High levels of multiresistance in quinolone resistant urinary tract isolates of Escherichia coli from Norway; a non clonal phenomen?

Abstract

BackgroundThe problem of emerging ciprofloxacin resistance is compounded by its frequent association with multiresistance, the reason for which is not fully understood. In this study we compare multiresistance, clonal similarities and phylogenetic group in urinary tract isolates of Escherichia coli sensitive and resistant to the quinolone antimicrobials nalidixic acid and ciprofloxacin.ResultsQuinolone resistant isolates were more resistant to non-quinolone antibiotics than sensitive isolates, with resistance to ampicillin, mecillinam, sulphonamide, trimethoprim, tetracycline, kanamycin and chloramphenicol significantly increased. Fifty-one percent of quinolone-resistant isolates were multiresistant. Although multiresistance was most prevalent (63%) in isolates showing high-level ciprofloxacin resistance, it was still highly prevalent (41%) in nalidixic acid resistant isolates with low-level ciprofloxacin resistance. Multiresistance was more frequent among singleton isolates (61%) than clonal isolates (40%) of quinolone resistant Escherichia coli. Ciprofloxacin resistance was associated with certain specific clones, among them the globally distributed clonal Group A. However, there was no significant difference in the overall degree of clonality between quinolone sensitive and resistant isolates. Ciprofloxacin resistance was positively associated with phylogroup D and negatively associated with phylogroup B2. This correlation was not associated with clonal isolates.ConclusionThis study supports earlier findings of association between ciprofloxacin resistance and resistance to other antibiotics. The prevalence of multiresistance in quinolone-resistant isolates that have not yet developed high-level ciprofloxacin resistance suggest that multiresistance arises early in the development of quinolone resistance. This is consistent with exposure to quinolones causing quinolone resistance by mutations and mobilization of multiresistance elements by induction of the SOS response. The spread of clones seems to be less important than previously reported in regard to emergence of quinolone resistance and multiresistance as both are associated primarily with singleton isolates.

Characteristics of ciprofloxacin-resistant Enterobacteriaceae isolates recovered from wastewater of an Algerian hospital

“…Phylogroups A and B1 are considered less virulent or even commensal compared to the B2 phylogroup and, to a lesser extent, the D phylogroup [47]. Moreover, A and B1 were described as the most frequently resistant to antibiotics, as shown in our results; indeed, it seems that there is a trade-off between antibiotic resistance, particularly to quinolones (ciprofloxacin), and virulence in E. coli [32].…”

“…The resistance to beta-lactams, aminoglycosides, tetracyclines, sulfonamides, and trimethoprim/sulfamethoxazole, resulting in multidrugresistance phenotype, supports the association between ciprofloxacin resistance and resistance to other antibiotics as previously reported [6,7,32]. Resistance to ciprofloxacin can even be used as a multidrug resistance marker [7].…”

“…This cross-resistance is related to shared mechanisms or genetic supports of resistance to ciprofloxacin and unrelated drugs. Multidrug resistance is also linked to the ability of ciprofloxacin to induce mutational changes in efflux regulatory genes [33] or mobilization of multiresistance elements through the SOS response [32].…”

Changes in antimicrobial susceptibility profile and prevalence of quinolone low-sensitive strains in subgingival plaque from acute periodontal lesions after systemic administration of sitafloxacin

“…Despite prescribing guidelines now recommending reserving fluoroquinolone use, resistance continues to rise and is a major problem encountered in clinical medicine [29,30]. The problem of emerging quinolone resistance is further compounded by its frequent association with multiresistance to other antibiotics [30]. It has been reported that quinolone-resistant strains have double point mutations within the quinolone resistance-determining regions of gyrA and parC [31,32].…”

“…Despite prescribing guidelines now recommending reserving fluoroquinolone use, resistance continues to rise and is a major problem encountered in clinical medicine [29,30]. The problem of emerging quinolone resistance is further compounded by its frequent association with multiresistance to other antibiotics [30].…”