Current Issue : January - March Volume : 2020 Issue Number : 1 Articles : 5 Articles
Hydroxide [Ag(OH)L] (L = IVL, VL, VIL, VIIL), oxide [{AgL}2}(micro-O)] (L = IL, IIL, IIIL,\nVL, VIL) or chloride [AgIIL]Cl, [Ag(VIL)2]Cl complexes were obtained from reactions of mono- or\nbicamphorimine derivatives with Ag(OAc) or AgCl. The new complexes were characterized by\nspectroscopic (NMR, FTIR) and elemental analysis. X-ray photoelectron spectroscopy (XPS), ESI\nmass spectra and conductivity measurements were undertaken to corroborate formulations. The\nantimicrobial activity of complexes and some ligands were evaluated towards Candida albicans\nand Candida glabrata, and strains of the bacterial species Escherichia coli, Burkholderia contaminans,\nPseudomonas aeruginosa and Staphylococcus aureus based on the Minimum Inhibitory Concentrations\n(MIC). Complexes displayed very high activity against the Candida species studied with the lowest\nMIC values (3.9 microg/mL) being observed for complexes 9 and 10A against C. albicans. A significant\nfeature of these redesigned complexes is their ability to sensitize C. albicans, a trait that was not\nfound for the previously investigated [Ag(NO3)L] complexes. The MIC values of the complexes\ntowards bacteria were in the range of those of [Ag(NO3)L] and well above those of the precursors\nAg(OAc) or AgCl. The activity of the complexes towards normal fibroblasts V79 was evaluated by\nthe MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay. Results showed that\nthe complexes have a significant cytotoxicity....
Objectives: The ceragenins, or CSAs, were designed to mimic the activities of antimicrobial\npeptides and represent a new class of antimicrobial agent. The aim of this study was to comparatively\ninvestigate the antimicrobial activities of first/second generation ceragenins and various antibiotics\nagainst multidrug-resistant (MDR) Klebsiella pneumoniae, including colistin-resistant bacteria. Also,\nthe synergistic effects of two ceragenins with colistin or meropenem were investigated with\nsix K. pneumoniae strains presenting different resistant patterns. Methods: Minimal inhibition\nconcentrations (MICs) were determined by the microdilution method according to the CLSI. Antibiotic\ncombination studies were evaluated by the time-kill curve method. Results: MIC50 and MIC90 values\nof tested ceragenins ranged from 8 to 32 mg/L and 16 to 128 mg/L. Overall, among the ceragenins\ntested, CSA-131 showed the lowest MIC50 and MIC90 values against all microorganisms. The MICs of\nthe ceragenins were similar or better than tested antibiotics, except for colistin. Synergistic activities\nof CSA-131 in combination with colistin was found for strains both at 1* MIC and 4* MIC. No\nantagonism was observed with any combination. Conclusions: First-generation ceragenins CSA-13\nand CSA-44 and second-generation ceragenins CSA-131, CSA-138 and CSA-142 have significant\nantimicrobial effects on MDR K. pneumoniae. Mechanisms allowing resistance to clinical comparator\nantibiotics like colistin did not impact the activity of ceragenins. These results suggest that ceragenins\nmay play a role in treating infections that are resistant to known antibiotics....
Urinary tract infections (UTI) are common worldwide and are becoming increasingly\ndifficult to treat because of the development of antibiotic resistance. Immunocompetent murine\nmodels of human UTI have been used to study pathogenesis and treatment but not for investigating\nresistance development after treatment with antibiotics. In this study, intravesical inoculation of\nuropathogenic Escherichia coli CFT073 in immunocompetent Balb/c mice was used as a model of human\nUTI. The value of the model in investigating antibiotic exposure on in vivo emergence of antibiotic\nresistance was examined. Experimentally infected mice were treated with 20 or 200 mg/kg ampicillin,\n5 or 50 mg/kg ciprofloxacin, or 100 or 1000 mg/kg of fosfomycin. Ampicillin and ciprofloxacin\nwere given twice daily at 8 h intervals, and fosfomycin was given once daily. Antibiotic treatment\nbegan 24 h after bacterial inoculation and ended after 72 h following the initial treatment. Although\nminimum inhibitory concentrations (MIC) for the experimental strain of E. coli were exceeded at\npeak concentrations in tissues and consistently in urine, low levels of bacteria persisted in tissues in\nall experiments. E. coli from bladder tissue, kidney, and urine grew on plates containing 1* MIC of\nantibiotic, but none grew at 3 *MIC. This model is not suitable for studying emergent resistance but\nmight serve to examine bacterial persistence....
In recent years, the incidence and severity of Clostridium difficile infections has increased.\nAdditionally, resistance of C. difficile to frequently used antibiotics is rising. To improve our\nunderstanding of C. difficile, there is a need for molecular characterization of different strains and\nantibiotic resistance testing. We investigated the efficacy of GenoType CDiff kit (Hain Lifesciences)\nin identification of C. difficile and its various strains in northern Israel. The kit involves a molecular\nassay that detects C. difficile from stool samples or colonies and identifies the different strains and\nmutations in the gyrA gene that cause moxifloxacin resistance. Forty-nine C. difficile positive samples\nwere examined by the kit following DNA extraction from both colonies and stool. The identification\nrate (95.9%) of C. difficile was much higher when DNA was extracted from colonies, compared to\nextraction from stool (46.9%). Low frequencies of ribotype027 strain (2%) and of ribotype078 strain\n(4%) were found. There was a high concordance between genotype (mutation in gyrA) and phenotype\n(Etest) for moxifloxacin resistance (Kappa = 0.72). A high percentage of moxifloxacin-resistant strains\nwas found. Our findings indicate that the GenoType CDiff kit is very effective in characterization of\nC. difficile strains and less effective for identification of C. difficile directly from stool samples....
The basis of drug resistance in Mycobacterium abscessus is still poorly understood.\nNevertheless, as seen in other microorganisms, the efflux of antimicrobials may also play a role\nin M. abscessus drug resistance. Here, we investigated the role of effluxpumps in clarithromycin\nresistance using nine clinical isolates of M. abscessus complex belonging to the T28 erm(41) sequevar\nresponsible for the inducible resistance to clarithromycin. The strains were characterized by drug\nsusceptibility testing in the presence/absence of the effluxinhibitor verapamil and by genetic analysis\nof drug-resistance-associated genes. Effluxactivity was quantified by real-time fluorometry. Efflux\npump gene expression was studied by RT-qPCR upon exposure to clarithromycin. Verapamil\nincreased the susceptibility to clarithromycin from����������...
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