coli (from 256 to 2 mg/L, fractional inhibitory concentration index (FICI)≤0.02) and by a factor of at least 64 in K. pneumoniae (from 1024 mg/L to 16 mg/L, FICI≤0.05). Synergy between PMBN and PBA enhanced ceftazidime activity 133 times in P. aeruginosa (from 16 mg/L to 0.12 mg/L, FICI≤0.03). As a consequence, MICs of all the antibiotics tested were brought down to therapeutic range. In addition, the combinations also reduced several orders of magnitude the amount of inhibitor needed for antibiotic sensitization. Ceftazidime/PBA/PMBN at 50 times the planktonic MIC caused a 10 million-fold reduction in the viability of mature biofilms. We proved that AMPs can synergize with BLIs and that this phenomenon can be exploited to sensitize bacteria to antibiotics. V.Currently, topical treatment with antibiotics is a major strategy for the decolonization of S. aureus, although it results in antibiotic resistance or recolonization of the organism. Recently, the application of bacteriophages in treatment of S. aureus infection has attracted attention; however, a single administration of bacteriophages did not effectively decolonize S. aureus in our first trial in vivo. Using a bacteriophage, pSa-3, and surfactant combination in vitro, we showed an increased (more than 8%) adsorption rate of the bacteriophage on the host. Moreover, the combination increased the eradication of immunoglobulin E-stimulated aggregation, as the surfactant promoted the dissociation of S. aureus aggregates by decreasing the size by 75 and 50% in the absence and presence of IgE, respectively. Furthermore, the combined treatment significantly decolonized the pathogen, with an efficacy double that of the phage-only treatment, and decreased the expression of pro-inflammatory cytokine genes (IL-1β, IL-12, and IFN- γ) for 5 days in the second in vivo trial. These results suggest that the bacteriophage-surfactant combination could act as an alternative to antibiotics for S. aureus decolonization in patients with dermatitis. V.Antibiotic collateral sensitivity (CS) occurs when a bacterium that acquires resistance to a treatment drug exhibits decreased resistance to a different drug. Here we identify reciprocal CS networks and candidate genes in Burkholderia multivorans. B. multivorans was evolved to become resistant to each of six antibiotics. The antibiogram of the evolved strain was compared to the immediate parental strain to determine CS and cross-resistance (CR). The evolution process was continued for each resistant strain. CS interactions were observed in 170 of 279 evolved strains. CS patterns grouped into two clusters based on the treatment drug being a beta-lactam antibiotic or not. Reciprocal pairs of CS antibiotics arose in at least 25% of all evolved strains. Sixty-eight evolved strains were subjected to whole-genome sequencing and the resulting mutation patterns were correlated with antibiograms. Cloperastine fendizoate solubility dmso Analysis revealed there was no single gene responsible for collateral sensitivity (CS), and that CS seen in B. multivorans is likely due to a combination of specific and non-specific mutations. The frequency of reciprocal CS, and the degree to which resistance changed, suggests a long-term treatment strategy; when resistance to one drug occurs, switch to use of the other member of the reciprocal pair. This switching could theoretically be continued indefinitely, allowing life-long treatment of chronic infections with just two antibiotics. V.BACKGROUND We aimed to describe the effect of initial antifungal therapy on the fatality and detail the current distribution and resistance patterns of Candida species among the patients with Candidemia. METHODS A prospective observational study was performed among the consequent patients with Candidemia from 10 medical centers, between January 2015 and November 2018. Primary outcome was defined as 10-day mortality. For species level identification Matrix Assisted Laser Desorption Ionization Time of Flight Mass Spectrometer (MALDI-TOF) was used. RESULTS A total of 342 patients with candidemia were included, 175 (51.2%) were males and 68 (20%) patients were under 18 years old. The most common Candida species were C. albicans (47%), C. parapsilosis (27%), C. tropicalis (10%), C. glabrata (7%). Among all Candida species, the 10-day case fatality rate (CFR) was 32%. The highest CFR was among the patients with C.albicans (57%), the lowest was among C. parapsilosis (22%). The rate of resistance against fluconazole was 13% in C.parapsilosis isolates with no significant effect on fatality. No resistance against echinocandins was detected. In multivariate analysis, being in intensive care unit (OR2.1, CI 1.32-3.57, p=0.002), renal failure (OR2.4, CI 1.41-3.97, p=0.001), total parenteral nutrition (OR2, CI 1.22-3.47, p=0,006) detection of C. albicans (OR1,7 CI 1.06- 2.82, p=0.027), using echinocandin as the primary agent (OR0.6, CI0.36-0.99, p=0.047) were found to be significantly associated with fatality CONCLUSIONS Candidemia is one of the most fatal infections. Resistance to fluconazole is emerging, although it was not related to fatality, significantly. Using echinocandins as the primary agent could be life saving. V.INTRODUCTION Co-existence of both virulence and multidrug-resistant (MDR) determinants on a self-transmissible plasmid facilitates simultaneous transfer of virulence and resistance in a single event and rapid emergence of virulent and MDR Klebsiella pneumoniae clones. METHOD This study identified extensively drug-resistant ST15 strains, KP17-15 and KP17-16, from clinical cases with microbiological and genomical approaches. RESULTS The chromosomes of KP17-15 and KP17-16 were highly homologous with 12 SNP differences, indicating that the two strains were derived from the same clone. Multiple plasmids existed in the isolates, including novel virulence plasmids p17-15-vir (479 kb) and p17-16-vir (290 kb) for KP17-15 and KP17-16, respectively. Notably, the plasmid p17-15-vir (479 kb) was a hybrid plasmid that might be formed by recombination of two homologous regions encoding group II intron reverse transcriptase and mobile element ISShes11 shared by p17-16-vir (290 kb) and a conjugative MDR plasmid p17-16-CTX (188 kb).