I thought it might be helpful to give some background on E. coli O157:H7 and the dangers it poses to our food supply, particularly in hamburger:
E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis[1] associated with consumption of hamburgers from a fast food chain restaurant.[2] 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.[3] In the ten years that followed there were approximately thirty outbreaks recorded in the United States.[4] 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.[5] As a result, only the most geographically concentrated outbreak would have garnered enough notice to prompt further investigation.[6]

The virulence of E. coli O157:H7 is a result of its ability to produce Shiga-like toxins.[7] It has been theorized that generic E. coli picked up this deadly ability through horizontal transfer of virulence genes from the Shigella bacteria.[8] 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.[9] The prospect of emerging pathogens as a significant public health threat has been emphasized by the CDC for some time.[10]
Foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections.[11] Surveys performed on feed lots have demonstrated that cattle can be infected with E. coli O157:H7 through close contact, and under muddy conditions.[12] The prevalence of E. coli O157:H7 among cattle in these feed lots can reach 63-100%, especially during the summer.[13] 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.”[14] 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 fever.[15] 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.[16] Infection can occur in people of all ages but is most common in children.[17] The duration of an uncomplicated illness can range from one to twelve days.[18] 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.[19]
What makes E. coli O157:H7 truly and decidedly deadly is its very low infectious dose,[20] and how relatively difficult it is to kill these bacteria.[21] 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.”[22] As few as twenty organisms have been said to be sufficient to infect a person and, as a result, possibly kill them.[23] 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.[24]
And, finally, to make it even more of a dangerous threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact.[25] 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.[26] 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 the cooking process.[27]
1. “[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, http://www.merck.com/mmhe/sec09/ch122/ch122b.html.
2. 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).
3. 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).
4. 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).
5. 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.”).
6. 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).
7. Griffin & Tauxe, supra note 10, at 61-62 (noting that the nomenclature came about because of the resemblance to toxins produced by Shigella dysenteriae).
8. Griffin & Tauxe, supra note 10, at 62 (using the more technical term “phage-mediated transfer”).
9. 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).
10. 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.
11. 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).
12. 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.”).
13. CDC, supra note 18, at 638 and nn.4 and 5.
14. Rangel, supra note 13, at 603.
15. Griffin & Tauxe, supra note 10, at 63.
16. 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.
17. Su & Brandt, supra note 9 (“the young are most often affected”).
18. Tauxe, supra note 23 at 1152.
19. Id.
20. Griffin & Tauxe, supra note 10, at 72 (“The general patterns of transmission in these outbreaks suggest that the infectious dose is low.”).
21. 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).
22. 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 http://www.fsis.usda.gov/oa/pubs/colortech.htm (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 http://www.hi-tm.com/Documents2001/hamburger-temp.pdf (“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.
23. 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.
24. Nestle, supra note 2, at 41.
25. 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).
26. 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 http://www.nap.edu/books/0309086272/html.
27. 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).