Isolation of a Staphylococcus aureus capsulated derivative after passage of non-encapsulated isolate HU-14 through the bloodstream using a mouse model of bacteremia.

Selection pressures exerted on Staphylococcus aureus by host factors during infection may lead to the emergence of regulatory phenotypes better adapted to the conditions encountered at the infection site. In the long run, traits convenient for bacteria to persist may be fixed by mutation in chronically infected patients thus turning these mutants into microevolution endpoints. This study was conducted to assess the feasibility that stable, non-encapsulated S. aureus mutants can regain the expression of key virulence factors for survival in the bloodstream. S. aureus agr mutant HU-14 (IS256 insertion in agrC) was recovered from a patient with chronic osteomyelitis. This strain was passed through the bloodstream of a mouse model of bacteriemia and derivative P3.1 was obtained after 3 consecutive passages. Strain P3.1 regained the production of capsular polysaccharide type 5 (CP5) and staphyloxanthin in spite of the fact that IS256 remained inserted in agrC. Both P3.1 and HU-14 strains failed to express RNAIII. Whereas the HU-14 strain expressed very low levels of asp23, the P3.1 derivative expressed significantly higher levels of asp23, as ascertained by qRT-PCR, which indicated that SigB had regained its nominal activity. Strain P3.1 have lost much of its osteoclastogenesis capacity, which indicated a decreased adaptability to bone compared with parental strain HU-14. Our results demonstrated that S. aureus organisms that escape the infected bone may recover the expression of one or more key virulence factors thus returning a supposedly harmless endpoint-of-microevolution bacteria back into a dangerous infective derivative.