Antibiotic Resistance in Extra Intestinal Pathogenic Escherichia Coli

In recent years, extra intestinal E. coli infection and a high level of drug resistance among such ExPEC is often seen in the World. The treatment of E. coli infections is increasingly becoming difficult because of the multi-drug resistance exhibited by the organism. As multidrug resistance has spread, we are already coming across infections that cannot be cured with any available antibiotics. Extended spectrum β-lactamase (ESBL) producing E. coli has spread as a major cause of hospital-acquired infections, as well as infections in outpatient settings [1]. Genes that encode ESBLs are often found on large plasmids that also carry genes for resistance to other antibiotics [2]. Beginning in the 1990s, the frequency of resistance to fluoroquinolone antibiotics, including ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin, and nalidixic acid in E. coli has increased worldwide [3]. Administration of ciprofloxacin or other fluoroquinolones is a risk factor for isolation of resistant strains of E. coli from patients undergoing long-term hospital care, and resistance is associated with treatment failure. In addition, multi-resistance, defined as resistance to norfloxacin in addition to two or three other antibiotics, has also increased [3,4]. Several reports have indicated that quinolone resistance in uropathogenic E. coli is associated with decreased prevalence or expression of virulence factors compared to quinolonesusceptible strains [5,6]. Vila suggested that a possible reason for this is that virulence genes could be lost concomitant with a mutation at codon 83 of the gyrA gene, which affects super coiling of DNA, leading to changes in gene expression. Another reason is that with exposure to quinolones and development of resistance to these agents, there is a concomitant increase in the deletion and transposition of pathogenicity islands (PAIs) [7]. Soto et al. [6] found that uropathogenic E. coli strains incubated with sub inhibitory concentrations of ciprofloxacin showed partial or total loss of virulence genes encoded within PAIs [6].