Shiga toxin-producing Escherichia coli: Epidemiology, microbiology, clinical manifestations, and diagnosis

Authors:: Lori R Holtz, MD, MSPH; Phillip I Tarr, MD
Section Editors:: Stephen B Calderwood, MD; Sheldon L Kaplan, MD
Deputy Editor:: Elinor L Baron, MD, DTMH

Literature review current through: Apr 2025. | This topic last updated: Aug 19, 2024.

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 cause severe disease including painful bloody diarrhea, as well as hemolytic uremic syndrome (HUS) in some cases. STEC with high risk for development of associated HUS include all E. coli O157:H7 and any non-O157 STEC containing a gene encoding Shiga toxin 2.

Other terms for STEC include enterohemorrhagic E. coli (EHEC), since these organisms often cause bloody diarrhea, and verotoxigenic E. coli (VTEC), because of the cell line (Vero) that was used to first demonstrate their cytotoxicity.

The epidemiology, microbiology (including toxin and pathogen nomenclature), clinical manifestations, and diagnosis of STEC infections are discussed here, focusing on the diarrheal phase of illness. The treatment and prevention of STEC infections are discussed separately. (See "Shiga toxin-producing Escherichia coli: Treatment and prevention".)

General issues related to evaluation of patients with acute diarrhea are discussed separately. (See "Diagnostic approach to diarrhea in children in resource-abundant settings", section on 'Acute diarrhea (typical duration <5 days)' and "Approach to the adult with acute diarrhea in resource-abundant settings", section on 'Evaluation'.)

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".)

EPIDEMIOLOGY

Burden of disease — Shiga toxin-producing Escherichia coli (STEC) are important causes of diarrheal illness globally. In a review from 10 of 14 World Health Organization (WHO) subregions, the global incidence of STEC infection was estimated at 2.8 million cases per year [1]. The most frequently recovered serogroups in the United States, Europe, and Argentina are summarized in the table (table 1).

In the United States in 2022, the incidence of STEC infection was 5.7 cases per 100,000 persons, an increase from 5.3 cases per 100,000 in 2016 to 2018 [2]. STEC O157:H7 infection has been reported more frequently in the northern regions [3]. This may reflect variations in detection and reporting infections as well as possibly proximity to cattle, which excrete abundant E. coli O157:H7 [4]. Most E. coli O157:H7 infections occur from June to September in the Northern Hemisphere, and cattle shed E. coli O157:H7 more frequently during the summer [5].

Transmission — Modes of STEC transmission include food and water, animal contact, and person-to-person.

The infectious dose of E. coli O157:H7 is low. As few as 10 viable E. coli O157:H7 can cause disease in humans [6].

●Food and water – The most important reservoir for E. coli O157:H7 is the gastrointestinal tract of cattle. Beef is contaminated when the intestinal contents from a colonized animal come in contact with meat during slaughter. Other ruminants, such as sheep, goats, and deer, carry E. coli O157:H7 in their gastrointestinal tracts and are potential sources of infection [7]. Swine can harbor and shed E. coli O157:H7, but pork causes only a small portion of STEC outbreaks [8,9].

Water and other food items can become contaminated by the feces of colonized animals. Non-beef outbreak sources include fresh produce (eg, spinach, lettuce, ready-to-eat salads, fruit, sprouts) [10-15], other uncooked or unpasteurized products (including raw milk, raw flour, raw dough), apple juice, soy nut butter, and falafel [16-20].

In the United States, detailed outbreak information can be found on the Centers for Disease Control and Prevention (CDC) website. Additional information is available from the US Food and Drug administration (FDA) website.

●Animal contact – STEC outbreaks have been associated with occupational exposure to animals, as well as recreational contact at county fairs, farms, and petting zoos, particularly in association with poor hand hygiene [21-26]. In a review of 55 outbreaks of enteric infection associated with animal contact in public settings, E. coli O157:H7 accounted for 58 percent [23].

Preventive measures for settings with animal exposure are discussed separately. (See "Shiga toxin-producing Escherichia coli: Treatment and prevention", section on 'Prevention'.)

●Person-to-person – Individuals at risk for transmission include household contacts, daycare contacts, and nursing home residents; outbreak attack rates have ranged from 10 to 22 percent [27-29].

Most individuals shed STEC for seven days or less, although occasional individuals, particularly younger children, shed the organism for three weeks or longer [30-34].

●Fecal microbiota transplant – Transmission of a non-O157:H7 STEC infection via fecal microbiota transplant (FMT) has been reported; the pathogen was transmitted through stool from a single donor that tested negative for Shiga toxin by enzyme immunoassay (EIA) but was subsequently found to be positive for a Shiga toxin gene by polymerase chain reaction (PCR) [35].

In the United States, the FDA recommends that all stool donated for FMT be screened for STEC with Shiga toxin molecular testing [36]. (See "Fecal microbiota transplantation for treatment of Clostridioides difficile infection", section on 'Stool donor selection'.)

Risk factors for sporadic cases — Most STEC infections are sporadic (ie, not linked to an identifiable outbreak). Risk factors include [37-46]:

●Travel

●Recreational water exposure

●Consumption of food from buffets, mobile stands, or table-service restaurants

●Private water supply and/or septic system

●Residence in a rural area

MICROBIOLOGY

Serogroups and serotypes

●O and H antigens – E. coli are classified by their O and H antigens.

•The O antigen is determined by the repeating polysaccharide chains that are part of the lipopolysaccharide (LPS) embedded in the outer leaflet of the outer membrane. E. coli strains expressing the same O antigen are categorized as a serogroup; for example, "E. coli O157" refers to a serogroup.

•The H antigen is defined by the antigenic specificity of the bacterial flagellum. A serotype includes information about the O antigen (serogroup) as well as the H antigen; for example, E. coli O157:H7 refers to a serotype. Identifying the presence of the H antigen is not needed for clinical care.

●Clinical isolates – A limited number of serotypes account for most human STEC isolates (table 2).

•Serogroup E. coli O157

-E. coli O157:H7 does not ferment sorbitol when grown on agar plates containing sorbitol as a carbon source. This distinctive phenotype facilitated an early understanding of the epidemiology and spectrum of infections caused this serotype. In general, E. coli O157:H7 causes more severe disease than non-O157 STEC.

-E. coli O157:HNM (non-motile; also called E. coli O157:H-) does ferment sorbitol so is not distinguishable on sorbitol-containing indicator agar. Therefore, these nonmotile strains, which are largely confined to Germany and the Czech Republic, do not have an appearance that distinguish them from commensal sorbitol-fermenting bacteria on agar plates. Phylogenetically, they are closely related to sorbitol-nonfermenting E. coli O157:H7 and are at least as virulent as E. coli O157:H7 in terms of hemolytic uremic syndrome (HUS) risk [47], but they must be detected using toxin assays or nucleic acid amplification technology.

•Non-O157 serogroups – Non-O157 serogroups are more difficult to detect than E. coli O157:H7 because few possess a phenotype as distinctive as the inability to ferment sorbitol. The major non-O157 STEC that cause human disease belong to serogroups that express lipopolysaccharide side chains O26, O45, O80 (confined to Europe), O92, O103, O111, O113, O121, and O145 (table 2 and table 3).

Techniques used to detect non-O157 serogroups include toxin enzyme immunoassays of overnight broth culture, nucleic acid amplification of Shiga toxin genes (directly from broth, or isolated colonies) [48], and chromogenic and selective and differentiating agars (table 3) [49].

Selective culture — We favor plating stool on selective and differentiating media, such as sorbitol-MacConkey (SMAC) agar (with or without cefixime and tellurite). E. coli O157:H7 ferments sorbitol slowly and appears as translucent colonies on this medium (picture 1). Such colonies can be easily tested for reaction with antisera to the O157 antigen and then confirmed as E. coli biochemically. Strains presumptively identified as E. coli O157:H7 should be sent to a reference laboratory for deoxyribonucleic acid (DNA) fingerprinting.

Chromogenic STEC agar is another selective media that can be used to detect E. coli O157:H7 as well as some non-O157:H7 STEC isolates, but it may not be as sensitive for certain non-O157:H7 STEC strains [49].

Shiga toxin — The cardinal virulence trait of STEC is the ability to produce Shiga toxin.

●Nomenclature – The term STEC refers to E. coli that produce Shiga toxin [50].

This term is confusing because providers may misinterpret detection of Shiga toxin to mean detection of Shigella [51]. However, the only Shigellae that synthesize Shiga toxin are Shigella dysenteriae serotype 1 (which are almost never detected in the United States) and rare isolates of Shigella sonnei and Shigella flexneri [52-55]. (See "Shigella infection: Epidemiology, clinical manifestations, and diagnosis".)

E. coli Shiga toxins belong to two families [56]:

•Shiga toxin 1 (and its variants) are nearly identical to Shiga toxin of S. dysenteriae serotype 1

•Shiga toxin 2 (and its variants) have approximately 57 percent homology to Shiga toxin 1

●Clinical categories – STEC fall into two clinically relevant categories (table 2):

•STEC with a gene encoding Shiga toxin 2 (high-risk STEC, with or without a gene encoding Shiga toxin 1) – These organisms are more virulent than STEC that produce only Shiga toxin 1. STEC that contain a gene encoding Shiga toxin 2 are often associated with bloody diarrhea and can cause HUS [57]. Therefore, E. coli of any serotype containing a gene encoding Shiga toxin 2 is regarded as a "high-risk" STEC (ie, high risk for development of HUS).

E. coli O157:H7 remains a leading cause of STEC infections worldwide and is the serotype most likely to be associated with epidemics and severe disease. Nearly all E. coli O157:H7 contain a gene encoding Shiga toxin 2 (and about two-thirds also contain a gene encoding Shiga toxin 1) [58,59]. Hence, all E. coli O157:H7 should be regarded as high-risk STEC.

Among the many non-O157:H7 STEC serotypes, only a subset of human isolates have the capacity to produce Shiga toxin 2 and cause severe disease.

Paradoxically, among STEC that contain a gene encoding Shiga toxin 2, those that also contain a gene encoding Shiga toxin 1 have somewhat lower risk of progressing to HUS [60,61].

•STEC that do not produce Shiga toxin 2 (ie, their only Shiga toxin gene encodes Shiga toxin 1) – These organisms are usually not associated with bloody diarrhea and carry minimal or no risk for HUS.

Many non-O157:H7 STEC contain do not produce Shiga toxin 2, and for this reason are considered "low risk".

●Laboratory detection of STEC – The likelihood of a high-risk STEC being detected depends on whether bloody diarrhea is present and whether E. coli O157:H7 has been excluded (table 4) [62-64].

•Available tools – Tools for laboratory detection of STEC are summarized in the table (table 3).

-Selective culture – Selective culture is most useful for the detection of E. coli O157:H7. (See 'Selective culture' above.)

-Molecular testing – Nucleic acid amplification tests (NAATs; on stool or stool broth culture) are increasingly available for detection of E. coli O157:H7 (by amplification of a gene encoding part of the O157 lipopolysaccharide O-side chain) and/or for detection of genes encoding Shiga toxins 1 and 2 [48].

If molecular testing indicates presence of a Shiga toxin gene but the genotype is not specified, the toxin type should be sought by the microbiology laboratory, to aid in determining if the patient is at risk of developing HUS.

-Immunoassay – Immunoassay (EIA; performed on overnight stool broth culture) can detect toxins that suggest the presence of O157:H7 as well as non-O157:H7 STEC. However, EIAs fail to detect up to 10 to 15 percent of E. coli O157:H7 that are detected on agar plating [63,65-70]. Therefore, EIA testing should be used in addition to, but not in place of, selective culture or nucleic acid amplification testing. Like NAAT, the toxin type might not be specified by a laboratory using a Shiga toxin immunoassay.

•Interpretation of laboratory results

-Ambiguous results – If a laboratory report states: "Shiga toxin-positive," "Shiga toxin 1/2 detected," or "Shiga toxin 1 and/or 2 detected," it is likely that the laboratory used an NAAT or immunoassay that is not formatted to report the specific toxin genotype. This ambiguity can complicate management, because an STEC that produces Shiga toxin 1, but not Shiga toxin 2, has little or no ability to cause HUS. However, reports that do not specify which toxin family is detected lends little clarity to these situations.

While awaiting microbiology results, we follow the strategy outlined in the figure (figure 1), which takes into account the spectrum of test results returned, the clinical condition of the patient, and the day of illness that the specimen was submitted.

Based on four studies of children with bloody and nonbloody diarrhea in which testing was adequate to detect the presence of STEC that produce Shiga toxin 1 and/or 2 independent of serogroup, it is estimated that, for a patient with bloody diarrhea and a nondifferentiated Shiga toxin test, the likelihood of infection with a high risk STEC was 87 percent [71]. If E. coli O157:H7 had been excluded, the likelihood decreased to 42 percent. Similarly, 40 percent of patients with nonbloody diarrhea in whom an STEC was identified were infected with a high-risk pathogen; after excluding E. coli O157:H7, the high-risk STEC rate fell to 20 percent.

When such ambiguous results are received, we encourage careful discussion with laboratory personnel to clarify that it is important to determine whether the pathogen produces Shiga toxin 2. It is also important that culture be obtained; pathogen isolation is important for epidemiologic analysis and outbreak tracing [72,73]. (See 'Selective culture' above.).

●False-negative results – In some situations, the infecting STEC may have cleared by the time the patient is tested. For patients with falling platelet counts in the absence of an alternative explanation, it may be reasonable to assume that the patient remains at risk of HUS and continue to manage accordingly. (See "Shiga toxin-producing Escherichia coli: Treatment and prevention".)

CLINICAL FEATURES —

Disease due to Shiga toxin-producing Escherichia coli (STEC) infection is most severe in children <10 years of age and older adults.

Incubation period — Following exposure, STEC infections have a median incubation period of three days, with a range of one to ten days [74]. However, many STEC infections cannot be linked to a specific vehicle or exposure, so the exact timing of ingestion is often unknown.

Typical findings during diarrhea phase — Infections with high-risk STEC (ie, all E. coli O157 and any non-O157 STEC containing a gene encoding Shiga toxin 2) are generally characterized by painful nonbloody diarrhea that becomes bloody after one to three days, often without fever.

●Gastrointestinal symptoms – The course of infection with high-risk STEC follows a patterned sequence of events (figure 2) [75]. We count the first day of illness as the first day of diarrhea (which informs management decisions); however, abdominal pain, vomiting, and fever can precede onset of diarrhea [62,76,77].

The initially nonbloody diarrhea typically becomes visibly bloody one to three days after onset. Uncommonly, patients with E. coli O157:H7 report only a few hours of nonbloody diarrhea before the stool becomes visibly bloody; rarely, some patients report the first loose stool was bloody [76].

Approximately 15 to 20 percent of patients infected with E. coli O157:H7 experience only nonbloody diarrhea.

STEC-related diarrhea generally resolves after about seven days, whether or not hemolytic uremic syndrome (HUS) ensues.

Though the preponderance of patients with STEC-related HUS have antecedent diarrhea, a small subset of patients with HUS have had little or no pre-HUS diarrhea [78-82].

●Lack of fever – Fever at the time of presentation is unusual in the setting of STEC infection [83]; however, many patients or their caregivers report a fever early in the course of illness, prior to seeking care. As an example, in a review of 260 cases of STEC infection, fever was self-reported in approximately 30 and 16 percent of O157:H7 and non-O157 E. coli cases, respectively [84].

Conversely, absence of fever at presentation does not distinguish infections caused by E. coli O157:H7 from other bacterial enteric infections [62]. Nonetheless, presence of high fever (>38.5°C or >101.3°F) in a patient with painful diarrhea increases the likelihood that the diarrhea is caused by other pathogens besides STEC (eg, Shigella, Campylobacter, or Salmonella). (See 'Clinical suspicion' below.)

●Laboratory findings – At the time of bloody diarrhea onset in patients with STEC infection, the platelet count, creatinine concentration, and hematocrit are typically normal, and there is no evidence of hemolysis on peripheral blood smear. However, abnormalities in coagulation and fibrinolysis suggestive of vascular injury are present at this point in illness. As infection progresses, the platelet count often falls, sometimes to values below the lower limit of normal, even if the patient does not develop HUS [85-89]. We use the day-to-day trend in platelet counts as indicators of HUS risk, and to guide treatment decisions.

Complications

Hemolytic uremic syndrome

●Definition – Hemolytic uremic syndrome (HUS) is characterized by the triad of nonimmune-mediated hemolytic anemia (hematocrit <30 percent), thrombocytopenia (platelet count <150,000/microL), and acute kidney injury (serum creatinine above the upper limit of normal for age).

●Associated serogroups – A subset of STEC serogroups cause HUS (table 3); these vary with geography (table 1). E. coli O157:H7 is the first or second most common precipitant of HUS; most clinical data are based on patients with sporadic or epidemic infection with this serotype.

●Risk varies with age – The likelihood of HUS in the setting of E. coli O157:H7 infection varies with age:

•Among children <10 years of age with culture-proven E. coli O157:H7 infection, HUS develops in 15 to 20 percent of cases [71,90-92].

•Among adolescents and adults, the rate of HUS is difficult to determine with confidence, because ascertainment of infection rates differ between children and adults, and STEC-associated HUS in adults may be misclassified as atypical HUS or thrombotic thrombocytopenic purpura [93-97]. It is important to differentiate the cause of thrombotic microangiopathy in adults and to re-direct therapies when an STEC is detected [98].

In 2022, the Centers for Disease Control and Prevention (CDC) reported that the incidence of diagnosed STEC infection fell from 17.8 cases per 100,000 children under age 5 years to approximately 5 cases per 100,000 persons for all subsequent years of life [99].

Even though HUS is less frequent among adults, high-risk STEC can cause severe disease at any age. Two outbreaks demonstrate the virulence of STEC in adults. The 2011 E. coli O104:H4 outbreak in Germany had a very high frequency of HUS among infected adults [100], as well as a high case fatality rate. In a 2018 North American outbreak including 210 patients with E. coli O157:H7 infection transmitted by Romaine lettuce, the median age was 28 years; 96 patients were hospitalized, 28 developed HUS, and 5 died [101]. Among elderly patients with HUS in the United States between 2000 and 2006, mortality rose from 30 percent (ages 65 to 74 years) to 50 percent (85 and older) [102]. A study from France observed that the increase in mortality among adults with STEC-associated HUS began at 40 years of age [103].

Potential explanations for this age distribution include variable exposure and transmission risk, age-specific toxin expression, presence of antibodies to Shiga toxin, and renal blood vessel diameter.

●Timing of clinical onset – Patients who develop HUS generally meet the case definition on a median of day 7 of illness, with a range between 5 and 13 days (the first day of illness is the first day of diarrhea) (figure 2) [104,105]. Occasionally patients with E. coli O157:H7 develop HUS on day 4 after the onset of diarrhea. Rarely, patients with HUS due to high-risk STEC E. coli have no diarrhea [78-82].

The clinical manifestations and diagnosis of STEC-associated HUS are discussed in detail separately. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children".)

●Role of Shiga toxin in HUS – Our current understanding suggests that circulating Shiga toxins are the cause of host systemic injury in HUS; STEC rarely invade the bloodstream. Toxin-mediated microangiopathic injury leads to a prothrombotic state, manifest by formation of intravascular microthrombi, which can cause acute kidney injury by occluding afferent renal vessels (picture 2). (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children", section on 'Kidney pathology'.)

Intussusception (rare) — Rarely, patients with STEC infection present with intussusception [106]. Intussusception is discussed in detail separately. (See "Intussusception in children".)

EVALUATION AND DIAGNOSIS

Clinical suspicion — Infection due to high-risk Shiga toxin-producing Escherichia coli (STEC; ie, all E. coli O157:H7 or non-O157 STEC that encodes a gene for Shiga toxin 2) should be suspected in the following circumstances [78-80]:

●Patients with acute bloody diarrhea and abdominal pain, usually in the absence of fever

●Patients with acute diarrhea (bloody or nonbloody) with relevant epidemiologic risk factors (these include contact with a patient with known STEC infection or recent exposure to animals at a farm or petting zoo)

●Patients with hemolytic uremic syndrome (HUS), even in the absence of diarrhea

Clinical features that reduce the likelihood of infection with a high-risk STEC include:

●Absence of abdominal pain

●Diarrhea that abates within several hours of presentation (even if bloody)

●Total duration of diarrhea greater than one week at time of presentation

●Findings suggesting a chronic process (such as microcytic anemia, weight loss)

●Contact with a patient with diarrhea caused by a bacterial pathogen other than STEC

Presence of fever (>38.5°C or >101.3°F) at the time of presentation is atypical of STEC infection; however, the possibility of STEC infection should not be discounted in the setting of fever.

Children with STEC infection often have symptoms severe enough to present for emergency evaluation but overall account for a small proportion of patients with acute diarrhea in that setting; thus STEC infection (and risk for HUS) is often under-recognized. As an example, one study of children with STEC presenting to pediatric emergency departments in the United States and Canada, one in seven developed HUS within a median of three days of presentation; nearly 30 percent of those who subsequently developed HUS were initially discharged [90].

Definitive diagnosis — In patients with acute diarrhea, a diagnosis of high-risk STEC infection is established in either of the following circumstances (figure 1):

●Isolation of E. coli O157:H7 in culture

●Detection of Shiga toxin 2 (or a gene encoding a Shiga toxin 2)

Until the toxin genotype is known, we consider an unspecified Shiga toxin from a patient with acute diarrhea to reflect high-risk STEC infection, especially in the setting of bloody diarrhea. (See 'Shiga toxin' above.)

Approach to evaluation — The initial evaluation of patients with suspected STEC infection includes history and physical examination, microbiologic testing for STEC and other bacterial pathogens via rectal swab or stool specimens, and general laboratory testing:

●History and physical examination – We aim to determine the first day the patient experienced loose stools; this is designated as the first day of illness (figure 2). Prodromal symptoms such as vomiting or abdominal pain often precede the first day of diarrhea; however, they are too nonspecific to serve as points of reference for subsequent phases of illness [107]. We also ask about visible blood in the stools and abdominal pain.

On physical examination, we focus on vital signs, heart and lung auscultation (in anticipation of volume expansion), and abdominal tenderness. The assessment should evaluate volume status and ability to tolerate oral fluids.

●Microbiologic testing – Prompt, reliable diagnostic test results early in illness are strongly associated with favorable clinical outcomes in E. coli O157:H7 infection [108]. Medical management is highly dependent on microbiology results; a guide to interpretation is presented in the figure (figure 1).

•Detection of STEC

-Acute diarrhea – For patients with acute diarrhea, stool specimens should be submitted for E. coli O157:H7 selective culture and Shiga toxin testing (by molecular testing or by immunoassay following overnight broth culture) (table 3) [109,110]. (See 'Microbiology' above.)

For patients who are unable to produce a stool specimen promptly, we obtain a rectal swab. This approach may expedite establishing a diagnosis, which is important for guiding management.

Among children, culture of rectal swab specimens may have higher diagnostic yield than culture of stool specimens [111]. Among adults, rectal swab specimens may have lower sensitivity than stool specimens [112]; however, some data suggest that the yield of swab specimens may be similar among children and adults [113]. Use of rectal swab specimens may preclude molecular panel testing.

-Persistent or chronic diarrhea – For patients with persistent or chronic diarrhea, the clinical relevance of STEC detection is uncertain and usually does not warrant specific clinical action, especially if the diarrhea is nonbloody.

•Other causes of diarrhea – Patients should also be evaluated for non-STEC bacterial pathogens that cause bloody diarrhea. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Inflammatory diarrhea'.)

•Patients with fever – Most patients with STEC infection are afebrile at the time of presentation with diarrhea and remain afebrile during the diarrhea phase of illness. Presence of fever at or after presentation should prompt evaluation for other causes of infection, tailored to clinical circumstances; we typically obtain blood cultures and chest radiograph.

●General laboratory testing – We obtain the following daily: complete blood count, electrolyte panel, serum creatinine [107,114]. These tests can demonstrate evidence of microangiopathy (manifesting initially as a falling platelet count, followed by hemolysis and azotemia), warranting inpatient management. (See "Shiga toxin-producing Escherichia coli: Treatment and prevention".)

Elevated serum lactate dehydrogenase (LDH) concentration could be a harbinger of hemolysis and has been used to monitor thrombotic microangiopathies of various etiologies [90], but data are insufficient to endorse routine use for risk stratification.

Elevated prothrombin time is rare in HUS, and fibrinogen is normal or elevated, so there is not a picture of disseminated intravascular coagulation (DIC).

●Role of radiographic imaging – In children, radiographic imaging with computed tomography (CT) rarely has a role in evaluating suspected or documented STEC infection; the low likelihood that the findings could inform management is outweighed by the risks of radiation and the potential nephrotoxicity of intravenous (IV) contrast.

In adults, CT (and other testing) may be useful for evaluation of noninfectious intestinal disorders presenting with bloody diarrhea [115].

DIFFERENTIAL DIAGNOSIS —

The differential diagnosis of acute bloody diarrhea predominantly includes other bacterial pathogens (such as Salmonella, Campylobacter, Shigella, and Yersinia spp). These are discussed in detail separately. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Inflammatory diarrhea'.)

Assessing these and other causes of acute diarrhea in children and adults is presented separately. (See "Diagnostic approach to diarrhea in children in resource-abundant settings", section on 'Acute diarrhea (typical duration <5 days)' and "Approach to the adult with acute diarrhea in resource-abundant settings", section on 'Bloody diarrhea'.)

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

●STEC definition – Escherichia coli that contain genes encoding Shiga toxins 1 and/or 2 are referred to as Shiga toxin-producing Escherichia coli (STEC). STEC with high risk for development of associated hemolytic uremic syndrome (HUS) include all E. coli that contain a gene encoding Shiga toxin 2. Shiga toxin 2 producing E. coli are termed high-risk STEC. All E. coli O157:H7 produce Shiga toxin 2 (and many also produce Shiga toxin 1). Only a subset of non-O157 STEC contain a gene encoding Shiga toxin 2 (table 2). (See 'Introduction' above.)

●Epidemiology – Modes of STEC transmission include food and water, animal contact, and person-to-person. The infectious dose of E. coli O157:H7 is low; as few as 10 viable E. coli O157:H7 can cause disease in humans. (See 'Epidemiology' above.)

●Clinical features

•Typical findings – High-risk STEC infection is usually characterized by painful diarrhea that becomes bloody (typically one to three days after onset); abdominal pain, vomiting, and fever can precede onset of diarrhea (figure 2). Fever at the time of presentation is unusual in the setting of STEC infection; however, many patients report a fever early in the course of illness, prior to seeking care. (See 'Typical findings during diarrhea phase' above.)

•Hemolytic uremic syndrome – HUS is characterized by the triad of nonimmune-mediated hemolytic anemia (hematocrit <30 percent), thrombocytopenia (platelet count <150,000/microL), and acute kidney injury (serum creatinine above the upper limit of normal for age). Among children <10 years of age with culture-proven E. coli O157:H7 infection, HUS develops in 15 to 20 percent of cases; older adults are also at increased risk. (See 'Hemolytic uremic syndrome' above.)

●Evaluation and diagnosis

•Clinical suspicion – High-risk STEC infection should be suspected in patients with acute bloody diarrhea and abdominal pain, usually in the absence of fever. It should also be suspected in individuals with acute diarrhea and known exposure to a patient with STEC. (See 'Clinical suspicion' above.)

•Definitive diagnosis – In patients with acute diarrhea, a diagnosis of high-risk STEC infection is established by isolation of E. coli O157:H7 in culture or detecting Shiga toxin 2 by an antigen test, or a gene encoding Shiga toxin 2. (See 'Differential diagnosis' above.)

•Approach to evaluation

-Microbiologic testing – Specimens should be submitted for E. coli O157:H7 selective culture and Shiga toxin testing (by molecular testing or by immunoassay following overnight broth culture). The preferred specimen type is stool; for patients who are unable to produce a stool specimen promptly, we obtain a rectal swab. Patients should also be evaluated for non-STEC bacterial pathogens that cause bloody diarrhea. (See 'Approach to evaluation' above and 'Microbiology' above.)

-General laboratory testing – A complete blood count, electrolyte panel, and serum creatinine should be obtained.

ACKNOWLEDGMENT —

The UpToDate editorial staff acknowledges Stephen Freedman, MD, PhD, who contributed to a revision of this topic review.

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Topic 2714 Version 45.0

خرید پکیج

Shiga toxin-producing Escherichia coli: Epidemiology, microbiology, clinical manifestations, and diagnosis

References