In the process of addressing this question, we found that the original ausA mutant contains an inadvertent mutation in saeS and, therefore, the observed involvement of aureusimines in staphylococcal virulence was due to that mutation in saeS.
The sae deletion mutant showed a moderate level of resistance not only to erythromycin but also to chloramphenicol, another antibiotic widely used in staphylococcal research (Fig. 5A).
More recently, defined mutants of S. aureus that lack WTA or have altered WTA structures have facilitated experiments to elucidate in greater detail the role of WTA in staphylococcal pathogenesis [6] [10].
Our results show that the previously reported roles of aureusimines in staphylococcal gene regulation and virulence were due to an unintended mutation in saeS, which was likely selected due to elevated resistance of the mutant to environmental stresses.
Some PSMs, such as the PSMα group of S. aureus or the PSMα peptide of S. epidermidis, efficiently lyse white and red blood cells., Consequently, deletion mutants of the psmα operon in S. aureus are severely attenuated in animal infection models, indicating a central role of PSM peptides in staphylococcal virulence.
The underlying reasons for this apparent ethnic disparity in staphylococcal disease are uncertain.
It is important to use an antibiotic combination including rifampin in staphylococcal infections.
Mutants lacking staphylococcal accessory regulator (Sar) and accessory gene regulator (Agr), which cause significantly less severe septic arthritis in murine models, were able to induce expression of several MMP mRNA comparable with that of their isogenic parent strain but induced notably higher levels of tissue inhibitors of metalloproteinases (TIMPs).
Furthermore, it seems that SCC mec element is involved in staphylococcal virulence.
Several authors have suggested that this indicates yet another potential epidemiological shift in staphylococcal infections.
