Sources, Characteristics, and Identification

E. coli is an archetypal commensal bacterial species that lives in mammalian intestines. E. coli O157:H7 is one of thousands of serotypes Escherichia coli.[1] The combination of letters and numbers in the name of the E. coli O157:H7 refers to the specific antigens (proteins which provoke an antibody response) found on the body and tail or flagellum[2]respectively and distinguish it from other types of E. coli.[3] Most serotypes of E. coli are harmless and live as normal flora in the intestines of healthy humans and animals.[4] The E. coli bacterium is among the most extensively studied microorganism.[5] The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping.[6] Pulsed-field gel electrophoresis (PFGE),[7] sometimes also referred to as genetic fingerprinting, is used to compare E. coli O157:H7 isolates to determine if the strains are distinguishable.[8] A technique called multilocus variable number of tandem repeats analysis (MLVA) is used to determine precise classification when it is difficult to differentiate between isolates with indistinguishable or very similar PFGE patterns.[9]

E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis[10] associated with consumption of hamburgers from a fast food chain restaurant.[11] Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one (1) isolationwith serotype O157:H7, and that was a case in 1975.[12] In the ten (10) years that followed there were approximately thirty (30) outbreaks recorded in the United States.[13] This number is likely misleading, however, because E. coliO157: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.[14] As a result, only the most geographically concentrated outbreak would have garnered enough notice to prompt further investigation.[15]

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-like toxins.[16] Shiga toxin (Stx) has multiple variants (e.g. Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells.[17] Shiga toxin is one of the most potent toxins known.[18] In addition to Shiga toxins, E. coli O157:H7 produces numerous other putative virulence factors including proteins, which aid in the attachment and colonization of the bacteria in the intestinal wall and which can lyse red blood cells and liberate iron to help support E. coli metabolism.[19]

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.[20]The rate of genetic mutation of E. coli O157:H7 indicates that the common ancestor of current E. coli O157:H7 clades[21] likely existed some 20,000 years ago.[22] E. coli O157:H7 is a relentlessly evolving organism,[23] constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat.[24] The CDC has emphasized the prospect of emerging pathogens as a significant public health threat for some time.[25]

Although foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coliO157:H7 infections[26], outbreak of illnesses have been linked to a wide variety of food items. For example, produce has, since at least 1991, been the source of substantial numbers of outbreak-related E. coli O157:H7 infections.[27] Other unusual vehicles for E. coli O157:H7 outbreaks have included unpasteurized juices, yogurt, dried salami, mayonnaise, raw milk, game meats, sprouts, and raw cookie dough. Leafy greens and other fresh produce have become leading vehicles: a 2018 outbreak linked to romaine lettuce from the Yuma, Arizona growing region sickened 210 people across 36 states, hospitalized 96, and caused 5 deaths—the largest U.S. E. coli O157:H7 outbreak since the 2006 spinach outbreak—and in 2024, slivered onions served on McDonald’s Quarter Pounders were linked to 104 illnesses across 14 states, including one death (CDC/FDA).[28]

According to a recent study, an estimated 93,094 illnesses are due to domestically acquired E. coli O157:H7 each year in the United States.[29] Estimates of foodborne acquired O157:H7 cases result in 2,138 hospitalizations and 20 deaths annually. These figures cover only the O157:H7 serotype; non-O157 Shiga toxin–producing E. coli (STEC) strains now account for the majority of STEC infections reported in the United States. In 2012, following petitions from food-safety advocates, the USDA’s Food Safety and Inspection Service declared six additional STEC serogroups—O26, O45, O103, O111, O121, and O145—adulterants in raw non-intact (ground) beef, extending the zero-tolerance policy previously applied only to O157:H7 (USDA/FSIS).[30] The colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within twenty-four (24) hours, and sometimes fevers.[31] The incubation period—which is to say the time from exposure to the onset of symptoms—in outbreaks is usually reported as three (3) to four (4) days, but may be as short as one (1) day or as long as ten (10) days.[32] Infection can occur in people of all ages but is most common in children.[33] The duration of an uncomplicated illness can range from one (1) to twelve (12) days.[34] 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 have occurred at nursing homes.[35]

What makes E. coli O157:H7 remarkably dangerous is its very low infectious dose,[36] and how relatively difficult it is to kill these bacteria.[37] 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,”[38] as few as twenty (20) organisms may be sufficient to infect a person and, as a result, possibly kill them.[39] And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44°F, survives freezing and thawing, is heat resistant, grows at temperatures up to 111°F, resists drying, and can survive exposure to acidic environments.[40]

And, finally, to make it even more of a threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact.[41] 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.[42] With this pathogen, there is ultimately no margin of error. It is for this precise reason that the USDA has repeatedly rejected calls from the meat industry to hold consumers primarily responsible for E. coli O157:H7 infections caused, in part, by mistakes in food handling or cooking.[43]

Hemolytic Uremic Syndrome (HUS)

E. coli O157:H7 infections can lead to a severe, life-threatening complication called hemolytic uremic syndrome (HUS).[44] HUS accounts for the majority of the acute deaths and chronic injuries caused by the bacteria.[45] HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins.[46] It is the most common cause of renal failure in children.[47] Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long term renal impairment.[48] The same number suffers severe brain damage.[49] While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes, can also occur.[50] There is no cure or effective treatment for HUS.[51]

HUS is believed to develop when the toxin from the bacteria, known as Shiga-like toxin (SLT), enters the circulation through the inflamed bowel wall.[52] 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.[53] Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain.[54]  By definition, 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).[55]

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.[56] Among survivors, at least five percent will suffer end stage renal disease (ESRD) with the resultant need for dialysis or transplantation.[57] But, “[b]ecause renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.”[58] 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.[59] Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not really available and remains controversial.[60] All that can be said for certain is that HUS causes permanent injury, including loss of kidney function, and it requires a lifetime of close medical-monitoring.

Other Medical Complications

Reactive Arthritis

The term reactive arthritis refers to an inflammation of one or more joints, following an infection localized at another site distant from the affected joints. The predominant site of the infection is the gastrointestinal tract. Several bacteria, including E. coli, induce septic arthritis.[61]The resulting joint pain and inflammation can resolve completely over time or permanent joint damage can occur.[62]

The reactive arthritis associated with Reiter Syndrome may develop after a person eats food that has been tainted with bacteria. In a small number of persons, the joint inflammation is accompanied by conjunctivitis (inflammation of the eyes), and urethritis (painful urination). Id. This triad of symptoms is called Reiter syndrome.[63] Reiter syndrome, a form of reactive arthritis, is an uncommon but debilitating syndrome caused by gastrointestinal or genitourinary infections. The most common gastrointestinal bacteria involved are Salmonella, Campylobacter, Yersinia, and Shigella. Reiter syndrome is characterized by a triad of arthritis, conjunctivitis, and urethritis, although not all three symptoms occur in all affected individuals.[64]

Although the initial infection may not be recognized, reactive arthritis can still occur. Reactive arthritis typically involves inflammation of one joint (monoarthritis) or four or fewer joints (oligoarthritis), preferentially affecting those of the lower extremities; the pattern of joint involvement is usually asymmetric. Inflammation is common at entheses – i.e., the places where ligaments and tendons attach to bone, especially the knee and the ankle.

Salmonella has been the most frequently studied bacteria associated with reactive arthritis. Overall, studies have found rates of Salmonella-associated reactive arthritis to vary between 6 and 30%.[65] The frequency of postinfectious Reiter syndrome, however, has not been well described. In a Washington State study, while 29% developed arthritis, only 3% developed the triad of symptoms associated with Reiter syndrome.[66] In addition, individuals of Caucasian descent may be more likely those of Asian descent to develop reactive arthritis,[67] and children may be less susceptible than adults to reactive arthritis following infection with Salmonella.[68]

A clear association has been made between reactive arthritis and a genetic factor called the human leukocyte antigen (HLA) B27 genotype. HLA is the major histocompatibility complex in humans; these are proteins present on the surface of all body cells that contain a nucleus and are in especially high concentrations in white blood cells (leukocytes). It is thought that HLA-B27 may affect the elimination of the infecting bacteria or an individual’s immune response.[69]HLA-B27 has been shown to be a predisposing factor in one-half to over two-thirds of individuals with reactive arthritis.[70] While HLA-B27 does not appear to predispose to the initial infection itself, it increases the risk of developing arthritis that is more likely to be severe and prolonged. This risk may be slightly greater for Salmonella and Yersinia-associated arthritis than with Campylobacter, but more research is required to clarify this.[71]

Irritable Bowel Syndrome

A recently published study surveyed the extant scientific literature and noted that post-infectious irritable bowel syndrome (PI-IBS) is a common clinical phenomenon first-described over five decades ago.[72] The Walkerton Health Study further notes that:

Between 5% and 30% of patients who suffer an acute episode of infectious gastroenteritis develop chronic gastrointestinal symptoms despite clearance of the inciting pathogens.[73]

In terms of its own data, the “study confirm[ed] a strong and significant relationship between acute enteric infection and subsequent IBS symptoms.”[74] The WHS also identified risk-factors for subsequent IBS, including younger age; female sex; and four features of the acute enteric illness – diarrhea for > 7days, presence of blood in stools, abdominal cramps, and weight loss of at least ten pounds.[75]

Irritable bowel syndrome (IBS) is a chronic disorder characterized by alternating bouts of constipation and diarrhea, both of which are generally accompanied by abdominal cramping and pain.[76] In one recent study, over one-third of IBS sufferers had had IBS for more than ten years, with their symptoms remaining fairly constant over time.[77]IBS sufferers typically experienced symptoms for an average of 8.1 days per month.[78]

As would be expected from a chronic disorder with symptoms of such persistence, IBS sufferers required more time off work, spent more days in bed, and more often cut down on usual activities, when compared with non-IBS sufferers.[79] And even when able to work, a significant majority (67%), felt less productive at work because of their symptoms.[80] IBS symptoms also have a significantly deleterious impact on social well-being and daily social activities, such as undertaking a long drive, going to a restaurant, or taking a vacation.[81] Finally, although a patient’s psychological state may influence the way in which he or she copes with illness and responds to treatment, there is no evidence that supports the theory that psychological disturbances in fact cause IBS or its symptoms.[82]

PREVENTION OF E. COLI O157:H7 INFECTION

    Because there is at present no vaccine against E. coli O157:H7, and because antibiotic treatment of an established infection is generally contraindicated and may itself increase the risk of hemolytic uremic syndrome, prevention remains the only reliable defense against the disease and its most devastating complications.[83] The organism’s very low infectious dose, its ability to survive freezing, drying, and acidic environments, and its resistance to conditions that would destroy many other pathogens leave essentially no margin for error.[84] Effective prevention therefore depends upon interrupting each of the routes by which the bacteria reach the mouth—through undercooked food, cross-contamination in the kitchen and along the supply chain, contaminated produce and water, unpasteurized dairy and juice, contact with animals and their environments, and person-to-person spread.

    Safe Cooking and the Prevention of Cross-Contamination

    Thorough cooking is the single most effective way to destroy E. coli O157:H7 in foods of bovine origin. The United States Department of Agriculture’s Food Safety and Inspection Service recommends that ground beef and other ground meats be cooked to an internal temperature of at least 160°F (71°C), that whole cuts of beef, pork, veal, and lamb reach 145°F (63°C) followed by a three-minute rest, and that all poultry reach 165°F (74°C).[85] Because the pathogen can survive in meat that is only slightly undercooked, and because the color of ground beef is not a reliable indicator of doneness, a food thermometer—rather than appearance—should be used to confirm that a safe internal temperature has in fact been reached.[86]

    Cooking alone, however, does not address the equally serious danger of cross-contamination. Raw meat and its juices should be kept separate from produce and other ready-to-eat foods; separate cutting boards and utensils should be used for raw meat; hands, counters, and utensils should be washed with hot, soapy water after any contact with raw meat; and perishable foods should be refrigerated promptly at or below 40°F. As discussed above, a persistent criticism of federal E. coli O157:H7 policy has been its historical emphasis on consumer cooking practices at the expense of the far less forgiving risks posed by cross-contamination—risks that arise both in the home kitchen and, well before that, throughout the supply chain.[87]

    Produce, Water, and Unpasteurized Products

    Cooking cannot protect against the growing number of E. coli O157:H7 vehicles that are ordinarily consumed raw. Fresh produce—particularly leafy greens such as romaine and spinach—has become a leading source of outbreaks, and because contamination can occur in the field and may become internalized within the plant, washing reduces but cannot be relied upon to eliminate the organism.[88] Consumers can lower their risk by refrigerating produce promptly and by discarding items subject to an active recall, but the primary safeguards for produce lie upstream—in agricultural water quality, worker hygiene, and the exclusion of livestock and wildlife intrusion from growing fields.

    Unpasteurized dairy and juice products present a distinct and readily avoidable hazard. Raw (unpasteurized) milk, cheeses made from raw milk, and unpasteurized juice and cider have repeatedly been implicated in E. coli O157:H7 outbreaks, and public health authorities uniformly recommend that consumers—especially young children, the elderly, pregnant women, and the immunocompromised—choose pasteurized products.[89] Water is a further recognized vehicle: swallowing contaminated drinking or recreational water can transmit the organism, as the Walkerton, Ontario tragedy—one of the largest E. coli O157:H7 outbreaks in the history of North America—grimly demonstrated.[90]

    Handwashing, Animal Contact, and Person-to-Person Transmission

    Because as few as twenty organisms may be sufficient to cause infection, and because the bacteria are readily transmitted from person to person, rigorous hand hygiene is an essential and often underappreciated line of defense.[91]Hands should be washed thoroughly with soap and running water after using the toilet, after changing diapers, before and after preparing food, and after any contact with animals or their surroundings.

    Direct and indirect contact with ruminant animals is a well-documented route of exposure. Cattle, sheep, and goats are natural reservoirs of E. coli O157:H7, and outbreaks have been traced to petting zoos, agricultural fairs, and farm visits; handwashing stations should be used after animal contact, and food and drink should be kept out of animal areas.[92] Finally, because infected individuals—particularly young children—may continue to shed the organism and infect others even after their own symptoms resolve, persons diagnosed with E. coli O157:H7 should be excluded from food handling and from child-care and health-care duties, and affected children should be kept out of group child-care settings, until they are cleared in accordance with applicable public health guidance.[93]

    [1]           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), http://www.cfsan.fda.gov/~ebam/bam-4.html. 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.

    [2]           Not all E. coli are motile. For example, E. coli O157:H7 which lack flagella are thus E. coli O157:NM for non-motile.

    [3]           CDC, Escherichia coli O157:H7, General Information, Frequently Asked Questions: What is Escherichia coli O157:H7?, http://www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_g.htm.

    [4]           Marion Nestle, Safe Food:  Bacteria, Biotechnology, and Bioterrorism, 40-41 (1st Pub. Ed. 2004).

    [5]           James M. Jay, MODERN FOOD MICROBIOLOGY at 21 (6th ed. 2000). (“This is clearly the most widely studied genus of all bacteria.”)

    [6]           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).

    [7]           Jay, supra note 5, at 220-21 (describing in brief the PFGE testing process).

    [8]           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 6, 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).

    [9]           Konno T. et al. Application of a multilocus variable number of tandem repeats analysis to regional outbreak surveillance of Enterohemorrhagic Escherichia coli O157:H7 infections. Jpn J Infect Dis. 2011 Jan; 64(1): 63-5.

    [10]         “[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, 2nd Home Ed. Online, http://www.merck.com/mmhe/sec09/ch122/ch122b.html.

    [11]         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).

    [12]         Riley, supra note 11 at 684. See also Patricia M. Griffin & Robert V. Tauxe, The Epidemiology of Infections Caused by Escherichia coliO157:H7, Other Enterohemorrhagic E. coli, and the Associated Hemolytic Uremic Syndrome, 13 Epidemiologic Reviews 60, 73 (1991).

    [13]         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).

    [14]         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.”)

    [15]         See Keene, supra note 14 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 were a total of 350 reported outbreaks from 1982-2002. Josef 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).

    [16]         Griffin & Tauxe, supra note 12, at 61-62 (noting that the nomenclature came about because of the resemblance to toxins produced by Shigella dysenteries).

    [17]         Sanding K, Pathways followed by ricin and Shiga toxin into cells, Histochemistry and Cell Biology, vol. 117, no. 2:131-141 (2002). Endothelial cells line the interior surface of blood vessels. They are known to be extremely sensitive to E. coli O157:H7, which is cytotoxigenic to these cells making them a primary target during STEC infections.

    [18]         Johannes L, Shiga toxins—from cell biology to biomedical applications. Nat Rev Microbiol 8, 105-116 (February 2010). Suh JK, et al. Shiga Toxin Attacks Bacterial Ribosomes as Effectively as Eucaryotic Ribosomes, Biochemistry, 37 (26); 9394–9398 (1998).

    [19]         Welinder-Olsson C, Kaijser B. Enterohemorrhagic Escherichia coli (EHEC). Scand J. Infect Dis. 37(6-7): 405-16 (2005). See alsoUSDA Food Safety Research Information Office E. coli O157:H7 Technical Fact Sheet:  Role of 60-Megadalton Plasmid (p0157) and Potential Virulence Factors, http://fsrio.nal.usda.gov/document_fsheet.php?product_id=225.

    [20]         Kaper JB and Karmali MA. The Continuing Evolution of a Bacterial Pathogen. PNAS vol. 105 no. 12 4535-4536 (March 2008). Wick LM, et al. Evolution of genomic content in the stepwise emergence of Escherichia coli O157:H7. J Bacteriol 187:1783–1791(2005).

    [21]         A group of biological taxa (as species) that includes all descendants of one common ancestor.

    [22]         Zhang W, et al. Probing genomic diversity and evolution of Escherichia coli O157 by single nucleotide polymorphisms. Genome Res 16:757–767 (2006).

    [23]         Robins-Browne RM. The relentless evolution of pathogenic Escherichia coli. Clin Infec Dis. 41:793–794 (2005).

    [24]         Manning SD, et al. Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks. PNAS vol. 105 no. 12 4868-4873 (2008). (“These results support the hypothesis that the clade 8 lineage has recently acquired novel factors that contribute to enhanced virulence. Evolutionary changes in the clade 8 subpopulation could explain its emergence in several recent foodborne outbreaks; however, it is not clear why this virulent subpopulation is increasing in prevalence.”)

    [25]         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.”)

    [26]         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).

    [27]         Rangel, supra note 15, at 605.

    [28]         Feng, supra note 13, at 49. See also USDA Bad Bug Book, Escherichia coli O157:H7, http://www.fda.gov/food/foodsafety/foodborneillness/foodborneillnessfoodbornepathogensnaturaltoxins/badbugbook/ucm071284.htm.

    [29]         Scallan E, et al. Foodborne illness acquired in the United States –major pathogens, Emerging Infect. Dis. Jan. (2011), http://www.cdc.gov/EID/content/17/1/7.htm.

    [30]         Id., Table 3.

    [31]         Griffin & Tauxe, supra note 12, at 63.

    [32]         Centers for Disease Control, Division of Foodborne, Bacterial and Mycotic Diseases, Escherichia coli general information, http://www.cdc.gov/nczved/dfbmd/disease_listing/stec_gi.html. 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”).

    [33]         Su & Brandt, supra note 11 (“the young are most often affected”).

    [34]         Tauxe, supra note 25, at 1152.

    [35]         Id.

    [36]         Griffin & Tauxe, supra note 12, at 72. (“The general patterns of transmission in these outbreaks suggest that the infectious dose is low.”)

    [37]         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 130°F, there is no bacterial destruction, and at 140°F, there is only a 2-log reduction of E. coli present).

    [38]         Griffin & Tauxe, supra note 12, at 72 (noting that, as a result, “fewer bacteria are needed to cause illness that for outbreaks of salmonellosis”). Nestle, supra note 4, at 41. (“Foods containing E. coli O17:H7 must be at temperatures high enough to kill all of them.”) (italics in original)

    [39]         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 4, 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.

    [40]         Nestle, supra note 4, at 41.

    [41]         Griffin & Tauxe, supra note 12, 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 15, at 605-06 (finding that 80% of the 50 reported person-to-person outbreak from 1982-2002 occurred in daycare centers).

    [42]         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), http://www.nap.edu/books/0309086272/html/.

    [43]         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).

    [44]         Griffin & Tauxe, supra note 12, 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).

    [45]         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). (“[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 http://www.pediatrics.org/cgi/content/full/100/1/e12.

    [46]         Tauxe, supra note 25, at 1152. See also Nasia Safdar, MD, et al. Risk of Hemolytic Uremic Syndrome After Treatment of Escherichia coliO157: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.”)

    [47]         Su & Brandt, supra note 11.

    [48]         Safdar, supra note 46, 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).

    [49]         Richard L. Siegler, MD, Postdiarrheal Shiga Toxin-Mediated Hemolytic Uremic Syndrome, 290 JAMA (No. 10) 1379, 1379 (Sept. 10, 2003).

    [50]         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”).

    [51]         Safdar, supra note 46, at 996. See also Siegler, supra note 49, 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.”)

    [52]         Garg, supra note 46, at 1360.

    [53]         Id. Siegler, supra note 45, at 1509-11 (describing what Dr. Siegler refers to as the “pathogenic cascade” that results in the progression from colitis to HUS).

    [54]         Garg, supra note 46, at 1360. See also Su & Brandt, supra note 11, at 700.

    [55]         Garg, supra note46, at 1360. See also Su & Brandt, supra note 11, at 700.

    [56]         Siegler, supra note 45, 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.”)

    [57]         Garg, supra note 46, at 1366-67.

    [58]         Siegler, supra note 45, at 1519.

    [59]         Id. at 1519-20. See also Garg, supra note 46, at 1366-67.

    [60]         Garg, supra note 46, at 1368.

    [61]         See J. Lindsey, “Chronic Sequellae of Foodborne Disease,” Emerging Infectious Diseases, Vol. 3, No. 4, Oct-Dec, 1997.

    [62]         Id.

    [63]         Id. See also Dworkin, et al., “Reactive Arthritis and Reiter’s Syndrome following an outbreak of gastroenteritis caused by Salmonella enteritidis,” Clin. Infect. Dis., 2001 Oct. 1;33(7): 1010-14; Barth, W. and Segal, K., “Reactive Arthritis (Reiter’s Syndrome),” American Family Physician, Aug. 1999, online at www.aafp.org/afp/990800ap/ 499.html.

    [64]         Hill Gaston JS, Lillicrap MS. (2003). Arthritis associated with enteric infection. Best Practices & Research Clinical Rheumatology. 17(2):219-39.

    [65]         Id.

    [66]         Dworkin MS, Shoemaker PC, Goldoft MJ, Kobayashi JM, “Reactive arthritis and Reiter’s syndrome following an outbreak of gastroenteritis caused by Salmonella enteritidis. Clin. Infect. Dis. 33(7):1010-14. 

    [67]         McColl GJ, Diviney MB, Holdsworth RF, McNair PD, Carnie J, Hart W, McCluskey J, “HLA-B27 expression and reactive arthritis susceptibility in two patient cohorts infected with Salmonella Typhimurium,” Australian and New Zealand Journal of Medicine 30(1):28-32 (2001).

    [68]         Rudwaleit M, Richter S, Braun J, Sieper J, “Low incidence of reactive arthritis in children following a Salmonella outbreak,” Annals of the Rheumatic Diseases. 60(11):1055-57 (2001).

    [69]         Hill Gaston and Lillicrap, supra Note 7.

    [70]         Id.; Barth WF, Segal K., “Reactive arthritis (Reiter’s syndrome),” American Family Physician, 60(2):499-503, 507 (1999).

    [71]         Hill Gaston and Lillicrap, supra Note 7.

    [72]         J. Marshall, et al., Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery, Gastro., 2006; 131; 445-50 (hereinafter “Walkerton Health Study” or “WHS”). The WHS followed one of the largest E. coli O157:H7 outbreaks in the history of North America. Contaminated drinking water caused over 2,300 people to be infected with E. coli O157:H7, resulting in 27 recognized cases of HUS, and 7 deaths. Id. at 445. The WHS followed 2,069 eligible study participants. Id. For Salmonella specific references, seeSmith, J.L., Bayles, D.O., Post-Infectious Irritable Bowel Syndrome: A Long-Term Consequence of Bacterial Gastroenteritis, Journal of Food Protection. 2007:70(7);1762-69.

    [73]         Id. at 445 (citing multiple sources).

    [74]         WHS, supra note 34, at 449.

    [75]         Id. at 447.

    [76]         A.P.S. Hungin, et al., Irritable Bowel Syndrome in the United States: Prevalence, Symptom Patterns and Impact, Aliment Pharmacol. Ther. 2005:21 (11); 1365-75.

    [77]         Id.at 1367.

    [78]         Id.

    [79]         Id. at 1368.

    [80]         Id.

    [81]         Id.

    [82]         Amy Foxx-Orenstein, DO, FACG, FACP, IBS—Review and What’s New, General Medicine 2006:8(3) (Medscape 2006) (collecting and citing studies). Indeed, PI-IBS has been found to be characterized by more diarrhea but less psychiatric illness with regard to its pathogenesis. SeeNicholas J. Talley, MD, PhD, Irritable Bowel Syndrome: From Epidemiology to Treatment, from American College of Gastroenterology 68th Annual Scientific Meeting and Postgraduate Course (Medscape 2003).

    [83]         There is at present no licensed vaccine for the prevention of E. coli O157:H7 infection in humans. As noted above, moreover, the administration of antibiotics to a person already infected is generally contraindicated because it appears to increase the risk of hemolytic uremic syndrome. See Safdar, supra note 46. See generally Ctrs. for Disease Control & Prevention, E. coli (Escherichia coli): Prevention, https://www.cdc.gov/ecoli/.

    [84]         See supra notes 39-40 (describing the pathogen’s low infectious dose and its ability to multiply at temperatures as low as 44°F, to survive freezing and thawing, to resist drying, and to withstand acidic environments).

    [85]         U.S. Dep’t of Agric., Food Safety & Inspection Serv., Safe Minimum Internal Temperature Chart (recommending an internal temperature of 160°F for ground meats, 145°F followed by a three-minute rest for whole cuts of beef, pork, veal, and lamb, and 165°F for all poultry), https://www.fsis.usda.gov/.

    [86]         See U.S. Dep’t of Agric., Food Safety & Inspection Serv., The Color of Cooked Ground Beef as It Relates to Doneness (color is not a reliable indicator of doneness, and a food thermometer should be used to verify a safe internal temperature). As noted above, E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection. See supra note 38.

    [87]         See supra notes 42-43 (discussing the criticism that federal policy has failed to focus adequately on the risks of cross-contamination as compared with those attributed to improper cooking).

    [88]         See supra notes 27-28 (describing produce, and leafy greens in particular, as leading vehicles for E. coli O157:H7 outbreaks).

    [89]         See U.S. Food & Drug Admin., The Dangers of Raw Milk: Unpasteurized Milk Can Pose a Serious Health Risk; U.S. Food & Drug Admin., Talking About Juice Safety: What You Need to Know (recommending pasteurized dairy and juice products), https://www.fda.gov/.

    [90]         See supra note 72 (describing the Walkerton, Ontario waterborne outbreak, in which contaminated drinking water infected more than 2,300 people with E. coli O157:H7, resulting in 27 recognized cases of HUS and 7 deaths).

    [91]         See supra notes 39, 41 (noting that as few as twenty organisms may be sufficient to infect a person and that the bacteria are easily transmitted by person-to-person contact).

    [92]         See Ctrs. for Disease Control & Prevention, Compendium of Measures to Prevent Disease Associated with Animals in Public Settings(recommending handwashing after animal contact and the separation of animal areas from areas where food and drink are consumed). Ruminant animals are the principal reservoir of E. coli O157:H7.

    [93]         See Ctrs. for Disease Control & Prevention, E. coli (Escherichia coli): Prevention, https://www.cdc.gov/ecoli/. Public health authorities recommend that symptomatic persons, and in certain circumstances asymptomatic carriers—particularly food handlers and young children in child-care settings—be excluded from high-risk activities until stool testing and applicable state requirements confirm that they are no longer shedding the organism, in order to prevent secondary transmission.

    Public Health is investigating an outbreak of Shiga toxin-producing E. coli O157 (called STEC) associated with food from Tokyo Stop Teriyaki. We are aware of five King County residents who have gotten sick with the same type of STEC using DNA fingerprinting (whole genome sequencing or WGS) after eating food from Tokyo Stop Teriyaki in Bellevue before becoming sick. It is likely these five people became sick from contaminated food served at Tokyo Stop Teriyaki.

    There is one additional person in King County whose illness matches the other five cases by WGS and did not report eating food from Tokyo Stop Teriyaki. This means their illness may have come from another source that is unrelated to Tokyo Stop Teriyaki or may be due to a contaminated food product served at this restaurant and elsewhere. 

    The investigation is still in progress, and we need your help. 

    If you ate at Tokyo Stop Teriyaki in November or December 2025, and later developed symptoms such as nausea, vomiting, stomach cramps, diarrhea (including bloody diarrhea), or fever, please fill out our survey: STEC Outbreak Questions. This may help us identify the potential source of STEC infections and prevent future outbreaks.

    The sick people reported signs of STEC, including nausea, vomiting, stomach cramps, diarrhea (including bloody diarrhea), and fever. Four people were hospitalized and recovered. 

    We have not found any sick restaurant workers at Tokyo Stop Teriyaki.

    On December 12, 2025, we asked the restaurant to close. We visited the restaurant on December 13 and found several problems that could have contributed to this outbreak:

    • Sinks for washing raw meat and vegetables were placed too close together
    • Tools and surfaces used for raw meat like chicken, weren’t sanitized properly

    We worked with the restaurant to improve their food safety practices and do a full cleaning and disinfection. When we returned on December 15, we confirmed that the cleaning was done properly and that they were following required food safety procedures. Based on this, they were allowed to reopen.

    All six people who became sick tested positive for the same type of STEC (O157), using DNA fingerprinting (whole genome sequencing or WGS).

    Will Humble, Executive Director, AZ Public Health Association, joined “Arizona Horizon” to share how changes in the State Health Department have led to health concerns, and how illnesses are seemingly tame for this time of year.

    The series of E. coli cases that occurred (possibly linked to State Fair petting zoo), because of the state fair, has raised cause for concern. Previously, vendors were required to have a flow through pattern, so kids had to wash their hands after exiting the exhibit, but that was no longer a requirement this year.

    Prevention for visitors to petting zoos and agricultural fairs

    Do:

    • Wash hands
    • Before eating or drinking or preparing foodAfter petting or being around animals or their pensSupervise children’s hand washing
    • Hand sanitizers are not a as effective as hand washing and shouldn’t be used as a substitute for hand washing!
    • Wash Clothing after visiting animals
    • Keep young children’s toys, pacifiers, and blankets outside of animal interaction areas.

    Don’t:

    • Eat or drink in animal areas.
    • Bring pacifier, strollers, toys or spill-proof bottles into animal areas.

    See www.fair-safety.com 

    November 13, 2025

    One additional Washington resident has been added to this outbreak, bringing the total to 10 cases – 9 Washington residents and 1 Oregon resident. All cases report illness onsets before the cheese was recalled on October 24, 2025. 

    November 6, 2025

    Samples of Twin Sisters Creamery cheese have tested positive for two different STEC strains associated with human cases: E. coli O103 and E. coli O26. 

    Two Washington residents and one Oregon resident have been infected with E. coli O103. Molecular fingerprinting of the E. coli O103 bacteria from the three cases is extremely similar to the E. coli O103 identified in both the Twin Sisters Creamery Farmhouse and Whatcom Blue cheeses. 

    Six Washington residents have been infected with E. coli O26. Molecular fingerprinting of the E. coli O26 bacteria from the six cases is extremely similar to the E. coli O26 bacteria identified in the Twin Sister’s Creamery Peppercorn Farmhouse cheese.   

    Twin Sisters Creamery brand cheese sampleWhere CollectedWhere TestedShiga
    Farmhouse variety (opened)Case’s HomeCommercial LabE. coli O103
    Whatcom Blue varietyRetail StoreWashington State Department of AgricultureE. coli O103
    Peppercorn Farmhouse variety (unopened)Case’s HomeFood and Drug AdministrationE. coli O26
    Farmhouse varietyRetail StoreWashington State Public Health LabE. coli NOS*

    *NOS: Not otherwise specified–this strain of Shiga toxin E. coli is not typeable at the Washington State Public Health Lab

    Two Whatcom County residents are known to have been sickened, and test results showed a genetic link between their illness and Twin Sisters Creamery products. An additional case in Oregon has also been genetically linked. One is a child under five years old, and two are adults. One person was hospitalized. All illnesses occurred between September 5 and September 16, 2025. Specific or additional products may be recalled or identified as a possible source of infection in the future.

    Multiple varieties of aged raw milk cheese from Twin Sisters Creamery are in the process of being recalled after testing linked E. coli bacteria from three cases to the company’s cheese. Twin Sisters Creamery is cooperating with the investigation. Additional products may be recalled or identified as a possible source of infection in the future. 

    All sizes of Whatcom Blue, Farmhouse, Peppercorn and Mustard Seed cheese varieties from Twin Sisters Creamery produced on or after May 27, 2025 are being recalled. 

    ◦ #450 Made on 5/27/2025 – Batch Code 250527B Whatcom Blue
    ◦ #452 Made on 6/10/2025 – Batch Code 250610B Whatcom Blue
    ◦ #454 Made on 6/18/2025 – Batch Code 250618B Whatcom Blue
    ◦ #455 Made on 6/24/2025 – Batch Code 250625B Whatcom Blue
    ◦ #451 Made on 6/03/2025 – Batch Code 250603F Farmhouse
    ◦ #453 Made on 6/16/2025 – Batch Code 250616B Farmhouse
    ◦ #451 Made on 6/03/2025 – Batch Code 250603P Peppercorn
    ◦ #453 Made on 6/16/2025 – Batch Code 250616 Mustard Seed

    Some cheese products were repackaged by grocery stores and markets, so the original label may not be present. In these instances, the grocery store/market label should list the cheese brand.

    Marler Clark has represented victims in several high-profile E. coli outbreaks linked to contaminated cheese. The firm’s history with these cases primarily involves raw-milk cheeses, but its broader work covers many foods. 

    Key lawsuits involving cheese

    • Bravo Farms Gouda Cheese (2010):Marler Clark represented multiple individuals sickened in a 2010 E. coli O157:H7 outbreak linked to Bravo Farms Dutch Style Gouda.
      • The contaminated cheese was sold at Costco stores, with at least 38 people in five states confirmed ill.
      • The firm filed multiple lawsuits against Bravo Farms on behalf of the victims, some of whom were seriously sickened after attending a Costco “cheese road show”.
    • Raw Farm Cheddar Cheese (2024): In 2024, Marler Clark filed a lawsuit on behalf of victims in a multistate E. coli O157:H7 outbreak linked to Raw Farm brand Raw Cheddar cheese.
      • The outbreak, which ended in March 2024, included 11 confirmed illnesses and five hospitalizations across multiple states. Two people developed hemolytic uremic syndrome (HUS), a life-threatening form of kidney failure.
      • While product tests by health officials were negative, epidemiological evidence strongly implicated the Raw Cheddar cheese as the source.
    • Canadian Raw Milk Cheese (2013): Marler Clark reported on an E. coli outbreak and death in Canada linked to raw milk cheese.
      • The recall included raw milk Gouda, Parmesan, and other cheeses from a manufacturer in British Columbia.
      • While the victims were in Canada, Marler Clark is experienced in cross-border foodborne illness litigation and covered the case through its blog. 

    Related raw dairy cases

    The firm’s work on E. coli illnesses from raw cheese is part of a larger focus on unpasteurized dairy products. Other similar cases include: 

    • Organic Pastures Raw Milk (2008): In 2008, Marler Clark filed E. coli lawsuits against Organic Pastures on behalf of children who developed HUS after drinking its raw milk products.
    • Dee Creek Farms Raw Milk (2005): The firm represented families of children who were severely injured by E. coli from unpasteurized milk from Dee Creek Farm in Washington State.
    • Cozy Valley Creamery Raw Milk (2012): Marler Clark filed a lawsuit on behalf of a child hospitalized with HUS after consuming raw milk from Cozy Valley Creamery in Washington. 

    Broader context of Marler Clark’s work

    Since its founding, the firm has represented victims in most major foodborne illness outbreaks in the United States. Its notable history includes: 

    • 1993 Jack in the Box E. coli Outbreak: The firm gained national prominence representing victims, including a record $15.6 million settlement for a young survivor.
    • 1996 Odwalla E. coli Outbreak: The firm represented most victims of the E. coli outbreak linked to unpasteurized apple juice.
    • Work with various food types: The firm has litigated E. coli cases involving ground beef, lettuce, spinach, and sprouts, alongside its numerous raw dairy cases. 
    https://www.marlerblog.com/files/2025/08/TN25-058-Outbreak-Summary_Final_7.31.25_Redacted.pdf

    Really well done investigation by Tennessee DOH – however, yet another example of a DOH NOT telling a victim of the cause of their illness. I made the call to the family of the child that died today. I do not understand why DOH would not have done this?

    Background

    On May 12, 2025, the Tennessee Department of Health’s (TDH) Foodborne and Enteric Diseases (FED) Program received a report of Hemolytic Uremic Syndrome (HUS) and Shiga toxin-producing E. coli (STEC) O157:H7 in a 4-year-old female from Henry County, TN. The case’s isolate was sent to the Kentucky Division of Laboratory Services for whole genome sequencing (WGS), and her isolate was compared to others in the National Center for Biotechnology Information (NCBI). In NCBI, a case from Texas matched the Tennessee case by zero single-nucleotide polymorphisms (SNPs). Since these two cases were indistinguishable by WGS, TDH initiated an outbreak investigation.

    Epidemiology

    The TDH FED nurse consultant received the initial case report through routine HUS surveillance. She interviewed the case’s mother to collect demographic, clinical, and exposure information (e.g. food eaten, places traveled, etc.) in the 7 days before illness onset. The FED Nurse Consultant reviewed NCBI to identify additional cases and contacted the Texas Department of Health (TXDH) to obtain information on a Texas resident who matched the TN case by 0 SNPs.

    A confirmed case was defined as a person with diarrheal illness and laboratory confirmed infection with the outbreak strain of STEC O157:H7 based on whole genome sequencing.

    Environmental Health

    The Tennessee Department of Agriculture (TDA) routine inspector for this facility and environmental health staff from TDH FED jointly performed a site visit at meat processing Facility L, which had processed venison consumed by both the Tennessee and Texas cases. The purpose of the site visit was to assess potential contributing factors that may have led to contamination of venison. During this visit, TDA performed a routine inspection and FED staff performed environmental sampling of the facilities and equipment used during venison processing.

    FED staff also collected the remaining frozen venison from the Tennessee case’s home and delivered to the Tennessee State Public Health Laboratory (SPHL) for STEC testing.

    Laboratory

    Stool specimens were tested at the Kentucky Division of Laboratory Services for the Tennessee case and at the Texas Department of State Health Services Public Health Laboratory for the Texas case. The Tennessee case’s stool was tested on a GI molecular panel (QIAstat-Dx) at the hospital laboratory. The isolate was sent to Kentucky Division of Laboratory Services where stool culture and subsequent whole genome sequencing were performed. The Texas case’s stool was culture positive ElA at a commercial laboratory then forwarded to a local health department’s laboratory with PFGE performed and positive ElA resulted. The sample was then sent to Texas DSHS, culture confirmed and whole genome sequenced performed inhouse.

    The TN SPHL tested 14 environmental swabs and processed venison meat samples using the FDA BAM method for STEC PCR a n d culture. A total of 23 packs of venison meat were received which included 17 ground meat, 5 backstrap, and 1 loin. To ensure all meat was tested, portions from two packs were pooled for testing, while the loin was tested separately. This strategy allowed for the testing of the entire 40 pounds of venison among 11 pooled ground meat and backstrap samples and 1 individual loin sample.

    Epidemiology

    The Tennessee case became ill on May 5, 2025, and symptoms included fever and hives. On May 7, 2025, she developed bloody diarrhea and was hospitalized at the Murray Calloway County Hospital in Murray, KY. A stool sample was collected on May 8, 2025, and tested positive for STEC O157:H7. On May 10, 2025, she was transferred to Vanderbilt Children’s Hospital in Nashville, TN and diagnosed with HUS. The case died at Vanderbilt Children’s Hospital on May 12, 2025.

    The case’s mother was interviewed with a standard case report form on May 13, 2025. Exposures reported by the case’s mother included daycare, eating chicken at a fast food and a Mexican restaurant, contact with a family member who worked as a farrier on farms in Kentucky and Tennessee, contact with a horse and a donkey at home, private well at home, likely eating venison processed at Facility L in Puryear, TN, drinking unpasteurized goat’s milk provided by a private individual, and eating fresh strawberries, raspberries and mangoes purchased at Wal-Mart. The case’s mother reported local travel only for daycare (Benton, KY) and restaurants (Murray, KY and Paris, TN). No recreational water exposure was reported. The case’s mother reported she had diarrhea the week before the child’s illness, the case’s father reported vomiting the week before the child’s illness, and the case’s 11-month-old sibling had fever and one day of diarrhea the week before the child’s illness. None were reported to seek treatment or testing.

    After finding the genetically related case in NCBI, TDH reached out to TXDH to see if the Texas case shared any common exposures. The Texas case’s illness onset was November 17, 2024. Symptoms experienced by the Texas case included bloody diarrhea, fever, vomiting, nausea, chills and abdominal pain. The Texas case visited the emergency room but was not hospitalized and did not develop HUS. The duration of illness was 15 days. The father stated the case, and her family traveled to Murray, KY, a week before her illness onset.

    Other exposures shared between cases were either eating or having contact with deer processed at meat processing Facility L, family members who are farriers, and the Texas case and her family traveled to the same area of Kentucky where the Tennessee case resided.

    Environmental Health

    No immediate violations or practices that could have contributed to m e a t contamination were identified during the site visit. The facility employs 10 people and noted no facility issues during their venison processing period.

    During deer season (end of October through early January), pork and beef processing is ceased at this facility to focus solely on venison. No venison is processed outside this window of time. When a deer is brought to the facility for custom meat processing, butchers on staff assess the deer visually to ensure the meat looks appropriate for processing (i.e., meat is appropriate color, no bugs). The deer is then field dressed (if not already done outside of the facility). brought inside, placed onto hooks, skinned, and offal removed prior to being placed in a walk-in blast cooler for at least 1-2 days at 32°F prior to further processing. The meat is then washed with a warm wash and sprayed with vinegar water before cooling again for 3-4 days at 35°F.

    Following cooling, the meat is brought into the processing room where it is cut into steaks or ground prior to being packaged in vacuum sealed packages or sausage casings according to the customer’s preferences. Any spices used are pre-packaged from a commercial spice supplier. The meat is then labeled and placed into a walk-in freezer for at least 36 hours to fully freeze prior to notifying the customer to pick it up.

    Each night, all equipment is disassembled, and the entire facility is cleaned by an independent cleaning service. No product is co-mingled other than in the machines – grinders and stuffers are not cleaned between individual deer.

    Environmental samples were collected in each of the processing rooms in places that would have had contact with venison meat. Of note, sampling was done over 5 months since the last deer oF the 2024-2025 deer season was processed at the facility.

    Laboratory

    The Kentucky Division of Laboratory Services and the Texas Department of State Health Services Public Health Laboratory isolated STEC O157:H7 from the Tennessee and Texas cases, respectively. Whole genome sequencing results for the clinical STEC isolates indicated relatedness within 0-5 SNPs and 0 alleles by cgMLST. No other isolates were closely related to these two clinical isolates in the NCBI dendrogram.

    Approximately 40 lbs. of frozen meat from one deer were collected from the Tennessee case’s home for testing. All samples were PCR and culture negative for STEC.

    One environmental sample was PCR positive for STEC, but STEC was not isolated by culture. Without a cultured isolate, no WGS could be performed on this sample to see if it matched the outbreak strain of STEC O157:H7. This sample was collected from a hide pull that is used exclusively for venison. The chain, floor plate, bolts, and plate-chain attachment were swabbed

    Discussion

    This STEC )157:H7 outbreak had a suspected link to contact with deer processed at the Facility L in Puryear, TN. Whole genome sequences of the two human stool STEC O157:H7 isolates were identical, indicating a common exposure that was epidemiologically identified through case interviews. Other common exposures may have contributed to illness, including travel to similar areas of Kentucky and Tennessee, and family members of both cases who worked as farriers. However, investigators could not find any connection where the farriers would have worked with one another or had contact with similar people. Also, there were no common restaurants or events in Kentucky a n d Tennessee shared by the two cases seven days before their illness onset.

    Furthermore, venison is a rare exposure among STEC cases in Tennessee, with approximately 2% of all STEC cases annually reporting contact with any wild game meat, including venison. The rarity of this shared exposure, combined with the link to a shared processing facility, contributed to a high level of suspicion of venison as the suspected source in this outbreak over other possible modes of transmission.

    The literature reports outbreaks of O157:H7 linked to venison contact and consumption (Kenne al., 1997; Smith-Palmer et al., 2018; Laidler 2013). Shiga toxin-producing E. coli. can colonize in the gastrointestinal tract of ruminant animals such as cattle, goats and deer, and be shed in their feces. Deer, like other ruminant animals such as cattle and goats, can shed STEC in their stool without being ill. Transmission can occur to humans who have contact with the animal’s f e c e s or ingest foods contaminated with their feces.

    The absence of STEC in venison from the Tennessee case’s household d o e s does not indicate that the venison was not contaminated. It is possible that the section of the deer that was contaminated was already consumed, or laboratory testing could not isolate the pathogen. Shiga toxin-producing E. coli was detected by PCR on a hide pull swab; however, STEC could not be isolated from this sample. Since STEC was not isolated, G S could not be performed to determine if it matched the outbreak strain. Shiga toxin-producing E. coli was not detected or identified in any venison samples or other environmental swabs from the production facility. This could have been due in part to the lag time between the two cases’ illness onset (November 2024 for the Texas case and May 2025 for the Tennessee case) and the fact that the facility was no longer processing deer for the season at the time of our investigation. Since no environmental samples were culture positive for STEC and no process breakdowns or issues of concern were identified at the facility, no additional public health control measures were implemented beyond the processes already in place.

    Safe food handling practices, such as cooking venison steaks and roasts to 145°F and ground venison to 160°F, combined with safe handling during processing, are the best way to prevent STEC and other infections since deer can carry STEC and other bacteria without appearing ill. Young children, older adults, pregnant women, and those who are immunocompromised should not eat undercooked meats and should wash their hands with warm water and soap after being in contact with raw meats or ruminant animals, such as deer. Our investigation found that venison was the most likely common source of infection in this outbreak; however, this could not be confirmed by environmental sampling and testing.

    References

    Keene WE, Sazie E, Kok J, Rice DH, Hancock DD, Balan VK, Zhao T, Doyle MP. An outbreak of Escherichia coli O157:H7 infections traced to jerky made from deer meat. JAMA. 1997 Apr 16;277(15):1229-31. doi: 10.1001/jama. 1997.03540390059036. PMID: 9103348.

    Smith-Palmer A, Hawkins G, Browning L, Allison L, Hanson M, Bruce R, McElhiney J, Horne J. Outbreak of Escherichia coli O157 Phage Type 32 linked to the consumption of venison products. Epidemiol Infect. 2018 Nov; 146(15):1922-1927. doi: 10.1017/S0950268818001784. Epub 2018 Jul 6. PMID: 29976259; PMCID: PMC6452997.

    Laidler MR, Tourdjman M, Buser GL, Hostetler T, Repp KK, Leman R, Samadpour M, Keene WE. Escherichia coli O157:H7 infections associated with consumption of locally grown strawberries contaminated by deer. Clin Infect Dis. 2013 Oct;57(8): 1129-34. doi: 10.1093/cid/cit468. Epub 2013 Jul 21. PMID: 23876397.

    The Pennsylvania Department of Agriculture warns consumers to immediately discard Byers Organic Dairy brand raw milk purchased between July 8 and July 10, 2025, with sell-by dates of July 22 and July 23, 2025. Routine milk samples were tested and confirmed to be contaminated with Shigatoxin-producing E. colibacteria.

    Milk was sold in plastic half-gallon and gallon containers at the farm’s store at 10139 Church Hill Road Mercersburg, Franklin County. The store has removed the milk from their shelves, but could not supply a list of customers who purchased it.

    Shigatoxin-producing E. coli can make people sick with diarrhea, urinary tract infections, pneumonia, sepsis, and other illnesses. Children under five, adults over 65, and people with compromised immune systems may be at risk.

    No reported illnesses have been attributed to the product. Anyone who consumed the raw milk should consult a physician if they become ill.

    On November 25, 2024, PulseNet coded an outbreak of E. coli O157:H7 2411MOEXH-2. At the time of closing, this investigation included 89 cases across 15 states: AR (2), CO (1), IL (7), IN (8), KS (1), KY (1), MO (50), MT (1), ND (2), NE (3), OH (8), PA (1), SD (1), TN (1), WI (2), all related within 0-4 alleles by cgMLST. Isolation dates ranged from November 7, 2024, to December 1, 2024. Reported onset dates (n=83) ranged from November 4, 2024, to November 30, 2024. Ages ranged from 4 to 90 years with a median age of 24. Sixty of 88 cases (68%) were female. Outcome information was available for 74 cases, of which 36 (49%) were hospitalized. There were 7 reported cases of HUS, and 1 death attributed to this outbreak.

    A case in this investigation was defined as infection with E. coli O157:H7 with an isolate related to the outbreak strain within 0-4 alleles by cgMLST and isolation date ranging from November 7 to December 1, 2024.

    This outbreak was related to six historical investigations: 2302MLEXH-1, 2210MLEXH-3, 2210MLEXH-2, 2209MLEXH-1, 2112MLEXH-1, and 2106CAEXH-1. The only vehicle identified was for 2112MLEXH-1, which was closed with a confirmed vehicle of organic power greens. The NCBI tree for this strain included numerous nonclinical beef isolates.

    This outbreak was coded following notification from colleagues in MO after they identified and investigated multiple illness linked to events catered by the same MO-based caterer. These events occurred between November 6 and November 8. All events included the same menu items with a few modifications. MO colleagues conducted a retrospective cohort study at 2 of the events and found that salads were the only statistically significant menu item across both events. Salads contained an iceberg/romaine lettuce blend, carrots, purple cabbage, onions, canned pimento, canned artichokes, parmesan cheese, and a house made salad dressing.

    In total, 7 subclusters were identified across the multistate outbreak. These included 3 MO catered events, an OH secondary school, an IN restaurant, and IL restaurant, and an IL event catered by a different MO-based caterer. Salads were the common link across all 7 subclusters, and cases in all subclusters ate an iceberg/romaine lettuce blend. CDC deployed a focused questionnaire on November 26, 2024; 27 questionnaires were returned. Epi information was available for 65 cases, of which 60 (95%) reported consuming any type of leafy green prior to illness. Of 57 cases who could remember the exact type of leafy green consumed, 50 (88%) consumed romaine lettuce. This is statistically significantly higher than the background rate of 49% from the FoodNet Population survey. 

    A traceback investigation was initiated in response to an E. coli O157 outbreak with leafy greens as the suspected vehicle. Each case included in the traceback investigation reported consumption of leafy greens prior to illness onset. Based on information available at the points of service (POS), the traceback focused on iceberg and romaine lettuce. The investigation consisted of three traceback legs representing twenty-eight cases and five POS. The three traceback legs identified four distribution centers, one broker, two processors, one grower, and one ranch. The traceback investigation determined that a sole processer sourced romaine lettuce from a single grower that would have been available at all points of service during the timeframe of interest. Additionally, romaine lettuce supplied to four of the five POS was traced back to a common ranch and lot. Through analysis of records, four lot of romaine lettuce were implicated, resulting in confirmation of romaine lettuce as the vehicle. 

    Epidemiologic and traceback data supported the conclusion that romaine lettuce was the source of illnesses in this outbreak. CDC closed this investigation on January 15, 2025, following the elapsing of the surveillance reporting lag period and lack of new uploads. CDC closed this investigation as an outbreak with a confirmed vehicle of romaine lettuce. This outbreak will be reported to NORS with NORS ID: 511856.

    Here is what I have been able to get from the CDC and FDA to date:

    https://www.marlerblog.com/files/2025/04/2411MOEXH-2-Romaine-CO-DPHE-Records.pdf

    https://www.marlerblog.com/files/2025/04/2411MOEXH-2-Romaine-E.-coli-FDA-Records.pdf

    The CDC has declared that an outbreak of E. coli O121:H19 infections traced to carrots from Grimmway Farms has ended.

    A total of 48 people were confirmed as victims in the outbreak. Patients were spread across 19 states. Twenty people were hospitalized. One person died, and another developed hemolytic uremic syndrome, a serious condition that can cause kidney failure and brain damage.

    The Centers for Disease Control and Prevention reported that illnesses started from Sept. 6 to Nov. 10. The outbreak investigation started on Oct. 15. Grimmway Farms initiated a recall on Nov. 16.

    According to the Food and Drug Administration, epidemiologic and traceback evidence showed that recalled carrots were the likely source of illnesses in this outbreak.

    The FDA inspected Grimmway Farms of Bakersfield, CA, and collected environmental samples. Two outside environmental samples were positive for Shiga toxin-producing E. coli (STEC). 

    “Although both strains of E. coli detected in the samples are capable of causing human illness, neither match the strain of E. coli causing illnesses in this outbreak. The strain of E. coli causing illnesses in this outbreak was not found in environmental samples,” according to the FDA’s outbreak update.

    The FDA is working with Grimmway Farms on corrective and preventive actions.

    In relation to the outbreak, Grimmway Farms recalled 35 brands and weight sizes of organic carrots and baby carrots. The recalled carrots were distributed nationwide and included popular brands sold at Walmart, Kroger, Whole Foods, Target, Sprouts, and other retailers.

    The true number of outbreak patients was likely much higher than those confirmed. The CDC reports that for every confirmed patient in an E. coli outbreak, 26 go unreported. This is because some people do not seek medical attention, and others are not specifically tested for E. coli infection.