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As an important opportunistic pathogen, Pseudomonas aeruginosa (P. aeruginosa, PA) was the most prevalent bacterial pathogens in infectious diseases, such as respiratory tract infections, bacteremia, pneumonia, urinary tract infections, cystic fibrosis, infections of burn, catheter infections and infections of heart valve.~ 1,2 Owing to mass usage of antibiotic agents, P. aeruginosa has shown intrinsic and acquired multi-drug resistance (MDR) that always causes failure in clinical therapy. P. aeruginosa MDR is more commonly due to mutation of antibiotic resistance gene ranging from mutation of type Ⅱ topoisomerase gene (gyrA)~3 to development of active efflux-mediated drug resistance (such as MexAB-OprM).~4 In addition, the formation of P. aeruginosa biofilms markedly enhances bacterial resistance to antibiotics agents.~5 P. aeruginosa biofilms are composed primarily of extracellular polymeric substance (EPS) as well as bacterial cells. This kind of compact substance prevents drugs to produce therapeutic effects.~6 However, in P. aeruginosa, the relationship between intrinsic drug resistance (including mutation of gyrA and active efflux of MexAB-OprM) and biofilms resistance is not clear. This work is to try to illuminate this relationship. We screened mutation of gyrA and active efflux of MexAB-OprM for studying the change of P. aeruginosa intrinsic resistance in process of bacterial biofilms development. Furthermore, we used biofilms strains to co-culture with intrinsic drug resistance strains and to demonstrate survival rate of biofilm strains and intrinsic resistance strains to ciprofloxacin.
As an important opportunistic pathogen, Pseudomonas aeruginosa (P. aeruginosa, PA) was the most prevalent bacterial pathogens in infectious diseases, such as respiratory tract infections, bacteremia, pneumonia, urinary tract infections, cystic fibrosis, infections of burn, catheter infections and infections of heart valve. ~ 1,2 Owing to mass usage of antibiotic agents, P. aeruginosa has shown intrinsic and acquired multi-drug resistance (MDR) that always causes failure in clinical therapy. P. aeruginosa MDR is more due due to mutation of antibiotic resistance gene ranging from mutation of type II topoisomerase gene (gyrA) ~ 3 to development to active efflux-mediated drug resistance (such as MexAB-OprM). 4 In addition, the formation of P. aeruginosa biofilms markedly enhances bacterial resistance to antibiotics agents. ~ 5 P. aeruginosa biofilms are fixed in extracellular polymeric substances (EPS) as well as bacterial cells. This kind of compact substance prevents drugs t This work between to aerobinosa, the relationship between intrinsic drug resistance (including mutation of gyrA and active efflux of MexAB-OprM) and biofilms resistance is not clear. This work is to try to illuminate this relationship. We, screened mutation of gyrA and active efflux of MexAB-OprM for studying the change of P. aeruginosa intrinsic resistance in process of bacterial biofilms development. Furthermore, we used biofilms strain to co-culture with intrinsic drug resistance strain and to demonstrate survival rate of biofilm strains and intrinsic resistance strains to ciprofloxacin.