Aim. The aim of our study was to analyze putative genes for virulence factors of Cutibacterium isolates obtained from implant-associated infections. Methods. We analyzed 64 isolates of Cutibacterium spp. (C. acnes (53/64), C. avidum (6/64), C. granulosum (4/64), C. namnetense (1/64)) using NextSeq 550 (Illumina, San Diego, CA, USA) and performed genomic analysis of 24 genes associated with virulence factors (VFs) of C. acnes previously reported in the literature. Most isolates were obtained from implant-associated infections (IAI) between 2012–2021 at the Institute of Microbiology and Immunology, Faculty of Medicine, Ljubljana. Additionally, we included the first C. namnetense isolated in our laboratory from surgical site infection. Results. C. acnes and C. namnetense have the highest number of VFs among those examined. The VFs gntK (shikimate kinase) and HYL-IB / II (hyaluronate lyase) are absent in phylotype IA. 1. (sequence types (ST) A, C, D according to the SLST scheme). Repressor gene of porphyrin synthesis, deoR is present in all Cutibacterium spp. isolates. The phylotypes II and IB show a similar distribution of VFs, with the presence of the VFs rcsB (compound for biofilm formation) and HYL-IA (hyaluronate lyase), which are absent in other C. acnes phylotypes and other Cutibacterium spp. In phylotypes IA. 1. and IB, the sequence of genes encoding VFs dsA1 and dsA2 does not have 100% genomic coverage, possibly indicating homologs between species. The isolates of C. acnes and C. namnetense possess all three CAMP (1,2,4) factors, which are not detected in other Cutibacterium spp. However, further analysis revealed species-specific CAMP factors in C. avidum and C. granulosum. Both species also have similar other genes for VFs, mainly encoding heat shock proteins and lipases, while VFs related to biofilm production are mostly absent (rcsB, ytpA). Conclusion. We found several differences in the distribution of VFs among Cutibacterium spp. isolated from IAI

Introduction. Long bone surgery and marrow instrumentation represent significant surgical insults, and may cause severe local and systemic sequelae following both planned and emergent surgery. Preconditioning is a highly conserved evolutionary endogenous protective mechanism, but finding a clinically safe and acceptable method of induction has proven difficult. Glutamine, a known inducer of the heat shock protein (HSP) response, offers pharmacological modulation of injury through clinically acceptable preconditioning. This effect has not been previously demonstrated in an orthopaedic model. Aims. The aim of the study was to test the hypothesis that glutamine preconditioning protects against the local and systemic effects of long bone trauma in a rodent model. Methods. Thirty two adult male Sprague-Dawley rats were randomised into four groups:. Control group which received trauma without preconditioning,. Normal Saline preconditioning 1 hour before trauma,. Glutamine preconditioning 1 hour before trauma, and. Glutamine preconditioning 24 hours prior to trauma. Trauma consisted of bilateral femoral fracture following intramedullary instrumentation. Blood samples were taken just prior to the insult, and at an interval four hours following this. The animals were then sacrificed, bronchioalveolar lavage (BAL) performed and skeletal muscle and lung harvested for evaluation. Results. Glutamine pretreated rats had lower CK levels at 4 hours than those treated with normal saline. Renal dysfunction was less in pre-treated animal, and there was a significant reduction in neutrophil infiltration into BAL fluid. Finally glutamine pre-treated rats showed less muscle and lung oedema. This effect was more pronounced for the group which received glutamine 24 hours before trauma than the group receiving glutamine one hour before trauma. Conclusion. This data suggests that preconditioning with a single bolus of intravenous glutamine prior to planned orthopaedic intervention may afford local and end-organ protection