Quinolone co-resistance in ESBL- or AmpC-producing Escherichia coli from an Indian urban aquatic environment and their public health implications

Abstract

Quinolone and β-lactam antibiotics constitute major mainstay of treatment against infections caused by pathogenic Escherichia coli. Presence of E. coli strains expressing co-resistance to both these antibiotic classes in urban aquatic environments which are consistently being used for various anthropogenic activities represents a serious public health concern. From a heterogeneous collection of 61 E. coli strains isolated from the river Yamuna traversing through the National Capital Territory of Delhi (India), those harboring blaCTX-M-15 (n = 10) or blaCMY-42 (n = 2) were investigated for co-resistance to quinolones and the molecular mechanisms thereof. Resistance was primarily attributed to amino acid substitutions in the quinolone resistance-determining regions (QRDRs) of GyrA (S83L ± D87N) and ParC (S80I ± E84K). One of the E. coli strains, viz., IPE, also carried substitutions in GyrB and ParE at positions Ser492→Asn and Ser458→Ala, respectively. The phenotypically susceptible strains nevertheless carried plasmid-mediated quinolone resistance (PMQR) gene, viz., qnrS, which showed co-transfer to the recipient quinolone-sensitive E. coli J53 along with the genes encoding β-lactamases and led to increase in minimal inhibitory concentrations of quinolone antibiotics. To the best of our knowledge, this represents first report of molecular characterization of quinolone co-resistance in E. coli harboring genes for ESBLs or AmpC β-lactamases from a natural aquatic environment of India. The study warrants true appreciation of the potential of urban aquatic environments in the emergence and spread of multi-drug resistance and underscores the need to characterize resistance genetic elements vis-à-vis their public health implications, irrespective of apparent phenotypic resistance.

Escherichia coli β-Lactamases: What Really Matters

“…Such global dissemination of the CTX-M type ESBLs has primarily been attributed to the extremely mobilizable genetic platforms which harbor bla CTX-M genes ( Cantón et al, 2012 ), association of these platforms with E. coli genotypes showing clonal dissemination ( Coque et al, 2008 ; Nicolas-Chanoine et al, 2008 ; Woodford et al, 2011 ), and frequent co-existence of bla CTX-M with genes conferring resistance to other classes of antibiotics like fluoroquinolones and aminoglycosides leading to high rates of co-selection ( Cantón and Ruiz-Garbajosa, 2011 ; Bajaj et al, 2015 ). Analysis of the genetic environments of bla CTX-M genes has revealed that the promoter sequence present in the upstream region significantly affects gene expression as well as its dissemination (summarized in Table 1 ).…”

Antimicrobial Resistance Patterns of Extended Spectrum Β-Lactamase Producing Klebsiellae and E. coli Isolates from a Tertiary Hospital in Ghana

“…Ciprofloxacin resistance was 29.5% in ESBL positive and 4.7% in ESBL-negative isolates and this difference was significant (p= <0.01), an indication that ciprofloxacin resistance in the isolates was closely associated with ESBLs (Shaikh et al, 2015). Common co-resistance has been found in ESBL-producing organisms to aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and sulfamethoxazole-trimethoprim (Bajaj et al, 2016). This is a demonstration of the emergence of epidemic clones harbouring several beta-lactamases simultaneously (Bla CTX-M , Bla SHV and Bla TEM ) and perhaps of other mechanisms of resistance.…”

Biodegradation of Antibiotics: The Balance Between Good and Bad

“…In addition, some studies point to the idea that ARGs involved in the expression of aminoglycoside-modifying and β-lactamase enzymes were present in the environment long before the use manmade antibiotics in a therapeutic scope [47,48,49] showed that βlactamase family shared a common origin with enzymes involved in cell wall biosynthesis. In spite of using the antibiotics and their presence in the environment, bacteria resistant to β-lactams are thriving and there are a constant presence in more and more countries [50,51,52]. The same emerging resistance pattern it is also observed for bacteria producing carbapenemase [53,54,55].…”