Escherichia coli O157:H7
A Shiga toxin-producing E. coli causing foodborne outbreaks and kidney failure.
Escherichia coli O157:H7 is a specific strain of the *E. coli* bacterium that produces Shiga-like toxins, making it a pathogen. It typically causes foodborne illness when people eat contaminated or raw foods, such as raw milk or undercooked ground beef. Infection can lead to bloody diarrhea or kidney failure, and has been known to be fatal in children under five, the elderly, and people with weakened immune systems.
The illness spreads through the fecal-oral route, often via contaminated raw leafy greens, undercooked meat, or unpasteurized milk. Symptoms usually include severe, acute bloody diarrhea (though non-bloody diarrhea is also possible) and abdominal cramps, with little to no fever. Most people recover in 5 to 10 days, but some cases are asymptomatic. In vulnerable groups—young children under five, older adults, and immunocompromised individuals—the infection can progress to hemolytic-uremic syndrome (HUS), which destroys red blood cells and causes acute kidney failure. About 2–7% of infections lead to this complication, and in the United States, HUS is the leading cause of acute kidney failure in children, most often linked to this strain.
Bacteriologically, O157:H7 is gram-negative and oxidase-negative like other *E. coli*, but it stands out because it cannot ferment sorbitol—a trait used in lab identification. Its ability to produce Shiga toxins comes from a prophage (a virus integrated into its DNA) that carries the toxin gene. Non-toxin-producing strains can acquire this ability if they are exposed to toxin-positive strains. The prophage appears to have infected the strain's ancestors relatively recently, and it can replicate when the bacterium is stressed, such as by antibiotics. All clinical isolates of O157:H7 carry a plasmid called pO157, which encodes a catalase enzyme that may boost the bacterium's virulence by protecting it from oxidative damage during infection. Non-hemorrhagic strains can become hemorrhagic through lysogenic conversion after being infected by a bacteriophage.
In nature, O157:H7 is relatively uncommon but can be found in the intestines of cattle, goats, and sheep. Cattle lack the Shiga toxin receptor, so they can carry the bacterium without symptoms. In North American feedlot herds, prevalence ranges from 0 to 60%.
Quick Facts
- Field
- Infectious disease
Facts from the source article.
Lore & Background
The common ancestor of Escherichia coli O157:H7 originated in the Netherlands around 1890, as estimated by molecular biologists. International spread is thought to have occurred through animal movements, such as Holstein Friesian cattle. The strain moved from Europe to Australia around 1937, to the United States in 1941, to Canada in 1960, and from Australia to New Zealand in 1966. The first recorded observation of human infection was in 1975, in association with a sporadic case of hemorrhagic colitis, but it was not identified as pathogenic then. It was first recognized as a human pathogen following a 1982 hemorrhagic colitis outbreak in Oregon and Michigan, in which at least 47 people were sickened by eating beef hamburger patties from a fast food chain that were found to be contaminated with it.
Reader's Guide
Escherichia coli O157:H7 is significant as a leading cause of foodborne illness and acute kidney failure in children in the United States. Its low infectious dose—fewer than 10 to 100 colony-forming units—makes it highly virulent compared to other pathogenic E. coli strains. The bacterium is transmitted via the fecal–oral route, often through contaminated raw leaf green vegetables, undercooked meat, and raw milk. Infection can lead to hemolytic–uremic syndrome (HUS), characterized by destruction of red blood cells and acute kidney failure, particularly in young children, older adults, and immunocompromised individuals. Approximately 2–7% of infections progress to HUS. The United States Department of Agriculture banned the sale of ground beef contaminated with the O157:H7 strain in 1994. Treatment focuses on fluid replacement and blood pressure support, as antibiotics may precipitate HUS and antidiarrheal agents may prolong infection. The pathogen results in an estimated 2,100 hospitalizations annually in the United States.
Did You Know?
- E. coli O157:H7 does not ferment sorbitol, which allows clinical differentiation on sorbitol-MacConkey agar.
- The bacterium's Shiga toxin genes are carried by a prophage, and nonproducing strains can become toxin-producing after incubation with toxin-positive strains.
- Some cattle are 'super-shedders,' excreting >10^3 to 10^4 CFU per gram of feces, and may account for >90% of all E. coli O157:H7 excreted in a feedlot.
- The common ancestor of E. coli O157:H7 originated in the Netherlands around 1890.
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