial clonality, although 26574517 both the present study and previous work showed that isolates within the same agr group may belong to genetically diverse CCs. In our study, isolates within agr II were significantly associated with invasive disease, and 50% of invasive isolates within agr II originated from patients with IE. Since agr II included isolates assigned to CC5 and CC15, and invasive isolates dominated within these clones, it is not possible to conclude whether this association is a consequence of clonality or assignment to agr group. A previous study by Jarraud et al also showed a positive relationship between agr II and IE. As expected, all isolates carried CP serotype 5 or 8. Among the isolates that displayed CP5, invasive isolates dominated which is consistent with a previous study in which a CP5-positive strain in a mouse model showed a higher bacteremia level as well as enhanced capacity to persist in the bloodstream, compared to a IMR-1 price CP8-positive strain. It is also worth noting the even stronger correlation between CP5 and IE. However, as for agr group, CP type is linked to the affiliation to CCs, and so the association between CP5 and invasive disease as well as IE could be a consequence of clonality. The absence of correlation between capsule serotypes and agr groups is also in line with results in a previous study. 7 CCs and Virulence Genes in Invasive S. aureus Due to the capacity of MSCRAMMs to bind extracellular matrix proteins, the significance of MSCRAMM genes for invasive disease and IE has been thoroughly examined previously. The present study showed a significant association 
between the presence 18201139 of fnbB as well as sasG and invasive disease, in accordance with previous studies. There was also a trend towards a higher prevalence of sasG among isolates from IE patients compared to other invasive isolates. The presence of sasG, but not fnbB, was in accordance with affiliation to CCs. The results are however difficult to interpret, due to the overlapping properties of many adhesins. Besides binding fibronectin, both FnbA and FnbB have the capacity to bind elastin; although unlike FnbA, FnbB has not been shown to promote platelet aggregation or bind fibrinogen. The overall capacity to bind fibronectin is not crucial based on whether the isolate carries one or both fnb genes. This may indicate that the additional role of FnbB, such as binding elastin, may be important for S. aureus invasive capacity. The lack of evidence for FnbB promoting platelet aggregation is consistent with our findings, which showed no difference in fnbB gene prevale
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