Staphylococcus epidermidis in Orthopedic Device Infections: The Role of Bacterial Internalization in Human Osteoblasts and Biofilm Formation

Abstract

Background Staphylococcus epidermidis orthopedic device infections are caused by direct inoculation of commensal flora during surgery and remain rare, although S. epidermidis carriage is likely universal. We wondered whether S. epidermidis orthopedic device infection strains might constitute a sub-population of commensal isolates with specific virulence ability. Biofilm formation and invasion of osteoblasts by S. aureus contribute to bone and joint infection recurrence by protecting bacteria from the host-immune system and most antibiotics. We aimed to determine whether S. epidermidis orthopedic device infection isolates could be distinguished from commensal strains by their ability to invade osteoblasts and form biofilms.Materials and MethodsOrthopedic device infection S. epidermidis strains (n = 15) were compared to nasal carriage isolates (n = 22). Osteoblast invasion was evaluated in an ex vivo infection model using MG63 osteoblastic cells co-cultured for 2 hours with bacteria. Adhesion of S. epidermidis to osteoblasts was explored by a flow cytometric approach, and internalized bacteria were quantified by plating cell lysates after selective killing of extra-cellular bacteria with gentamicin. Early and mature biofilm formations were evaluated by a crystal violet microtitration plate assay and the Biofilm Ring Test method.ResultsNo difference was observed between commensal and infective strains in their ability to invade osteoblasts (internalization rate 308+/−631 and 347+/−431 CFU/well, respectively). This low internalization rate correlated with a low ability to adhere to osteoblasts. No difference was observed for biofilm formation between the two groups.ConclusionOsteoblast invasion and biofilm formation levels failed to distinguish S. epidermidis orthopedic device infection strains from commensal isolates. This study provides the first assessment of the interaction between S. epidermidis strains isolated from orthopedic device infections and osteoblasts, and suggests that bone cell invasion is not a major pathophysiological mechanism in S. epidermidis orthopedic device infections, contrary to what is observed for S. aureus.

Rifamycin Derivatives Are Effective Against Staphylococcal Biofilms In Vitro and Elutable From PMMA

“…1). In addition to the activity against biofilms, rifampin and the rifamycin derivatives at a concentration of 32 lg/mL were able to reduce the number of intracellular S. aureus, an important source of organisms contributing to persistent and recurrent infections [26,55] compared with vancomycin at 4 and 24 hours after infection ( Figs. 2A, 2C).…”

A new host cell internalisation pathway for SadA‐expressing staphylococci triggered by excreted neurochemicals

“…Exemplified of S. pseudintermedius ED99, we identified a new concept of host cell internalisation that plays a role especially in animalpathogenic staphylococcal species expressing SadA or nonaureus staphylococcal strains (Maali et al, 2016;Valour et al, 2013). In contrast to all published pathways, this pathway does not involve a staphylococcal surface protein that interacts with a corresponding host cell receptor to trigger invasion.…”

Coagulase-Negative Staphylococci

“…epidermidis strains were also shown to be internalized by bone cells (338). However, in contrast to S. aureus, S. epidermidis orthopedic device infection strains exhibited only a low internalization rate (compared to commensal, nasal carriage isolates), suggesting that bone cell invasion is not a major pathophysiolog-ical mechanism in S. epidermidis orthopedic device infections (339).…”