**1. Introduction**

Increasing resistance to antimicrobial drugs is of major concern worldwide. For many developing countries, the possibility of having cheap antibiotics available may now be threatened. There are antimicrobial resistance issues with most pathogenic bacteria and in virtually all of the opportunistic bacterial-caused infections. This translates into increased healthcare costs. These costs include extended length of hospital stay and increased costs for medical supplies including more expensive antimicrobial drugs. In addition, antimicrobial drug-resistant infections lead to higher rates of mortality, especially in patients who had recent prior exposure to antibiotics [1].

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Antimicrobial drugs are classified into groups according to the type of antimicrobial activity. These groups include drugs that inhibit bacterial cell wall synthesis, depolarize the cell membrane, inhibit bacterial protein synthesis, inhibit bacterial nucleic acid synthesis, and inhibit bacterial metabolic pathways. The improper use of these drugs has helped to create resistant bacterial strains. Factors that contribute to resistance include the increased use of all antimicrobial drugs and improper antimicrobial prescribing. Many of the less expensive drugs that have fewer side effects have been used too commonly. Improper prescribing may be choosing broad spectrum or ineffective drugs [2–4].

**2.1. Diffusely adherent** *Escherichia coli* **(DAEC)**

**2.2. Enteroaggregative** *Escherichia coli* **(EAEC)**

which may also result in fluid secretion [16–18].

**2.3. Enterohemorrhagic** *Escherichia coli* **(EHEC)**

**2.4. Enteroinvasive** *Escherichia coli* **(EIEC)**

cause HUS [19–21].

These strains are sometimes referred to as enteroadherent *E. coli* (EAEC) (not to be confused with the enteroaggregative strains, which are sometimes referred to as EAggEC). While not known to cause severe diarrheal disease, the DAEC, which are probably a group of related strains, are thought to be responsible for some types of persistent diarrhea in infants. Whether they possess true virulence factors is still under debate, but these bacteria are able to bind to enterocytes (probably via adhesins such as Afa/Dr) and elicit a response in which the microvilli extend and wrap around the bacteria. Diarrhea in association with DAEC has also shown

Antimicrobial Mechanisms of *Escherichia coli*

http://dx.doi.org/10.5772/67363

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The EAEC strains were so named because of their tendency to adhere to enterocytes in dense clusters. The bacteria attach to the microvilli and also to other EAEC bacteria. The EAEC are also a heterogeneous group of strains with a similar pathogenesis, resulting in non-bloody diarrhea. Infection is established by adhering to the microvilli via fimbriae (the aggregative adherence fimbriae—AAF), inducing increased mucus production and biofilm formation, inducing an inflammatory response and production of toxins. The main toxins of the EAEC strains are the EAEC heat-stable enterotoxin (EAST1), which enters the enterocytes and activates guanine cyclase, resulting in increased levels of cGMP in the cell and loss of fluid into the intestinal lumen; the plasmid-encoded toxin (Pet), which disrupts the enterocyte cytoskeleton, resulting in cell detachment; and a *Shigella*-like enterotoxin (ShET1), a heat-stable toxin

The most publicized strain of pathogenic *E. coli* is the EHEC strain. EHEC serotype O157:H7 is well known as the causative agent of outbreaks of food-associated severe diarrhea. Infection with O157:H7 results in sever abdominal cramps and bloody diarrhea and may lead to hemolytic-uremic syndrome (HUS) which can be life-threatening. The most common foods associated with transmission of these bacteria are undercooked meat (especially ground beef), raw milk, and raw vegetables. The EHEC strains do not directly invade the enterocytes, but produce toxins that do enter and severely damage these cells. The responsible cytotoxins are verotoxins I and II (designated as Shiga toxins, Stx-1 and Stx-2). The Shiga toxins are capable of inactivating ribosomes, blocking protein synthesis, and emerging through the basolateral membrane into the subepithelial region. Stx-2 is seen most often in the EHEC strains that

In infections with EIEC, the bacteria invade by directly entering M cells. The bacteria pass through these cells and then are able to invade the enterocytes via the basolateral membrane, causing severe damage to the intestinal mucosa. The bacteria are also able

an ability to induce the production of inflammatory cytokines, such as IL-8 [13–15].

Many strains of *Escherichia coli* are not harmful. In fact, these commensal strains in the gut are necessary for the synthesis of vitamin K2 , which is an important clotting factor [5]. However, there are pathogenic strains, and these strains may become a larger threat if they possess or acquire certain antimicrobial mechanisms. The main ones of concern are the extended-spectrum β-lactamase (ESBL)-producing strains and the carbapenem-resistant Enterobacteriaceae (CRE) strains. The ESBL strains are resistant to most β-lactam drugs, and the CRE strains are resistant to most carbapenem drugs. Greatly increased healthcare costs are associated with the ESBL and CRE strains. Various studies have shown a hospital stay of up to twice as long and increased costs of 1.5–2.5 times as much [6–8]. One study in the United States estimated the increased costs to be \$16,450 per patient [6].

All of the pathogenic strains of *E. coli* are armed with the same types of potential virulence factors. These factors include a capsule (in some strains), flagella, the lipopolysaccharide (LPS) cell wall, fimbriae, outer membrane proteins (OMPs), a hemolysin, cytolysins, and siderophores. The specific types of some of these virulence factors plus the possession of other toxins and effectors may vary with each individual pathogenic strain [9].
