Shiga toxin-producing Escherichia coli: Treatment and prevention

INTRODUCTION — 

Escherichia coli that contain genes encoding Shiga toxins 1 and/or 2 are important human pathogens; these are referred to as Shiga toxin-producing Escherichia coli (STEC). Some strains, such as E. coli O157:H7, cause severe disease including painful bloody diarrhea, as well as hemolytic uremic syndrome (HUS) in some cases.

The treatment and prevention of STEC infections are discussed here, focusing on the diarrheal phase of illness and management to reduce the likelihood of adverse outcomes. The epidemiology, microbiology, clinical manifestations, and the many considerations in the diagnosis of STEC infections are discussed separately. (See "Shiga toxin-producing Escherichia coli: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Issues related to STEC-associated HUS in children are discussed separately. (See "Overview of hemolytic uremic syndrome in children" and "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children" and "Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children".)

Issues related to STEC-associated HUS in adults are discussed separately. (See "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy (TMA)" and "Thrombotic microangiopathies (TMAs) with acute kidney injury (AKI) in adults: CM-TMA and ST-HUS".)

MANAGEMENT OF CHILDREN — 

Management of infection due to high-risk Shiga toxin-producing Escherichia coli (STEC; ie, all E. coli O157:H7 and any non-O157 STEC containing a gene encoding Shiga toxin 2) focuses on reducing the likelihood of developing hemolytic uremic syndrome (HUS), by careful fluid management and close monitoring for evidence of microangiopathy.

Site of care — Ideally, patients with known or suspected STEC infection (acute onset of bloody diarrhea and abdominal pain, or acute onset of nonbloody diarrhea with known exposure to a patient with STEC) (figure 1) should be managed in a setting where they can receive close laboratory monitoring and attention to volume status (algorithm 1).

●Inpatient management - Inpatient management is warranted in the following circumstances:

•Patients who appear dehydrated (table 1), are vomiting, or have severe abdominal pain.

Findings suggestive of dehydration include dry mucous membranes, persistent tachycardia after a bolus of isotonic crystalloid, and/or elevated hematocrit (early in illness).

•Patients with laboratory tests demonstrating evidence of emerging microangiopathy, especially progressive thrombocytopenia, hemolysis, or persistent azotemia after volume expansion.

•Patients who cannot be reassessed readily as outpatients with daily laboratory tests (complete blood count [CBC], chemistries) and physical examination.

●Outpatient management - Outpatient management with oral rehydration therapy is reasonable for patients who are well hydrated, not vomiting, do not have severe abdominal pain, do not have evidence of microangiopathy (thrombocytopenia or hemolysis) or renal injury, and can be reassessed daily with repeat laboratory tests (CBC, chemistries) and physical examination – with feasibility to hospitalize if there is clinical or laboratory deterioration. (see "Oral rehydration therapy"):

●Monitored fluid management not required - Monitored fluid management is not required in the following circumstances:

•Patients with STEC infection who present on or after day 10 of illness; in such cases, monitoring is not necessary if there is no evidence of HUS and diarrhea is improving or has resolved.

•Patients with rapid resolution of bloody diarrhea (eg, within a few hours of presentation); in such cases, the risk of STEC infection is low, since bacterial diarrhea does not typically improve so rapidly. In such patients, intensive monitoring might reasonably be discontinued early.

Initial volume resuscitation — For children with known or suspected high-risk STEC, initial management consists of restoring the circulating fluid deficit.

●Intravenous access - For children receiving parenteral fluid, a peripheral intravenous (IV) catheter is usually sufficient. In some cases a peripherally inserted central catheter (PICC) can forestall access challenges due to peripheral edema. We discourage phlebotomy from the antecubital vein in the event it needs to be used for a PICC line.

●Estimating the volume deficit - The extent of volume deficit can be difficult to estimate. If possible, we compare the patient's weight to prior baseline; if this is not possible, signs of dehydration can be used as treatment targets to restore volume. For example, if there is hemoconcentration, adequacy of volume restoration could be demonstrated by a decrease in the hematocrit. If there is tachycardia, effective volume restoration would reduce the heart rate. If the creatinine is mildly elevated on presentation, a bolus of fluids should reduce this value.

●Restoring volume - To restore volume, we administer boluses (20 mL/kg) of isotonic crystalloid (0.9 percent NaCl, Lactated Ringer, or other balanced salt solution) if we are confident the patient does not have central volume overload; in the first four days of illness, volume contraction is much more common than volume overload. (See 'Choice of intravenous fluid' below.)

●Monitoring - Children receiving fluid therapy require careful clinical and laboratory monitoring. (See 'Monitoring' below.)

Subsequent volume management

Selecting an approach — Once circulating volume has been restored, options for preserving intravascular volume include conservative fluid management (with a goal of achieving euvoleumia) or hyperhydration (with a goal of proactive volume expansion to reduce the risk of renal injury).

Whether one approach is superior to the other is uncertain and the subject of an ongoing clinical trial at 26 pediatric institutions (including the authors’). Health care providers who are associated with one of these sites (listed at clinicaltrials.gov, study NCT05219110) should follow the treatment protocols of the trial at their center [1].

Otherwise, the approach is at the discretion of the provider. However, we do not use hyperhydration for children younger than <9 months prior to microbiologic confirmation of STEC infection.

Conservative fluid management — Conservative fluid management consists of administering fluids with the goal of achieving euvolemia, once the circulating fluid deficit has been restored (see 'Initial volume resuscitation' above),

●Outpatients - Conservative fluid management for outpatients consists of maintenance fluid administered orally. (See "Oral rehydration therapy".)

●Inpatients - Conservative management for inpatients consists of intravenous fluid (isotonic crystalloid with 5 percent dextrose). (See 'Choice of intravenous fluid' below.)

•Calculating the maintenance fluid rate – The maintenance fluid rate is determined based on the Holliday-Segar formula (100 mL/kg/day for the first 10 kg of a patient's weight, 50 mL/kg/day for the next 10 kg of a patient's weight, and 20 mL/kg/day for each kg over 20 kg of a patient's weight) [2]. (See "Maintenance intravenous fluid therapy in children".)

•Modifying the infusion rate – In general, central volume overload (heart failure, pulmonary edema) is uncommon in the setting of conservative fluid management; manifestations include tachypnea and hypoxemia. In the setting of central volume overload, the fluid infusion rate should be reduced. (See "Prevention and management of acute kidney injury in children", section on 'Hypervolemia'.)

Guidance for discontinuation of fluids is discussed below. (See 'Discontinuing therapy' below.)

Management of children with STEC-related HUS is discussed separately. (See "Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children".)

Hyperhydration (anticipatory volume expansion)

●Definition and rationale – Hyperhydration consists of anticipatory intravascular volume expansion. This is a proactive approach to maintaining renal perfusion; it accounts for the usual maintenance fluid requirements (related to diarrheal losses and variable oral intake), as well anticipates the ongoing threat to intravascular volume by vascular leakage. This approach may reduce the risk of renal injury.

Hyperhydration is done in inpatient settings, once the estimated circulating deficit is restored. 

The need for hyperhydration should be evaluated daily. Hyperhydration should discontinued when there is evidence that the vascular injury is abating (ie, a rising platelet count) in patients who do not develop HUS, or once specific criteria for modifying the infusion rate are met.

●Drawbacks and contraindications – Potential drawbacks of hyperhydration include risk of volume overload, as well as the cost of hospitalization and monitoring for children with known or suspected high-risk STEC (most of whom do not develop HUS) [1].

We do not use hyperhydration for children younger than <9 months prior to microbiologic confirmation of STEC infection, because STEC infection is rare in this age group, and experience with this approach in such young children is limited.

●Supporting evidence – Use of hyperhydration (anticipatory volume expansion) for children with STEC infection is supported by the following evidence, derived from observational studies:

•In a meta-analysis of eight observational studies including 1511 children with STEC-associated HUS, IV fluid administration was associated with a decreased risk of renal replacement therapy (odds ratio [OR] 0.26, 95% CI 0.11-0.60); in addition, clinically dehydrated patients had an OR of death of 3.71 (95% CI, 1.25-11.03) [3]. Additional studies also suggest that volume expansion is beneficial [4-8].

•In two prospective cohort studies of children with HUS, volume expansion prior to onset of HUS was associated with lower rates of anuria [9,10]. As anuric HUS is categorically worse than non-anuric HUS [11-22], interventions that avert this outcome have merit if HUS develops.

•In studies of children who presented with established HUS, better outcomes have been observed among those managed with volume expansion than those managed with fluid restriction [8,23,24].

The rationale for conservative fluid management is discussed separately. (See "Maintenance intravenous fluid therapy in children".)

●Clinical approach - Our approach to hyperhydration (using isotonic crystalloid with 5 percent dextrose) is as follows:

•Calculating the hyperhydration fluid infusion rate – We administer two times the maintenance fluid rate, not to exceed 250 mL/hour. Calculation of the maintenance fluid rate is usually based on the Holliday-Segar formula, which defines maintenance volume as 100 mL/kg/day for the first 10 kg of a patient's weight, 50 mL/kg/day for the next 10 kg of a patient's weight, and 20 mL/kg/day for each kg over 20 kg of a patient's weight [2].

As an example, for a patient who weighs 23 kg, maintenance volume over 24 hours would be 1560 mL (1000 mL plus 500 mL plus 60 mL), or 65 mL/hour; the infusion rate for hyperhydration would be twice maintenance volume, or 3120 mL over 24 hours, or 130 mL/hour.

•Modifying the infusion rate – We reduce the infusion rate in the following circumstances:

-The hematocrit has fallen by 20 percent from baseline at outset of volume expansion, and the patient's weight exceeds 110 percent of the admission weight. We use this dual target since an isolated decline in hematocrit may be attributable to a microangiopathic process or other causes.

Once this dual target is met (in the absence of central volume overload), we reduce the fluid infusion rate to maintenance and continue laboratory monitoring for development of HUS (see 'Discontinuing therapy' below).

-There are signs of central volume overload (heart failure, pulmonary edema). Manifestations of central volume overload include as tachypnea and hypoxemia. In the setting of central volume overload, the fluid infusion rate should be reduced. (See "Prevention and management of acute kidney injury in children", section on 'Hypervolemia'.)

Guidance for discontinuation of fluids is discussed below. (See 'Discontinuing therapy' below.)

Management of children with STEC-related HUS is discussed separately. (See "Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children".)

Choice of intravenous fluid

●Fluid selection based on stage of clinical management

•For restoring the circulating fluid deficit, we administer isotonic crystalloid (0.9 percent NaCl or Lactated Ringer, or other balanced salt solution) as a bolus. (See 'Initial volume resuscitation' above.)

•For preserving intravascular volume, we administer isotonic crystalloid with 5 percent dextrose. (See 'Subsequent volume management' above.)

●Choice of isotonic crystalloid – We favor 0.9 percent NaCl or Lactated Ringer (or other balanced salt solution) over hypotonic fluid; the goal of parenteral volume expansion is to preserve kidney blood flow, which is better achieved with isotonic fluids.

•Normal serum sodium concentration – For patients with normal serum sodium concentration, we prefer a balanced salt solution (such as Lactated Ringer); vigorous volume expansion using 0.9 percent NaCl can contribute to hyperchloremic metabolic acidosis since chloride is the exclusive anion.

•Hyponatremia – For patients with hyponatremia, we prefer 0.9 percent NaCl; the sodium concentration of Lactated Ringer solution is considerably less than the sodium concentration in 0.9 percent NaCl (130 versus 154 mEq/L).

●Hypokalemia – Options for managing hypokalemia include infusing potassium chloride from a separate bag, collaborating with a pharmacist to increase the potassium concentration of the balanced salt solution, or using 0.9 percent NaCl with added potassium.

Monitoring — Tools for following the clinical trajectory of STEC infection include physical examination and laboratory tests.

Clinical monitoring — The following clinical parameters should be monitored at least daily [25]:

●Symptoms (diarrhea, vomiting, abdominal pain)

●Volume status (including heart rate, respiratory rate, and chest auscultation) (see "Prevention and management of acute kidney injury in children", section on 'Hypervolemia')

●Weight (if admitted)

●Intake (oral and intravenous) and output (urine and stool; if admitted)

Volume contraction in patients with STEC infection should not be attributed to fluid loss from diarrhea; STEC diarrhea is rarely voluminous.

Capillary leakage can occur, often in advance of azotemia, and even with a normal serum creatinine concentration. Therefore, peripheral edema should not prompt fluid restriction in the absence of central volume overload [1].

Laboratory monitoring

●Ordering laboratory tests – At least daily, we obtain a complete blood count (CBC), electrolytes, and creatinine concentration.

Serum albumin concentrations are sometimes helpful, especially if there is peripheral edema, as albumin infusions might expand intravascular volume and reduce peripheral edema. (See 'Hypoalbuminemia' below.)

●Laboratory definition of HUS [26,27]:

•Hematocrit <30 percent

•Platelet count <150,000/microL

•Serum creatinine concentration greater than the upper limit of normal for the patient's age

Issues related to diagnosis and management of HUS are discussed further separately. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children", section on 'Diagnosis' and "Treatment and prognosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children".)

●Interpreting laboratory test results – Laboratory values must be interpreted in the context of the day of illness.

•Creatinine – Early in the course of STEC infection (on or before day 4 of illness), an elevated serum creatinine concentration in the absence of thrombocytopenia likely reflects volume contraction without renal injury; in such cases, the creatinine should decrease if volume is restored. In the setting of persistent evidence for renal injury, nephrology should be consulted.

A rising creatinine in the setting of concomitant thrombocytopenia should raise concern for HUS; in this case, the increasing creatinine concentration cannot be attributed solely to volume contraction. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children", section on 'Diagnosis'.)

•Platelet count – The trend in the platelet count (even within a range that is normal), is an important leading indicator of microangiopathy as well as of injury resolution. If the platelet count is stable or rising on or after the fifth day of illness, HUS is very unlikely to ensue.  

•Hematocrit – Within the first few days of illness, the trend in the hematocrit may be used to evaluate hydration status; with fluid repletion, it should remain constant or diminish. For patients who begin to demonstrate evidence of microangiopathy (usually after day four of illness), the hematocrit is a less reliable indicator of volume status because hemolysis reduces circulating red cell mass.

Discontinuing therapy — The decision to discontinue monitored inpatient and outpatient management depends on the stage of the illness, platelet count trajectory, and clinical improvement.

A decrease in platelet count is often the first laboratory manifestation of HUS. Rising platelet counts in the middle phase of diarrhea suggest that the risk for HUS is lessening.

We count the first day of illness as the first day of diarrhea (not the first day of bloody diarrhea) (figure 2 and algorithm 2):

●Days 1 through 4 of illness (early phase) – We continue daily clinical and laboratory assessment through the first four days of illness.

●Days 5 through 10 of illness (middle phase) – If the patient's clinical condition has improved (resolving diarrhea and abdominal pain), and the platelets have increased by at least 5 percent compared with the day prior, we discontinue daily clinical and laboratory assessment (and intravenous fluids if underway).

In some cases, we obtain a CBC on the day after discharge to ensure there is no decrease in the platelet count reflecting late deterioration. This is unusual, but if it does occur, we typically readmit patients for an additional day or two of IV fluids.

●Day 11 or later of illness (late phase) – If the patient's clinical condition has improved, we discontinue monitoring (even if the platelets have not increased by more than 5 percent compared with the day prior).

We obtain a repeat stool culture (or swab) prior to discharge in patients who may need to document a negative culture prior to returning to daycare, school, or work.

MANAGEMENT OF ADULTS — 

For adults with Shiga toxin-producing Escherichia coli (STEC), the approach to management is the same as for other causes of hypovolemia, and should also be informed by other clinical considerations (in particular, any cardiopulmonary issues that could be exacerbated). Peripheral edema is expected, but we do not aggressively administer fluids if there are signs of central volume overload.

Issues related to fluid management for adults with diarrhea are discussed separately. (See "Approach to the adult with acute diarrhea in resource-abundant settings" and "Approach to the adult with acute diarrhea in resource-limited settings" and "Maintenance and replacement fluid therapy in adults".)

AVOIDING POTENTIALLY HARMFUL INTERVENTIONS

Antibiotics — We do not treat confirmed or suspected Shiga toxin-producing Escherichia coli (STEC) infection (E. coli O157:H7 or non-O157:H7) with antibiotics [28]. For patients who received empiric antibiotics prior to diagnosis of STEC infection, we discontinue antibiotic therapy.

This approach is based on repeated associations between antibiotics and the development of hemolytic uremic syndrome (HUS) in patients with STEC infection. The risk was illustrated by a meta-analysis of mainly observational studies that included over 1800 patients with STEC infection [29]. When all studies were pooled, there was a nonsignificant trend toward a higher risk of HUS with antibiotic use (pooled OR 1.33, 95% CI 0.89-1.99); however, among five studies that employed a stringent definition of HUS and were deemed to have low risk of bias, the association between antibiotic use and development of HUS was stronger (32 versus 18 percent; pooled OR 2.24, 95% CI 1.45-3.36).

Data in adults are sparser; in three studies among adults that were included in the meta-analysis discussed above and were considered high quality, antibiotics administered early in STEC infection were associated with subsequent development of HUS [29-32].

We are unaware of any study that has convincingly demonstrated that antibiotic administration reduces the chances of developing HUS in patients with a high-risk STEC infection. In addition, antibiotics have not been shown to reduce symptoms or other complications associated with STEC infection [33].

For some coincident bacterial infections (such as otitis media, group A streptococcal pharyngitis, or an enteric co-infection such as C. difficile, Campylobacter, Salmonella, or Shigella), deferral of antibiotic treatment is preferred. However, for patients with serious coinfection (such as invasive pneumococcal infection [10] or Clostridium septicum infection [34-37]), antibiotic therapy is warranted.

For patients who develop HUS (especially anuric HUS), antibiotics may be used if indicated. In such cases we avoid ceftriaxone since HUS results in a pigment load that can lead to biliary stones [38], and ceftriaxone may lead to accumulation of biliary sludge.

Other medications — We avoid several medications given their lack of benefit and/or suggestion of potential harm in patients with STEC infection:

●Antimotility agents (including opioids) – These agents have been associated with a higher risk of HUS and, among those who develop HUS, complicated HUS (eg, with central nervous system dysfunction) [39-41]. In one study, they were also associated with prolongation of gastrointestinal symptoms [39].

●Nonsteroidal anti-inflammatory drugs (including ketorolac) – These agents can diminish kidney blood flow and thus can theoretically exacerbate ischemic damage to the kidney that likely underlies kidney failure in HUS. They are demonstrated to cause kidney injury in children with gastroenteritis from all causes [42], and abdominal discomfort is unlikely to respond to these agents.

●IV ondansetron – This serotonin 5-H₃ receptor antagonist can prolong the QT interval. Given that a subset of deaths during HUS are sudden, we believe that it is prudent to avoid this potentially arrhythmogenic agent [43]. Orally administered ondansetron is safer but, in our experience, rarely stops vomiting associated with STEC infections.

ADDITIONAL MANAGEMENT ISSUES

Pain control — Abdominal pain may be attributable in part to intestinal ischemia; therefore, an intravenous bolus of isotonic crystalloid might be helpful. We avoid opioids and nonsteroidal anti-inflammatory drugs. (See 'Other medications' above.)

Hypoalbuminemia — Many patients with Shiga toxin-producing Escherichia coli (STEC) infection are hypoalbuminemic. For patients with peripheral edema or diminishing urine output and serum albumin concentration <3 g/dL, albumin may be infused judiciously (0.5 g/kg once, and then repeated several hours or a day later) to draw extracellular fluid into blood vessels and increase circulating blood volume. (See "Evaluation and management of edema in children", section on 'Intravenous albumin infusion' and "Causes and treatment of refractory edema in adults", section on 'Albumin infusion for hypoalbuminemia'.)

In the absence of cardiopulmonary overload, we do not administer albumin with a diuretic in the pre-hemolytic uremic syndrome (HUS) phase.

Anemia or thrombocytopenia without azotemia — Occasionally, severe anemia from hemolysis can precede, or occur in the absence of, elevations in serum creatinine (ie, before criteria for HUS have been met or in situations in which HUS does not develop).

●Anemia – In the absence of tachycardia or hypoxemia, we defer red cell transfusion. Almost all patients with STEC-related HUS ultimately require at least one red blood cell transfusion, but we favor delaying this intervention if feasible since the added pigment load from ongoing hemolysis may be nephrotoxic. (See "Red blood cell transfusion in infants and children: Indications" and "Indications and hemoglobin thresholds for RBC transfusion in adults".)

●Thrombocytopenia – Patients with high-risk STEC infection can develop profound thrombocytopenia in the absence of azotemia or prior to development of azotemia. We discourage platelet transfusion unless there is severe bleeding, which is unusual. As HUS is a thrombotic injury, clinically consequential hemorrhagic complications are rare, and platelet infusions theoretically could exacerbate the thrombotic state.

PREVENTION

In health care settings — Hospitalized patients with Shiga toxin-producing Escherichia coli (STEC) infection should be placed on contact precautions to reduce person-to-person transmission [44]. (See "Infection prevention: Precautions for preventing transmission of infection", section on 'Contact precautions'.)

The local public health authorities should be notified of any patient diagnosed with STEC or hemolytic uremic syndrome (HUS); this is important for outbreak tracking and source identification.

In the community

Reducing transmission risk — Tools for exposure reduction include (see "Shiga toxin-producing Escherichia coli: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Epidemiology'):

●Food safety – Food safety measures to reduce STEC exposure include proper handling of raw beef and meats and cooking ground meats to internal temperatures of ≥160°F (71°C) (table 2).

Individuals should also avoid consuming raw milk or other unpasteurized dairy and juice products, raw flour or dough, and other foods that are implicated in ongoing outbreaks. In the United States, information on specific outbreaks can be found on the Centers for Disease Control and Prevention (CDC) website on E. coli outbreak investigations.

●Animal exposure – In settings with animal exposure (including occupational as well as recreational contact), exposure reduction measures include hand hygiene, personal protective wear, thorough hygiene practices, and implementation of workflow patterns with discrete contaminated and clean areas.

Return to school or work — Local health jurisdictions have varying policies regarding exclusion from daycare and food handling jobs to prevent post-infectious transmissions of these pathogens. Physicians should defer to their policies.

A negative stool culture is often requested prior to return to daycare, school, or other sensitive settings (eg, occupation with food preparation). For children, we typically obtain a stool culture prior to discharge from the hospital, as this is more convenient than submitting an outpatient specimen.

Exposed individuals — For individuals exposed to an outbreak source and for household contacts of infected patients, there is no role for preemptive post-exposure intervention in the absence of diarrhea. Patients should be advised to seek medical care if they develop diarrhea, and should alert their provider of STEC exposure.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in adults" and "Society guideline links: Acute diarrhea in children".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: E. coli diarrhea (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Management of children – Management of infection due to high-risk Shiga toxin-producing Escherichia coli (STEC; E. coli O157:H7 and non-O157 STEC containing a gene encoding Shiga toxin 2) focuses on reducing the likelihood of developing hemolytic uremic syndrome (HUS), by careful fluid management and close monitoring for evidence of microangiopathy. (See 'Management of children' above.)

•Site of care – Inpatient management is warranted in the following circumstances (algorithm 1) (see 'Site of care' above):

-Patients who appear dehydrated (table 1), are vomiting, or have severe abdominal pain.

-Patients with laboratory tests demonstrating thrombocytopenia or other evidence of microangiopathy (coagulation abnormalities, fibrinolysis, and/or hemolysis).

-Patients who cannot be reassessed readily with daily laboratory tests (CBC, chemistries) and physical examination

Outpatient management is reasonable for patients who are well hydrated, not vomiting, and can be reassessed daily with repeat laboratory tests (complete blood count [CBC], chemistries) and physical examination.

•Fluid management – Approaches to fluid management for children with STEC include hyperhydration (anticipatory volume expansion) or conservative fluid management (targeting euvolemia by restoring volume in response to hypovolemia). The optimal approach is uncertain; a trial is underway.

For patients who present to a center that is not participating in the trial, the management approach should be selected at the discretion of the health care provider. (See 'Selecting an approach' above.)

•Clinical and laboratory monitoring

-Clinical approach – We monitor clinical parameters (symptoms, volume status, weight, fluid intake, fluid output) and laboratory parameters (CBC, electrolytes, and creatinine concentration at least daily) for development of HUS, defined as follows: hematocrit <30 percent, platelet count <150,000/microL, and serum creatinine concentration greater than the upper limit of normal for the patient's age. (See 'Monitoring' above.)

-Timing for discontinuation – The decision to discontinue monitored fluid management depends on the stage of the illness, the inter-day platelet count change, and clinical improvement (algorithm 2). (See 'Discontinuing therapy' above.)

●Management of adults – The approach to fluid management in adults with STEC is the same as for other causes of hypovolemia. (See "Approach to the adult with acute diarrhea in resource-abundant settings" and "Approach to the adult with acute diarrhea in resource-limited settings" and "Maintenance and replacement fluid therapy in adults".)

●Avoiding harmful interventions

•Antibiotics – For patients with high-risk STEC infection, we recommend not treating with antibiotics (Grade 1B), given data suggesting an association between antibiotic use and increased risk for progression to HUS. We also do not use empiric antibiotics in patients with suspected STEC infection, pending microbiologic testing. Antibiotics have not been shown to reduce symptoms or complications of STEC infection. (See 'Antibiotics' above.)

•Other medications – We discourage the use of antimotility agents, narcotics, and intravenous ondansetron. These agents have little benefit and can have important adverse effects. (See 'Other medications' above.)

●Prevention

•Infection control – Hospitalized patients with STEC infection should be placed on contact precautions to reduce person-to-person transmission. (See 'In health care settings' above.)

•Reducing transmission risk – Measures for prevention of STEC infection consist of exposure reduction, including attention to food safety measures and measures to reduce exposure associated with animals. (See 'Reducing transmission risk' above.)