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.
Highlights
Staphylococcus epidermidis, coagulase-negative staphylococci, have been considered innocuous commensals of human skin and mucous membranes but are accepted as the leading opportunistic pathogens responsible for numerous nosocomial infections [1]
Internalization of S. epidermidis in Human Osteoblasts MG63 osteoblasts were infected with increasing multiplicity of infection (MOI) of the reference strain NCTC11047, and the results demonstrated that the number of bacteria that are internalized was MOIdependent, where more S. epidermidis was internalized when the MOI rose from 250:1 to 500:1
The abilities of S. epidermidis to internalize in osteoblasts and to form biofilms failed to distinguish S. epidermidis strains isolated from infected orthopedic devices from nasal carriage isolates
Summary
Staphylococcus epidermidis, coagulase-negative staphylococci, have been considered innocuous commensals of human skin and mucous membranes but are accepted as the leading opportunistic pathogens responsible for numerous nosocomial infections [1]. The contrast between the low incidence of S. epidermidis orthopedic device infection and the highly prevalent S. epidermidis carriage suggests that S. epidermidis bone and joint infections might either correspond to accidental events due to colonizing strains or to a specific, more virulent sub-population of commensal isolates. The existence of such specificity could be crucial because it may impact the prevention and management of these severe infections. 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
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