**3. Shiga toxin-producing** *E. coli* **(STEC)**

#### **3.1 An overview of STEC**

Shiga toxin-producing *E. coli* (STEC), also known as verocytotoxin-producing *E. coli* (VTEC) was first identified as a pathogen in 1982 and is defined by the presence of Shiga toxin genes (*stx1* and *stx2*) that are known to be encoded on lambdoid prophages [52]. STEC had since emerged as a major enteric foodborne and zoonotic pathogen causing gastroenteritis and enterocolitis. STEC-related infection could progress to hemolytic-uremic syndrome (HUS) that in some cases could be fatal or result in renal failure in children (**Table 1**) [3]. Enterohemorrhagic *E. coli* (EHEC) is associated with hemorrhagic colitis which makes it a subset of STEC pathotype [3, 53]. STEC causes more than one million cases annually with about 30% of such

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

cases found in the United States [54]. According to Blanco et al. [55], 435 STEC serotypes strains have been identified but only a few are frequently associated with human infection among which are O26, O45, O103, O111, O121, O145, and O157 [56, 57]. STEC O157:H7 has been widely studied most likely because it is frequently implicated in STEC foodborne outbreaks. Although a series of outbreaks that are mostly caused by STEC O157:H7 have been reported globally in developed and developing countries, some are believed to go undetected or underreported [54, 58].

The main reservoir for STEC strains causing infection in humans are known to be ruminant food production animals including cattle, sheep, and goats. These animals are asymptomatic carriers and shedders as the vascular receptor that facilitate the transportation of the Shiga toxins to organs are absent. This *E. coli* pathotype is also common in the gastrointestinal tracts of poultry, pigs as well as some companion animals such as dogs and cats [59]. Other STEC asymptomatic carriers have been reported in other ruminant and monogastric animals, as well as in insects, suggesting their roles in the food contamination, dissemination, and transmission of different strains of this pathotype to humans (**Figure 2**) [59, 60]. Since STEC is part of the intestinal flora of food-production animals and is readily shed through feces, direct contact with contaminated environmental matrices and/or the consumption of contaminated products including undercooked meat, unpasteurized dairy products, vegetables, and/or water are a potential route of transmission of different strains of this pathotype to humans [61, 62]. STEC transmission due to direct contact with infected person or animals or their environments or products has been documented [63].
