BUSCADOR RECOLECTA

Membrane surface modification on recycled ultrafiltration membrane was conducted using statistical design of experiments by two levels full factorial design. Dip-coting using catechol (CA) and polyetylenimine (PEI) was chosen as the membrane surface modification method because its simplicity, energy saving characteristics and bio-based character. The factors studied were: CA and PEI concentration (1g/l and 4 g/l), temperature (30ºC and 50ºC) and reaction time (2 and 7 hours). The studied responses were the relative permeability (Pr) and the flux recovery ratio (FRR). A model with good validity was obtained for both responses. Membranes were deeply characterized using several techniques: Scanning electron microscopy (SEM); Attenuated total reflectance–Fourier transform infrared (ATR–FTIR) spectroscopy; X-ray photoelectron spectroscopy (XPS) and Atomic force microscopy (AFM). Statistical design of experiments resulted on a useful tool to understand how the factors affect the surface modification. Surface modification conducted at mild conditions (2 hours; 30 ºC and 1g/l) improved membrane permeability and flux recovery ratio. Moreover, interaction between factors turned out to be significant in the modification process which was an unexplored field in previous works. Modification of recycled membranes is an innovative process that follows a Circular Economy approach.

The appearance of carbapenem-resistant Klebsiella pneumoniae has increased the use of colistin as a last-resort antibiotic for treating infections by this pathogen. A consequence of its use has been the spread of colistin-resistant strains, in several cases carrying colistin resistance genes. In addition, when susceptible strains are confronted with colistin during treatment, mutation is a major cause of the acquisition of resistance. To analyze the mechanisms of resistance that might be selected during colistin treatment, an experimental evolution assay for 30 days using as a model the clinical K. pneumoniae kp52145 isolate in the presence of increasing amounts of colistin was performed. All evolved populations presented a decreased susceptibility to colistin, without showing cross-resistance to antibiotics belonging to other structural families. We did not find any common mutation in the evolved mutants, neither in already known genes, previously known to be associated with the resistance phenotype, nor in new ones. The only common genetic change observed in the strains that evolved in the presence of colistin was the amplification of a 34 Kb sequence, homologous to a prophage (Enterobacteria phage Fels-2). Our data support that gene amplification can be a driving force in the acquisition of colistin resistance by K. pneumoniae.