• To date, 25 STEC probable and confirmed cases have been reported to VDH
  • 21 cases were reported in Virginia residents from the Central, Northern and Northwest regions of the state
  • Four cases were reported in residents of other states
  • Most cases (76 percent) have occurred in children younger than 18 years of age

The Virginia Department of Health (VDH) is providing an update on the outbreak of Shiga toxin-producing Escherichia coli (STEC) in people who were in the Lake Anna area on and after the Memorial Day weekend. To date, 25 STEC probable and confirmed cases have been reported to VDH: 21 in Virginia residents from the Central, Northern, and Northwest regions of the state and four in residents of other states. Most cases (76%) have occurred in children younger than 18 years of age. Severe STEC infections can progress to hemolytic uremic syndrome (HUS), which can be particularly serious. To date, five HUS cases have been reported to VDH, all in children who required hospitalization.

VDH has been partnering with the Department of Environmental Quality (DEQ) in the collection of water samples at six priority locations in Lake Anna. There was an increase of STEC cases in the Rappahannock Health District during the first week of June. Soon after, the Office of Environmental Health Services initiated an investigation and began tracking the results. The first sampling event occurred on June 11 and the second event is planned for June 17. Water column samples were analyzed for bacteria, including E. coli, by the Department of General Services Division of Consolidated Laboratory Services (DCLS), the state laboratory. Results for samples collected June 11 indicate all fecal bacteria concentrations were well below a public health level of concern. A map of the six sampled areas and the test results is available on the VDH outbreak website that was launched today.

VDH’s investigation is ongoing. No single cause of the outbreak has been identified, and it is possible we might not be able to identify the source. There is no indication that contaminated food was the source of the outbreak. Environmental pollution from heavy rains, livestock, failing septic systems, boating discharge, and swimmers are potential sources of illness when swimming in natural waters. Avoid swimming where livestock are present.

If you were in the Lake Anna area on Memorial Day weekend (May 24–27, 2024) or since and you experienced gastrointestinal illness (such as stomach cramps and diarrhea), contact your local health department and seek medical care if you are still experiencing symptoms.

To prevent illness when swimming and boating in natural waters, people should:

  • Never drink untreated water, and don’t swim if skin has cuts or open wounds. Natural waters such as rivers, lakes, and oceans contain germs and contaminants, which can cause illness.
  • Wash their hands after using the bathroom and before preparing and eating food.
  • Avoid swimming near storm drains (pipes that drain polluted water from streets).
  • Avoid swimming if they are vomiting or have diarrhea.
  • Avoid going in water if there is a green film on the water and keep pets out as well. This may indicate an algal bloom and some algae produce toxins that can make people sick.
  • Shower or bathe after swimming to wash off possible germs and contaminants.
  • Avoid swimming for three days after a heavy rain. Germs can come from overflowing sewage, polluted storm water & runoff from land.
  • Properly dispose of human waste by discharging boat sewage at marinas with a pump-out unit or dump station.
  • If your body’s ability to fight germs is already affected by other health problems or medicines, check with your healthcare provider before swimming in oceans, lakes, rivers, and other natural bodies of water.

VDH will provide future updates on our outbreak website on Tuesdays and Thursdays.

Visit www.SwimHealthyVA.com for more healthy and safe swimming tips.

Food manufacturers are recalling at least 60 types of pre-packed sandwiches, wraps and salads sold in major supermarkets because of possible contamination with E. coli. 

E. coli bacteria have not been detected in the products, but they are being recalled as a precaution. It is understood these are items containing salad leaves.

Retailers involved include Aldi, Asda, Co-op and Morrisons.

As of 11 June, there have been a further 98 cases associated with this outbreak of STEC O145 in the UK, bringing the total number of confirmed cases to 211. All cases had sample dates before 31 May, but we expect this figure to rise as whole genome sequencing is ongoing to find any further cases which may be linked to the outbreak.

  • 147 in England
  • 27 in Wales
  • 35 in Scotland
  • 2 in Northern Ireland (for these cases, evidence suggests that they acquired their infection while visiting England)

Based on information from 160 cases to date, 42% were admitted to hospital.

UKHSA has worked closely with the Food Standards Agency (FSA), Food Standards Scotland and the devolved public health agencies to investigate the incident, carrying out epidemiological investigations and whole genome sequence analysis to help identify foods commonly consumed by the cases.

As a result of evidence gathered to date, product recall information notices have been published by FSA as a precaution.

Trish Mannes, Incident Director at UKHSA, said:

We would like to thank all the cases who have provided information that has enabled us, through epidemiological analysis of questionnaire data and food tracing investigations, to narrow down the likely food product linked to this outbreak.

Symptoms of infections with STEC include severe and sometimes bloody diarrhoea, stomach cramps, vomiting and fever. If you are unwell, have eaten salad leaves recently and are concerned about any symptoms, follow NHS.uk guidance on when to seek help and the steps you can take to avoid further spread to family and friends.

While diarrhoea and vomiting can have a range of causes, there are simple steps you can take to reduce your risk and risk of infecting others. Washing your hands with soap and warm water and using disinfectants to clean surfaces will help stop any further spread of infection. If you are unwell with diarrhoea and vomiting, you should not prepare food for others while unwell and avoid visiting people in hospitals or care homes to avoid passing on the infection in these settings. Do not return to work, school or nursery until 48 hours after your symptoms have stopped.

Darren Whitby, Head of Incidents at the FSA, said: 

Sandwich manufacturers are taking a precautionary measure to recall various sandwiches, wraps, subs and rolls in response to findings from investigations by the Food Standards Agency (FSA), Food Standards Scotland (FSS) and UK Health Security Agency (UKHSA) who are working to identify the cause of an ongoing outbreak caused by shiga toxin-producing E.coli (STEC). The full list of products can be found in the product recall information notice (PRIN).  

This is a complex investigation, and we have worked swiftly with the relevant businesses and the local authorities concerned to narrow down the wide range of foods consumed to a small number of salad leaf products that have been used in sandwiches, wraps, subs and rolls. Following thorough food chain analysis, these products are being recalled as a precaution.  

Infections caused by STEC bacteria can cause severe bloody diarrhoea and, in some cases, more serious complications. We therefore advise any consumers who have any of these products not to eat them.  

The FSA is here to ensure that food is safe. If there are products on the market that are not, we won’t hesitate to take action to remove them.

The National Cattlemen’s Beef Association (NCBA) needs a new motto: “Ignoring reality does not make reality go away.”

Clearly the NCBA, must have read a different report than I did and posted yesterday. The NCBA also must have missed this from this other FDA report a few years ago:

“We released our preliminary findings earlier this year that noted this investigation found the outbreak strain in a sample of cattle feces collected on a roadside about a mile upslope from a produce farm. This finding drew our attention once again to the role that cattle grazing on agricultural lands near leafy greens fields could have on increasing the risk of produce contamination, where contamination could be spread by water, wind or other means. In fact, the findings of foodborne illness outbreak investigations since 2013 suggest that a likely contributing factor for contamination of leafy greens has been the proximity of cattle. Cattle have been repeatedly demonstrated to be a persistent source of pathogenic E. coli, including E. coli O157:H7.”

According to the recent FDA Report on Yuma:

… there is a Concentrated Animal Feeding Operation (CAFO) with more than 80,000 head of cattle and an associated compost operation in proximity to some of the produce production areas studied. 

Key Findings 

  • Airborne Pathogens: Airborne transmission of viable STEC was documented on numerous occasions at several locations adjacent to and at incremental distances from a nearby large livestock and composting operation (80,000+ cattle). In addition, air, water, and lettuce leaf microbiome analysis demonstrated deposition of dust from cattle pens to the nearby water and land, suggesting that dust from CAFOs may play a role in STEC transmission in this part of the region. These findings indicate that STEC can survive in the air and that dust can act as a transfer mechanism for both pathogens and indicator organisms (e.g. generic E. coli) from adjacent and nearby land to water, soil, and plant tissue. Additionally, distance played an important factor in the likelihood of STEC being detected in collected airborne dust, with percentage of positive samples declining steadily as air sampling moved in an incremental manner away from concentrated animal operations.
  • Water Quality: The research team repeatedly observed that generic E. coli concentrations and STEC prevalence and isolation frequency increased as irrigation canal water flowed past an adjacent livestock and compost operation. In addition, these changes in water quality occurred absent other explanations such as surface run-off or other direct contamination, which indicates that airborne disposition of dust from a nearby CAFO was potentially a factor in the contamination of the irrigation water. Similar findings were not observed from samples obtained concurrently from a different nearby irrigation canal that flows south of the CAFO and associated compost operation suggesting the important role of localized southerly winds in transferring CAFO-associated dust in northward  directions.

However, the NCBA chooses to ignore reality.

NCBA Responds to FDA’s Longitudinal Study on the Yuma Valley Leafy Greens Growing Region

JUNE 13, 2024

On June 5, 2024, the U.S. Food and Drug Administration (FDA) released preliminary findings from a multi-year study investigating the spread of bacteria to leafy greens being grown in Yuma County, Arizona.

The study was undertaken after a 2018 E. coli outbreak that was linked to romaine lettuce from the Yuma, AZ, growing area. The investigation into that outbreak found samples of canal water that tested positive for the outbreak strain of E. coli. However, that strain of E. coli was not found at a nearby cattle feeding operation and the investigation ultimately found “no obvious route for contamination” from the feeding operation. 

“Despite those 2018 investigative findings, we are concerned that some have erroneously interpreted the new FDA study as suggesting that the cattle industry is responsible for the outbreak, even though the scientific evidence does not support such a conclusion,” said NCBA CEO Colin Woodall. “In fact, FDA has expressly stated that the multi-year study did not identify the specific source and route of contamination that contributed to the 2018 outbreak.”

On the surface, cattle operations appear to be an easy target, but cattle and beef producers are already subject to countless local, state, and federal regulations that govern their operations to minimize the environmental impact and ensure that the food supply is safe. 

“The cattle and beef industry takes its responsibility for food and consumer safety seriously. Clearly, more scientific data is needed, but we must not allow ourselves to get ahead of science and play the blame game,” said Woodall. “Farmers and ranchers dedicate significant resources toward identifying and implementing practices that protect the environment, while also supporting food safety.”

I call “bullshit!”

According to a recent FDA Report:

In 2019, the FDA, in collaboration with the University of Arizona, the Wellton-Mohawk Irrigation and Drainage District, local growers, industry groups, and others, began a multi-year study in Yuma County, Arizona – which grows many of the leafy greens sold in the United States. The study was designed to improve understanding of the environmental factors that may impact the presence of foodborne pathogens in the Southwest agricultural region. The research team was particularly interested in identifying new information about factors that significantly contribute to the introduction, persistence, growth, spread, and die-off of pathogens that could contaminate produce prior to harvest in this region.

The study involved collecting environmental samples throughout a five-year period. Samples were collected from irrigation waters, soil, sediments, air/dust, animal fecal material, wildlife scat, and other sources across approximately a 54 mile (7,000 acres) area of the southwest growing region, which also represents about 12% of the Wellton-Mohawk Irrigation and Drainage District’s agricultural production area. Water sampling occurred from the headworks of the Wellton-Mohawk canal and at multiple points as the canal splits and flows thru the Gila Valley and Texas Hill area. Other select surface water sites were also sampled. Special attention was given to the geography of the study region and the types and locations of agricultural and other adjacent and nearby land use activities relative to produce production areas.  For example, there is a Concentrated Animal Feeding Operation (CAFO) with more than 80,000 head of cattle and an associated compost operation in proximity to some of the produce production areas studied. In addition, research plots of romaine lettuce were grown within the study area over several seasons to capture data on pathogen prevalence and persistence as well as to evaluate the influence of specific growing and harvesting practices. Pertinent meteorological information (air temperature, wind speed and direction, rainfall, etc.) was also logged. 

Collected samples were analyzed using microbial culture methods, metagenomics, and whole genome sequencing to identify pathogens and microorganisms that can be indicators of unhygienic conditions. Through repeated sample collection, testing, measurement, and analysis, we observed fluctuations in the types and prevalence of pathogens and indicator organisms over time and location, including variability across different seasons. 

The findings of this study contribute to a better understanding of the impact various environmental factors can have on food safety and may be used to refine best practices for growers to continually improve produce safety.

Key Findings 

The research team conducted over 100 sampling events at 55 sites resulting in more than 5,000 unique samples collected and 15,000 individual tests for detection of generic EcoliSalmonella, and Shiga toxin-producing Ecoli (STEC), including Ecoli O157:H7.The research team then performed whole genome sequencing and analyzed isolated strains to determine their genetic relatedness as well as distribution across the study region. The research scientists are continuing to analyze data from this study, however preliminary key findings include:

  • Airborne Pathogens: Airborne transmission of viable STEC was documented on numerous occasions at several locations adjacent to and at incremental distances from a nearby large livestock and composting operation (80,000+ cattle). In addition, air, water, and lettuce leaf microbiome analysis demonstrated deposition of dust from cattle pens to the nearby water and land, suggesting that dust from CAFOs may play a role in STEC transmission in this part of the region. These findings indicate that STEC can survive in the air and that dust can act as a transfer mechanism for both pathogens and indicator organisms (e.g. generic E. coli) from adjacent and nearby land to water, soil, and plant tissue. Additionally, distance played an important factor in the likelihood of STEC being detected in collected airborne dust, with percentage of positive samples declining steadily as air sampling moved in an incremental manner away from concentrated animal operations.
  • Water Quality: The research team repeatedly observed that generic E. coli concentrations and STEC prevalence and isolation frequency increased as irrigation canal water flowed past an adjacent livestock and compost operation. In addition, these changes in water quality occurred absent other explanations such as surface run-off or other direct contamination, which indicates that airborne disposition of dust from a nearby CAFO was potentially a factor in the contamination of the irrigation water. Similar findings were not observed from samples obtained concurrently from a different nearby irrigation canal that flows south of the CAFO and associated compost operation suggesting the important role of localized southerly winds in transferring CAFO-associated dust in northward  directions.
  • Wildlife Contributions: Over 1,000 samples of wildlife fecal material, including from a wide variety of mammals and birds, were collected to study the role wildlife in this region may contribute to pathogen dissemination. A special emphasis was placed on birds, both native and migratory, given their presence and ability to access both terrestrial areas including produce fields and livestock areas, and various surface water locations including irrigation canals. In total, over 40 different bird species were sampled, with red-winged black birds being the only species testing positive for STEC in very few of the nearly 60 samples collected from this bird species. Therefore, birds and other wildlife do not appear to be significant sources of STEC or Ecoli O157:H7 in or around the part of the Southwest growing region evaluated. However, continued monitoring is warranted to reduce potential risk to produce, the environment and water sources.
  • Whole genome sequencing results: More than 40 different STEC serotypes were recovered from roughly 500 different samples representing all the matrices examined in this study. STEC strains detected in water, sediment, and plant tissue harvested from our research plots genetically matched strains isolated in air samples providing evidence that bacteria in air can transfer to other locations and surfaces.

The research team is continuing to analyze data from the study. For instance, meteorological data were collected at the time of sampling and are being used to evaluate whether factors such as wind speed and direction are drivers for both the positive and negative results obtained. As more information and findings become available this page will be updated.

Post-Study Actions

The preliminary results of this study stress the interconnectedness between people, animals and the environment and serve as an important model for how to foster productive dialogue among diverse stakeholders to improve food safety. Just as collaboration across the Southwest agricultural community was key to the development and execution of this study, continued collaboration among stakeholders including livestock managers/producers, fresh produce growers, academia, extension, retailers, and federal, state, and local government partners will be important to help control and mitigate potential contamination via environmental transmission including air/dust from adjacent and nearby land.

Members of the Arizona leafy greens industry will be working through the Desert Food Safety Coalition to continue to collaborate with the Arizona Department of Agriculture, University of Arizona Extension, Yuma Fresh Vegetable Association, Yuma Safe Produce Council, Arizona Farm Bureau, Arizona Leafy Green Marketing Agreement (AZ LGMA), Western Growers, USDA-APHIS Wildlife Services, Arizona Cattle Feeders’ Association, additional grower and landowner coalition members and other agricultural community stakeholders to engage the industry and inform best practices to improve food safety in the region.

While the results are regionally specific, the findings may also help us to address some knowledge gaps identified in the Leafy Green STEC Action Plan, particularly concerning adjacent and nearby land use. As additional data analysis is completed, FDA plans to engage with stakeholders to further explore the data and information gathered from this study.

The research team intends to present additional details about this study during the International Association for Food Protection annual meeting July 14-17, 2024. As final data analysis occur, we intend to publish manuscripts on this in the scientific literature. Additional information and publications will be added to this page as they become available.

The Food and Drug Administration’s Inspection and Recall Process Should Be Improved To Ensure the Safety of the Infant Formula Supply

What OIG Found

FDA had inadequate policies and procedures or lacked policies and procedures to identify risks to infant formula and respond effectively through its complaint, inspection, and recall processes. For example, FDA had not developed an organizational structure or assigned responsibilities to handle whistleblower complaints in an efficient and effective manner and took more than 15 months to address a February 2021 Abbott facility whistleblower complaint. In addition, FDA did not escalate an October 2021 whistleblower complaint to senior leadership, resulting in a nearly 4-month delay before senior leadership was aware of the complaint. We also found that FDA did not have policies and procedures to establish timeframes for the initiation of mission-critical inspections, which contributed to one inspection being initiated 102 days after a whistleblower complaint was received. Further, FDA did not have sufficient policies and procedures on how to initiate an infant formula recall under its FDA-required recall authority.

What OIG Recommends

We made nine recommendations to FDA, including that it: (1) maintain the National Consumer Complaint Coordinator’s (NCCC’s) continuity of operations by cross-training staff on whistleblower policies and procedures and NCCC duties, (2) develop and implement policies and procedures requiring periodic reporting to senior leadership on the status of open whistleblower complaints, (3) develop policies and procedures that FDA can use during future public health emergencies to identify how and when it is necessary to conduct mission-critical inspections and ensure that they are conducted in a timely manner, and (4) design and implement policies and procedures specific to the use of its FDA-required infant formula recall authority. The full recommendations are in the report. FDA concurred with all nine of our recommendations.

Findings

  • FDA did not have adequate policies and procedures or lacked policies and procedure
  • FDA did not have adequate policies and procedures to identify the February 2021 Whistleblower Complaint
  • FDA did not have adequate policies and procedures to escalate to the October 2021 Whistleblower Complaint
  • FDA did not have adequate policies and procedures to communicate consumer complaints to investigators
  • FDA did not have adequate policies and procedures to identify and correct infant formula consumer complaint data inaccuracies
  • FDA policies and procedures did not identify specific factors to determine which adverse event complaints should be communicated to the NCCC
  • FDA did not have policies and procedures to establish timeframes for the initiation of mission-critical inspections
  • FDA did not have adequate policies and procedures for initiating an FDA-required recall
  • FDA did not have the authority to require individuals and manufacturers to provide information that may have helped FDA to identify and respond to risks in the infant formula supply

See full report – https://oig.hhs.gov/documents/audit/9908/A-01-22-01502.pdf

The Virginia Department of Health (VDH) is investigating 20 confirmed cases of Shiga toxin-producing E. coli (STEC) from people who visited Lake Anna in Virginia over the Memorial Day weekend.  The VDH is still investigating all potential sources of the outbreak.

The health authority stated that five people developed hemolytic-uremic syndrome (HUS), which can lead to kidney failure and nine have been hospitalized. Ten cases are still under investigation and could lead to a higher number of confirmed illnesses.

I am lucky to have an epidemiologist on staff. Perhaps Fresh Start needs one too.

Let me make a prediction, Fresh Start will eat its press release because the FDA will find more cucumbers that test positive for either Africana, Braenderup or Bareilly in states other than Pennsylvania and there will be more clinical (human) positives for Africana, Braenderup and Bareilly.

Let’s start with the basics. The Salmonella Africana found in samples of the 196 victims of this outbreak share the same whole genome sequence (WGS). This showed that bacteria from sick people’s samples are closely related genetically. This means that people in this outbreak likely got sick from the same type of food. However, after the Pennsylvania Department of Agriculture released test results showing that the Fresh Start cucumbers it tested were positive for a different strain of SalmonellaSalmonella Bareilly. This DOES NOT mean that Fresh Start cucumber are not the source to the Salmonella Africana outbreak and Fresh Start may well also be the source of a different outbreak – Salmonella Braenderup – linked to its cucumbers too. Epidemiology will tell that tale as well.

So Fresh Start do not crow too loudly of your innocence. WGS and epidemiology do not lie. Here is what the FDA and CDC have said to date:

Based on epidemiological information collected by CDC for the Salmonella Africana investigation, as of June 12, 196 people infected with the outbreak strain of Salmonella Africana have been reported from 28 states and the District of Columbia. Of the 85 people interviewed, 63 (74%) reported eating cucumbers. 

CDC and FDA are also investigating an outbreak of Salmonella Braenderup infections, with 185 illnesses in 24 states. The two outbreaks share several similarities, including where and when illnesses occurred and the demographics of ill people. Investigators are working to determine whether the two outbreaks could be linked to the same food vehicle. Information will be provided on the source of the Salmonella Braenderup outbreak as it becomes available.

As part of the Salmonella Africana investigation, state partners in the Pennsylvania Department of Agriculture collected samples of cucumbers from several retail locations in their state. One sample supplied by Fresh Start Produce Sales, Inc., of Delray, Florida, tested positive for Salmonella. The specific strain of Salmonella found on Fresh Start Produce Sales, Inc. recalled cucumbers was identified as Salmonella Bareilly and does not match any ongoing outbreaks.  

Fresh Start Produce take a deep breath, talk to an epidemiologist and follow the science. That is what the folks at health departments in 28 states, the FDA and the CDC are doing.

The FDA and CDC, in collaboration with state and local partners, are investigating a multistate outbreak of Salmonella Africana infections potentially linked to cucumbers. 

Based on epidemiological information collected by CDC for the Salmonella Africana investigation, as of June 12, 196 people infected with the outbreak strain of SalmonellaAfricana have been reported from 28 states and the District of Columbia. Of the 85 people interviewed, 63 (74%) reported eating cucumbers. 

CDC and FDA are also investigating an outbreak of Salmonella Braenderup infections, with 185 illnesses in 24 states. The two outbreaks share several similarities, including where and when illnesses occurred and the demographics of ill people. Investigators are working to determine whether the two outbreaks could be linked to the same food vehicle. Information will be provided on the source of the Salmonella Braenderup outbreak as it becomes available.

As part of the Salmonella Africana investigation, state partners in the Pennsylvania Department of Agriculture collected samples of cucumbers from several retail locations in their state. One sample supplied by Fresh Start Produce Sales, Inc., of Delray, Florida, tested positive for Salmonella. The specific strain of Salmonella found on Fresh Start Produce Sales, Inc. recalled cucumbers was identified as Salmonella Bareilly and does not match any ongoing outbreaks.  

The investigations are ongoing to determine the source(s) of contamination and what products are linked to illnesses. FDA will update this advisory should additional consumer safety information become available. 

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 10 years that followed there were approximately thirty (30) outbreaks recorded in the United States.[13] This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987 when Washington became the first state to mandate its reporting to public health authorities.[14] As a result, only the most geographically concentrated outbreak would have garnered enough notice to prompt further investigation.[15]

The E. coli O157:H7 Bacteria

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. coli O157: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.[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.[30] The colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within 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 to four days, but may be as short as one day or as long as 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 to 12 days.[34] In reported outbreaks, the rate of death is 0-2 percent, with rates running as high as 16-35 percent 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 degrees F, survives freezing and thawing, is heat resistant, grows at temperatures up to 111 degrees 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 percent of victims, primarily children, with onset five to 10 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 percent 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 5 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 readily 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 percent.[65] The frequency of postinfectious Reiter syndrome, however, has not been well described. In a Washington State study, while 29 percent developed arthritis, only 3 percent 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 percent and 30 percent 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 more than 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 10 years, with their symptoms remaining 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 percent), 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]


[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.htmlSee 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 alEpidemiology 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 alPredictors 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 alRisk 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 alLong-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 note 46, 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]         IdSee 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).