**1. Introduction**

*Escherichia coli* inhabits and adapts to different hosts, a quest that resulted in the acquisition and loss of genes, which further drive diversity in this bacterium and contribute to the evolution of harmless strains to pathogenic lifestyles [1]. While *E. coli* is an integral part of the microbiota of different hosts, it can also cause severe infections in humans and animals [2, 3]. A subgroup of *E. coli* that are pathogenic can cause a broad range of human diseases due to evolution that resulted in the development of patho-features enabling it to adapt and survive in different environments. These environments range from the gastrointestinal tract to extraintestinal sites such as the urinary tract, or meninges, [4] in addition to fecal contamination of food that could cause enteric infection resulting from food poisoning or contamination [5]. Based on the type of infection they cause, pathogenic *E. coli* are divided into intestinal or diarrheagenic *E. coli* (DEC) that cause diarrheal illness and extraintestinal *E. coli* (ExPEC) that are implicated in infections such as urinary tract infections [3]. Diarrheal illness constitutes a public health burden and

is a leading cause of mortality worldwide, causing >300 million illnesses and about 200,000 deaths annually, particularly in children in developing countries, including sub-Saharan and Southeast Asian countries (**Figure 1**) [6, 7].

The treatment of *E. coli* associated illness is toppled by its growing resistance to antibiotics, culminated by either the acquisition of resistance determinants or mutations that encodes for low uptake and tolerance to a higher concentration of the antimicrobials. Hence, *E. coli* could serve as a major reservoir of resistance genes not only for other *E. coli* strains but also for Enterobacteriaceae [8]. In addition, virulence determinants and genes that are associated with stringent response in nutrient low environments could also be acquired, thereby contributing to the survival and persistence of this bacterium in its environment [9]. Transmission of these antibiotic-resistant or pathogenic *E. coli* strains between different hosts, particularly in animals and humans could be through several routes such as direct contact with fecal-contaminated samples or other secretions from animals, or via the consumption of contaminated food [5].

Assessing the antimicrobial resistance, virulence, and transmission dynamics of *E. coli* requires characterization of this bacterium. A widely accepted classic method for characterizing *E. coli* is the serotyping technique that is based on the Kauffman classification scheme, where the O (somatic) polysaccharides and H (flagellar) surface antigens are determined [10, 11]. Other methods of typing and assessing the genetic relatedness and detecting outbreaks of *E. coli* strains are pulsed-field gel electrophoresis (PFGE) [12], multilocus enzyme electrophoresis (MLEE) [13], multilocus variable-number tandem repeat analysis (MVLA) [14], or multilocus sequence typing (MLST) [15]. These methods have proven to be effective in the epidemiological investigation of pathogenic *E. coli* [16] and the assessment of the emergence and dissemination of multidrug-resistant clones. However, none of these methods can accurately define the evolutionary relationships between *E. coli* strains, hence the need for a tool with a higher resolution. The advent of whole-genome sequencing (WGS) technologies has greatly enhanced not only the epidemiological investigation of outbreaks and the global spread of multidrug resistant and pathogenic clones of *E. coli* [17], but also our understanding of the physiology and evolutionary history of how some pathogenic strains evolve from commensal *E.coli* strains.

#### **Figure 1.**

*Global mortality rate from diarrhea in children under 5 years in 2016. Data represent the analysis of diarrhea burden in 195 countries in 1990–2016, showing the regions most affected by the illness. Reprinted from Troeger et al. [6] which was published under Creative Commons License.*

*The Biology and the Evolutionary Dynamics of Diarrheagenic* Escherichia coli *Pathotypes DOI: http://dx.doi.org/10.5772/intechopen.101567*

Based on clinical manifestation, presence of specific virulence determinants and phylogenetic profiles, diarrheagenic *E. coli* are categorized into six main pathotypes namely, enterotoxigenic *E. coli* (ETEC), enterohaemorrhagic *E. coli* (EHEC) or Shiga toxin-producing *E. coli* (STEC), enteropathogenic *E. coli* (EPEC), enteroaggregative *E. coli* (EAEC), entero-invasive *E. coli* (EIEC), and diffusely adherent *E. coli* (DAEC) [3, 7]. This chapter provides a snapshot of the biology of *E. coli* by focusing on the resistome, virulome, as well as the population structure of diarrheagenic *E. coli* pathotypes.
