**1. Introduction**

Since its identification in 1885, *Escherichia coli* (*E. coli*) has become one of the most com‐ prehensively studied bacterial species. While *E. coli* is widely found in the environment and foods and is an important member of the commensal microbiota of mammals, some strains have evolved to include pathogenic mechanisms that cause significant diseases in humans and animals. In humans, *E. coli* strains can cause diverse enteric/diarrheagenic or extra‐intestinal infections by means of virulence factors that affect a wide range of cellular processes. Pathogenic *E. coli* associated with gastrointestinal illness have been divided into eight pathotypes based on their virulence profiles: (i) enteropathogenic *E. coli* (EPEC), (ii) enterohaemorrhagic *E. coli* (EHEC), (iii) enterotoxigenic *E. coli* (ETEC), (iv) enteroinvasive *E. coli* (EIEC), (v) enteroaggregative *E. coli* (EAEC), (vi) diffusely adherent *E. coli* (DAEC), (vii) adherent invasive *E. coli* (AIEC) and (viii) Shiga toxin‐producing enteroaggregative *E. coli* (STEAEC) [1]. This chapter will cover only two of them: ETEC and EHEC, which show opposite trends during their pathogenic processes. Even if in both cases human infections are primarily acquired through consumption of contaminated food products or drinking water, ETEC is a major cause of infantile diarrhea in developing countries, while EHEC is one of the main *E. coli* pathotypes associated with food poisoning outbreaks in the devel‐ oped world.

To cause human illness, pathogenic enteric *E. coli* must not only survive the passage through the human gastrointestinal (GI) tract but also accomplish their pathogenic process by a com‐ plex and coordinated multistage strategy, including adherence to the host intestine and toxin/ virulence protein production. The current chapter will provide a state of the art of ETEC and EHEC physiopathology, then focus on pathogen survival in the human digestive tract and regulation of virulence determinants by GI cues. As studies on humans are ethically incon‐ ceivable and small animal models do not recapitulate human pathogenesis, we will introduce the potential of dynamic *in vitro* digestion systems for increasing our understanding of ETEC and EHEC pathogenesis in a physiologically relevant GI environment.

ETEC cause approximately 280 million episodes of diarrhea worldwide, leading to hundreds of thousands of deaths per year [4]. With regard to EHEC, it is estimated that the pathogen is responsible for 2,801,000 acute illnesses, 3890 cases of haemolytic and uremic syndrome (HUS), 270 cases of permanent end‐stage renal disease, and 230 deaths worldwide [3]. For both pathogens, infants less than 5 years old are a high‐risk population. ETEC are respon‐ sible for 20–25% of diarrhea in young children, mostly in low‐income countries, and up to 40% of traveler's diarrhea [5]. In developing countries, children suffer from diarrhea attacks 7–8 times a year, with a peak incidence occurring between 6 and 18 months, and ETEC strains are responsible for one of each three attacks [6, 7]. In such countries, ETEC infections have then shown to play a significant part in the complex association between malnutrition and repeated bouts of diarrheal illness among young children. The impact of EHEC is also greater in infants and children, compared to other ages with 42% of cases of HUS and 29% of deaths

**Figure 1.** ETEC and EHEC pathogenesis including epidemiological data on the infections and at‐risk populations, reservoir, mode of transmission and virulence factors of the pathogen, and clinical signs are described. A/E: Attaching and effacing; CFTR: cystic fibrosis transmembrane regulator; GC‐C: guanylyl cyclase C; GM1: monosialoganglioside

Enterotoxigenic and Enterohemorrhagic *Escherichia coli*: Survival and Modulation of Virulence in the Human...

http://dx.doi.org/10.5772/intechopen.68309

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While the lack of ongoing monitoring systems makes it difficult to understand ETEC pathogenesis worldwide, dedicated surveillance systems of human EHEC infections have been developed in most of the industrialized areas of the world [8]. In Europe, the surveillance of EHEC infections is embedded in the Food and Waterborne Diseases and Zoonoses (FWD) surveillance system coor‐ dinated by the European Center for Disease Prevention and Control (ECDC). FWD is a passive surveillance system, collecting data on EHEC infections including laboratory‐confirmed cases, probable cases, and possible cases. Cases of HUS are specifically recorded through a network of pediatric nephrologists and infection‐control practitioners on the basis of clinical diagnosis.

occurring in children between the ages of 0 and 4 years [3].

receptor; LT: heat‐labile enterotoxins; ST: heat‐stable enterotoxins; Stx: Shiga toxin.
