Search

Achromobacter spp. can establish occasional or chronic lung infections in patients with cystic fibrosis (CF). Chronic colonization has been associated with worse prognosis highlighting the need to identify markers of bacterial persistence. To this purpose, we analyzed phenotypic features of 95 Achromobacter spp. isolates from 38 patients presenting chronic or occasional infection. Virulence was tested in Galleria mellonella larvae, cytotoxicity was tested in human bronchial epithelial cells, biofilm production in static conditions was measured by crystal violet staining and susceptibility to selected antibiotics was tested by the disk diffusion method. The presence of genetic loci associated to the analyzed phenotypic features was evaluated by a genome-wide association study. Isolates from occasional infection induced significantly higher mortality of G. mellonella larvae and showed a trend for lower cytotoxicity than chronic infection isolates. No significant difference was observed in biofilm production among the two groups. Additionally, antibiotic susceptibility testing showed that isolates from chronically-infected patients were significantly more resistant to sulfonamides and meropenem than occasional isolates. Candidate genetic biomarkers associated with antibiotic resistance or sensitivity were identified. Achromobacter spp. strains isolated from people with chronic and occasional lung infection exhibit different virulence and antibiotic susceptibility features, which could be linked to persistence in CF lungs. This underlines the possibility of identifying predictive biomarkers of persistence that could be useful for clinical purposes.

Cystic fibrosis (CF) is the most common rare disease caused by a mutation of the

Several advances in the medical field are often dependent on the ability to fight infections with the use of antibiotics, including joint replacements, organ transplants, and cancer therapy. The capacity of the bacteria to adapt to and escape from the mechanisms of action of antibiotics makes the antimicrobial resistance a serious public health problem worldwide. Polymyxin E colistin has rarely been used because of its nephrotoxicity and neurotoxicity. More recently, the emergence of multi-drug resistant bacteria as carbapenem-resistant Klebsiella pneumoniae, Acinetobacter baumannii and Pseudomonas aeruginosa and the re-evaluation of its pharmacokinetic properties have led to a resurgence of colistin as a treatment option, contributing to select resistant strains. Investigating the phenomenon of colistin-resistance in gram-negative bacteria, especially P. aeruginosa, is now mandatory, particularly after identification of a plasmid-mediated mechanism for the resistance to colistin (mcr) in Enterobacteriaceae strains, a mechanism transferable to other species. In this study, we investigated colistin-resistance in gram-negative bacteria isolated from respiratory secretions of cystic fibrosis patients in follow-up at Children’s Hospital Bambino Gesù of Rome.

Serum thromboxane-B2 (TxB2), together with arachidonic acid (AA)-induced platelet aggregation, are, at the moment, the most used tests to identify patients displaying high on-aspirin treatment platelet reactivity (HAPR). Both tests are specific for aspirin action on cyclooxygenase-1. While the correlation between serum TxB2 assay and clinical outcome is established, data are conflicting with regard to aspirin treatment and a possible association with AA-stimulated platelet markers and clinical outcome. To understand such discrepancy, we performed a retrospective study to compare both assays. We collected data from 132 patients receiving a daily dose of aspirin (100 mg/day) and data from 48 patients receiving aspirin on alternate days. All Patients who received a daily dose of aspirin were studied for AA-induced platelet aggregation together with serum TxB2 levels and AA-induced TxB2 formation was also studied in 71 patients out of entire population. Consistent with recommendations in the literature, we defined HAPR by setting a cut-off point at 3.1 ng/ml for serum levels of thromboxane B2 and 20% for AA-induced platelet aggregation. According to this cut-off point, we divided our overall population into two groups: (1) TxB23.1 ng/ml and (2) TxB23.1 ng/ml. We found low agreement between such tests to identify patients displaying HAPR. Our results show that AA-induced platelet aggregation20% identify a smaller number of HAPR patients in comparison with TxB2. A good correlation between serum TxB2 and arachidonic acid-induced TxB2 production was found (r = 0.76619).

Scientific object The epidemic diffusion of diabetes mellitus has raised serious concerns about the deleterious effects of its complications. Diabetic retinopathy (DR) is a severe progressive ocular pathology and the leading cause of blindness in adults. There is a significant limitation in specific biomarkers for DR, thus, implying that DR diagnosis occur when vision is already compromised. Poor glycemic control, with elevated hemoglobin A1c (HbA1c), and hypertension are recognized risk factors, however the implication of inflammatory processes in DR pathogenesis has prompt interest in the identification of biomarkers of disease within the immune system.