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The widespread presence of plasmid-mediated quinolone resistance determinants, particularly  qnr  genes, has become a current issue. By protecting DNA-gyrase from quinolones, Qnr proteins confer a low level quinolone resistance that is not sufficient to explain their emergence. Since Qnr proteins were hypothesized to act as DNA-binding protein regulators,  qnr  genes could have emerged by providing a selective advantage other than antibiotic resistance. We investigated host fitness of  Escherichia coli  isogenic strains after acquisition of the  qnrA3  gene, inserted either alone onto a small plasmid (pBR322), or harbored on a large conjugative native plasmid, pHe96( qnrA3 ) found in a clinical isolate. The isogenic strains were derived from the susceptible  E. coli  CFT073, a virulent B2 group strain known to infect bladder and kidneys in a mouse model of pyelonephritis.  In vitro  experiments included growth analysis by automatic spectrophotometry and flow cytometry, and competitions with CFU enumeration.  In vivo  experiments included infection with each strain and pairwise competitions in absence of antimicrobial exposure. As controls for our experiments we used mutations known to reduce fitness ( rpsL  K42N mutation) or to enhance fitness ( tetA  deletion in pBR322).  E. coli  CFT073 transformed with pBRAM(PBR322- qnrA3 ) had significantly higher maximal OD than  E. coli  CFT073 transformed with pBR322 or pBR322Δ tetA , and  in vivo  competitions were more often won by the  qnrA3  carrying strain (24 victories vs. 9 loss among 42 competitions, p = 0.001). In contrast, when pHe96( qnrA3 ) was introduced by conjugation in  E. coli  CFT073, it exerted a fitness cost shown by an impaired growth observed  in vitro  and  in vivo  and a majority of lost competitions (33/35, p<0.0001). In conclusion,  qnrA3  acquisition enhanced bacterial fitness, which may explain  qnr  emergence and suggests a regulation role of  qnr . However, fitness was reduced when  qnrA3  was inserted onto multidrug-resistant plasmids and this can slow down its dissemination without antibiotic exposure.

Plasmidic qnrA3 Enhances Escherichia coli Fitness in Absence of Antibiotic Exposure