## 1 Introduction  
Sheep and other ruminants are regular carriers of commensal _Escherichia coli_; however, they may harbor some pathogenic _E. coli_ and cause either, diarrhea or extraintestal illness [1]. The relevance of these diarrheagenic _E. coli_ (DEC) isolates as causative agents of food-borne diseases (FBD) was recently studied in Latin America, although there is a lack of information in some countries regarding the main reservoirs and infection routes [2]. Animal products, like sheep and beef meat, are at risk of contamination by poor hygiene practices during the slaughtering process in the abattoirs, hence, the implementation of good production practices (GPP) and good manufacture practices (GMP) are essential to prevent bacterial contamination of carcasses and ensure food safety [3]. Sheep without diarrhea are usually asymptomatic carriers of zoonotic pathogens and reservoirs of DEC, which could enter the production line, especially in the critical control points [4]. The animals that arrive at the slaughterhouse are the principal focus of contamination towards drinking water and animal products, allowing the direct transmission of zoonotic microorganisms to the human population [5]. At least five _E. coli_ pathotypes are related to gastrointestinal illness in humans: Shigastoxin-producing _E. coli_ (STEC), enteropathogenic _E. coli_ (EPEC), enterotoxigenic _E. coli_ (ETEC), enteroinvasive _E. coli_ (EIEC), and enteroaggregative _E. coli_ (EAEC) [6]. These pathotypes are classified according to their virulence factors. The principal virulence factor of STEC is the production of a toxin that inhibits protein synthesis coded by _stx1_ and _stx2_ genes and their variants; moreover, other virulence factors like the intimin (encoded by _eae_ gene) or autoagglutinating adhesins can be found [7]. Shiga toxins are classified as _stx1_ and _stx2_. The _stx1_ toxins are a homogeneous group with three subtypes: _stx1a_, _stx1c_, and _stx1d_. On the other hand, _stx2_ toxins are more heterogeneous with a greater number of subtypes that include _stx2a_, _stx2b_, _stx2c_, _stx2d_, _stx2e_, _stx2f_ and _stx2g_, with _stx2c_ and _stx2d_ being the most strongly associated with hemolytic uremic syndrome (HUS). Other relevant virulence factors include the intimin (encoded by _eae_ gene), a plasmid-carried enterohaemolysin (encoded by _eltxA_ gene), and putative adhesins genes like _Tox B_, _sa_, _espC_, and _espP_[8, 9]. The presence or absence of the _eae_ gene in STEC strains allows classifying them into the typical virulent (t-STEC) or atypical strains of low virulence (a-STEC). STEC strains induce gastroenteritis and further complications such as HUS or hemorrhagic colitis (HC), which can lead to chronic kidney dysfunction, especially in infants and the elderly [6]. EPEC produces the attachment and effacing (A/E) lesions onto intestinal mucosa. This pathotype is divided into two categories based on the presence or absence of the bundle-forming pilus (_bfp_) gene; strains that contain this gene are classified as typical (t-EPEC), while the ones that lack this gene are atypical (a-EPEC). Curiously, the a-EPEC strains are more common in developing countries; in contrast, t-EPEC causes diarrhea in children from developed countries [10]. The main feature of ETEC is the production of two enterotoxins: the heat labile-toxin (LT) and the heat-stable toxin (ST). The ETEC strains are the leading cause of traveler's diarrhea and also related to children's diarrhea [11]. The EIEC group and _Shigella_ spp. are biochemically and genetically related. The pathogenicity mechanism is through the invasion of the colon's epithelium; several involved proteins like Ipa and others are encoded in the 140 MDa plasmid _plnv_. Generally, watery diarrhea is observed, but in some cases, inflammatory colitis can occur [12]. Finally, EAEC strains are characterized by aggregative adherence (AA) to Hep-2 cells, wherein bacteria are seen in stacked brick aggregates attaching to cells.