After ingestion of E. coli O157: H7, the bacteria bind to the intestinal mucosa and begin releasing Shiga toxin. The toxin, in turn, disrupts protein synthesis in the epithelial cells lining intestinal mucosa, leading to cell death, sloughing of the mucosa, and eventual bloody diarrhea.  Following exposure to the Shiga toxin, diarrhea, often the hemorrhagic variety, develops three days after exposure to the contaminated food specimen. After three days of diarrheal symptoms, diarrhea will become bloody in approximately 90% of affected patients. Hemorrhagic diarrheal symptoms will often resolve after seven days, with 85% of patients having a spontaneous resolution; the remainder 15%, often children, will develop systemic manifestations, most often HUS. Chronic colonization with the post-symptomatic shedding of E. coli O157: H7 may continue to occur, leading to a persistent risk of transmission and re-infection.

Patients will classically present with acute onset of bloody diarrhea and abdominal cramping, usually without fever. Diarrhea initially may not be bloody, often being watery in consistency. Most patients will not manifest a temperature during the initial presentation and evaluation. As a result of nausea, vomiting, and profuse diarrhea, patients will often note dehydration, asthenia, and decreased urine output. Patient history should include assessment of risk factors including (1) consumption of raw or undercooked meats or dairy products, especially unpasteurized milk, (2) exposure to ruminant animals or petting zoos, and (3) exposure to other farm scenarios.

Abdominal tenderness on physical examination reflects E. coli 0157: H7 Shiga toxin-induced intestinal vasculitis and inflammation. The abdominal discomfort from enterohemorrhagic E. coli generally manifests more severely than other forms of enteritis as a result of the hemorrhagic vasculitis. Systemic signs of dehydration such as dry mucous membranes, tachycardia, decreased skin turgor, slow capillary refill, cold extremities, and delirium, presage worsened morbidity, particularly in children.

Initial laboratory evaluation should include a complete blood count to rule out leukocytosis, hemolysis, and thrombocytopenia. A complete metabolic profile will aid in ruling out dehydration, electrolyte disturbance, and uremia. The majority of patients with E. coli 0157:H7 colitis will have a leukocytosis above 10,000/microL. Initial diagnosis of E. coli O157: H7 utilizes the stool culture of a diarrheal sample within the first days after onset. Most cultures positive for E. coli 0157:H7 will come from patients complaining of hemorrhagic diarrhea or grossly bloody diarrheal samples. Despite the Centers for Disease Control and Prevention recommendation that all diarrheal samples submitted for culture undergo screening for E. coli O157: H7, many laboratories will not routinely screen for this organism necessitating the clinician to request testing for E. coli 0157:H7 specifically. Culture the diarrheal specimen with sorbitol MacConkey agar, which allows for differentiation of non-pathogenic E. coli from pathogenic E. coli O157 based on the latter’s inability to metabolize sorbitol. Diagnostic confirmation utilizes testing for the presence of E. coli O157: H7 antigens in the stool or toxin genes with polymerase chain reaction. Commercially available enzyme-linked immunosorbent assays can detect Shiga toxins in hemorrhagic stool samples.[8][9][10]

Treatment of E. coli 0157: H7 gastrointestinal infection focuses on supportive care and maintenance of hydration status. Most enterohemorrhagic E. coli diarrheal patients recover without treatment within ten days other than fluid replacement. Antibiotic therapy has not had a beneficial effect in speeding resolution or preventing complications from E. coli 0157: H7; additionally, evidence exists that antibiotics worsen outcomes by increasing the likelihood of development of HUS, possibly secondary to antibiotic-induced lysis of infectious organisms with the sudden release of Shiga toxin into the systemic circulation. Patients with severe manifestations of HUS may benefit from hemodialysis to treat volume, electrolyte, and uremia issues related to acute renal failure. Limited data suggest that the monoclonal antibody eculizumab may expedite recovery from E. coli 0157: H7 HUS. Eculizumab acts by inhibiting the complement cascade, thereby interfering with the recruitment of inflammatory cells and attenuating damage to the renal vasculature. Notably, eculizumab, an extremely expensive pharmaceutical with a primary indication for treatment of paroxysmal nocturnal hematuria, lacks clinical consensus for the treatment of E. coli O157 associated HUS and typically gets utilized as a rescue agent in the sickest patients. Antiperistaltic agents, such as loperamide or dicyclomine, slow intestinal motility, and increase the risk of systemic complications; clinicians should avoid their utilization in this setting.[4][11]

The differentiation of E. coli O157: H7 from other invasive intestinal bacterial pathogens inducing hemorrhagic dysenteries such as Salmonella, Shigella, Campylobacter, Yersinia, and C. difficile has a meaningful clinical impact in that antibiotic therapy often aids in recovery from these other pathogens. Noninfectious etiologies of hemorrhagic diarrhea such as ischemic colitis, mesenteric ischemia, Crohn disease, and ulcerative colitis merit consideration as well.

Enterohemorrhagic E. coli colitis has a good prognosis for recovery when patients do not have systemic manifestations of diarrheal illness. HUS complicates up to 10% of E. coli 0157:H7 cases, with higher risk reported for younger children, especially those under 5 years old. When patients develop HUS complications, the risk of mortality approaches 5%.

Although most with enterohemorrhagic diarrhea-associated HUS recover from the acute illness episode, these patients have the potential for persistent, long-term renal dysfunction and extrarenal complications, including seizures, diabetes, chronic colitis, and hypertension. HUS, the most frequent, severe complication of E. coli O157: H7 colitis, occurs most commonly in children, especially young children less than 5 years old, and in the elderly. HUS manifests 5 to 10 days following the onset of hemorrhagic diarrhea and presents with the triad: hemolytic anemia, acute kidney failure, and thrombocytopenia. Approximately 10% of children with an E. coli O157: H7 infection will develop HUS, which carries an annual 5% mortality rate, and those who survive have an increased risk for developing chronic kidney disease. Shiga toxin enterohemorrhagic-induced HUS in the elderly causes significant morbidity and mortality. E. coli 0157:H7 infections result in healthcare costs in the United States of over US$ 400 million annually. As 10% of E. coli 0157:H7 hemorrhagic colitis cases progress to HUS with worsened prognosis, prevention of Shiga toxin enterohemorrhagic infections would improve health outcomes and reduce healthcare expenditures.

Nephrology consultation has merit if patients develop HUS, as up to 50% require hemodialysis if acute renal impairment occurs. Gastroenterology or infectious disease consultations may also provide expert guidance, especially in the initial diagnostic evaluation patient care phase, when trying to differentiate E. coli O157: H7 from other infectious, inflammatory, or ischemic etiologies of bloody diarrhea.

Potential means of preventing HUS include minimizing fecal Shiga toxin enterohemorrhagic shedding in animals and transmission of infection to humans. Public health measures to safeguard food and water from contamination remain essential in addition to personal hygiene and special care of food preparation and storage. Preventing the spread of E. coli 0157:H7 hemorrhagic colitis includes isolation of potentially infectious contacts in school or within institutions to minimize infectious transmission. Ample evidence suggests that personal hygiene, particularly handwashing, effectively prevents infectious acquisition and spread of E. coli 0157:H7 infections in the community, thereby altering the risk of HUS. Public health education, guidelines, and legislation to safeguard food and water against Shiga toxin enterohemorrhagic E. coli food and water contamination and to ensure safe food production, preparation, and storage of food will benefit society as a whole.  Research investigating altering bovine intestinal conditions with different feeds as a means of reducing fecal E. coli 0157:H7 shedding has demonstrated that cattle fed hay rather than grain for a brief period before slaughter has reduced fecal shedding of pathogenic E. coli. Developing a human vaccine to prevent enterohemorrhagic E. coli infection may eventually provide herd immunity, protect against HUS, and provide value in low-income, high-risk dysentery settings.

The management of E Coli 015: H7 infection is by an interprofessional team that includes an emergency department physician, an infectious disease consultant, a nephrologist, an internist. The majority of patients are treated with supportive measures that include hydration. Antibiotics are not beneficial in most cases. However, patients with severe manifestations of HUS may benefit from hemodialysis to treat volume, electrolyte, and uremia issues related to acute renal failure. Limited data suggest that the monoclonal antibody eculizumab may expedite recovery from E. coli 0157: H7 HUS. The outcome in healthy patients is good, but in those patients with suppression of immunity, the prognosis is guarded. (Level V)