Persistent Staphylococcus aureus isolates from two independent cases of bacteremia display increased bacterial fitness and novel immune evasion phenotypes.
Bottom Line: Several novel traits were associated specifically with both independent sets of persistent S. aureus isolates compared to both the initial isolates and the isolates from resolved infections (resolved isolates).These traits included (i) increased growth under nutrient-poor conditions; (ii) increased tolerance of iron toxicity; (iii) higher expression of cell surface proteins involved in immune evasion and stress responses; and (iv) attenuated virulence in a Galleria mellonella larva infection model that was not associated with small-colony variation or metabolic dormancy such as had been seen previously.Overall, our data indicate a novel role for MprF function during development of S. aureus persistence by increasing bacterial fitness and immune evasion.
Affiliation: Department of Genetics and Infection, Immunity of Inflammation, University of Leicester, Leicester, United Kingdom.Show MeSH
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Mentions: Host cell invasion and intracellular persistence have both been implicated as mechanisms of persistence (39, 40); therefore, we assessed these phenotypes using an H9C2 rat myocardium cell line infection assay (Fig. 6). No differences in adhesion or invasion rates were observed between the initial, persistent, and control resolved EMRSA-15 bacteremia isolates; in fact, resolved isolate RB4-1 showed a significantly higher invasion level than PB3-1, which was the isolate with the next highest invasion rate (P < 0.05). Furthermore, in contrast to previous studies, both the PB1- and PB3-associated persistent isolates actually showed reduced levels of intracellular persistence compared with the respective initial isolates (PB1-15-1, P < 0.01; PB1-15-2, P < 0.05; PB3-32-1, P < 0.05). These data show that there was no association between adhesion, invasion, or intracellular persistence capabilities and persistence in this study.
Affiliation: Department of Genetics and Infection, Immunity of Inflammation, University of Leicester, Leicester, United Kingdom.