Escherichia coli are the most numerous aerobic commensal inhabitants of the large intestine. Certain strains cause diarrhea, and all can cause infection when they invade sterile sites (eg, the urinary tract). Diagnosis is by standard culture techniques. Toxin assays may help identify the cause of diarrhea. Treatment with antibiotics is guided by susceptibility testing.

Diseases caused by E. coli : Most commonly, E. coli cause UTIs, which usually represent ascending infection (ie, from the perineum via the urethra).

E. coli normally inhabit the GI tract; however, some strains have acquired genes that enable them to cause intestinal infection. When ingested, the following strains can cause diarrhea:

• Enterohemorrhagic: These strains (eg, type O157:H7—see Gram-Negative Bacilli: E. coli O157:H7 Infection) produce several cytotoxins, neurotoxins, and enterotoxins, including Shiga toxin, and cause bloody diarrhea; hemolytic-uremic syndrome develops in 2 to 7% of cases (see Thrombocytopenia and Platelet Dysfunction: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)). Such strains have most often been acquired from undercooked ground beef but may also be acquired from infected people by the fecal-oral route when hygiene is inadequate.
• Enterotoxigenic: These strains can cause watery diarrhea, particularly in infants and travelers (see Gastroenteritis: Traveler's Diarrhea).
• Enteroinvasive: These strains can cause inflammatory diarrhea.
• Enteropathogenic: These strains can cause watery diarrhea, particularly in infants.
• Enteroaggregative: Some strains are emerging as potentially important causes of persistent diarrhea in patients with AIDS and in children in tropical areas.

Other strains are capable of causing extraintestinal infection if normal intestinal anatomic barriers are disrupted (eg, by ischemia, inflammatory bowel disease, or trauma), in which case the organism may spread to adjacent structures or invade the bloodstream. Hepatobiliary, peritoneal, cutaneous, and pulmonary infections also occur. E. coli bacteremia may also occur without an evident portal of entry.

In neonates, particularly preterm infants, E. coli bacteremia and meningitis (caused by strains with the K1 capsule, a marker for neuroinvasiveness) are common (see Neonatal Meningitis on see Infections in Neonates: Neonatal Bacterial Meningitis and Neonatal Sepsis on see Infections in Neonates: Neonatal Sepsis).

Diagnosis

• Culture

Samples of blood, stool, or other clinical material are sent for culture. If an enterohemorrhagic strain is suspected, the laboratory must be notified because special culture media are required.

Treatment

• Various antibiotics depending on site of infection and susceptibility testing

Treatment must be started empirically based on the site and severity of infection (eg, mild bladder infection, urosepsis) and then modified based on antibiotic susceptibility testing. Many strains are resistant to ampicillinSome Trade Names
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PRINCIPEN
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and tetracyclines, so other drugs should be used; they include ticarcillinSome Trade Names
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, piperacillinSome Trade Names
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, cephalosporins, aminoglycosides, trimethoprim/sulfamethoxazoleSome Trade Names
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(TMP/SMX), and fluoroquinolones.

Surgery may be required to drain pus, debride necrotic lesions, or remove foreign bodies.

E. coli O157:H7 Infection

E. coli O157:H7 typically causes acute bloody diarrhea, which may lead to hemolytic-uremic syndrome. Symptoms are abdominal cramps and diarrhea that may be grossly bloody. Fever is not prominent. Diagnosis is by stool culture and toxin assay. Treatment is supportive; antibiotic use is controversial.

Epidemiology

Although > 100 serotypes of E. coli produce Shiga and Shiga-like toxins, E. coli O157:H7 is the most common in North America. In some parts of the US and Canada, E. coli O157:H7 infection may be a more common cause of bloody diarrhea than shigellosis or salmonellosis. E. coli O157:H7 infection can occur in people of all ages, although severe infection is most common among children and the elderly.

E. coli O157:H7 has a bovine reservoir, so outbreaks and sporadic cases occur after ingestion of undercooked beef (especially ground beef) or unpasteurized milk. Food or water contaminated with cow manure or raw ground beef can also transmit infection. The organism can also be transmitted by the fecal-oral route, especially among infants in diapers (eg, via inadequately chlorinated children's wading pools).

After ingestion, E. coli O157:H7 and similar strains of E. coli (termed enterohemorrhagic E. coli) produce high levels of various toxins in the large intestine; these toxins are closely related to the potent cytotoxins produced by Shigella dysenteriae type 1. These toxins appear to directly damage mucosal cells and vascular endothelial cells in the gut wall. If absorbed, they exert toxic effects on other vascular endothelia (eg, renal).

Symptoms and Signs

E. coli O157:H7 infection typically begins acutely with severe abdominal cramps and watery diarrhea that may become grossly bloody within 24 h. Some patients report diarrhea as being “all blood and no stool,” which has given rise to the term hemorrhagic colitis. Fever, usually absent or low grade, occasionally reaches 39° C. Diarrhea may last 1 to 8 days in uncomplicated infections.

About 5% of cases (mostly children < 5 yr and adults > 60 yr) are complicated by hemolytic-uremic syndrome (see Thrombocytopenia and Platelet Dysfunction: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)), which typically develops in the 2nd wk of illness. Death may occur, especially in the elderly, with or without this complication.

Diagnosis

• Stool cultures
• Sometimes rapid stool assay for Shiga toxin

E. coli O157:H7 infection should be distinguished from other infectious diarrheas by isolating the organism from stool cultures. Often, the clinician must specifically ask the laboratory to test for the organism. Because bloody diarrhea and severe abdominal pain without fever suggest various noninfectious etiologies, E. coli O157:H7 infection should be considered in suspected cases of ischemic colitis, intussusception, and inflammatory bowel disease. A rapid stool assay for Shiga toxin may help. Patients at risk of noninfectious diarrheas may need sigmoidoscopy. If done, sigmoidoscopy may reveal erythema and edema; barium enema typically shows evidence of edema with thumbprinting.

Treatment

• Supportive care

The mainstay of treatment is supportive. Although E. coli is sensitive to most commonly used antibiotics, antibiotics have not been shown to alleviate symptoms, reduce carriage of the organism, or prevent hemolytic-uremic syndrome. Fluoroquinolones are suspected of increasing release of enterotoxins.

In the week after infection, patients at high risk of developing hemolytic-uremic syndrome (eg, children < 5 yr, the elderly) should be observed for early signs, such as proteinuria, hematuria, red cell casts, and rising serum creatinine. Edema and hypertension develop later. Patients who develop complications are likely to require intensive care, including dialysis and other specific therapies, at a tertiary medical center.

Prevention

Correct disposal of the stool of infected people, good hygiene, and careful hand washing with soap limit spread of infection. Preventive measures that may be effective in the day care setting include grouping children known to be infected with E. coli O157:H7 or requiring 2 negative stool cultures before allowing infected children to attend. Pasteurization of milk and thorough cooking of beef prevent food-borne transmission.

Reporting outbreaks of bloody diarrhea to public health authorities is important because intervention can prevent additional infections.

Last full review/revision August 2009 by Burke A. Cunha, MD

Content last modified February 2012