Antimicrobial Resistance inEscherichia coli

Abstract

Multidrug resistance in Escherichia coli has become a worrying issue that is increasingly observed in human but also in veterinary medicine worldwide. E. coli is intrinsically susceptible to almost all clinically relevant antimicrobial agents, but this bacterial species has a great capacity to accumulate resistance genes, mostly through horizontal gene transfer. The most problematic mechanisms in E. coli correspond to the acquisition of genes coding for extended-spectrum β-lactamases (conferring resistance to broad-spectrum cephalosporins), carbapenemases (conferring resistance to carbapenems), 16S rRNA methylases (conferring pan-resistance to aminoglycosides), plasmid-mediated quinolone resistance (PMQR) genes (conferring resistance to [fluoro]quinolones), and mcr genes (conferring resistance to polymyxins). Although the spread of carbapenemase genes has been mainly recognized in the human sector but poorly recognized in animals, colistin resistance in E. coli seems rather to be related to the use of colistin in veterinary medicine on a global scale. For the other resistance traits, their cross-transfer between the human and animal sectors still remains controversial even though genomic investigations indicate that extended-spectrum β-lactamase producers encountered in animals are distinct from those affecting humans. In addition, E. coli of animal origin often also show resistances to other-mostly older-antimicrobial agents, including tetracyclines, phenicols, sulfonamides, trimethoprim, and fosfomycin. Plasmids, especially multiresistance plasmids, but also other mobile genetic elements, such as transposons and gene cassettes in class 1 and class 2 integrons, seem to play a major role in the dissemination of resistance genes. Of note, coselection and persistence of resistances to critically important antimicrobial agents in human medicine also occurs through the massive use of antimicrobial agents in veterinary medicine, such as tetracyclines or sulfonamides, as long as all those determinants are located on the same genetic elements.

Population structure and antimicrobial resistance traits of avian‐origin mcr‐1 ‐positive Escherichia coli in Eastern China, 2015 to 2017

“…Antimicrobial resistance is one of the major global threats to public and animal health (Poirel et al, ). The emergence and rapid spread of MDR and XDR bacteria is causing public concerns around the world.…”

Extensive antimicrobial resistance and plasmid-carrying resistance genes in mcr-1-positive E. coli sampled in swine, in Guangxi, South China

“…The results were shown in Table 3 Interestingly, there is evidence that ESBL E. coli has a higher level of mcr-1 than non-ESBL E. coli, and the rapid rise in ESBL also significantly increases the selective pressure for colistin resistance [17]. In this study, 63.6% (21/33) of MCRPEC strains were detected to contain different ESBL genes E. coli is by nature sensitive to almost all clinically relevant antimicrobial agents, but this bacterium has a great capacity to accumulate resistance genes, mainly through horizontal gene transfer [36]. In this study, 11 plasmids carrying non-lactam genes were found in MCRPEC, including fluoroquinolone (qnrA, qnrB, qnrS, aac(6')-Ib-cr), tetracycline (tetA, tetB), sulfonamide (sul1, sul2), aminoglycoside (aadA), and chloramphenicol (floR), suggesting that the effect of MCRPEC on spreading non-β-lactam genes should not be underestimated.…”

Occurrence and Antibiogram of Extended-Spectrum Cephalosporin- and Cephamycin-Resistant Escherichia coli in Asymptomatic University Students

“…Therefore, finding the CTZ resistance without ESBL production in this study suggested selection of oxyiminocephalosporin (3GC) by other mechanisms of β-lactam resistance such as production of other β-lactamases, change in cell wall permeability, expression of active efflux pumps, gene mutations and/or alteration of penicillin binding protein receptors. 2,7,33 However, production of AmpC could be the mechanism by which the 6 FOXresistant isolates in this study preferred to CTZ since resistance to ESCs is mediated majorly by ESBL and/or AmpC which confers FOX resistance. 7,10,11,25 The finding of 30% FOX-resistant (putative AmpC-producers) E. coli in this study also calls for concern because AmpC-P enterobacteria are MDR as also observed in the current experiment.…”

“…Escherichia coli, a member of Enterobacterales is a natural inhabitant of the intestinal tract of humans and animals and thus found in various ecological niches such as soil, water, vegetables and so on. [1][2][3] Escherichia coli is a useful indicator organism for antimicrobial resistance surveillance (because it easily acquires and transfers resistance genes) and it is versatile, being facultatively pathogenic with the pathogenic variants associated with intestinal (enteritis) and extra-intestinal infections, including urinary tract infection, meningitis, peritonitis, and septicemia in humans. 1,2,4 Extendedspectrum cephalosporins (ESCs) which include the third (e.g., ceftazidime, cefpodoxime), fourth and fifth generation cephalosporins, and cephamycin (cefoxitin: FOX) are critically-important antibacterial agents of the highest priority in managing serious E. coli infections in humans and animals.…”

“…[1][2][3] Escherichia coli is a useful indicator organism for antimicrobial resistance surveillance (because it easily acquires and transfers resistance genes) and it is versatile, being facultatively pathogenic with the pathogenic variants associated with intestinal (enteritis) and extra-intestinal infections, including urinary tract infection, meningitis, peritonitis, and septicemia in humans. 1,2,4 Extendedspectrum cephalosporins (ESCs) which include the third (e.g., ceftazidime, cefpodoxime), fourth and fifth generation cephalosporins, and cephamycin (cefoxitin: FOX) are critically-important antibacterial agents of the highest priority in managing serious E. coli infections in humans and animals. [5][6][7] In Enterobacterales, extendedspectrum β-lactamases (ESBL) inhibited by clavulanic acid and Ampicillinase C (AmpC) which is not inhibited by clavulanic acid mediate resistance to ESCs, but cephamycin (FOX) resistance is conferred only by AmpC.…”