While the commensal bacterium Propionibacterium acnes (P. acnes) is involved in the maintenance of a healthy skin, it can also act as an opportunistic pathogen in acne vulgaris. The latest findings on P. acnes shed light on the critical role of a tight equilibrium between members of its phylotypes and within the skin microbiota in the development of this skin disease. Indeed, contrary to what was previously thought, proliferation of P. acnes is not the trigger of acne as patients with acne do not harbour more P. acnes in follicles than normal individuals. Instead, the loss of the skin microbial diversity together with the activation of the innate immunity might lead to this chronic inflammatory condition. This review provides results of the most recent biochemical and genomic investigations that led to the new taxonomic classification of P. acnes renamed Cutibacterium acnes (C. acnes), and to the better characterisation of its phylogenetic cluster groups. Moreover, the latest data on the role of C. acnes and its different phylotypes in acne are presented, providing an overview of the factors that could participate in the virulence and in the antimicrobial resistance of acne-associated strains. Overall, this emerging key information offers new perspectives in the treatment of acne, with future innovative strategies focusing on C. acnes biofilms and/or on its acne-associated phylotypes.

Although prosthetic joint infection (PJI) is a rare event after arthroplasty, it represents a significant complication that is associated with high morbidity, need for complex treatment, and substantial healthcare costs. An accurate and rapid diagnosis of PJI is crucial for treatment success. Current diagnostic methods in PJI are insufficient with 10-30% false-negative cultures. Consequently, there is a need for research and development into new methods aimed at improving diagnostic accuracy and speed of detection. In this article, we review available conventional diagnostic methods for the diagnosis of PJI (laboratory markers, histopathology, synovial fluid and periprosthetic tissue cultures), new diagnostic methods (sonication of implants, specific and multiplex PCR, mass spectrometry) and innovative techniques under development (new laboratory markers, microcalorimetry, electrical method, reverse transcription [RT]-PCR, fluorescence in situ hybridization [FISH], biofilm microscopy, microarray identification, and serological tests). The results of highly sensitive diagnostic techniques with unknown specificity should be interpreted with caution. The organism identified by a new method may represent a real pathogen that was unrecognized by conventional diagnostic methods or contamination during specimen sampling, transportation, or processing. For accurate interpretation, additional studies are needed, which would evaluate the long-term outcome (usually >2 years) with or without antimicrobial treatment. It is expected that new rapid, accurate, and fully automatic diagnostic tests will be developed soon.

Presence of an insertion sequence upstream of ampC in A. baumannii clinical isolates, possibly including a strong promoter, has the potential to cause over-expression of AmpC, resulting in high-level ceftazidime resistance.

The genetic structures surrounding the plasmid-carried bla OXA-23 oxacillinase gene, encoding resistance to carbapenems, were studied in Acinetobacter baumannii. ISAba1 and the novel element ISAba4 were detected upstream of the bla OXA-23 gene, providing promoter sequences for its expression. These insertion elements were likely involved in transposition processes at the origin of acquisition of this ␤-lactamase gene.Acinetobacter baumannii is a typical opportunistic pathogen, often involved in nosocomial outbreaks, for which resistance to carbapenems is increasingly reported (23) and may be linked to the production of Ambler class B metallo-␤-lactamases (30) but also to the production of carbapenem-hydrolyzing class D ␤-lactamases (CHDLs) (18,31). Although integrons are associated with many metallo-␤-lactamase or oxacillinase genes, they are likely not the genetic vehicles for acquisition of CHDL genes since these genes are not in the form of gene cassettes (10,22,23). Three main acquired CHDL gene clusters have been described for A. baumannii, namely, the bla OXA-23 -, bla OXA-24 -, and bla OXA-58 -like genes, whereas the bla OXA-51 gene cluster is naturally occurring and chromosomally located in A. baumannii (5,6,11,16,23,29). The bla OXA-23 gene has been identified worldwide in A. baumannii (4,8,9,13,15,27) and in Proteus mirabilis in France (3). Whereas the bla OXA-24 -like genes have been identified as chromosomally encoded, the bla OXA-23 and bla OXA-58 genes are mostly found on plasmids (23). The acquisition of bla in an A. baumannii isolate from France has been associated with a homologous recombination process (21,22).ISAba1 has been found upstream of bla , bla OXA-51 -like, and bla ampC genes in A. baumannii and is involved in their expression (7,12,23,26,28). ISAba1 belongs to the IS4 family of insertion sequences, possesses two 16-bp imperfect inverted repeats (IRs), and generates a 9-bp target site duplication upon transposition. Its transposase is made of two open reading frames, encoding 189 and 178 amino acids, leading to a functional protein when a frameshift occurs during the translation process (12).The aim of this study was to analyze the genetics of acquisition and expression of the bla OXA-23 gene in unrelated A. baumannii isolates recovered from different countries (Table 1). Genes coding for CHDLs were searched for by PCR, using primers specific for the bla OXA-23 -like, bla OXA-24 -like, and bla OXA-58 genes (15). Two bla

The role of Propionibacterium acnes in acne and in a wide range of inflammatory diseases is well established. However, P. acnes is also responsible for infections involving implants. Prolonged aerobic and anaerobic agar cultures for 14 days and broth cultures increase the detection rate. In this paper, we review the pathogenic role of P. acnes in implant-associated infections such as prosthetic joints, cardiac devices, breast implants, intraocular lenses, neurosurgical devices, and spine implants. The management of severe infections caused by P. acnes involves a combination of antimicrobial and surgical treatment (often removal of the device). Intravenous penicillin G and ceftriaxone are the first choice for serious infections, with vancomycin and daptomycin as alternatives, and amoxicillin, rifampicin, clindamycin, tetracycline, and levofloxacin for oral treatment. Sonication of explanted prosthetic material improves the diagnosis of implant-associated infections. Molecular methods may further increase the sensitivity of P. acnes detection. Coating of implants with antimicrobial substances could avoid or limit colonization of the surface and thereby reduce the risk of biofilm formation during severe infections. Our understanding of the role of P. acnes in human diseases will likely continue to increase as new associations and pathogenic mechanisms are discovered.

Our understanding of the role of Cutibacterium acnes in the pathophysiology of acne has recently undergone a paradigm shift: rather than C. acnes hyperproliferation, it is the loss of balance between the different C. acnes phylotypes, together with a dysbiosis of the skin microbiome, which results in acne development. The loss of diversity of C. acnes phylotypes acts as a trigger for innate immune system activation, leading to cutaneous inflammation. A predominance of C. acnes phylotype IA 1 has been observed, with a more virulent profile in acne than in normal skin. Other bacteria, mainly Staphylococcus epidermis , are also implicated in acne. S. epidermidis and C. acnes interact and are critical for the regulation of skin homeostasis. Recent studies also showed that the gut microbiome is involved in acne, through interactions with the skin microbiome. As commonly used topical and systemic antibiotics induce cutaneous dysbiosis, our new understanding of acne pathophysiology has prompted a change in direction for acne treatment. In the future, the development of individualized acne therapies will allow targeting of the pathogenic strains, leaving the commensal strains intact. Such alternative treatments, involving modifications of the microbiome, will form the next generation of ‘ecobiological’ anti-inflammatory treatments.

BackgroundBacteremia, or bloodstream infection (BSI), is a leading cause of death among patients with certain types of cancer. A previous study reported that intestinal domination, defined as occupation of at least 30 % of the microbiota by a single bacterial taxon, is associated with BSI in patients undergoing allo-HSCT. However, the impact of the intestinal microbiome before treatment initiation on the risk of subsequent BSI remains unclear. Our objective was to characterize the fecal microbiome collected before treatment to identify microbes that predict the risk of BSI.MethodsWe sampled 28 patients with non-Hodgkin lymphoma undergoing allogeneic hematopoietic stem cell transplantation (HSCT) prior to administration of chemotherapy and characterized 16S ribosomal RNA genes using high-throughput DNA sequencing. We quantified bacterial taxa and used techniques from machine learning to identify microbial biomarkers that predicted subsequent BSI.ResultsWe found that patients who developed subsequent BSI exhibited decreased overall diversity and decreased abundance of taxa including Barnesiellaceae, Coriobacteriaceae, Faecalibacterium, Christensenella, Dehalobacterium, Desulfovibrio, and Sutterella. Using machine-learning methods, we developed a BSI risk index capable of predicting BSI incidence with a sensitivity of 90 % at a specificity of 90 % based only on the pretreatment fecal microbiome.ConclusionsThese results suggest that the gut microbiota can identify high-risk patients before HSCT and that manipulation of the gut microbiota for prevention of BSI in high-risk patients may be a useful direction for future research. This approach may inspire the development of similar microbiome-based diagnostic and prognostic models in other diseases.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-016-0301-4) contains supplementary material, which is available to authorized users.

There is no standard method for the diagnosis of prosthetic joint infection (PJI). The contribution of 16S rRNA gene PCR sequencing on a routine basis remains to be defined. We performed a prospective multicenter study to assess the contributions of 16S rRNA gene assays in PJI diagnosis. Over a 2-year period, all patients suspected to have PJIs and a few uninfected patients undergoing primary arthroplasty (control group) were included.