Balancing the Virulence and Antimicrobial Resistance in VISA DAP-R CA-MRSA Superbug.

Background: Methicillin-resistant (MRSA) with intermediate resistance to Vancomycin (VISA) is reported worldwide. These strains frequently emerge among hospital-associated (HA)-MRSA and rarely within community-acquired (CA)-MRSA. Here, the genomic and transcriptomic adaptations distinguishing VISA daptomycin resistant (DAP-R) CA-MRSA, which emerged in a hospitalized patient under glycopeptide treatment, were explored.

Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Lineages.

The treatment of multidrug-resistant Gram-negative infections is based on colistin. As result, COL-resistance (COL-R) can develop and spread. In , a crucial step is to understand COL-R onset and stability, still far to be elucidated.

Genomic Characterization of a New Biofilm-Forming and Adhesive ST398 Human-Adapted MSSA Lineage Causing Septic Knee Arthritis Following Surgical Reconstruction.

Methicillin-susceptible (MSSA) and methicillin-resistant (MRSA) is a pathogen commonly found in bone and joint infections, including septic arthritis. virulence and the frailty of affected patients can cause several complications; a prompt and specific antibiotic treatment can positively affect the outcome of patients. We carried out an in-depth genomic characterization by Illumina whole genome sequencing and bioinformatics of two biofilm-producing M1 and M2 ST398 MSSA causing septic knee arthritis not-responding to antimicrobial therapy.

Genomic and Long-Term Transcriptomic Imprints Related to the Daptomycin Mechanism of Action Occurring in Daptomycin- and Methicillin-Resistant Under Daptomycin Exposure.

Daptomycin (DAP) is one of the last-resort treatments for heterogeneous vancomycin-intermediate (hVISA) and vancomycin-intermediate (VISA) infections. DAP resistance (DAP-R) is multifactorial and mainly related to cell-envelope modifications caused by single-nucleotide polymorphisms and/or modulation mechanisms of transcription emerging as result of a self-defense process in response to DAP exposure. Nevertheless, the role of these adaptations remains unclear.

COL sRNA Signatures: Computational Comparative Identification and Biological Targets.

Multidrug-Resistant (MDR) and Extensively Drug Resistant (XDR) () represent a serious cause of healthcare-associated infections worldwide. Currently, the available treatment options are very restricted and colistin-based therapies are last-line treatments of these infections, even though colistin resistant (COL) have rarely been isolated yet. In bacteria, small non-coding RNAs (sRNAs) have been implicated in regulatory pathways of different biological functions, however, no knowledge exists about the sRNA role on the biological adaptation in COL .

Titration of Igs contained in an intravenous IgM-enriched preparation against selected pathogens involved in sepsis.

The goal of our work was to titer the IgG, IgM and IgA in Pentaglobin® (a preparation enriched in IgM), targeting specific surface antigens of Gram-positive and Gram-negative bacteria as well as a C. albicans strain. Lipopolysaccharides from Gram-negative bacteria, peptidoglycan and lipoteichoic acid from the other microorganisms were extracted and used in several ELISA assays in order to determine the titration of immunoglobulins in Pentaglobin® directed towards the aforementioned surface antigens.

Colistin Resistant : Genomic and Transcriptomic Traits Acquired Under Colistin Therapy.

Even though colistin-based treatment represents the antimicrobial-regimen backbone for the management of multidrug-resistant Gram-negative infections, colistin resistance is still rare, at least as a full resistance, in (). We investigated the genomics and transcriptomics of two clinical Extensively Drug Resistance (XDR) colistin-susceptible/resistant (COL-S/R) strain-pairs in which COL-resistance was developed after exposure to colistin therapy. The molecular characterization of the strains showed that all strains belonged to PFGE-A, ST-281, OXA-23 producers, Global Clone-II, and were resistant to imipenem, meropenem, ampicillin/sulbactam, ciprofloxacin, gentamicin, amikacin, trimethoprim/sulfamethoxazole, and susceptible to tigecycline, in agreement with NGS-acquired resistome.