980-E. coli 0157:H7

Course # DL-980: What You Always Wanted to Know About E. coli 0157:H7 Infection

by James I. Mangels, MA, CLS, MT(ASCP) - Consultant - Microbiology Consulting Services Santa Rosa, CA

Approved for 3.0 CE
Level of Difficulty: Intermediate


The Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia estimates that 76 million Americans become ill, 300,000 are hospitalized, and 5,000 people die from foodborne illnesses each year (2). According to the CDC’s data, 24% of foodborne disease outbreaks are caused by bacteria, 5.4% by chemicals, 0.7% by parasites, 4.2% by viruses, and 68% are of unknown etiology (2). The most commonly reported bacterial agents of foodborne infections are, Campylobacter, Salmonella, Clostridium perfringens, and E. coli O157:H7 (2).

First described in 1982 after a foodborne outbreak involving undercooked hamburgers, E. coli O157:H7 is now recognized as a significant cause of foodborne and waterborne illness in the industrialized world (2). Each year, E. coli O157:H7 and other Shigella toxin-producing E. coli (STEC) strains cause an estimated 73,000 cases of hemorrhagic colitis and 60 deaths in the United States (likely an underestimate because many laboratories do not routinely include selective media for this organism, as this course will describe). As many as 8-18% of victims with E. coli O157:H7 infection—particularly young children or the elderly—go on to develop a disease called hemolytic uremic syndrome (HUS) (1,5,6). These patients may require kidney dialysis, transfusions or transplant, and some are left with chronic renal failure and neurological damage. Three to 5% of patients with HUS die (5,6).

Over 100 serotypes of E. coli produce Shigella toxins, and over 50 serotypes have been associated with hemorrhagic colitis or HUS (4). In the United States, E. coli O157:H7 is the most frequently isolated E. coli producing Shigella toxin (Shiga-toxin E. coli or STEC), but increasingly other non-O157 STEC organisms are being identified as causes of outbreaks and sporadic illness. Because most current laboratory methods for the detection of O157 STEC do not also detect non-O157 STEC, the incidence of documented non-O157 infections is undetermined (1,3, 4).

In some countries, non-O157 STEC serotype strains are more commonly isolated, although most outbreaks and most cases of HUS are attributed to O157 STEC. In Europe and Australia, non-O157 serotypes predominate, especially 0111:H, 026, and 0103:H5, among others.

Clinical laboratories play a key role in the detection and surveillance of outbreaks. To protect the public health, it is critical that clinical laboratories are able to identify or rule out pathogens like E. coli O157:H7 during outbreaks. However, surveys have shown that laboratories vary widely in their stool culture protocol and in their ability to reliably isolate and correctly identify this organism (1,5,6). In some geographic areas and age groups in the United States, the rate of isolation of E. coli O157 from fecal specimens equals that of Campylobacter and exceeds that of Salmonella and Shigella.

This distance learning course will review some of the history of E. coli O157:H7 infection, where the isolates are found, how the organism is spread, the clinical symptoms of the disease, how the organism is isolated and identified by the clinical laboratory, and some steps people can take to reduce the risk of infection.


After completing this course the participant will be able to

  1. discuss the incidence of E. coli O157:H7 infection.
  2. outline the history of E. coli O157:H7 infections.
  3. explain how E. coli O157:H7 is acquired and spread.
  4. outline the clinical features of E. coli O157:H7 infection and some of the potential consequences of the disease.
  5. explain how the organism is isolated and identified.
  6. state methods to prevent or avoid infection from this organism.


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