**2. AMR trends**

Capability of bacterial species to resist the action of a particular antimicrobial agent is referred to as antimicrobial resistance, and this phenomenon has been remarkably proliferated over the years**.** The availability and usage of antimicrobial have contributed in the increased incidence of resistant strains [9]. Though antimicrobial resistance is a natural phenomenon and was considered under control in the past but recently it is envisaged a high-level risk for world health [10]. Mainly three reasons responsible for antimicrobial resistance are; (a) increase usage of antibiotics, (b) due to unseriousness of the patients about treatments being suggested, (c) replacement of the existing class of antibiotics with a new one. Bacterial resistance to antimicrobial agents is classified into three types, namely intrinsic resistance, adopted resistance, and acquired resistance see in **Figure 1**.

The most common example of an intrinsic resistance system is the Acr AB/Tol C EPs in *E. coli*, which has a wide substrate specificity and can export antibiotics, detergents, dyes, and various disinfectants [11]. *E. coli*, Tol C has many efflux systems including the resistance-nodulation-division (RND) pumps as well as the main facilitator superfamily (MFS) systems [12]. RND pumps function as proton antiporters and confer resistance to tetracyclines, chloramphenicol, some β-lactams, vancomycin, and fluoroquinolones being supported by intrinsic resistance [13, 14]. While adopted

*Antimicrobial Resistance in* Escherichia coli *DOI: http://dx.doi.org/10.5772/intechopen.101583*

#### **Figure 1.**

*Three types of antimicrobial resistance transmission and virulence factors can be classified into 1. adaptive resistance, 2. intrinsic resistance, and 3. acquired resistance. The adaptive resistance includes, environmentally induced EG (encoded genes) as two phases of bacteria 1) PT represents (planktonic), and BF (biofilms) can induce physiological changes at the cellular level (CP represents cellular process), and cause (a) enhanced mutation levels, (b) modification in metabolic genes and processes of the regulation, (c) classic determinants and a host antibiotic inactivation. Where EF shows efflux, OT (overprotection at the target site), MT (modification at the target site), MT (mutation at the target), DA represents the degradation of antibiotics and II represents impaired influx. This type of resistance increased infections which can potentially be transferred between E. coli strains leading to acquired resistance. Acquired resistance is transmitted through HGT among bacteria.*

resistance contains environmentally induced genetic variations such as biofilm and persisted development, enzymatic driven inactivation of antibiotic see in **Figure 1** [15]. Due to adopted resistance, *E. coli* revealed resistance toward aminoglycoside encoded by *arm-A*, *npm-A*, *rmt-A*, *rmt-B*, *rmt-C*, and *rmt-D* resistant genes [16, 17]. The *rmt* gene provides resistance to gentamicin and amikacin, while *npm-A* provides resistance to gentamicin, neomycin, amikacin, and apramycin. While the most common ESBL gene in *E. coli* isolates of human origin is *blaCTX-M-15* and ST-131 clone and are mainly involved in dissemination AMR [18]. Similarly, the acquired resistance is usually influenced by HGT and may include plasmid-encoded specific EPs and enzymes that alter antibiotics [19, 20]. The increase in carbapenems (CPE) is mainly associated with the extensive dissemination of acquired CPE. CPE encoding genes are usually located in mobile genetic elements (MGEs), implying in the emergence of MDR and XDR strains [21]. Furthermore, colistin believes as a choice of drug for the treatment of resistant pathogens its resistance is facilitated through variations in lipopolysaccharides (LPS). *E. coli* the first pathogen in which plasmid-mediated colistin resistance was observed, through the acquisition of the *MCR-1* gene [6] The *MCR-1* gene could swiftly propagate and can impart resistance to other strains. *MCR-1* protein expression leads to the addition of a phosphor-ethanolamine group to lipid A. This produces a change in the charge of LPS, which in turn reduces the affinity of


**Table 1.**

*Antimicrobial resistance, MGEs, and their associated virulence factors.*

#### Escherichia coli *- Old and New Insights*

*Antimicrobial Resistance in* Escherichia coli *DOI: http://dx.doi.org/10.5772/intechopen.101583*

colistin for LPS [22]. Resistance to colistin can be due to mutations in chromosomal genes or it may be acquired. Furthermore, quinolones and fluoroquinolones are important antimicrobial agents implied for treating pathogenic microbes associated with humans and animals. Resistance to these antimicrobial agents is generally due to mutations in the drug targets, namely, DNA gyrase and topoisomerase IV genes seen in **Table 1** [30]. All such changes will lead to the transfer of resistance genes from chromosomal DNA into a plasmid, which will have more chances of dissemination in the human population. Additionally, it will be prone more harmful to human health due to variation in their resistance determinant transfer like from chromosome into plasmid, will definitely bring variation in expression pattern and dispersal [28, 31]. Another well-documented example is a transfer of the chromosomal β-lactamase gene *Amp C* to a plasmid and their subsequent global dissemination see in **Table 1** [28].
