The E. coli O157:H7 Bacteria

E. coli O157:H7 is one of hundreds of strains of the bacterium Escherichia coli. Most strains of E. coli are harmless and live as normal flora in the intestines of healthy humans and animal. The E. coli bacterium is among the most extensively studied microorganism. The combination of letters and numbers in the name of the E. coli O157:H7 refers to the specific markers found on its surface and distinguishes it from other types of E. coli. The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping. Pulsed-field gel electrophoresis (“PFGE”), sometimes also referred to as genetic fingerprinting, is used to compare E. coli O157:H7 isolates to determine if the strains are distinguishable.

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 isolation 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. As a result, only the most geographically concentrated outbreak would have garnered enough notice to prompt further investigation.

The virulence of E. coli O157:H7 is a result of its ability to produce Shiga-like toxins. It has been theorized that generic E. coli picked up this deadly ability through horizontal transfer of virulence genes from the Shigella bacteria. Genome sequencing of E. coli O157:H7 has since confirmed that gene transfer did in fact occur, and that the evolution of ever more virulent forms of bacteria will likely continue to occur. The CDC has emphasized the prospect of emerging pathogens as a significant public health threat for some time.

Foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections. Surveys performed on feedlots have demonstrated that cattle can be infected with E. coli O157:H7 through close contact, and under muddy conditions. The prevalence of E. coli O157:H7 among cattle in these feed lots can reach 63-100%, especially during the summer. The prevalence of E. coli O157:H7 in the summer, which is when outdoor grilling of hamburgers becomes most common, is a significant public safety risk.

According to a recent study, an “estimated 73,480 illnesses due to E. coli O157:H7 infections occur each year in the United States, leading to an estimated 2,168 hospitalizations and sixty-one deaths annually.” The hemorrhagic colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within twenty-four hours, and sometimes fevers. The typical incubation period—which is to say the time from exposure to the onset of symptoms—in outbreaks is usually reported as three to eight days. Infection can occur in people of all ages but is most common in children. The duration of an uncomplicated illness can range from one to twelve days. In reported outbreaks, the rate of death is 0-2%, with rates running as high as 16-35% in outbreaks involving the elderly, like those at nursing homes.

What makes E. coli O157:H7 truly and decidedly dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. Unlike Salmonella, for example, which usually requires something approximating an “egregious food handling error, E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.” As few as twenty organisms have been said to 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 degrees Fahrenheit, survives freezing and thawing, is heat resistant, grows at temperatures up to 111 degrees Fahrenheit, resists drying, and can survive exposure to acidic environments.

And, finally, to make it even more of a dangerous threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact. There is also the serious risk of cross-contamination between raw meat and other food items intended to be eaten without cooking. Indeed, a principle and consistent criticism of the USDA E. coli O157:H7 policy is the fact that it has failed to focus on the risks of cross-contamination versus that posed by so-called improper cooking. With this pathogen, there is ultimately no real margin of error, and the cost of error can be death. It is for this precise reason that the USDA has repeatedly rejected calls from the meat industry to hold consumers responsible for E. coli O157:H7 surviving after cooking.

Hemolytic Uremic Syndrome (HUS)

E. coli O157:H7 infections can lead to a severe, life-threatening complication called hemolytic uremic syndrome (“HUS”). HUS accounts for the majority of the acute and chronic illness and death caused by the bacteria. HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. 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 can also occur. There is no cure or effective treatment for HUS. And, tragically, as too many parents can attest, children with HUS too often die.

HUS develops when the toxin from the bacteria, known as Shiga-like toxin (“SLT”), enters the circulation through the inflamed bowel wall. SLT, and most likely other chemical mediators, attach to receptors on the inside surface of blood vessel cells (endothelial cells) and initiate a chemical cascade 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. By definition, when fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and acute renal failure (loss of kidney function).

As already noted, there is no known therapy to halt the progression of HUS. HUS is a frightening complication that even in the best American centers has a notable mortality rate. Among survivors, 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 really available and remains controversial. All that can be said for certain is that HUS causes permanent injury, and it requires a lifetime of close medical monitoring.


– E. coli bacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich. Feng, Peter, Stephen D. Weagant, Michael A. Grant, Enumeration of Escherichia coli and the Coliform Bacteria, in BACTERIOLOGICAL ANALYTICAL MANUAL (8th ed. 2002), available online at Dr. Escherich also showed that certain strains of the bacteria were responsible for infant diarrhea and gastroenteritis, an important public health discovery. – Id. Although the bacteria were initially called Bacterium coli, the name was later changed to Escherichia coli to honor its discoverer. Id.
– Marion Nestle, Safe Food:Bacteria, Biotechnology, and Bioterrorism, 40-41 (1st Pb. Ed. 2004).
– James M. Jay, MODERN FOOD MICROBIOLOGY at 21(6th ed. 2000) (“This is clearly the most widely studied genus of all bacteria.”)
– CDC, Escherichia coli O157:H7, General Information, Frequently Asked Questions: What is Escherichia coli O157:H7?,
– Beth B. Bell, MD, MPH, et al., A Multistate Outbreak of Escherichia coli O157:H7-Associated Bloody Diarrhea and Hemolytic Uremic Syndrome from Hamburgers: The Washington Experience, 272 JAMA (No. 17) 1349, 1350 (Nov. 2, 1994) (describing the multiple step testing process used to confirm, during a 1993 outbreak, that the implicated bacteria were E. coli O157:H7).
– Jay, supra note 3, at 220-21 (describing in brief the PFGE testing process).
– Id. Through PFGE testing, isolates obtained from the stool cultures of probable outbreak cases can be compared to the genetic fingerprint of the outbreak strain, confirming that the person was in fact part of the outbreak. Bell, supra note 5, at 1351-52. Because PFGE testing soon proved to be such a powerful outbreak investigation tool, PulseNet, a national database of PFGE test results was created. – Bala Swaminathan, et al., PulseNet: The Molecular Subtyping Network for Foodborne Bacterial Disease Surveillance, United States, 7 Emerging Infect. Dis. (No. 3) 382, 382-89 (May-June 2001) (recounting the history of PulseNet and its effectiveness in outbreak investigation).
“ [A] type of gastroenteritis in which certain strains of the bacterium Escherichia coli (E. coli) infect the large intestine and produce a toxin that causes bloody diarrhea and other serious complications.” The Merck Manual of Medical Information, Second Home Edition Online,
– L. Riley, et al., Hemorrhagic Colitis Associated with a Rare Escherichia coli Serotype, 308 New. Eng. – J. Med. 681, 684-85 (1983) (describing investigation of two outbreaks affecting at least 47 people in Oregon and Michigan both linked to apparently undercooked ground beef); Chinyu Su, MD & Lawrence J. Brandt, MD, Escherichia coli O157:H7 Infection in Humans, 123 Annals Intern. Med. (Issue 9), 698-707 (describing the epidemiology of the bacteria, including an account of its initial discovery).
– Riley, supra note 9 at 684. See also Patricia M. Griffin & Robert V. Tauxe, The Epidemiology of Infections Caused by Escherichia coli O157:H7, Other Enterohemorrhagic E. coli, and the Associated Hemolytic Uremic Syndrome, 13 Epidemiologic Reviews 60, 73 (1991).
– Peter Feng, Escherichia coli Serotype O157:H7: Novel Vehicles of Infection and Emergence of Phenotypic Variants, 1 Emerging Infect. Dis. (No. 2), 47, 47 (April-June 1995) (noting that, despite these earlier outbreaks, the bacteria did not receive any considerable attention until ten years later when an outbreak occurred 1993 that involved four deaths and over 700 persons infected).
– William E. Keene, et al., A Swimming-Associated Outbreak of Hemorrhagic Colitis Caused by Escherichia coli O157:H7 and Shigella Sonnei, 331 New Eng. J. Med. 579 (Sept. 1, 1994). See also Stephen M. Ostroff, MD, John M. Kobayashi, MD, MPH, and Jay H.Lewis, Infections with Escherichia coli O157:H7 in Washington State: The First Year of Statewide Disease Surveillance, 262 JAMA (No. 3) 355, 355 (July 21, 1989) (“It was anticipated the reporting requirement would stimulate practitioners and laboratories to screen for the organism.”)
– See Keene, supra note 12, at 583 (“With cases scattered over four counties, the outbreak would probably have gone unnoticed had the cases not been routinely reported to public health agencies and investigated by them.”). With improved surveillance, mandatory reporting in 48 states, and the broad recognition by public health officials that E. coli O157:H7 was an important and threatening pathogen, there was a total of 350 reported outbreaks from 1982-2002. Josefa M. Rangel, et al., Epidemiology of Escherichia coli O157:H7 Outbreaks, United States, 1982-2002, 11 Emerging Infect. Dis. (No. 4) 603, 604 (April 2005).
– Griffin & Tauxe, supra note 10, at 61-62 (noting that the nomenclature came about because of the resemblance to toxins produced by Shigella dysenteriae).
– Griffin & Tauxe, supra note 10, at 62 (using the more technical term “phage-mediated transfer”)
– Nicole T. Perna, et al., Genome Sequence of enterohaemorrhagic Escherichia coli O157:H7, 409 Nature 529 (Janote 25, 2001) (finding that E. coli O157:H7 has 1, 387 genes not found in non-pathogenic E. coli). See also Robert V. Tauxe, Emerging Foodborne Diseases: An Evolving Public Health Challenge, 3 Emerging Infect. Dis. 425 (1997) (arguing that the epidemiology of foodborne disease will continue to change, requiring increased collaboration of regulatory agencies and Meat Industry, and the strengthening of surveillance and research efforts).
– Robert A. Tauxe, Emerging Foodborne Diseases: An Evolving Public Health Challenge, 3 Emerging Infect. Dis. (No. 4) 425, 427 (Oct.-Dec. 1997) (“After 15 years of research, we know a great deal about infections with E. coli O157:H7, but we still do not know how best to treat the infection, nor how the cattle (the principal source of infection for humans) themselves become infected.”). The FSIS failed to respond to the problem of microbial pathogens in the ten years after the 1982 E. coli O157:H7 outbreak even though a 1985 report by the National Academy of Sciences concluded that the Agency’s organoleptic inspection methods were inadequate to detect pathogens like E. coli O157:H7. See General Accounting Office, Food Safety: Risk-Based Inspection and Microbial Monitoring Needed for Meat and Poultry, GAO-94-110, at 5.
– CDC, Multistate Outbreak of Escherichia coli O157:H7 Infections Associated With Eating Ground Beef—United States, June-July 2002, 51 MMWR 637, 638 (2002) reprinted in 288 JAMA (No. 6) 690 (Aug. 14, 2002)
– Id. See also Nestle, supra note 2, at 44-45 (“Animals from many locations arrive at the slaughterhouse together and remain in close contact until killed; their carcasses remain in close contact until processed. Contact alone favors the spread of pathogens.”).
– CDC, supra note 18, at 638 and nn.4 and 5.
– Rangel, supra note 13, at 603.
– Griffin & Tauxe, supra note 10, at 63.
– Robert V. Tauxe, et al., Foodborne Disease, in MANDELL, DOUGLAS AND BENNETT’S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASE 1150, 1152 (5th ed. 2000). See also PROCEDURES TO INVESTIGATE FOODBORNE ILLNESS, 107 (IAFP 5th Ed. 1999) (identifying incubation period for E. coli O157:H7 as “1 to 10 days, typically 2 to 5”). In the Sizzler outbreak, the mean incubation period was 4.04 days, with a range of 2 to 24 days.
– Su & Brandt, supra note 9 (“the young are most often affected”)
– Tauxe, supra note 23 at 1152.
– Id.
– Griffin & Tauxe, supra note 10, at 72 (“The general patterns of transmission in these outbreaks suggest that the infectious dose is low.”).
– V. K. Juneja, O.P. Snyder, A. C. Williams, and B.S. Marmer, Thermal Destruction of Escherichia coli O157:H7 in Hamburger, 60 J. Food Prot. (vol. 10). 1163-1166 (1997) (demonstrating that, if hamburger does not get to 130F, there is no bacterial destruction, and at 140F, there is only a 2-log reduction of E. coli present).
– Griffin & Tauxe, supra note 10, at 72 (noting that, as a result, “fewer bacteria are needed to cause illness that for outbreaks of salmonellosis”); Nestle, supra note 2, at 41 (“Foods containing E. coli O17:H7 must be at temperatures high enough to kill all of them.”) (italics in original). The use of the term “undercooked” here, and elsewhere, should be recognized as the tautology it is—i.e., undercooked means cooking that resulted in enough bacteria surviving to cause infection. While “undercooked” can imply negligence on the part of the person preparing the ground beef, especially as the term is often used by the those in the Meat Industry, this implication ignores the complexity of the heat destruction of this bacteria in a non-homogenous medium like ground beef. For example, after telling cooks for years to use color as an indicator of doneness, in June 1997 the USDA issued a press release retracting its previous advice and recommended in its place that a thermometer should be used to ensure “thorough” cooking. See FSIS Technical Publication, Color of Cooked Ground Beef as it Relates to Doneness, available online at (citing the studies that prompted the changed recommendation). The USDA’s current recommendations are still not without some learned and well-respected critics. See, e.g. O. Peter Snyder, Ph.D., The Dangerous Bi-Metallic Thermometer, available at (“USDA-recommended bimetallic coil thermometer is an inaccurate, awkward, and complicated device for measuring the temperature of highly contaminated, government-inspected and improved raw foods that cooks must pasteurize”). Consequently, it must be remembered that the USDA’s zero-tolerance policy for the presence of E. coli O157:H7 in ground beef is premised on the finding that ground beef, as “customarily cooked,” does not ensure that it will free of the bacteria when consumed, and that “an E. coli O157:H7-contaminated product must not be distributed until it has been processed into a ready-to-eat product—i.e., a food product that may be safely consumed without any further cooking or preparation.” See USDA, Beef Products Contaminated with Escherichia coli O157:H7, 64 Fed. Reg. 2803, at 2804 (Jan. 19, 1999). That is why all ground beef that contains E. coli O157:H7 is per se adulterated within the meaning of the Federal Meat Inspection Act. Id.
– Patricia M. Griffin, et al., Large Outbreak of Escherichia coli O157:H7 Infections in the Western United States: The Big Picture, in RECENT ADVANCES IN VEROCYTOTOXIN-PRODUCING ESCHERICHIA COLI INFECTIONS, at 7 (M.A. Karmali & A. G. Goglio eds. 1994) (“The most probable number of E. coli O157:H7 was less than 20 organisms per gram.”). There is some inconsistency with regard to the reported infectious dose. Compare Chryssa V. Deliganis, Death by Apple Juice: The Problem of Foodborne Illness, the Regulatory Response, and Further Suggestions for Reform, 53 Food Drug L.J. 681, 683 (1998) (“as few as ten”) with Nestle, supra note 2, at 41 (“less than 50”). Regardless of these inconsistencies, everyone agrees that the infectious dose is, as Dr. Nestle has put it, “a miniscule number in bacterial terms.” Id.
– Nestle, supra note 2, at 41.
– Griffin & Tauxe, supra note 10, at 72. The apparent “ease of person-to-person transmission…is reminiscent of Shigella, an organism that can be transmitted by exposure to extremely few organisms.” Id. As a result, outbreaks in places like daycare centers have proven relatively common. – Rangel, supra note __, at 605-06 (finding that 80% of the 50 reported person-to-person outbreak from 1982-2002 occurred in daycare centers).
– See, e.g. National Academy of Science, Escherichia coli O157:H7 in Ground Beef: Review of a Draft Risk Assessment, Executive Summary, at 7 (noting that the lack of data concerning the impact of cross-contamination of E. coli O157:H7 during food preparation was a flaw in the Agency’s risk-assessment), available at
– Kriefall v. Excel, 265 Wis.2d 476, 506, 665 N.W.2d 417, 433 (2003) (“Given the realities of what it saw as consumers’ food-handling patterns, the [USDA] bored in on the only effective way to reduce or eliminate food-borne illness”—i.e., making sure that “the pathogen had not been present on the raw product in the first place.”) (citing Pathogen Reduction, 61 Fed. Reg. at 38966).
– Griffin & Tauxe, supra note 10, at 65-68. See also Josefa M. Rangel, et al., Epidemiology of Escherichia coli O157:H7 Outbreaks, United States, 1982-2002, 11 Emerging Infect. Dis. (No. 4) 603 (April 2005) (noting that HUS is characterized by the diagnostic triad of hemolytic anemia—destruction of red blood cells, thrombocytopenia—low platelet count, and renal injury—destruction of nephrons often leading to kidney failure); Richard L. Siegler, MD, The Hemolytic Uremic Syndrome, 42 Ped. Nephrology, 1505 (Dec. 1995) (noting that the diagnostic triad of hemolytic anemia, thrombocytopenia, and acute renal failure was first described in 1955).
– Siegler, supra note 35 at 1505. (“[HUS] is now recognized as the most frequent cause of acute renal failure in infants and young children.”) See also Beth P. Bell, MD, MPH, et al., Predictors of Hemolytic Uremic Syndrome in Children During a Large Outbreak of Escherichia coli O157:H7 Infections, 100 Pediatrics 1, 1 (July 1, 1997), at
– Tauxe, supra note 17, at 1152. See also Nasia Safdar, MD, et al., Risk of Hemolytic Uremic Syndrome After Treatment of Escherichia coli O157:H7 Enteritis: A Meta-analysis, 288 JAMA (No. 8) 996, 996 (Aug. 28, 2002). (“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.”); Amit X. Garg, MD, MA, et al., Long-term Renal Prognosis of Diarrhea-Associated Hemolytic Uremic Syndrome: A Systematic Review, Meta-Analysis, and Meta-regression, 290 JAMA (No. 10) 1360, 1360 (Sept. 10, 2003). (“Ninety percent of childhood cases of HUS are…due to Shiga-toxin producing Escherichia coli.”)
– Su & Brandt, supra note 9.
– Safdar, supra note 37, at 996 (going on to conclude that administration of antibiotics to children with E. coli O157:H7 appeared to put them at higher risk for developing HUS).
– Richard L. Siegler, MD, Postdiarrheal Shiga Toxin-Mediated Hemolytic Uremic Syndrome, 290 JAMA (No. 10) 1379, 1379 (Sept. 10, 2003).
– Pierre Robitaille, et al., Pancreatic Injury in the Hemolytic Uremic Syndrome, 11 Pediatric Nephrology 631, 632 (1997) (“although mild pancreas involvement in the acute phase of HUS can be frequent”).
– Safdar, supra note 37, at 996; see also Siegler, supra note 35, at 1379. (“There are no treatments of proven value, and care during the acute phase of the illness, which is merely supportive, has not changed substantially during the past 30 years.”)
– Su & Brandt, supra note 9 (“the mortality rate is 5-10%”). See also Kriefall, 265 N.W.2d at 483 (“three-year old Brianna Kriefall died from food that everyone party to this appeal…recognize was cross-contaminated by E. coli O157:H7 bacteria from meat sold by Excel.”)
– Garg, supra note 37, at 1360.
– Id. Siegler, supra note 35, at 1509-11 (describing what Dr. Siegler refers to as the “pathogenic cascade” that results in the progression from colitis to HUS).
– Garg, supra note 37, at 1360; see also Su & Brandt, supra note 9, at 700.
– Garg, supra note 37, at 1360; Su & Brandt, supra note 9, at 700.
– Siegler, supra note 35, at 1519 (noting that in a “20-year Utah-based population study, 5% dies, and an equal number of survivors were left with end-stage renal disease (ESRD) or chronic brain damage.”)
– Garg, supra note 37, at 1366-67.
– Siegler, supra note 35, at 1519.
– Id. at 1519-20; Garg, supra note 37, at 1366-67.
– Garg, supra note 37, at 1368.