E. coli O157:H7—a foodborne pathogen
E. coli O157:H7 is one of thousands of serotypes of Escherichia coli.
E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis associated with consumption of hamburgers from a fast-food chain restaurant. Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolate with serotype O157:H7, and that was a case in 1975. In the ten years that followed, there were approximately thirty outbreaks recorded in the United States. This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987, when Washington became the first state to mandate its reporting to public health authorities. Consequently, an outbreak would not be detected if it was not large enough to prompt investigation.
E. coli O157:H7’s ability to induce injury in humans is a result of its ability to produce numerous virulence factors, most notably Shiga toxin (Stx), which is one of the most potent toxins known to man. Shiga toxin has multiple variants (e.g., Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells. Endothelial cells line the interior surface of blood vessels and are known to be extremely sensitive to E. coli O157:H7, which is cytotoxigenic to these cells.
E. coli O157:H7 evolved from enteropathogenic E. coli serotype O55:H7, a cause of non-bloody diarrhea, through the sequential acquisition of phage encoded Stx2, a large virulence plasmid, and additional chromosomal mutations. The rate of genetic mutation indicates that the common ancestor of current E. coli O157:H7 clades likely existed some 20,000 years ago. E. coli O157:H7 is a relentlessly evolving organism, constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat.
Although foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections, outbreaks of illnesses have been linked to a wide variety of food items. For example, produce has been the source of substantial numbers of outbreak-related E. coli O157:H7 infections since at least 1991. Outbreaks have been linked to alfalfa, clover and radish sprouts, lettuce, and spinach. Other vehicles for outbreaks include unpasteurized juices, yogurt, dried salami, mayonnaise, raw milk, game meats, hazelnuts, and raw cookie dough.
E. coli O157:H7 bacteria and other pathogenic E. coli mostly live in the intestines of cattle, but E. coli bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coli O157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. Over 7% of pest fly pools also tested positive for E. coli O157:H7. Shiga toxin-producing E. coli does not make the animals that carry it ill. The animals are merely the reservoir for the bacteria.
According to a study published in 2011, an estimated 93,094 illnesses are due to domestically acquired E. coli O157:H7 each year in the United States. Estimates of foodborne-acquired O157:H7 cases result in 2,138 hospitalizations and 20 deaths annually.
What makes E. coli O157:H7 remarkably dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. “E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.” As few as 20 organisms may be sufficient to infect a person and, as a result, possibly kill them. And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44° Fahrenheit, survives freezing and thawing, is heat-resistant, grows at temperatures up to 111 F, resists drying, and can survive exposure to acidic environments. And, finally, to make it even more of a threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact.
Cattle as Reservoirs
Beef and dairy cattle are known reservoirs of E. coli O157:H7 and non-O157 STEC strains. In reviews of STEC occurrence in cattle worldwide, the prevalence of non-O157 STECs ranged from 4.6 to 55.9% in feedlot cattle, 4.7 to 44.8% in grazing cattle, and 0.4 to 74% in dairy cattle feces. The prevalence in beef cattle going to slaughter ranged from 2.1 to 70.1%. While most dairy cattle-associated foodborne disease outbreaks are linked to milk products, dairy cattle still represent a potential source of contamination of beef products when they are sent to slaughter at the end of their useful production life (termed “cull” or “spent” dairy cows); this “dairy beef” is often ground and sold as hamburger.
The high prevalence of E. coli O157 and non-O157 STEC in some cattle populations, combined with the lack of effective on-farm control strategies to reduce carriage, represents a significant risk of contamination of the food supply and the environment. Non-O157 STEC are also harbored in other ruminants, including swine.
Numerous Shiga toxin-producing E. coli serotypes known to cause human illness are of bovine origin, thus putting the beef supply at-risk. Both E. coli O157:H7 and non-O157 STEC may colonize the gastrointestinal tract of cattle, and potentially contaminate beef carcasses during processing. Although not as well studied, the risk factors for contamination of beef products from cattle colonized with non-O157 STECs are probably the same or very similar to E. coli O157:H7. For example, cattle hides contaminated with E. coli O157:H7 during slaughter and processing are a known risk factor for subsequent E. coli O157:H7 contamination of beef products. One study showed that the prevalence of non-O157 STEC (56.6%) on hides is nearly as high as that found for E. coli O157:H7 (60.6%).
A review of published reports from over three decades found that non-O157 STEC were more prevalent in beef products compared with E. coli O157. In this study, the prevalence of non-O157 STEC ranged from 1.7 to 58% in packing plants, from 3 to 62.5% in supermarkets, and an average of 3% in fast food restaurants. In a recent survey of retail ground beef products in the United States, 23 (1.9%) of 1,216 samples were contaminated with non-O157 STEC. In another study, researchers found a 10 to 30% prevalence of non-O157 STEC in imported and domestic boneless beef trim used for ground beef.
Environmental Sources of E. coli
E. coli O157:H7 bacteria and other pathogenic E. coli are believed to mostly live in the intestines of cattle, but these bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coliO157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. Over seven percent of pest fly pools also tested positive for E. coli O157:H7. Shiga toxin-producing E. coli does not make the animals that carry it ill, the animals are merely the reservoir for the bacteria.
A Life-Threatening Complication—Hemolytic Uremic Syndrome
E. coli O157:H7 infections can lead to a severe, life-threatening complication called the hemolytic uremic syndrome (HUS). HUS accounts for most of the acute deaths and chronic injuries caused by the bacteria. HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. “E. coli serotype O157:H7 infection has been recognized as the most common cause of HUS in the United States, with 6% of patients developing HUS within 2 to 14 days of onset of diarrhea.” And it is the most common cause of renal failure in children.
Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long term renal impairment. The same number suffers severe brain damage. While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes, also occurs. There is no cure or effective treatment for HUS. And, tragically, children with HUS too often die, with a mortality rate of five to ten percent.
Once Shiga toxins attach to receptors on the inside surface of blood vessel cells (endothelial cells), a chemical cascade begins that results in the formation of tiny thrombi (blood clots) within these vessels. Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain. Consequently, organ injury is primarily a function of receptor location and density.
Once they move into the interior of the cell (cytoplasm), Shiga toxins shut down protein machinery, causing cellular injury or death. This cellular injury activates blood platelets too, and the resulting “coagulation cascade” causes the formation of clots in the very small vessels of the kidney, leading to acute kidney failure.
The red blood cells are either directly destroyed by Shiga toxin (hemolytic destruction) or are damaged as cells attempt to pass through partially obstructed micro-vessels. Blood platelets become trapped in the tiny blood clots, or they are damaged and destroyed by the spleen.
When fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and renal failure (loss of kidney function). Although recognized in the medical community since at least the mid-1950s, HUS first captured the public’s widespread attention in 1993 following a large E. coli outbreak in Washington State that was linked to the consumption of contaminated hamburgers served at a fast-food chain. Over 500 cases of E. coli were reported; 151 were hospitalized (31%), 45 persons (mostly children) developed HUS (9%), and three died.
Of those who survive HUS, at least five percent will suffer end stage renal disease (ESRD) with the resultant need for dialysis or transplantation. But “[b]ecause renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.” Other long-term problems include the risk for hypertension, proteinuria (abnormal amounts of protein in the urine that can portend a decline in renal function), and reduced kidney filtration rate. Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not available and remains controversial.
How is an E. coli Infection Diagnosed?
Infection with E. coli O157:H7 or other Shiga toxin-producing E. coli is usually confirmed by the detection of the bacteria in a stool specimen from an infected individual. Most hospitals labs and physicians know to test for these bacteria, especially if the potentially infected person has bloody diarrhea. Still, it remains a good idea to specifically request that a stool specimen be tested for the presence of Shiga toxin-producing E. coli.
Treatment for an E. coli Infection
In most infected individuals, symptoms of a Shiga toxin-producing E. coli infection last about a week and resolve without any long-term problems. Antibiotics do not improve the illness, and some medical researchers believe that these medications can increase the risk of developing HUS. Therefore, apart from supportive care, such as close attention to hydration and nutrition, there is no specific therapy to halt E. coli symptoms. The recent finding that E. coli O157:H7 initially speeds up blood coagulation may lead to future medical therapies that could forestall the most serious consequences. Most individuals who do not develop HUS recover within two weeks.
What to do to protect yourself and your family from E. coli
Since there is no fail-safe food safety program, consumers need to “drive defensively” as they navigate from the market to the table. It is no longer enough to take precautions only with ground beef and hamburgers; anything ingested by family members can be a vehicle for infection. Shiga toxin-producing E. coli are so widely disseminated that a wide variety of foods can be contaminated. Direct animal-to-person and person-to-person transmission is not uncommon. Following are steps you can take to protect your family.
- Practice meticulous personal hygiene. This is true not only for family members (and guests), but for anyone interfacing with the food supply chain. Remember that E. coli bacteria are very hardy (e.g., can survive on surfaces for weeks) and that only a few are sufficient to induce serious illness. Since there is no practical way of policing the hygiene of food service workers, it is important to check with local departments of health to identify any restaurants that have been given citations or warnings. The emerging practice of providing sanitation “report cards” for public display is a step in the right direction.
- Be sure to clean and sanitize all imported and domestic fruits or vegetables. All can be carriers of disease. If possible, fruits should be skinned, or at least vigorously scrubbed and/or washed. Vegetables (and of course meat) should be cooked to a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds. If not cooked, fruits and vegetables should be washed to remove any dirt or other material, and then soaked in chlorinated water (1 teaspoon of household bleach in one quart of water, soaked for at least 15 minutes). They can then be rinsed in clean water to remove the chlorine taste. This will remove most, but not all, bacteria. In the case of leafy vegetables, bacteria may not be limited to the leaf’s surface, but can reside within the minute circulatory system of the individual vegetable leaves.
- Be careful to avoid cross contamination when preparing and cooking food, especially if beef is being served. This requires being very mindful of the surfaces (especially cutting boards) and the utensils used during meal preparation that have met uncooked beef and other meats. This even means that utensils used to transport raw meat to the cooking surfaces should not be the same that are later used to remove the cooked meat (or other foodstuffs) from the cooking surfaces.
- Do not allow children to share bath water with anyone who has any signs of diarrhea or “stomach flu”. And keep any toddlers still in diapers out of all bodies of water (especially wading and swimming pools).
- Do not let any family members touch or pet farm animals. Merely cleaning the hands with germ “killing” wipes may not be adequate!
- Wear disposable gloves when changing the diapers of any child with any type of diarrhea. Remember that E. coliO157:H7 diarrhea initially is non-bloody, but still very infectious. If gloves are not available, then thorough hand washing is a must.
- Remember that achieving a brown color when cooking hamburgers does not guarantee that E. coli bacteria have been killed. This is especially true for patties that have been frozen. Verifying a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds is trustworthy. Small, disposable meat thermometers are available, a small investment compared to the medical expense (and grief) of one infected family member.
- Avoid drinking (and even playing in) any non-chlorinated water. There is an added risk if the water (well, irrigation water or creek/river) is close to, or downstream from any livestock.