Escherichia coli, a facultatively anaerobic gram-negative bacillus, is a major component of the normal intestinal flora and is ubiquitous in the human environment. First described in 1885, E coli has become recognized as both a harmless commensal and a versatile pathogen.
In contrast to the essential and beneficial role of most E coli isolates in the human intestine, pathogenic E coli are responsible for a broad spectrum of human disease. E coli has emerged as an important cause of diarrheal illness, with diverse phenotypes and pathogenic mechanisms. Hemolytic-uremic syndrome (HUS) is a potentially devastating consequence of enteric infection with specific E coli strains. E coli is also a commonly identified cause of urinary tract infections (UTIs), as well as neonatal sepsis and meningitis.
Uropathogenic E coli (UPEC) has the ability to colonize the uroepithelium by means of surface fimbriae. Although only partially understood, UPEC has been suggested to cause either direct cellular damage or direct invasion of the renal epithelial cells. 
Five pathotypes have of diarrheagenic E coli have been recognized; each pathotype has a distinct pathogenesis. The pathotypes are as follows:
Enterotoxigenic E coli (ETEC)
Enterohemorrhagic E coli (EHEC)
Enteropathogenic E coli (EPEC)
Enteroinvasive E coli (EIEC)
Enteroaggregative E coli (EAEC)
ETEC adheres to the small bowel mucosa by means of several different fimbrial colonization factor antigens (CFAs). Once colonization is achieved, one or both of the enterotoxins are released (ie, heat labile toxin [LT] and heat stable toxin [ST]). These toxins draw fluid and electrolytes from the small bowel mucosa. ST is reportedly the more virulent of the toxins.  LTs are closely related in structure and function to the enterotoxin expressed by Vibrio cholerae. Immunity develops to ETEC surface antigens, confining most disease to immunologically naïve travelers and weaning infants.
EHEC, also known as Shiga-toxin producing E coli (STEC), induces an attaching and effacing (AE) lesion in the large bowel. Once established in the colon, EHEC releases one or more toxins known as Shiga-like toxin (Stx). Stx is related to the Shiga toxin of Shigella dysenteriae and is cytotoxic to the vascular endothelium. The systemic circulation of Stx accounts for the potential development of HUS but is not required for EHEC hemorrhagic colitis to occur. E coli O157:H7 is the most virulent of the EHEC. [2, 1]
HUS consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. HUS typically develops in the second week of illness (range, 2-14 d), often after the diarrhea has resolved. Patients present with pallor, weakness, irritability, and oliguria or anuria.
EPEC also produce AE lesions; however, it does so in the absence of Shiga toxin production. The pathogenesis includes colonization of the small intestine, followed by the formation of AE lesions and a subsequent net secretory state. [2, 1]
The pathogenesis of EIEC mimics that of the Shigella species. The EIEC invades the large bowel epithelial cells, producing secretogenic enterotoxins and subsequent colonic epithelial cell death. These enterotoxins are typically lactose nonfermenting and are responsible for the local colonic inflammatory response. [2, 1] Invasiveness derives from a virulence plasmid closely related to that possessed by Shigella species.
EAEC adheres to the small and large bowel by means of aggregative adherence fimbriae (AAFs), and colonization ensues. This colonization produces enterotoxins and cytotoxins, which, in turn, damages the intestinal mucosa. [2, 1]
Systemic infections caused by E coli are frequently seen in neonates either by means of vertical or horizontal transmission. The characteristic serotype of this pathogenic E coli displays the K1 antigen, which is responsible for 40% of the cases of bacteremia and 80% of the cases of meningitis caused by E coli.  The virulent activity of the K1 antigen reduces the ability of the host to develop an antibody specific response and to activate the alternative complement system. In addition, S fimbriae have been associated with many of the E coli of patients with CNS infections. S fimbriae enhance the ability of E coli to adhere to vascular epithelium as well as the spread of the bacterium within the CNS. 
Statistics on pathogenic E coli strains reflect increasing recognition and surveillance over the past 2 decades. According to the Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Disease Control and Prevention (CDC) Emerging Infections Program, in 2007, the incidence of Shiga-toxin–producing Ecoli (O157) was 1.20 cases per 100,000 population, and the incidence of Shiga-toxin–producing E coli (non-O157) was 0.57 cases per 100,000 population). Since the beginning of surveillance in 1996, the incidence of Shiga-toxin–producing E coli (O157) has decreased 25%. 
Many strains of diarrheagenic E coli primarily affect developing nations due to inadequate sanitary conditions. Statistics on the prevalence of the strains vary by location and surveillance activity. Worldwide, enterotoxigenic E coli are estimated to cause more than 600 million cases of diarrhea annually and 700,000 deaths in children younger than 5 years.
ETEC is the most common enteropathogen in developing countries, accounting for approximately 210 million diarrhea episodes and approximately 380,000 deaths. [4, 5] Traveler’s diarrhea is primarily caused by ETEC; thus, persons traveling to endemic areas regularly import the pathogen to the developed world. [6, 7, 8, 9, 10]
The outbreak of gastroenteritis and hemolytic uremic syndrome caused by Shiga-toxin–producing E coli in Germany in May, June, and July, 2011 was linked to the consumption of sprouts.  Reported were 3816 cases, which included 54 deaths; 22% involved hemolytic uremic syndrome, which occurred predominantly in female adults. 
Several E coli pathotypes have been implicated in chronic diarrhea among severely immunocompromised patients (eg, patients with human immunodeficiency virus [HIV]). [13, 14, 15] ETEC causes more dehydrating diarrhea cases among infants in developing countries than any other pathotype. [16, 17]
People of any age can become infected. Very young individuals and the elderly are the most likely groups to become seriously ill and to develop HUS.
What would you like to print?