Two years after children were sickened and some nearly died, insurance companies and the lawyers they hire continue to deny justice to the victims – that will not last long.


In March 2017, the Centers for Disease Control and Prevention (CDC) and several state health departments attributed a multi-state outbreak of Shiga toxin-producing Escherichia coli O157:H7 to I.M. Healthy brand SoyNut Butter manufactured by Dixie Dew and sold at retail on online outlets.

Outbreak investigators collected open containers of SoyNut Butter from the homes of sick people, and unopened containers from retail locations. Containers of SoyNut Butter from lots #243162 and 244161 tested positive for E. coli O157:H7. Whole genome sequencing revealed that the same strain of E. coli O157:H7 was found in clinical isolates from sick people and containers of I.M. Healthy SoyNut Butter. Epidemiologic investigation determined that 32 people ill with this strain of E. coli had been infected by eating or attending a facility that served I.M. Healthy SoyNut Butter. This included residents of Arizona (4), California (5), Florida (2), Illinois (1), Massachusetts (1), Maryland (1), Missouri (1), New Jersey (1), Oregon (11), Virginia (2), Washington (2), and Wisconsin (1).

The damage caused by this outbreak has been considerable. Twelve people were hospitalized due to their infection, and nine developed hemolytic uremic syndrome (HUS). HUS is a debilitating condition caused by E. coli that is commonly characterized by kidney failure, but may also lead to brain damage, seizures, and diabetes. Children less than 10 years of age are particularly at risk for developing HUS.

I.M. Healthy brand SoyNut Butter filed for bankruptcy in 2017 and 2018 respectively.


The causal link between Julian Murph’s E. coli O157 infection and I.M. Healthy brand SoyNut Butter is clear. Julian’s parents purchased a container of I.M. Healthy brand SoyNut Butter on February 12, 2017. Julian regularly consumed this during February and March.

Julian began to experience bloody diarrhea and stomach cramps on March 2, 2017. A stool specimen collected on March 6 at Pediatric Associates of the Northwest tested culture positive at Oregon State Public Health Laboratory for shiga toxin-producing E. coli O157 (Case ID#557072). A sample of SoyNut Butter from Julian’s container also tested positive for E. coli. Genetic testing revealed that Julian’s E. coli was the same as the E. coli found in his SoyNut Butter (PFGE pattern EXHX01.2652\EXHA26.3972). This PFGE pattern matched that of the multi-state SoyNut Butter outbreak.

Julian was identified as a confirmed case in the I.M. Healthy SoyNut Butter E. coli outbreak (CDC cluster ID#1702CAEXH-1) by the Multnomah County Health Department.

The causal link between Finley Oleksiak’s E. coli infection and I.M. Healthy brand SoyNut Butter is clear. Finley attends the Montessori of Alameda preschool in Portland, Oregon, where he is classmates with Julian Murph, a child confirmed to be infected with E. coli from consuming contaminated I.M. Healthy brand SoyNut Butter. Finley did not ingest SoyNut Butter but acquired his E. coli infection through secondary transmission from Julian Murph.

Finley began to experience bloody diarrhea, nausea, and stomach cramps on March 3, 2017. A stool specimen collected on March 14 at Legacy Emmanuel Medical Center tested culture positive at Oregon State Public Health Laboratory for shiga toxin-producing E. coli O157 (Case ID#556818). Genetic testing revealed that Finley’s E. coli was the same as the E. coli found in contaminated SoyNut Butter (PFGE pattern EXHX01.2652\EXHA26.3972). Finley was identified as a confirmed case in the I.M. Healthy SoyNut Butter E. coli outbreak (CDC cluster ID#1702CAEXH-1) by the Multnomah County Health Department.


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. coliO157: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. coliculturesobtained between 1973 and 1982 found only one (1) isolationwith serotype O157:H7, and that was a casein 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. 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]

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. coliO157: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 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.


Finley Oleksiak just turned three years old. He lives in Portland, Oregon with his mother Elizabeth and father Joseph, and attended daycare at Montessori of Alameda in the winter of 2017. One of Finley’s Montessori classmates at the time was Julian Murph, whose family purchased and fed him soy nut butter products contaminated by E. coli O157:H7. Ultimately, a number of children in Finley and Julian’s classroom were counted as confirmed and probable outbreak victims.

Finley is Elizabeth and Joseph’s first and only child. They describe him as an intelligent, empathetic, kind, energetic and happy boy:

As first-time parents, you naturally think these things, but when random grandmothers in grocery stores reiterate our sentiments, it is hard not to believe you have something extraordinary.

Symptom Onset

Finley began to show symptoms of loose stool on Thursday, March 3, 2017, just as his parents were putting him to bed. Initially this was the only symptom he exhibited and, because it was mild, they were not initially concerned. Over the next couples of days, his diarrhea became more prominent and Finley began to display a noticeably-more-subdued demeanor. He was not interested in taking part in the activities he usually loved, such as gymnastics or going to the library.

Finley’s symptoms took a more ominous turn when Elizabeth and Joseph noticed that he did not want to eat, even his most favorite foods. By Friday evening, they noticed unusual symptoms. Finley was not able to sleep throughout the night, waking up every twenty to thirty minutes with diarrhea, and telling them that he had to go to the bathroom. Elizabeth recalls a long and frightening night:

What initially began to worry us was the unusual amount of runny stool he was passing and the pain he was complaining of when toileting. Because we had recently begun toilet training, he insisted on using the toilet each time he felt the urge rather than letting us use diapers. Needless to say, no one slept well that night. We felt as sleep deprived as we had been two years ago when he was an infant.

The next morning, Finley’s diarrhea continued at the same frequency, and Elizabeth noticed small amounts of mucousy blood in his diapers. At first, she and Joseph attributed this to his rectum being irritated from the previous night’s frequent bathroom sessions. But Finley was still not acting like his spunky, jovial self, and only found comfort in lying on the couch with Daddy. As his symptoms worsened, it quickly became clear to them that their baby needed medical attention. That evening, Elizabeth called his primary care physician and the on-call nurse directed her to take Finley straight to the children’s emergency room. She recalls:

Hearing this made us panic. We left the house immediately with our coats and wallet and headed for the emergency room.

Randall Children’s Hospital at Legacy Emanuel Hospital

It was just before 7 PM on Saturday, March 4, 2017 when Finley was checked in Randall Children’s Hospital, where Michael Stone, MD evaluated him in the pediatric emergency department for bloody diarrhea. Elizabeth and Joseph described the onset and character of Finley’s diarrhea illness, with the only other recent illnesses being a cold the week before and an otherwise unremarkable medical history.

In the ER, Dr. Stone found Finley acting miserable and complaining of pain. He did not have a fever and his vital signs were stable. Dr. Stone told Elizabeth and Joseph that the range of problems they could be looking at included intussusception, perforated appendicitis, enteroinvasive enteritis, among other serious illnesses. Dr. Stone ordered a CBC to check Finley for anemia or leukocytosis [elevated white count], as well as a metabolic panel to check his sodium levels, renal function, and electrolyte imbalances. He also requested a urinalysis to rule out infection or a kidney source of bleeding. He started Finley on IV fluids while awaiting abdominal imaging.

Elizabeth recalls the ER as a traumatic experience for Finley:

We spent the remainder of Saturday night in the emergency room, awaiting answers to Finley’s ailments. By this time, Finley was in so much discomfort and pain, it was difficult to manage. He continued to cry every time he had to go to the bathroom, which was about every 20 minutes at this point. Nurses and doctors were poking and prodding him, trying to determine his diagnosis, which he did not handle well. Several times during our emergency department stay, we had to hold him down while he screamed and flailed his arms and legs, so that the medical staff could exam him, draw blood, insert an IV for dehydration, and complete diagnostic imaging tests. This was excruciating for both Finley and us, it is difficult to rationalize with a two-year-old, but next to impossible explaining the purpose behind what he was experiencing. Little did we know at this point; this was just the beginning of a 20-day hospitalization and an intensely traumatic physical and emotional roller coaster for our entire family.

At 8 PM, radiologist James Gilmore, MD performed an ultrasound that identified significant bowel wall thickening but no definite intussusception. Jafri Mubeen, MD from pediatric surgery evaluated Finley and recommended that he be admitted to the pediatric hospitalist service for IV fluid hydration and serial abdominal exams by the surgical team. He requested a GI PCR Panel. James P. McCord, MD accepted Finley for admission, but it was not until almost 10:30 PM when Megan Rae Durham, MD formally admitted him to the hospital with a preliminary diagnosis of gastroenteritis/colitis.

Dr. Durham reviewed the labs drawn in the ER, noting nothing that stood out as alarming, with a normal white count, no anemia, and normal kidney function. She thought the ultrasound could represent either an infectious process or “self-reduced intussusception,” with a reassuring read by the surgery department. A KUB (kidney-urethra-bladder) x-ray was confirmatory and showed a nonobstructive gas pattern. Nevertheless, surgery wanted Finley to have nothing by mouth (NPO) as a precaution in case things changed overnight. There was mostly a concern for an infectious process at this point, and the plan was to collect a stool specimen for culture as soon as possible, with blood cultures if Finley ran a fever over 101.5ºF. They would also keep a close eye on his urinary output.

Randall Children’s Hospital Pediatric Unit – Day 1

On Sunday, March 5, 2017 at a little after midnight, Shannon Lowell, MD of the surgical team looked in on Finley, finding him somewhat more comfortable after having been given intranasal pain medication (oxycodone) and IV fluids in the ER. She discussed his labs with Louis Le, MD, pediatric surgery fellow and pediatric hospitalist Angelique Murphy, MD, and they agreed on a care plan that included serial abdominal exams with a repeat abdominal ultrasound if Finley’s pain recurred.

Later during morning rounds, Dr. Murphy noted that Finley had not tolerated fluids orally. He initially seemed to be improving and expressed hunger; however, after some sips of “clears,” his abdominal pain returned, and he had vomiting and continued diarrhea with scant blood streaking. Dr. Murphy commented that Finley awoke from sleep with obvious stomach cramping and pain, crying out “oweeeoweeeowee,” and he was tender throughout his abdomen. He seemed to be the most painful over the right and left lower quadrants. A urine sample was collected just after midnight that was reflective of dehydration, with ketones and high specific gravity. A stool sample was also sent to the lab and was pending culture results, as well as PCR testing for C. difficile and a GI PCR Panel.

Later that evening, pediatric hospitalist Kathryn Cox, MD came in with Dr. Murphy and noted Finley moaning in his sleep and “awakened as if in pain,” and she was able to discern abdominal contractions. Elizabeth and Joseph remained at Finley’s bedside and were able to console him. Dr. Murphy also thought the toddler’s abdomen was mildly distended, without any obvious peritoneal sounds. She discussed Finley with pediatric gastroenterologist Kathryn Moyer, MD, who felt pretty certain this was most likely infectious acute gastroenteritis (AGE) and did not require immediate gastroenterology involvement. However, she put herself on standby if Finley took a turn for the worse.

Elizabeth recalls the watchful waiting, as Finley became more and more uncomfortable:

As the medical team was trying to determine his correct diagnosis, they decided to admit Finley overnight for observation. After we were admitted, Finley continued to experience high levels of pain and discomfort. Initially our care team was unsure of the reason behind his symptoms and thought it could potentially be a surgical issue, the attending physician ordered that Finley not consume food or liquid until they could determine if he would need surgery. Not being allowed to eat or drink was very difficult for Finley, as he did not understand the reasoning behind this decision, and would desperately ask for food and milk, and then would proceed to cry and moan when we told him he could not have any. This was hard for us as his parents as well, since our primary duty is to provide and care for our child. It broke our hearts that we could not give him what he wanted, especially something as basic as food. His frequent diarrhea and pain continued throughout the weekend.

Randall Day 2 – Confirmation of E. coli O157:H7

Just past midnight on Monday, March 6, 2017, Dr. Murphy received notice that the hospital lab had just reported a positive stool PCR result from the GI Panel, showing that he had tested positive for E. coli O157, as well as Shiga-toxin-producing E. Coli (STEC).

Angela Pickens, MD was summoned to Finley’s bedside at 1 AM to re-evaluate and make changes to his care plan. She responded to the E. coli results by discussing Finley with GI and surgery and alerted Elizabeth and Joseph to his diagnosis. The discussion included the risks of his developing hemolytic uremic syndrome, which they would be watching for closely. Finley’s C. difficile test came back negative. Dr. Pickens adjusted Finley’s IV fluids to compensate for electrolyte losses and put the nursing staff on high alert for signs of HUS.

Through the day, the doctors continued to watch Finley for any decrease in his urinary output. They increased his IV fluids as he was unable to take anything orally. Nephrology was notified of Finley’s diagnosis but had yet to formally consult.

Elizabeth recalls hearing the news of Finley’s STEC-positive stool test:

It took about 24 hours from the time we were admitted for his blood culture to come back with a diagnosis of E. Coli. By this point, no one had slept more than an hour or two since Thursday and we were having a hard time absorbing the information we were receiving. When the medical team told us that they had confirmed his diagnosis as being E. Coli 0157-H7, “the scary type of E. Coli with Shiga toxin” and asked if we had any questions, we remember not even being able to gather our thoughts and formulate questions. We were so tired and emotional. It felt as if everything was happening so fast, yet our minds were not processing the information quickly enough. We had heard of E. coli but did not have a clue as to how serious it could be. When the provider left the room, we quickly googled it and began to panic! We were both terrified for our son and felt the mixed emotions of guilt and fear. Thoughts were running through our heads such as: Will he be okay? Is he going to die? Should we have been more in tune with his symptoms and brought him in earlier for medical attention? Did we do this to him? Etc.

By this point, Finley would not engage with us, he did not want to use the bathroom, walk or eat, rather he would lay in bed moaning with pain. The frequency of his diarrhea increased, and he would often be pooping while we were changing his diaper. His bottom was very sore, and his rectum began to prolapse causing a lot of pain and discomfort during diapering. We cannot erase the image of our child’s rectum protruding out of his anus. Because he had been pooping so much at this point, he did not have any stool left, but instead discharged a rather horrid smelling secretion.

Randall Day 3 – Nephrology Consultation

On Tuesday, March 7, 2017, Weiwen Vivian Shih, MD came in for pediatric nephrology, noting that Finley had been improving slowly overall, but they were monitoring him for signs of HUS. His morning labs had returned a number of concerning results, with a downtrending in his platelets and an increase in his serum creatinine (PLT 109 and CR 0.84). His white blood cell count was also marginally elevated at 18.9K, and he was mildly anemic with a hemoglobin of 10.5 and hematocrit 32.3%. Dr. Shih examined Finley, and he was crying out “owie, owie,” and did not want his abdomen touched. She talked to Elizabeth and Joseph about their toddler’s abnormal labs, making a point of telling them: “To be clear, Finley at this time does NOT definitively have HUS.” She explained that HUS was defined as the presence of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. “Thus far, Finley has acute kidney injury and downtrending platelet count and hemoglobin, but he does not show clear evidence of hemolytic anemia or definitive thrombocytopenia at this time.”

Dr. Shih explained, and wrote in her chart notes:

Most commonly HUS is caused by infection, as would be so in Finley’s case given his stool culture positive for E. Coli O157:H7, although less commonly it could be caused by primary complement dysregulation. Most commonly in HUS, the hemolytic anemia is quite pronounced with a Hgb < 8 with a negative Coombs test and a peripheral blood smear demonstrating hemolysis. Thrombocytopenia typically does not involve signs of active bleeding or purpura. From a renal perspective, the involvement of the kidney is quite wide ranging from minor hematuria and proteinuria to severe renal failure with oligoanuria. Hypertension is quite common. Many patients will have hematuria that can be either microscopic or gross.

Dr. Shih advised Elizabeth and Joseph that, once a patient develops HUS, there was no actual treatment that was curative, only supportive, thus it was crucial to monitor Finley closely. After telling Finley’s parents that their son did NOT have HUS, she went on to explain that, based on his falling blood counts (hemoglobin and hematocrit) she suspected that he probably DID have HUS, but “…since we really only have two data points, it will be helpful for us to gather more information. Discussed that while his renal function is abnormal, he is still making good urine with stable electrolytes.”

Elizabeth expressed her concern about whether Finley was going to need dialysis, and Dr. Shih reassured them that they were “nowhere near requiring dialysis at this time.” In response to Elizabeth’s queries about how long the course of HUS was, and Dr. Shih “…gave a general idea of 5-7 days but reiterated that every patient is different and it [could] last much longer. In specific, even once the HUS itself is resolved, it can take patients significantly more time to be ready for discharge particularly when it comes to taking adequate nutrition.”

Dr. Shin recommended the avoidance of nephrotoxic agents such as NSAIDs, CT contrast medium, etc., and serial measurements of Finley’s blood pressure with the administration of isradipine if they became elevated over 120 systolic. She was concerned about how much pain Finley seemed to be exhibiting, especially as it was limiting his oral intake. She discussed the possibility of starting total parenteral nutrition (TPN) via a peripherally inserted central catheter (PICC) line, or via a nasogastric tube (NG).

Randall Day 4 – Hemolytic Uremic Syndrome

On Wednesday, March 8, 2017, Dr. Shih came back in to see Finley and check on his morning lab test results. She observed that he did “pretty well” overnight, but he had gained “quite a bit” of weight and so was given one dose of Lasix, a diuretic. The phlebotomists were having some difficulty getting blood from Finley, so Dr. Shih ordered the insertion of a PICC line that afternoon. Finley’s blood pressures were mostly in normal range, but he had some elevations if he was upset and crying.

Elizabeth recalls the difficulties with Finley’s blood draws:

Finley was not a fan of regular blood draws or taking oral pain medicine. At one point, the nursing staff was trying to start an IV to draw blood and could not easily find a vein that would work due to his swelling. They stuck him several times with no success and then asked us to help hold him down while the vascular access team tried a third time. Finley was screaming and we were crying. This was not going to be a sustainable option for drawing blood going forward as he would not be able to tolerate multiple blood draws. Because of this, the doctor recommended Finley get a PICC line placed and a NG tube for feeding and oral medicines.

Unfortunately, that morning Dr. Shih identified the telltale signs that Finley now met the criteria for Shiga-toxin-associated hemolytic uremic syndrome secondary to E. coli O157:H7. She noted that the disease had evolved over the prior 24 hours, now with significant thrombocytopenia, hemolytic anemia, and acute kidney injury. Finley’s platelets were down to 51K, and his hemoglobin/hematocrit were down to 7.8/22.6. His kidney function was worsened, with a BUN and creatinine of 34 and 2.38. His liver function tests were also abnormal, with an ALT/AST 98/125 and total bilirubin 1.6. Finley’s peripheral blood smear also exhibited schistocytes that day, and a haptoglobin was recommended to help quantify his hemolysis. Dr. Shih also recommended testing his LDH. This came back elevated at 886. His urine output remained “brisk” with minimal use of diuretics. Dr. Shih felt it was time to initiate NG tube feeds since Finley could not or would not eat or drink, starting slowly as he tolerated the feeds and supplementing with TPN via a PICC line.

At 12:13 PM, John McCreary, MD took Finley to the operating room in order to insert a PICC line under general anesthesia, and new blood samples were taken for laboratory analysis. They took the opportunity to insert an NG tube while Finley was sleep. The NG tube placement in his stomach was confirmed to be correct with fluoroscopy. A chest x-ray showed the tip of the PICC line properly placed just distal to the superior vena cava. After the procedure, TPN was started through the PICC line.

Elizabeth recalls how stressful it was for her and Joseph to watch their toddler son endure procedures that would scare any adult:

Going through this procedure and taking Finley down to the OR procedure room of the hospital was one of the more scary and unforgettable moments of our hospital stay. Finley gripped on to his favorite stuffed panda bear and hid his face in his father’s chest as we carried him down to the OR. The surgeon discussed the plan, risks and benefits of surgery and then asked us to carry Finley into the OR and hold him while they gave him anesthesia. Finley was so scared, that while being given the anesthesia, he tried to negotiate with us by saying he would rather have Tylenol. If you know Finley, you know that he does not like taking medicine and fights us when we have to give it to him. We held him while they put him to sleep and his body went limp. We then left the OR to wait for Finley’s PICC line and NG tube to be placed.

When we got to the hall outside of the surgery suite, we hugged each other and cried. Watching your son being medically induced into a sleeping state is the most heart wrenching and helpless feeling. We waited for the procedure to finish, which seemed like eternity, and then held him in the recovery room while he woke up from the anesthesia. We will never forget when we first saw him with tubes coming out of his nose and arm. He looked so weak and helpless.

Pediatric hospitalist Ann Loeffler, MD looked in on Finley later in the day. She reviewed his labs, noting “brisk ongoing hemolysis” and commented that “the only really good news is that he is maintaining urinary output.” She ordered a blood transfusion of packed red blood cells (PRBCs). Finley’s post-transfusion hemoglobin was improved to 11.1, but his serum creatinine had worsened to 2.85. A recheck of Finley’s urine output late that evening showed a “fairly steep decline,” so Dr. Loeffler ordered an additional dose of Lasix at 10 PM.

Elizabeth recalls the panic she and Joseph felt, watching Finley’s condition decline:

At this point, we were hopeful that the E. Coli would pass and that he would quickly recover. Our experience was quite the contrary. Finley’s health continued to deteriorate and at a very rapid pace. It seemed that every time his lab results came back, we would have bad news. We were scared to leave the hospital or even leave Finley’s side. This is a terrifying feeling thinking that if we leave the room, even for a minute something could happen to our son. We remember taking a needed break to call our parents and not being gone more than 5 minutes before getting a call from the attending physician that we needed to come back to his room because his medical condition had worsened. The stress and anxiety associated with this, was something we have never experienced previously. We were completely dependent on our friends and family to bring us food and clothes, as we would not leave the hospital.

Randall Day 5

On Thursday, March 9, 2017, Finley’s morning labs returned showing worsening kidney function, with a BUN and creatinine of 52 and 3.09, increasing further in the afternoon to 62 and 3.5. His LDH was up to 2892. A dose of Lasix was given in the morning with only minimal urinary response. He exhibited increased edema throughout his body, but especially in his lower extremities. Finley also was obviously more uncomfortable, whimpering and moaning.

Dr. Loeffler came in to talk to Elizabeth and Joseph, explaining the meaning of Finley’s lab results, particularly his downtrending platelets and ongoing hemolysis, as well as the current smear that showed an increased number of schistocytes. She expected that Finley’s hemoglobin would continue to downtrend and he was going require another transfusion the next day. Dr. Loeffler told Elizabeth and Joseph that platelets were typically the cell line that recovered first. As such, she thought that they were still relatively early in the course of Finley’s HUS course.

The doctor then turned to a discussion about when dialysis might be indicated, including electrolyte abnormalities, acid base problems, uremia that was concerning for mental status changes, or volume overload. She explained that, at least currently, Finley’s electrolytes and acid-base balance were not a problem. Dr. Loeffler stated that fluid overload was the most concerning, given Finley’s poor response to the morning dose of Lasix. She explained that dialysis required the placement of a dialysis catheter, typically in either the groin or the neck. The plan would be to have a temporary catheter placed by Interventional Radiology or Surgery.

Randall Day 6 – Transfer to Legacy Emanuel

On Friday, March 10, 2017, Dr. Shih came in for pediatric nephrology and noted that Finley had been given several additional doses of Lasix with little urinary response. His parents reported that, overall, Finley appeared to be worsening. He was fussy and increasingly difficult to console. The nursing staff reported his condition to the medical staff, who ordered his feeds turned off overnight in preparation for the insertion of a hemodialysis catheter that day. Dr. Shih reviewed Finley’s lab results from blood drawn at 4:39 AM, which showed ongoing hemolytic anemia (H/H 9.2 and 25.8), platelets at 21K, BUN and creatinine 73 and 4.20, ALT and AST 172 and 333, and total bilirubin 4.6.

With Finley facing hemodialysis, Dr. Shih discussed his case with pediatric critical care specialist Bahareh. E. Keith, DO and the two agreed it would be best to transfer him over to the PICU at Legacy Emanuel Medical Center. The doctors discussed this with Elizabeth and Joseph, who indicated their agreement and understanding. At 1 PM, Jeffrey Leon, MD took Finley to Interventional Radiology for insertion of a hemodialysis catheter under general anesthesia. Jason Bauer, MD performed the insertion of a tunneled dialysis catheter.

Elizabeth recalls the placement of Finley’s dialysis catheter as nothing short of traumatic, not just for her son but for her and Joseph as well:

[Finley] was diagnosed with hemolytic uremic syndrome, the really scary side effect of the E. Coli with Shiga toxin. His red blood cells were depleting as well. At this point, his nephrologist advised us that Finley was going to need hemodialysis to help his kidneys filter toxins, and they were going to need to place the port before his platelets and red blood levels dropped to critical levels. Hearing this news and knowing that the procedure was time sensitive, made us panic. We quickly agreed that we would proceed with the dialysis catheter placement and were rushed off to surgery again.

It was like Deja vu! We held our scared little boy on the operating room surgical table, as the anesthesiologist again put him into a medically induced sleep and the surgeon prepared to place the catheter. We were both frightened and anxious wondering if Finley would ever recover from this horrible disease. When Finley awoke from the surgery, he was in a lot of pain and he had two tubes coming out of his neck. How do you explain to a two-year-old why this is happening or why we cannot remove these tubes? Seeing him like this, with tubes coming out of his arm, nose and neck made our hearts sick. The medical team transferred us to the intensive care unit immediately after surgery, so they could monitor him more closely and he could start hemodialysis. Everything was happening so quickly!

Legacy Emanuel – PICU Day 1 – A Disastrous Introduction to Hemodialysis

Finley was moved to the PICU after the HD catheter placement, and Peter Quint, MD formally admitted him to the unit. Dr. Quint noted that the toddler was no longer receiving enteral feeds and was transferred to the pediatric ICU for concern of need for dialysis. He admitted Finley to the pediatric ICU for ongoing care for his diagnoses of hemolytic uremic syndrome with thrombocytopenia, anemia, and oliguria. Finley was started on Epogen to help support the manufacture of his own red blood cells.

Nephrologist Dr. Shih resumed Finley’s care in the Legacy Emanuel PICU and oversaw his first dialysis run; however, Finley struggled with increased arterial pressures. They were able to continue for about 15 minutes but only at lower blood-flows, as a result. Because they were unable to return all the blood in the circuit, tPA was instilled in the catheter and a pRBC transfusion started. The HD catheter was noted to be kinked at the hub, likely due to Finley’s movement. IR attending Mark Buchholz, MD was summoned to the bedside and, with sedation, he was able to reposition Finley’s HD catheter and restart dialysis at 7:10 PM.

The events that occurred during Finley’s first hemodialysis were beyond horrifying to his parents, especially after the trauma they all just experienced getting the catheter inserted in the first place. Elizabeth recalls:

Finley’s first dialysis treatment was horrific. The medical team hooked him up to the dialysis machine and could not get the appropriate pressure in the lines for the treatment to work. He lost all of the blood in the machine, and they could not complete the initial treatment. They quickly realized that the catheter that was placed in his neck was twisted and it was going to have to be replaced. The problem with this was that we were running out of time and Finley’s condition was worsening. His weak little body would not be able to be put under general anesthesia again and his low platelet count made it risky to redo the catheter in the operating room. The physician care team determined their only option was to consciously sedate him and do a bedside procedure to fix the catheter. We looked at our physician’s worried demeanor and thought we were going to get sick. How could this be happening? Were we going to be able to fix it in time? Was he going to die? We began praying to God for our son to be okay! If we could have traded places with him, we would have done so in a heartbeat so that he did not have to suffer. The intensivist and interventional radiologist gave Finley something to manage the pain and began to do the bedside procedure with both of us around the bed. Finley’s face looked terrified! We knew we had to hide our emotions and be strong for our son. We didn’t want him to see how scared we were. Because we were in the ICU, they were not able to fully sedate him. When the physician began to cut in to his neck to fix the catheter, his poor body would twitch and move in response to the pain. We held his little hand and tried to be strong.

Legacy Emanuel – PICU Day 2 – Hospital Day 7

On Saturday, March 11, 2017, Dr. Quint reviewed Finley’s morning labs, which showed a BUN and creatinine of 68 and 4.04, a hemoglobin and hematocrit of 9.5 and 26.1%, and a normalized WBC count of 13.5K. He observed that Finley was not on any antibiotics and the primary current issues, apart from hemodialysis, were to determine if ongoing blood replacement was needed. The plan was to replace Finley’s platelets if they fell below 10K or he was bleeding.

Dr. Shih came in for pediatric nephrology and was happy to see that hemodialysis was ultimately completed the evening before and Finley was able to get some sleep overnight. He required multiple doses of Fentanyl for pain and currently had “adequate” urinary output. She thought he looked jaundiced, but his fluid retention was better with less periorbital edema evident. He was receiving TPN but had not yet resumed NG tube feeds. Dr. Shih wanted to get a direct bilirubin test along with the rest of his labs after the next dialysis. She advised a hemoglobin and hematocrit measurement two hours before dialysis to determine if Finley needed a blood transfusion during the procedure. Dr. Shih was worried about the elevation in Finley’s bilirubin, so she ordered an abdominal ultrasound to rule out an obstructive process as the cause of his hyperbilirubinemia.

At 7 PM, radiologist Paul Marten, MD performed a complete ultrasound of Finley’s abdomen, during which he identified enlarged echogenic kidneys without evidence of hydronephrosis (urinary backup). He saw sludge in Finley’s gallbladder with distention of the organ but no conspicuous stones. Dr. Marten thought the ultrasound was most reflective of known medical renal disease. He observed no signs of biliary tract obstruction or liver pathology.

Dr. Shih returned to see Finley after a partially completed hemodialysis run. Unfortunately, three minutes prior to its completion, the HD filter clotted, and they were unable to return his blood from the machine. A CBC drawn right before this happened showed Finley’s hemoglobin was quite low at 6.9. She ordered a transfusion of pRBC’s and a repeat CBC and bilirubin after that was done, followed by the administration of Bumex and Diuril, both diuretics. For the third HD run the next day, she ordered heparin anticoagulation to avoid a repeat of the HD events of the past two days.

Elizabeth and Joseph had no choice but to sit by their son’s side and wait this out, hoping he was going to survive a devastating illness that not all children did. She recalls:

We stayed in the ICU for several days so that Finley could start his dialysis treatment. He was in so much pain that he was given OxyContin and Fentanyl to bridge the pain between regular doses of Tylenol. Nurses would ask us if he needed more pain medicine. This is terrifying since as a parent as you cannot be certain of your child’s exact level of pain. On one hand, you do not want your child to experience pain, but you also don’t want to over medicate him.

Legacy Emanuel – Leaving the PICU on Day 3 – Hospital Day 8

On Sunday, March 12, 2017, Dr. Quint reviewed Finley’s morning lab results, which showed a hematocrit of 24%, platelets 28K, and white count 12.8K. His BUN and creatinine were 69 and 3.61. His peripheral smear continued to show “many” schistocytes. His ALT was 82 and total bilirubin 6.1. Finley was receiving Fentanyl to keep him comfortable and had not required Versed in the prior 24 hours for agitation. Finley had urinated during the night about 596 mL, so he was responding to the increased diuretic therapy implemented the day before. He was receiving TPN and taking sips of fluid. He was mildly hypertensive, but he had not required medication for this, and his pressures were improving with hemodialysis. Dr. Quint planned to ask nephrology when they could resume NG tube feedings and/or oral feedings. Dr. Shih responded that Finley could be started on NG tube feedings after dialysis later that day.

Repeat labs that afternoon showed continued hemolytic anemia and thrombocytopenia, with a hemoglobin 8.1, hematocrit 21.6% and platelets at 14K; however, these values did not meet the criteria for an additional blood transfusion. His BUN was up to 73 on recheck that afternoon. Dr. Shih thought Finley tolerated hemodialysis well that afternoon and deemed him stable enough to move back to a regular pediatric bed and out of the PICU.

Elizabeth recalls the transfer out of ICU did not spell an end to invasive and traumatic procedures for their son:

Finley was eventually transferred back to the medical/renal unit of the children’s hospital and continued to receive blood transfusion, dialysis and platelets. He remained bed ridden and was fed primarily through his PICC line. He could not walk or even sit up without assistance. He had no desire to eat or drink fluids and was provided needed nourishment and fluids through his PICC line. We continued to monitor his pain around the clock and tried to comfort him. It was many days of little sleep and Disney movies and books for entertainment.

As Finley started to become more conscious and aware of what was going on, it only became more difficult. He became very emotional and distressed every time a physician or nurse entered the room. Even bandage changes became a difficult task. We would be asked to hold down our son while he was kicking and screaming “I can’t like this!” while the nursing staff checked vitals, cleaned his ports, changed bandages or gave him medication. Because Finley was positive for E. Coli, the hospital placed us on contact precaution and Finley was unable to leave the hospital room. He would cry when people walked in and out of the room. He would tell us that he wanted to go home. We would hold him for hours to try and comfort him.

Legacy Emanuel Day 4 – Hospital Day 9 – Continued Dialysis and Blood Transfusions

On Monday, March 13, 2017, pediatric nephrologist Joyce Lee, MD saw Finley in the medical/renal unit, where he continued to receive hemodialysis. His morning labs showed a post transfusion hemoglobin and hematocrit of 9.4 and 25.1, and his platelets were at 12K. Dr. Lee noted that, while Finley’s white count was in normal range, his differential exhibited increased bands. His BUN and creatinine were 48 and 2.68. He still had standing orders for blood pressure medications, but he had needed none in the past 24-48 hours. Dr. Lee encouraged Finley to take more fluids orally and discontinued his NG tube feedings, while he continued to receive 85% of his nutrition via TPN. He was urinating more volume and his diuretics were able to be cut back overnight. He required some supplementation for electrolyte imbalances. Dr. Lee observed that Finley had required blood transfusions of pRBC’s on the 8th, 10th, 11th and 12th for his hemolytic anemia. His morning labs continued to exhibit hemolysis, including the presence of schistocytes, and she anticipated he was going to need another transfusion with his next dialysis treatment.

Legacy Emanuel Day 5 – Hospital Day 10 – Febrile to 102.9ºF – Antibiotics

On Tuesday, March 14, 2017, Dr. Lee came in to see Finley in the morning and noted that he had spiked a fever overnight of 102.9ºF. Blood cultures were sent to the lab as a result, and he was given a dose of IV antibiotics (ceftriaxone) and Dr. Lee ordered repeat daily doses until further notice. Finley was producing urine (1342 mL overnight) but his diuretics had to be discontinued when he exhibited hypokalemia (low potassium). She ordered a stool collection for re-culture before the antibiotics were given, given his fever.

Dr. Lee observed that Finley’s oral intake remained minimal; however, he was tolerating cheerios, pieces of orange, and Fig Newtons that morning. He appeared to be intermittently uncomfortable and fussy, with response to Tylenol and oxycodone. Finley’s WBC count was stable with decreasing bands, despite the fever. His hemoglobin and hematocrit were stable at 7.3 and 19.5, and his BUN and creatinine were 63 and 3.37. His platelets were 12K and he still exhibited schistocytes on his peripheral smear. His bilirubin was improved at 1.7. Dialysis was planned for the afternoon, with heparin added to prevent the problems with kinking and clotting in the line that was experienced in prior runs. Dr. Lee wanted to repeat his blood chemistries that afternoon to guide diuretic therapy.

Dr. Lee came in to oversee Finley’s dialysis that afternoon, which proceeded without problems, and he was transfused with additional pRBC’s during the procedure. He experienced a spike in his heart rate and his blood pressure registered 130/115, causing Dr. Lee to comment: “BP generous following rinse back, but also while quite agitated/mad.” Finley had standing orders to receive isradipine for persistently elevated blood pressures.

Legacy Emanuel Day 6 – Hospital Day 11 – Ultrasound and GI Consultation

Finley continued to spike fevers overnight and had repeat blood cultures drawn. He received his second dose of ceftriaxone. His peripheral IV infiltrated during the night and had to be discontinued. On Wednesday, March 15, 2017, Dr. Lee saw Finley in the morning and was happy to see that he continued to tolerate some fruit. He was producing urine on diuretic augmentation (Diuril). Finley’s post transfusion blood counts were stable (Hgb 9.0, Hct 26.3, platelets 17K), and his BUN and creatinine were improved at 37 and 2.11. Dr. Lee wanted to see how Finley did without diuretics that day, switching to oral Lasix to be given only as needed. She noted his blood pressures were creeping up with a number of diastolic pressures in the 90’s, but he had not required any isradipine. He continued to have a low-grade fever and she continued his ceftriaxone order.

Dr. Lee was concerned about the amount of pain Finley was in, and she requested a gastroenterology consultation, along with an ultrasound to look for a possible abdominal abscess and re-evaluation of Finley’s gallbladder. Radiologist Richard B. Hesla, MD performed a repeat ultrasound during the afternoon, during which he identified an enlarged gallbladder that was notable for likely sludge but no stones. Dr. Hesla also observed a small amount of right lower quadrant and midline free pelvic fluid under Finley’s liver, but he saw no loculated fluid collections to suggest an abscess. The appearance of Finley’s gallbladder was not significantly different from the imaging on the 11th.

Matthew Riley, MD came in for a pediatric gastroenterology consultation and examined Finley, who appeared to be having generalized, colicky abdominal pain through the day. Finley responded to the pain by getting up on all-fours and curling his abdomen. His stools were no longer bloody, but they were still loose. Dr. Riley looked at the ultrasound results and noted that Finley’s liver function labs showed a mildly elevated GGT, normal ALT, and now-normal bilirubin. He agreed that the ultrasound showed no cholecystitis or biliary obstruction, and no stones; however, he opined that Finley was at risk for the development of gallstones. Dr. Riley concluded that the likeliest cause of Finley’s current abdominal pain was infectious enteritis, and he saw no evidence of a surgical emergency. He recommended the addition of Ursodiol to Finley’s medications, a bile acid medication used to prevent the formation of gallstones.

Legacy Emanuel Day 7 – Hospital Day 12 – Dialysis Deferred

On Thursday, March 16, 2017, Dr. Lee came in and thought Finley was stable, seeing no additional concerns during the night. His morning labs continued to exhibit hemolysis, with a hemoglobin and hematocrit 7.4 and 21.9, platelets 54K. His BUN and creatinine were 53 and 2.68. Finley continued to produce urine without diuretics overnight, and Dr. Lee decided they could go without hemodialysis that day. However, Finley still needed a transfusion of pRBC’s. Dr. Lee requested the involvement of the hospital dietician to work with Finley, as he was dependent on TPN for his current nutritional needs and she wanted to get him transitioned to taking oral fluids and greater solid food intake

Stool Culture Positive E. coli O157:H7

At 2:17 PM on March 16, 2017, the hospital laboratory reported that Finley’s stool culture from a collection on the 4th was finalized and confirmed positive for Escherichia coli, serogroup O157. It was also positive for Shiga toxin 2, and negative for Shiga toxin 1. The isolate was sent to the Oregon State Public Health Lab for confirmation.

Legacy Emanuel Day 8 – Hospital Day 13

On Friday, March 17, 2017, Finley continued to require analgesia on a regular basis to keep him comfortable. Dr. Lee noted that he was showing some increased interest in oral intake, but it was still very inadequate. His post transfusion labs showed a hemoglobin and hematocrit 10.4 and 30.5, and his platelets were up to 120K. His BUN and creatinine were 55 and 2.53. Dr. Lee thought Finley had done well off dialysis the day before, but he had gained weight overnight and appeared puffy around his eyes.

Gastroenterologist Dr. Riley stopped back in to see Finley in the afternoon, and he spoke with Elizabeth and Joseph. They had noticed their son seemed a bit better since the day before and was eating a few small bites of food. He still had abdominal pain, but it appeared lessened. They reported he had a large, liquid, nonbloody stool early that morning. Dr. Riley reviewed Finley’s lab results, including the positive culture for E. coli O157:H-(nonmotile) with confirmation of Shiga toxin. Dr. Riley encouraged Finley to eat and drink, suggesting a retrial of trophic [minute volume] NG tube feedings, in consultation with dietary given his acute kidney injury.

Legacy Emanuel Day 9 – Hospital Day 14

On Saturday, March 18, 2017, Dr. Lee came in and noted that Finley had been more uncomfortable during the night; however, he felt much better after some Tylenol and oxycodone—and a large BM. His parents reported an increase in Finley’s interest in food the day before. His morning labs were stable, and his platelets were in normal range at 220K. His BUN and creatinine were slowly improving at 46 and 1.91. He remained off dialysis and had not required a blood transfusion since the 16th. Unfortunately, all that good news was offset somewhat by an increase in Finley’s fluid overload, which required the administration of Lasix to relieve the edema in his face and extremities. Finley had also had blood pressure spikes during the night that required two doses of isradipine. Dr. Lee wanted to transition him to amlodipine (Norvasc, also a calcium channel blocker) in the next few days, in anticipation of discharging him home.

Dr. Riley came in to see Finley around midday and noted the NG tube feedings had been started, which he recommended the day before. He advised a further increase and encouraged Finley to take in more oral fluids as well.

Legacy Emanuel Day 10 – Hospital Day 15

On Sunday, March 19, 2017, Dr. Lee came in to see Finley and was told he pulled out his NG tube overnight and had to have it replaced under conscious sedation with Versed. Afterwards, he tolerated NG Suplena, a liquid nutrition replacement. Finley’s morning labs showed a stable blood count and normal platelets, and his creatinine improved further to 1.38. Dr. Lee started him on oral amlodipine for his blood pressure control. Finley was taking sufficient enteric/oral fluids and nutrition to discontinue his TPN. He continued to require diuretics to manage his volume overload.

Legacy Emanuel Day 11 – Hospital Day 16

On Monday, March 20, 2017, Melissa Sheiko, MD came in for pediatric gastroenterology and was happy to see that Finley was eating more and tolerating his NG tube feeds, although she did not think he was drinking enough fluids. She recommended that they reduce the amount of fluids and food he was receiving in the tube feeds so his natural appetite would stimulate his interest in eating.

Sharon Su, MD came in for pediatric nephrology. She noted that a repeat stool culture taken on the 15th had not grown any pathogens; however, that had been while he was on antibiotics (Ceftriaxone). She requested another stool culture be sent to the lab that day. Finley had not required any hemodialysis or blood transfusions for four days at this point, and Dr. Su thought he could be discharged soon. The next few days would determine whether he needed to go home with a PICC line or not. She noted that his HD catheter had been removed on the 19th. Dr. Su changed Finley from twice daily to once daily Lasix dosing. He was doing better taking oral fluids and was tolerating some solids with limited emesis and nausea.

Legacy Emanuel Day 12-13 – Hospital Day 17-18

On Tuesday, March 21, 2017, Dr. Su came back in to see Finley. His morning labs showed a hemoglobin and hematocrit of 9.8 and 29.3, and his platelets were still in normal range. His BUN and creatinine were 35 and 0.91. His LDH was measured over the past few weeks, with a slow downtrend towards normal, now still high but improved at 642. Dr. Su noted that Finley’s stool sample from the 20th was positive for Shiga toxin 2 but it had grown only normal fecal flora and no enteric pathogens. On the 22nd, the isolate looked the same and was sent to the Oregon State Public Health Lab for confirmation. Dr. Su discussed the negative result from the 15th with Finley’s parents and told them it was probably a false negative because of the antibiotics, as it did exhibit a positive Shiga toxin 2 result. Finley was going to need two consecutive negative stool cultures to be able to return to school, so at least one or two more cultures were going to be needed. Dr. Su discontinued Finley’s diuretics that day. He pulled out his NG tube again that night, but this time it was not replaced.

Legacy Emanuel Day 14 – Hospital Day 19

On Thursday, March 23, 2017, Finley continued to be stable and his morning labs reflected that. He continued to be hypertensive, so Dr. Su increased his amlodipine to keep his pressures under control. She no longer thought Finley looked fluid overloaded off diuretics and he was producing urine, despite a less-than-adequate oral fluid intake. He continued to receive Epogen, as he had been since he was first admitted to the PICU. Dr. Su wanted to try to limit his blood draws at this point, since Finley was stable, and she wanted to conserve his blood volume while he was struggling to meet his fluid demands orally. Dr. Shih was still Finley’s primary nephrologist, so Dr. Su discussed discharge planning with her to try and coordinate the need for outpatient labs and nephrology visits. She anticipated weekly blood pressure checks in the clinic to monitor Finley’s hypertension.

Legacy Emanuel Day 15 – Hospital Day 20 – Going Home!

On Friday, March 24, 2017, Dr. Su came in to evaluate Finley for discharge from the hospital. His labs that morning showed continued stability, with a WBC 6.6 (normal), hemoglobin and hematocrit 9.8 and 30.1, platelets 386K, BUN and creatinine 28 and 0.63. His last stool culture was negative for bacterial growth of pathogens but still showed positive for Shiga toxin 2. She reminded Finley’s parents that he needed two consecutive negative stool cultures before he could return to school. Dr. Su made arrangements for Finley to come to the nephrology clinic on the 28th for a recheck, and to bring a stool sample with him then. She discharged him from the hospital that afternoon.

Randall Children’s Outpatient Nephrology

On March 28, 2017, Finley went to see Dr. Shih for a Pediatric Nephrology follow-up visit to check on his recovery from HUS. She remembered him well from his hospitalization at Randall before being transferred to Legacy Emanuel, finding it notable that he had spent almost three weeks in the hospital. Dr. Shih was happy to see that Finley seemed back to his “normal self,” eating and drinking well. His mom Elizabeth reported that he did not complain of further abdominal pain, and he had not been vomiting or passing blood in his stools.

The only physical observation that stood out to Dr. Shih was that Finley was still not walking totally normally: “… seems to be very deliberate with his steps, but unsure if this is just because he was sick for a while.” Elizabeth stated he was “throwing temper tantrums,” which was unusual for the toddler. Also, he reportedly said “owie” when he urinated, although he had no fevers or systemic signs of infection. They had no plans to send Finley back to the same school and were going to work with him at home with his grandmas. Finley objected vigorously to taking his amlodipine for his blood pressure, finding that they could not fool him by hiding in food or drinks. He would just spit it out, so his family had resorted to holding his nose and just making him take it. Because of that, Elizabeth did not know for sure how much of it actually went down. Finley also balked at taking his Ursodiol [bile acid sequestrant]. They were not taking his blood pressures at home.

Dr. Shih turned to Finley’s discharge lab results from the 24th, observing a “clearly still not normal” creatinine clearance, with a serum creatinine of 0.63. She emphasized to Elizabeth and Joseph that Finley was still at long term risk for chronic kidney disease, including hypertension, proteinuria, and renal insufficiency. Since it was hard to tell if Finley’s exclamations of “owie” actually reflected dysuria, so she wanted to get a clean catch urine in addition to checking his renal function labs, blood count (he was still anemic), and LDH. Dr. Shih also requested a repeat stool culture and suggested a repeat bladder ultrasound in the future for monitoring.

For Finley’s blood pressure, Dr. Shih thought they should continue his amlodipine suspension, suggesting they tried crushed tablets if the liquid continued to present problems because of taste. She set the family up with an automated blood pressure cuff so they could monitor Finley’s pressures at home, with instructions to withhold his BP med for systolic pressures under 85, and to call her if they were over 120. Dr. Shih also continued Finley’s Ursodiol as per gastroenterology’s instructions. She wanted to wait on recommendations regarding public outings until she could discuss this with infectious disease. Dr. Shih wanted to see Finely back in the Pediatric Nephrology Clinic in two months.

Finley’s lab results after Dr. Shih’s visit reflected continued abnormal kidney function (BUN 49, creatinine 0.93, LDH 468). On April 3rd, his BUN was 27, creatinine 0.50, LDH 253. A stool culture was reported positive for Shiga toxin 2, negative for Shiga toxin 2, on April 4th. Finley was back in the clinic on the 14th for a BP monitor calibration check and to check his logs, which showed his pressures were in the desired range on his current dose of medication.

On April 17th, Finley’s stool was negative for Shiga toxins 1 and 2 and the culture failed to grow any significant pathogenic bacteria. (On May 1, 2017, a second stool culture continued to be negative for Shiga toxins 1 and 2, and the culture was similarly negative for the growth of pathogens.)

Northwest Pediatric Gastroenterology

On April 18, 2017, Finley presented to Northwest Pediatric Gastroenterology, where Melissa Sheiko, MD saw him in follow-up of his hospitalization for E. coli O157:H7 associated HUS, but particularly to recheck the gallbladder sludge seen on two different ultrasounds. She found him clinically improved, and his “his labs have really returned to normal.” She expected his gallbladder sludging to resolve has he improved further. Dr. Sheiko discussed with Elizabeth and Joseph that Finley might need another abdominal ultrasound to make sure it was gone or at least improving, so he could stop taking the Ursodiol. She also discussed that taking probiotics might be helpful in clearing the E. coli HUS.

Randall Children’s Outpatient Nephrology

On May 31, 2017, Finley returned to see Dr. Shih and they went over his most recent labs. These included the ones just after his last visit, which showed an increase in his serum creatinine. Repeat labs done on the 30th were improved but still abnormal (BUN 27, creatinine 0.40). The second set of labs reflected an improvement after Dr. Shih talked to the family and encouraged them to increase Finley’s fluid intake; they had also switched from liquid BP medication to crushed tablets, which was working out much better for them. Finley still sometimes exclaimed “owie!” when urinating, but Elizabeth wondered if he was just responding to the sensation of the need to urinate. He was almost fully potty trained and no longer wore a diaper.

Dr. Shih was happy with the trending of Finley’s renal function labs, but she cautioned the family they still had to be on the alert for complications of his HUS. They discussed avoidance of nephrotoxic medications as before. Gastroenterology was coordinating an abdominal/renal ultrasound that was coming up soon.

Legacy Emanuel Hospital

On June 2, 2017, Finley underwent an abdominal ultrasound, during which radiologist Richard Hesla, MD identified a prominently sized gallbladder without sludge or stones. He noted that, since the last ultrasound on March 11th, there was interval resolution of the previously observed sludge, as well as in the size of the gallbladder and common bile duct, and now-absent free fluid.

Randall Children’s Outpatient Nephrology

On September 29, 2017, Dr. Shih saw Finley in follow-up of his recovery from HUS. His mom Elizabeth reported that, starting in August, Finley started spitting out his amlodipine every day and they could not get him to take it at all. They had been monitoring his blood pressures and his values remained in the desired target range. Finley was reportedly urinating well and was taking fluids well. A urinalysis that day was negative for protein, although the pH was up a bit. Finley’s urine total protein/creatinine ratio was elevated at 0.401 (RR 0.000-0.200), but because the sample was more than 24 hours old, Dr. Shih did not trust the numbers. She was happy with the ultrasound appearance of his kidneys in June, and she found it encouraging that his blood pressures were normal off the medications.

Dr. Shih was satisfied with Finley’s progress and asked his parents to bring him back to see her in another six months.


Elizabeth and Joseph’s Thoughts on Finley’s early recovery:

The hospitalization has had many lingering physical and emotional effects on Finley, and he has regressed in many ways as a result of this medical crisis. Because he was bed ridden for three weeks, he had difficulties standing and walking. He worked with physical therapy while we were in the hospital learning how to stand and walk again. Balance, walking and other normal physical activities continued to be challenging even after discharge. Finley continues to have high blood pressure, as a result of his kidney injury and gallbladder issues. We expect that he will need continued medical monitoring for the unforeseeable future and are unsure of his long-term prognosis. Before we went into the hospital Finley was almost completely potty trained. Even now, almost three months after his discharge, we continue to have challenges in this area. Finley will often complain of pain when he uses the bathroom. It is common for Finley to have night terrors since his hospital stay, screaming or crying in his sleep in the middle of the night. When we take him to medical appointments, he panics and becomes hysterical when medical staff put on blue gloves. He will tell us that “he can’t like it,” which is his way of telling us that he doesn’t like the situation. He was never afraid of going to the doctor prior to his E. coli experience.

Even though he was released from the hospital after 20 days, he was positive for E. Coli for over 70 days. This was both socially and financially hard on Finley and our family.

Socially it was very difficult for Finley as well. He was not able to engage with other children because of his illness or participate in his normal activities such as gymnastics, story time at the library, the children’s museum, swimming lessons or play dates with friends. He was very isolated and had limited social interaction with anyone outside of his family circle. People who are not familiar with this disease are afraid that they might catch E. Coli and distance themselves, so we have had limited interactions with friends and neighbors. Not being involved in a school setting has limited his educational development as well.

Prior to this experience, Finley was enrolled in a Spanish Immersion Montessori program, developing both his English and Spanish language. He has not been involved in this since his hospital stay.

We cannot even begin to describe the impact Finley’s medical condition has had on our family, friends and neighbors. We struggled with trying not to panic or worry them, when we were barely able to control our own emotions. Their pain and suffering were evident in their voices and expressions every time we interacted with them. We heard countless stories of church groups and others who were praying that Finley would live thru this ordeal and recover. We relied on this network of family and friends, and we will never be able to adequately thank them for their love and support.

Pediatric Associates of the Northwest

On December 15, 2017, Finley’s parents brought him to see their pediatrician Scott Spencer, MD for his three-year-old well child exam. Elizabeth and Joseph reported that Finley had been off his blood pressure medication (amlodipine) since he was last seen by the pediatric nephrologist in September. They discussed how Finley had been doing since he was discharged from the hospital nine months earlier for his severe E. coli infection complicated by HUS. Finley had exhibited numerous behavioral problems since he was so sick, which his parents described as “lots of tantrums” and “meltdowns.” He had also been hitting other children in his daycare, where the providers were reluctant to assign any “repercussions” to deal with it. Finley was also having sleep problems, which Dr. Spencer outlined in his chart note:

Won’t fall asleep without significant tantrums, mom has to go in and [lie down] with Finn. Bedtime is 8PM but sometimes won’t fall asleep until 10:30PM. Much worse after being in the hospital but did have some sleep problems prior.

On a positive note, Finley’s physical exam reflected that of a well 36-month-old, despite having been hospitalized with such a severe illness less than a year before. However, his blood pressure was relatively for his age, even after a recheck, falling into the 99th percentile for systolic and >95th percentile for diastolic pressures on the pediatric blood pressure chart.

Dr. Spencer surmised that Finley’s significant sleep problems could be related to his behavioral issues, which in turn he thought might still be linked to his hospitalization, daycare settings, or perhaps lack of sleep. He added the sleep issues to Finley’s “Problem List,” terming it “Circadian rhythm sleep disorder,” and also added “initial high BP” to his list of diagnoses.

Regarding Finley’s high blood pressure, Dr. Spencer placed a call to pediatric nephrologist Dr. Lee to discuss it, who recommended that Elizabeth and Joseph pick up a new blood pressure cuff from their clinic to monitor Finley’s pressures at home. For Finley’s sleep, Dr. Spencer hoped that trying a melatonin supplement before bed might help some. Turning to the behavioral issues, Elizabeth and Joseph told Dr. Spencer that Finley was starting a new school soon, and he suggested they discuss their discipline methods with the new school to try to align the two environments with a unified approach to the various issues. Dr. Spencer returned Finley to routine well-child follow-up.

Dr. Spencer did not specify what follow-up was needed for Finley’s blood pressure; however, at Randall Children’s Outpatient Nephrology on September 29th, Dr. Shih ended the visit with a request for his parents to bring him back to see her in another six months. That would make his next nephrology visit due around the end of February 2018.

Randall Children’s Hospital Nephrology

On February 16, 2018, Weiwen Vivian Shih, MD saw Finley in follow-up, noting that since his last clinic visit on September 29, 2017, he had been doing well with respect to his blood pressure and renal issues. Dr. Shih was aware of Finley’s slightly elevated blood pressure (110/73) at his PCP visit in December, but he was found to need a larger blood pressure cuff when rechecked at the nephrology office because he had outgrown the smaller cuff. His mom had been checking his blood pressures at home since then, and the highest systolic pressure noted had been in the low 100’s. He had been off amlodipine since September 2017. Finley’s urinary output appeared to be normal, and he was not completely potty trained with only occasional nighttime accidents. Dr. Shih noted that Finley’s mom was understandably worried about his developing kidney disease later on, but she was doing everything she knew how to do (re diet, etc.) to prevent that.

Since Finley had not had any blood work done since May of 2017, Dr. Shih checked his serum creatinine at this visit. She asked his mom to bring in a urine sample so they could recheck his urine protein/creatinine ratio sometime soon. Dr. Shih told Finley’s parents that they could now begin checking his blood pressures intermittently and to call if there were systolic pressures consistently over 110, or diastolic above 70.

On February 28, 2018, Dr. Shih sent a message to Finley and his parents that his blood work looked good, and he had no proteinuria. His urine protein/creatinine ratio was also normal.

And, the future – well, it is uncertain.


[1]           E. colibacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich. Feng, Peter, Stephen D. Weagant, Michael A. Grant, Enumeration of Escherichia coliand the Coliform Bacteria, in BACTERIOLOGICAL ANALYTICAL MANUAL (8thEd. 2002), 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 colito honor its discoverer. Id.

[2]           Not all E. coliare motile. For example, E. coliO157:H7 which lack flagella are thus E. coliO157:NM for non-motile.

[3]           CDC, Escherichia coliO157:H7, General Information, Frequently Asked Questions: What is Escherichia coliO157:H7?,

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

[5]           James M. Jay, MODERN FOOD MICROBIOLOGY at 21 (6thed. 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 coliO157: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. coliO157:H7).

[7]           Jay, supranote 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, supranote 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 coliO157: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, 2ndHome Ed. Online,

[11]         L. Riley, et al.Hemorrhagic Colitis Associated with a Rare Escherichia coliSerotype, 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 coliO157: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, supranote 11at 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 coliSerotype 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 coliO157:H7 and Shigella Sonnei, 331 New Eng. J. Med. 579 (Sept. 1, 1994). See alsoStephen M. Ostroff, MD, John M. Kobayashi, MD, MPH, and Jay H. Lewis, Infections with Escherichia coliO157: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]         SeeKeene, supranote 14at 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. coliO157: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 coliO157:H7 Outbreaks, United States, 1982-2002, 11 Emerging Infect. Dis. (No. 4) 603, 604 (April 2005).

[16]         Griffin & Tauxe, supranote 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. coliO157: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. coliO157:H7 Technical Fact Sheet:  Role of 60-Megadalton Plasmid (p0157) and Potential Virulence Factors,

[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 coliO157: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 ofEscherichia coliO157 by single nucleotide polymorphisms. Genome Res 16:757–767 (2006).

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

[24]         Manning SD, et al.VariationinvirulenceamongcladesofEscherichia coliO157:H7associatedwithdiseaseoutbreaks. 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 inthe clade 8 subpopulation could explainits emergence inseveral recent foodborne outbreaks; however, it is not clear why this virulent subpopulation is increasinginprevalence.”)

[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. coliO157: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 coliO157: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, supranote 15, at 605.

[28]         Feng, supranote 13, at 49. See alsoUSDA Bad Bug Book, Escherichia coliO157:H7,

[29]         Scallan E, et al.Foodborne illness acquired in the United States –major pathogens, Emerging Infect. Dis. Jan. (2011),

[30]         Id., Table 3.

[31]         Griffin & Tauxe, supranote 12, at 63.

[32]         Centers for Disease Control, Division of Foodborne, Bacterial and Mycotic Diseases, Escherichia coligeneral information, See alsoPROCEDURES TO INVESTIGATE FOODBORNE ILLNESS, 107 (IAFP 5thEd. 1999) (identifying incubation period for E. coliO157:H7 as “1 to 10 days, typically 2 to 5”).

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

[34]         Tauxe, supranote 25, at 1152.

[35]         Id.

[36]         Griffin & Tauxe, supranote 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 coliO157: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. colipresent).

[38]         Griffin & Tauxe, supranote 12, at 72 (noting that, as a result, “fewer bacteria are needed to cause illness that for outbreaks of salmonellosis”). Nestle, supranote 4, at 41. (“Foods containing E. coliO17: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 coliO157:H7 Infections in the Western United States: The Big Picture, in RECENT ADVANCES IN VEROCYTOTOXIN-PRODUCING ESCHERICHIA COLIINFECTIONS, at 7 (M.A. Karmali & A. G. Goglio eds. 1994). (“The most probable number of E. coliO157: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, supranote 4, at 41.

[41]         Griffin & Tauxe, supranote 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, supranote 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 coliO157: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. coliO157:H7 during food preparation was a flaw in the Agency’s risk-assessment),

[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, supranote 12, at 65-68. See alsoJosefa 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 alsoBeth 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

[46]         Tauxe, supranote 25, at 1152. See alsoNasia 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. coliserotype 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, supranote 11.

[48]         Safdar, supranote 46, at 996 (going on to conclude that administration of antibiotics to children with E. coliO157: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, supranote 46, at 996. See alsoSiegler, supranote 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, supranote 46, at 1360.

[53]         Id. Siegler, supranote 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, supranote 46, at 1360. See alsoSu & Brandt, supranote 11, at 700.

[55]         Garg, supranote46, at 1360. See also Su & Brandt, supranote 11, at 700.

[56]         Siegler, supranote 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, supranote 46, at 1366-67.

[58]         Siegler, supranote 45, at 1519.

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

[60]         Garg, supranote 46, at 1368.