Shigatoxigenic Escherichia coli (STEC)


Shigatoxigenic Escherichia coli (STEC) and verotoxigenic E. coli (and sometimes cause a severe complication called hemolytic-uremic syndrome (HUS).

STEC is distinguished from other strains of intestinal pathogenic E. coli including enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and diffusely adherent E. coli (DAEC).

The best known STEC strain is O157:H7.

The non-O157 strains of STEC caused an estimated 36,000 illnesses, 1,000 hospitalizations and 30 deaths in the United States yearly.

0157 is the most commonly identified serogroup in the stool of symptomatic persons worldwide it is identified in 84% of HUS cases in the US.

0157 can be detected by DNA amplification studies.

E. coli O26 causes less than 3% of cases of each US in the US.

Food safety specialists recognize 6 major strains: O26; O45; O103; O111; O121; and O145.

The O145 and O104 strains can cause hemolytic-uremic syndrome (HUS).

The O145 strain shown to account for 2% to 51% of known HUS cases.

Shiga toxin 1 and Shiga toxin 2 have different implications. 

Shiga toxin 2 produces serotypes that are much more virulent than Shiga toxin 1 producing serotypes, which rarely lead to HUS unless they also produce Shiga toxin 2.

The incidence of STEC infection peaks during summer and fall and his greatest among children younger than five years of age, the group at highest risk for the development of HUS.

Eneropathogeneic E. Coli induces bloody diarrhea leads to HUS in 10% of cases.

The manifestations of postdiarrheal HUS include acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia.

The verocytotoxin , shiga-like toxin,can directly damage renal and endothelial cells.

With HUS:

Thrombocytopenia occurs as platelets are consumed by clotting.

Hemolytic anemia results from intravascular fibrin deposition, increased fragility of red blood cells, and fragmentation.

Antibiotics have not shown to be of clear clinical benefit in HUS.

FLuoroquinolones, and other anti-biotics that interfere with DNA synthesis induce the Stx-bearing bacteriophage and cause increased production of toxins.

Plasma exchange is possibly helpful treatment in HUS.

The use of antimotility agents in children under 10 years of age or in elderly patients should be avoided, as they increase the risk of HUS with EHEC infections.

HUS presentation ranges from a mild and uncomplicated diarrhea to a hemorrhagic colitis with severe abdominal pain.

Serotype O157:H7 may trigger an infectious dose with 100 bacterial cells or fewer.

Infections are most common in warmer months.

Infection in children under five years of age are usually acquired from uncooked beef and unpasteurized milk and juice.

STEC initially presents as a non-bloody diarrhea after the bacterium attaches to the epithelium or the terminal ileum, cecum, and colon.

Production of toxins mediates the bloody diarrhea.

Patients may have abdominal pain, vomiting, and fever before the diarrhea phase of disease.

A median three day interval occurs between exposure to high risk STEC and the first loose stool.

Blood appears in the stool in nearly 2/3 of patients between 1 to 3 days after diarrhea begins.

Median number of stools in the 24 hours before presentation ranges from 7 to 11, and the diarrhea usually abates by day seven of illness.

Defecation is often painful.

Fever is reported in 30 to 50% of infected children.

In children, cytotoxins can attack the cells in the gut, allowing bacteria to leak out into the blood and cause endothelial injury in locations such as the kidney by binding to globotriaosylceramide, causing the hemolytic uremic syndrome.

HUS develops in 15 to 20% of infected children, with the greatest risk among those who were younger than five years of age.

HUS almost always manifest between days five and 14 of illness.

Rapid and progressive thrombocytopenia is the sentinel and universal hematologic abnormality in patients  with HUS and as often accompanied by hemoglobinuria and elevated serum LDH.

Hemoglobinuria reflects  intravascular hemolysis, the depletion of circulating haptoglobin, and plasma, hemoglobin levels that exceeded the reaborption capacity of the kidneys.

Microvascular endothelium activation is suspected to be the major contributor to the G.I. manifestations of STEC infections with superficial inflammation, focal necrosis, suggesting ischemia.

Ischemia may be the consequence of prothrombotic and pro-inflammatory injury during the initial diarrhea phase triggered by the Shiga toxin circulation, with subsequent damage to the microvascular endothelium.

Thrombotic microvascular injury is a major factor in the progression to HUS with microvascular thrombosis in the kidneys, brain, heart, and other extra intestinal organs.

Early diagnosis of STEC infection is important and stool samples from all patients with hematochezia and from children with non-bloody diarrhea, accompanied by tenesmus, orsevere abdominal pain should be sent for bacterial pathogen detection.

Stool swabs are the initial specimen, but stool collection when available.


enterohemorrhagic E. coli EHEC

hemolytic uremic syndrome–associated enterohemorrhagic E. coli HUSEC

shiga toxin–producing E. coli STEC

shigatoxigenic E. coli STEC

shiga-like toxin–producing E. coli SLTEC

verotoxin-producing E. coli VTEC

verotoxigenic E. coli VTEC

verocytotoxin-producing E. coli VTEC

verocytotoxigenic E. coli VTEC

Complement activation induced by the intestinal infection or by SHIGA toxin itself may play a role in STC related HUS.

During the acute illness a decrease in C3 and C4 occur along with increasing complement breakdown products.


Initial assessment for STEC infection includes CBC, chemistry profile, and blood smearto identify a microangiopathy.

Serial  blood tests can help monitor the process of finding decreasing platelet counts, hemoglobin levels or increasing creatinine levels.

An elevated LDH is associated with it progression to HUS.

Many interventions are potentially harmful in patients with possible or  confirmed. STEC infection: antibiotic administration increases the risk of HUS, narcotics and anti-motility drugs prolong bloody diarrhea, and increase the risk of HUS and neurologic complications, nonsteroidal, anti-inflammatory drugs, increased risk of kidney injury, and use of ondansetron increases the frequency of diarrhea and may prolong QT interval.

Patients with high relative hematocrit or hemoglobin values have worse outcomes, and are more likely to receive kidney replacement therapy and increased risk of neurologic complications and death, so such children should have administration of intravenous isotonic fluids, pending results of blood tests confirming HUS.

More than 50% of patients with STEC related HUS receive kidney replacement therapy.

Hemodialysis and peritoneal dialysis are equivalent with respect to survival benefit with acute kidney injury, and the choice depends on individual characteristics, expertise and resources.

Packed RBC transfusions are given to most patients with STEC associated HUS.

Platelet infusions are limited to patients with significant bleeding related to the possibility of causing thrombotic injury.

Sugar toxin is a therapeutic target in patients if the Shiga toxin 2 has been identified in serum.

Using eculizumab or plasma exchange does not seem to benefit patients with STEC-HUS.

Risk factors for the development of HUS-STEC  infected patients include: age less than five years and greater than 75 years, female sex, the presence of bloody diarrhea, vomiting, the presence of Shiga toxin 1, leucocytosis, and a platelet count below 250,000 per cubic millimeter.




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