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Shiga toxin-producing Escherichia coli: Microbiology, pathogenesis, epidemiology, and prevention

Shiga toxin-producing Escherichia coli: Microbiology, pathogenesis, epidemiology, and prevention
Literature review current through: May 2024.
This topic last updated: Aug 03, 2023.

INTRODUCTION — Escherichia coli that contain one or more genes encoding Shiga toxins are important human pathogens. They first came to medical attention in 1983 with two nearly simultaneous reports, one of which identified E. coli O157:H7 in the stools of patients with bloody diarrhea who had been exposed to undercooked hamburgers [1], and the other identified E. coli O157:H7 and Shiga toxin-producing E. coli (STEC) belonging to other serotypes in the stools of children with hemolytic uremic syndrome [2].

The microbiology, pathogenesis, epidemiology, and prevention of STEC infections will be reviewed here. The clinical manifestations, diagnosis (including clinical diagnostic microbiology), and treatment of STEC infections are discussed separately. (See "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment".)

MICROBIOLOGY

Nomenclature — We use the term STEC to refer to the E. coli that produce Shiga toxins [3].

Shiga toxin is the principal extracellular cytotoxin of Shigella dysenteriae serotype 1. E. coli Shiga toxins belong to two families:

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

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

Shiga toxins consist of a pentameric (B) subunit, which binds to globotriaosylceramide on the surface of eukaryotic cells, and an enzymatically active A subunit, which is a ribotoxin that inhibits protein synthesis.

STEC are also variably termed verotoxigenic E. coli (VTEC), because of the cell line (Vero) that was used to first demonstrate their cytotoxicity, and enterohemorrhagic E. coli (EHEC), because they often cause bloody diarrhea. Shiga toxins are synonymous with verotoxins. The terms Shiga-like toxins and Shiga-like toxin-producing E. coli have fallen into disuse.

STEC nomenclature has been confusing and problematic. As an example, STEC that produce Shiga toxin 1 but do not produce Shiga toxin 2 rarely cause bloody diarrhea, so "enterohemorrhagic" is an inaccurate term for such organisms.

"STEC" is also a confusing term because providers sometimes interpret the detection of Shiga toxin to mean that a patient is infected with Shigella [4]. Shigella dysenteriae serotype 1, which is almost never detected in the United States, and rare isolates of Shigella sonnei and Shigella flexneri are the only Shigella species that synthesize Shiga toxin [5-8]. (See "Shigella infection: Epidemiology, clinical manifestations, and diagnosis".)

Serotypes — E. coli strains and lineages are classified by their O and H antigens. The O antigen is defined serologically and determined by the repeating polysaccharide chains that are part of the lipopolysaccharide (LPS) embedded in the outer leaflet of the outer membrane. The H antigen is defined serologically by the antigenic specificity of the bacterial flagellum. Members of a clone of bacteria that express the same O antigen are described as a serogroup. When the serogroup and the H (flagellar) antigen are mentioned in unison, the designation becomes a serotype. E. coli O157:H7 refers to a serotype, and E. coli O157 refers to a serogroup.

E. coli O157:H7 is the most commonly studied serotype of STEC. This serotype does not ferment sorbitol when grown on agar plates containing sorbitol as a carbon source. This easily detectable property facilitated an early understanding of the epidemiology and spectrum of infections caused by strains of this serotype. A number of other E. coli serogroups produce Shiga toxin ("non-O157 STEC"). These non-O157 STEC have been identified less frequently because few possess a phenotype as distinctive as the inability to ferment sorbitol on agar plates. Newer diagnostic microbiology technology increasingly detects non-O157 STEC infections, and knowledge of the illnesses they cause is growing. These STEC are associated with a broader spectrum of illness than E. coli O157:H7 and are usually less severe (table 1). E. coli O157:H7 remains, nevertheless, a leading serotype worldwide, and, in general, causes more severe disease than non-O157 STEC, as discussed elsewhere. (See 'Shiga toxin type' below.)

One STEC of note is the sorbitol-fermenting (SF), nonmotile E. coli O157:NM (also called E. coli O157: H negative), a serotype that is largely confined to Germany and the Czech Republic and is closely related phylogenetically to sorbitol-nonfermenting E. coli O157:H7 [9]. Technically, it is an E. coli O157 STEC, though is not detected on sorbitol-MacConkey agar. SF E. coli O157:NM is at least as virulent as E. coli O157:H7 in terms of hemolytic uremic syndrome (HUS) risk.

Other non-O157 STEC isolated from humans are much less closely related to E. coli O157:H7. The major non-O157 STEC that cause human disease belong to E. coli serogroups that express the lipopolysaccharide side chains O26, O45, O92, O103, O111, O113, O121, and O145. Many additional non-O157:H7 STEC are found in food and in the environment and have minimal or no association with human disease.

As discussed, the predominance of E. coli O157:H7 partly relates to the ease with which this serotype can be detected on sorbitol MacConkey (with or without supplementation with cefixime and tellurite) or other differentiating and selective agar. Techniques used to detect non-O157:H7 STEC serotypes include toxin enzyme immunoassays of overnight broth cultures of stools, nucleic acid amplification of Shiga toxin genes directly from stool, broth, or isolated colonies [10], and chromogenic and selective and differentiating agars [11]. Methods for detecting STEC in clinical situations and guidance for interpreting results, which are critical components of patient care, are discussed in detail elsewhere. (See "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment", section on 'Microbiologic diagnosis'.)

For E. coli O157:H7 and non-O157:H7 STEC alike, identifying the presence of the H antigen is not needed for clinical care. Note also that a small number of sorbitol-nonfermenting E. coli O157 are nonmotile [12], but these organisms can be considered identical for clinical and diagnostic purposes to classic sorbitol-nonfermenting E. coli O157:H7.

Shiga toxin type — STEC infections fall into two clinically relevant categories:

Infections caused by E. coli that contain a gene encoding Shiga toxin 2 (with or without a gene encoding Shiga toxin 1) – STEC that contain the gene encoding Shiga toxin 2 are often recovered from patients with bloody diarrhea. They can also cause HUS independent of serogroup. Hence, bloody diarrhea is a reasonable surrogate indicator of the presence of an STEC that contains a gene encoding Shiga toxin 2.

Infections caused by E. coli that contain a gene encoding Shiga toxin 1 but do not contain a gene encoding Shiga toxin 2 – These usually do not cause bloody diarrhea or HUS, but there are exceptions [13].

Almost all E. coli O157:H7 contain a gene encoding Shiga toxin 2; about two-thirds of this serotype also contain a gene encoding Shiga toxin 1 [14,15]. Hence, all E. coli O157:H7 isolated from humans should be assumed to possess a gene encoding Shiga toxin 2 and be highly pathogenic. Interestingly, E. coli O157:H7 that contain the genes encoding both Shiga toxin 1 and Shiga toxin 2 are associated with a lower risk of developing HUS than those that contain only Shiga toxin 2 [14,16-18]. However, the difference in risk between a STEC is not sufficient to make a clinical decision that a patient will not develop HUS if infected with a STEC that produces both Shiga toxins.

In contrast, non-O157:H7 STEC isolated from humans usually contain a gene encoding Shiga toxin 1; only a subset contains a gene encoding Shiga toxin 2. Shiga toxin 2-producing non-O157:H7 STEC are more pathogenic than the larger group of non-O157:H7 STEC that do not contain this gene. The illnesses these Shiga toxin 2–producing E. coli cause are as serious as those caused by E. coli O157:H7. An appreciable subset of non-O157:H7 STEC infections involve multiple enteric pathogens [19].

We use the term "high-risk STEC" to refer to any E. coli that contains a gene encoding Shiga toxin 2, including all E. coli O157:H7, sorbitol-fermenting E. coli O157:NM, and E. coli of other serogroups that contain a gene encoding Shiga toxin 2, given their association with severe human disease, especially HUS.

PATHOGENESIS

Infectious dose — The infectious dose of E. coli O157:H7 is low. One study has estimated that as few as 10 viable E. coli O157:H7 can cause disease in humans [20].

Toxin production — The cardinal virulence trait of STEC is their ability to produce Shiga toxins. Systemic host injury is the likely consequence of toxemia, as STEC rarely invade extraintestinal sites or the bloodstream. Many serotypes of E. coli have genes encoding Shiga toxins 1 and/or 2, but a limited number of serotypes account for most human STEC isolates (table 1).

Shiga toxins 1 and 2 each have multiple allelic variants. In this topic, we refer to the Shiga toxin 1 and Shiga toxin 2 families, not a specific allele. Shiga toxin 1 is highly homologous to the principal extracellular cytotoxin of S. dysenteriae serotype 1; Shiga toxin 2 has 58 percent homology at the amino acid level to Shiga toxin 1 [21]. Shiga toxin 2 is more potent and much more frequently associated with severe human disease than Shiga toxin 1. (See 'Shiga toxin type' above.)

Shiga toxins have an AB5 subunit structure, with a pentameric B subunit that binds a sphingolipid, globotriaosylceramide (GB3), on eukaryotic cell surfaces, and an enzymatically active A subunit that enters the cell. Shiga toxins are N-glycosidases and inhibit protein synthesis in eukaryotic cells; their structure and mechanism of action resemble those of ricin [22]. A variety of interventions directed at Shiga toxins have been investigated, including those that neutralize circulating toxin and those that attenuate the effects of the internalized toxin, but none have advanced to clinical practice [23,24].

Toxemia has been thought to be a short-lived event early in STEC illness [25], though some data suggest toxin circulation later in illness [26,27]. Moreover, the concentrations of E. coli O157:H7 and free Shiga toxin in patients' stools generally diminish in the days following presentation [28].

Host injury is probably the consequence of systemic toxin-mediated microangiopathic injury. (See 'Hemolytic uremic syndrome' below.)

Other virulence factors — Extensive study of the genomes of E. coli O157:H7 demonstrates multiple virulence loci in addition to Shiga toxin [29,30].

E. coli O157:H7 possess a gene encoding intimin, which is located on the locus of enterocyte effacement and is the principal adhesin of E. coli O157:H7 [31].

The E. coli O157:H7 genome also encodes other adherence factors [32] and the enterohemorrhagic E. coli (EHEC)-hemolysin (a pore-forming toxin encoded on a large plasmid termed pO157) [33]. E. coli O157:H7 also form outer membrane vesicles that deliver virulence factors to host cells [34].

Non-O157:H7 STEC contain, by definition, genes encoding Shiga toxin 1 and/or 2 and a variable set of virulence factors, some of which are shared with E. coli O157:H7. However, from a clinical standpoint, the only relevant issue is whether or not Shiga toxin 2 is present. (See 'Shiga toxin type' above.)

Hemolytic uremic syndrome — Current understanding of pathogenesis suggests that systemic host injury is the consequence of circulating Shiga toxins, as STEC rarely invade extraintestinal organs or the bloodstream.

Toxin-mediated microangiopathic injury leads to a prothrombotic state in the human host, manifest by the formation of intravascular microthrombi. The prothrombotic abnormalities consist of elevated circulating activity of plasminogen activator-inhibitor type 1; elevated concentrations of circulating d-dimers, prothrombin activation fragment 1 + 2 [35], platelet activating factor [36], sheared Von Willebrand Factor [37], and chemokine ligand stromal cell-derived factor-1 [38]; and dysregulated angiopoietin 1 and 2 [39]. Intravascular microthrombi, if extensive, can cause acute kidney injury by critically occluding afferent renal vessels (picture 1). The working hypothesis is that the prothrombotic state that exists at the time of presentation with an infection caused by a high-risk STEC precedes and can lead to the hemolytic uremic syndrome (HUS), a complication that develops in approximately 15 to 20 percent of E. coli O157:H7-infected children. (See "Clinical manifestations and diagnosis of Shiga toxin-producing Escherichia coli (STEC) hemolytic uremic syndrome in children", section on 'Kidney pathology'.)

These vascular derangements are also present, though usually to lesser extents, in children whose STEC infections do not progress to HUS.

There is no credible clinical evidence that STEC-related or treatable abnormalities in complement regulatory systems cause HUS following STEC infections [40-43] or that HUS and thrombotic thrombocytopenic purpura share a common pathophysiology [37].

EPIDEMIOLOGY

Burden of disease — STEC are important causes of diarrheal illness globally, mostly because of the severity of the illnesses they cause rather than the absolute number of people they infect. Reliable data from all parts of the world are limited, but in a review of studies and databases from 10 of 14 World Health Organization subregions, the global incidence of STEC infection was estimated at 2.8 million cases per year [44].

In the United States, the Centers for Disease Control and Prevention (CDC) FoodNet project reports the frequency of laboratory-confirmed causes of acute foodborne illnesses based on data collected from 10 sites. During 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 [45].

The rank order of the four serogroups most frequently recovered from all patients are E. coli O26, O80, O157, and O145 (Europe); O157 (83.7 percent), O111 (5.9 percent), O145 (3.9 percent), O121 (2.5 percent; United States) [46], and O157 (73.6 percent), O145 (16.8 percent), O121 (5.4 percent), and O26 and O103 (tied; Argentina) [47].

STEC O157:H7 infection has been reported more frequently in the northern regions of the United States [48]. The reasons for this difference might include variations in detection and reporting of infected people and possibly proximity to cattle, which are termed "super shedders" because they excrete abundant E. coli O157:H7 [49]. Most E. coli O157:H7 infections occur between June and September. Notably, cattle shed E. coli O157:H7 mostly during the summer [50], and this seasonality correlates with higher prevalence of the organism on hides in processing plants [51].

Affected age groups — STEC infection occurs in patients of all ages. About one-third of E. coli O157:H7 infections occur in patients 20 to 59 years old [16]. However, the greatest burden of hemolytic uremic syndrome (HUS) occurs in children <5 years of age, followed by adults >60 years old [16,52-54]. The reasons why these age groups are most commonly and severely affected are unknown, but potential explanations include exposure, transmission, the ability of specific strains to establish disease in specific populations, age-specific expression on cells of receptors for toxins, and diameters of renal blood vessels.

The median ages of patients infected with non-O157:H7 and O157:H7 STEC are similar [55].

Transmission — Transmission of STEC is primarily through food and person-to-person or animal contact. Vegetables (18 percent), animal (11 percent), person to person (9 percent), beef (6 percent), and water (5 percent) exposures are the most common sources of E. coli O157:H7 infections acquired in outbreaks. For non-O157:H7 outbreaks, the corresponding exposures are person to person (20 percent), vegetables grown in rows (9 percent), animal (5 percent), and water (2 percent); beef accounted for only 1 percent of outbreaks [56].

Foodborne — The proportion of STEC outbreaks associated with consumption of beef has decreased [57], and the number of outbreaks caused by non-beef food products has risen and include fresh produce (eg, spinach, lettuce, ready-to-eat salads, fruit, sprouts) [58-63], other uncooked or unpasteurized products (such as raw milk, raw flour, raw dough [both prepackaged and homemade]), apple juice, soy nut butter, and falafel [64-68]. Non-beef meats, in particular pork and pork products, cause only a small portion of STEC outbreaks [69].

The most common reservoir for E. coli O157:H7 is the gastrointestinal tract of cattle, and beef is contaminated when the intestinal contents from a colonized animal contaminate the meat during harvest. Other ruminants, such as sheep, goats, and deer, carry E. coli O157:H7 in their gastrointestinal tracts and are potential sources of infection [70], and swine can also harbor and shed E. coli O157:H7 [71], but pork is rarely incriminated as an outbreak vehicle. Other food items and water can become contaminated when they encounter the feces of colonized animals.

In the United States, detailed information on current and recent outbreaks linked to specific food products can be found on the CDC website on E. coli outbreak investigations. Additional information is available from the US Food and Drug administration 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 [72-77]. In a review of 55 outbreaks of enteric infection associated with animal contact in public settings, E. coli O157:H7 accounted for 58 percent [74].

Investigation of an outbreak of E. coli O111 in a Colorado prison suggested that inmates were infected through fecally contaminated clothing and other items that were brought into food preparation areas by inmates who were employed at an onsite dairy and had extensive cattle contact [78]. This report highlights the importance of infection control measures during and after occupational animal contact, such as personal protective wear, thorough hygiene practices, and implementation of workflow patterns with discrete contaminated and clean areas.

Person-to-person — The low infectious dose of E. coli O157:H7 facilitates person-to-person transmission. Household and daycare contacts of STEC-infected patients are at particular risk and should seek medical care if they develop diarrhea. Secondary attack rates in outbreaks have ranged from 10 to 22 percent, particularly among children and adults in daycare centers and nursing homes [79,80], and households [81]. Hospitalization of STEC-infected patients has been proposed to reduce secondary infections in the community [82].

Person-to-person transmission of a non-O157:H7 STEC infection through fecal microbiota transplant 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) [83]. In the United States, the Food and Drug Administration recommends that all stool donated for fecal microbiota transplantation be screened for STEC with Shiga toxin molecular testing [84]. (See "Fecal microbiota transplantation for treatment of Clostridioides difficile infection", section on 'Stool donor selection'.)

Risk factors for sporadic cases — It is important to note that most STEC infections are sporadic, ie, they cannot be linked to an identifiable outbreak. A prospective case-control study evaluating children with sporadic bacterial diarrhea identified domestic travel, home septic systems, recreational water exposure, and consumption of food from self-serve buffets, mobile stands, or table-service restaurants as risk factors for E. coli O157:H7 infection [85].

Other studies have identified proximity to livestock, rural residence, and water (private supply) [86,87].

Residing in a rural area increases the risk for E. coli O157:H7 infection [88,89]. It is plausible that this increased risk is related to environmental transmission. E. coli O157:H7 can persist within cattle farms and spread to neighboring farms [90,91]. Geogenomic trends suggest clusters of related STEC infections over time, which likely arise from a common, persistent environmental reservoir [92].

Exposures to private water supplies, international travel, farm animals, raw sausage, and beef [87,93,94] have been proposed to be sources of sporadic non-O157:H7 STEC infections, though the literature is less extensive than for sporadic E. coli O157:H7 infections.

PREVENTION — STEC infection is primarily prevented through exposure reduction. Food safety measures to reduce 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 website on E. coli outbreak investigations.

Hand hygiene is also thought to reduce transmission. Most individuals shed STEC for seven days or less, although occasional individuals, particularly younger children, shed the organism for three weeks or longer [82,95-98].

Infection control measures for hospitalized patients and public health considerations are discussed elsewhere. (See "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment", section on 'Infection control measures'.)

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 5th to 6th 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 10th to 12th 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

Shiga toxin-producing Escherichia coli (STEC) cause serious disease characterized by bloody diarrhea; hemolytic uremic syndrome (HUS) is the major complication. Those that contain a gene encoding Shiga toxin 2 are more virulent (table 1). (See 'Shiga toxin type' above and 'Toxin production' above.)

E. coli strains can be classified by their O and H antigens into serotypes. E. coli O157:H7 is the most important STEC serotype in much of the world. It has been the most commonly isolated serotype and the leading cause of HUS, though data from Europe demonstrate that E. coli O26 is an increasingly common cause of HUS. Infections due to non-O157:H7 serotypes are increasingly recognized. (See 'Serotypes' above.)

The greatest burden of severe STEC infection and HUS occurs in children <5 years of age, followed by adults >60 years old. (See 'Affected age groups' above and 'Burden of disease' above.)

The most common route of transmission is foodborne; transmission also occurs through contact with colonized animals, infected individuals, and contaminated water. Beef has traditionally been the most common source of foodborne outbreaks, but many non-beef food products have also been implicated in STEC outbreaks. These mainly include fresh produce and other uncooked or unpasteurized products. (See 'Transmission' above.)

STEC infection is primarily prevented through exposure reduction. Preventive strategies include cooking beef and other meats adequately; avoiding consumption of unpasteurized dairy and juice products, raw flour or dough, and other foods that are implicated in outbreaks; and using proper hand hygiene. (See 'Prevention' above.)

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Topic 2711 Version 39.0

References

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