Acapsular Staphylococcus aureus with a non-functional agr regains capsule expression after passage through the bloodstream in a bacteriemia mouse model

CARLOS M SULIGOY; DIAZ R; GEHRKE, A; GONZALO YEBRA; JOANA ALVES; GOMEZ MARISA INES; SINDY WENDLER; J FITZGERALD; LORENA TUCHSCHERR; BETTINA LÖFFLER; DANIEL O. SORDELLI; NOTO LLANA M; FERNANDA ROXANA BUZZOLA

Scientific Reports

EEUU

Año: 2020

Selection pressures exerted on Staphylococcus aureus by host factors during infection may lead tothe emergence of regulatory phenotypes better adapted to the infection site. traits convenient forpersistence may be fixed by mutation thus turning these mutants into microevolution endpoints. Thefeasibility that stable, non‑encapsulated S. aureus mutants can regain expression of key virulencefactors for survival in the bloodstream was investigated. S. aureus agr mutant HU-14 (IS256 insertionin agrC) from a patient with chronic osteomyelitis was passed through the bloodstream using abacteriemia mouse model and derivative P3.1 was obtained. Although IS256 remained insertedin agrC, P3.1 regained production of capsular polysaccharide type 5 (CP5) and staphyloxanthin.Furthermore, P3.1 expressed higher levels of asp23/SigB when compared with parental strain HU-14.Strain P3.1 displayed decreased osteoclastogenesis capacity, thus indicating decreased adaptability to bone compared with strain HU- 14 and exhibited a trend to be more virulent than parental strain HU- 14. Strain P3.1 exhibited the loss of one IS256 copy, which was originally located in the HU-14noncoding region between dnaG (DNA primase) and rpoD (sigA). this loss may be associated with the observed phenotype change but the mechanism remains unknown. in conclusion, S. aureus organisms that escape the infected bone may recover the expression of key virulence factors through a rapid microevolution pathway involving SigB regulation of key virulence factors