Aim

The aim of this study was to confirm that Mirra's criterion (≥ 5 Polymorphonuclears (PMNs) per field in 5 high power fields (HPFs)) is not adequate for diagnosis of chronic bone and joint infections (BJIs) due to Cutibacterium acnes (C. acnes). The second objective was to determine if plasma-cell infiltration, that is a classical marker of chronic inflammation, could be useful for the diagnosis of chronic BJIs due to C. acnes.

Aim

Bone and joint infections (BJI) need frequently prolonged antibiotic treatment at high dosage for a total of 6 or 12 weeks depending the type of infection. Impact of such prolonged antibiotic exposure on the gut microbiota has never been assessed.

Aim

Staphylococcus epidermidis (S. epidermidis) is one of the main pathogens responsible for bone and joint infections especially those involving prosthetic materials (PJI). Although less virulent than S. aureus, S. epidermidis is involved in chronic infections notably due to its ability to form biofilm. Moreover, it is frequently multiresistant to antibiotics. In this context, the development of additional or alternative antibacterial therapies targeting the biofilm is a priority.

Aim

Staphylococcus aureus is the first causative agent of bone and joints infections (BJI). It causes difficult-to-treat infections because of its ability to form biofilms, and to be internalized and persist inside osteoblastic cells. Recently, phage therapy has emerged as a promising therapy to improve the management of chronic BJI. In the present study, we evaluated the efficacy of an assembly of three bacteriophages previously used in a clinical case report (Ferry, 2018) against S. aureus in in vitro models of biofilm and intracellular osteoblast infection.

Aim

Leading etiology of Bone and Join infections (BJI), Staphylococcus aureus (SA) is responsible for difficult-to-treat infections mainly because of three persistence factors: (i) biofilm formation, (ii) persistence within bone cells and (iii) switch to the small colony variant (SCV) phenotype. The impact of rifampin on these mechanisms gave it a prominent place in orthopedic device-associated BJI. However, resistance emergence, intolerance and drug interactions cause significant concerns. In this context, other rifamycins – namely rifapentine and rifabutin – have poorly been evaluated, particularly toward their ability to eradicate biofilm-embedded and intracellular reservoirs of SA.

Aim

Staphylococcus aureus (SA) chronic bone and joint infections (BJI) are characterized by a progressive destruction of bone tissue associated to SA persistence which results in a large number of relapses (10–20%). The main factors proposed for these failures are: i) a weak diffusion of antibiotics in bone tissue, ii) formation of biofilm, iii) the bacterial internalization by the cells responsible for bone mineralization, namely the osteoblasts (OB).

Our in vitro and in vivo work aimed at providing new information on the impact of SA, more specifically of internalized SA, on bone homeostasis.

Aim

Toxin-antitoxin (TA) systems are small genetics elements found in the majority of bacteria which encode a toxin causing bacterial growth arrest and an antitoxin counteracting the toxic effect. In Salmonella and E. coli, TA systems were shown to be involved in the formation of persisters. Persisters are a bacterial subpopulation with low growth rate and high tolerance to antibiotics. They could be responsible for antibiotic treatment failure in chronic infections and relapses, notably in bone and joint infections (BJI) caused by Staphylococcus aureus. Currently, two type II TA system families were described in S. aureus, mazEF and axe/txe, but their physiological roles are not well described. In this work, we studied the importance of mazEF in the intracellular survival of S. aureus inside osteoblasts, one of the mechanisms considered in the chronicity of S. aureus BJI.