I was reading on Food Safety News, “Yuma romaine growers hopeful harvest will end without E. coli issues” https://www.foodsafetynews.com/2019/03/yuma-romaine-growers-hopeful-harvest-will-end-without-e-coli-issues/ and could not help but think that what was missing was a story of a customer.  Here one is:

Jordan Anglen is a 24-year-old young man residing in Meridian, Idaho with his girlfriend Josie. Jordan was among those who became severely ill after consuming E. colicontaminated romaine lettuce. On March 25, 2018, Jordan purchased and ate a Chicken Caesar Salad containing E. coli-contaminated romaine lettuce at the Costco Food Court at 2051 S. Cole Rd., Boise, Idaho.

Primary Health Medical Group

On March 29, 2018, Jordan presented to Primary Health Medical Group, where Shannon Bordes, FNP evaluated him for a chief complaint of “diarrhea, back pain, body achy,” which he stated had begun the night before. Jordan described a two-day history of symptoms, which had also included joint pain, lightheadedness, lack of appetite, lower back pain, fever, and chills. He stated he had taken ibuprofen the previous afternoon at 5:30 PM for his symptoms. He was currently tolerating oral fluids and had been able to eat a small amount of food that morning. He had not been vomiting but was intermittently nauseated. On exam, NP Bordes found Jordan afebrile with a mostly unremarkable exam, which was significant mainly for a rapid heartbeat of 100 and a marginally elevated blood pressure of 137/81. He was mildly febrile with a temperature of 99.3ºF.[1]

NP Bordes thought Jordan’s clinical presentation was most consistent with viral gastroenteritis, which seemed to be already improving. She approved the use of Imodium to slow down his diarrhea, advising him to follow a clear liquid diet, and increase his intake slowly with electrolyte-containing fluids. Once his diarrhea was resolved, she told him he could advance his diet to more solid foods. If he had worsening symptoms, such as increasing fevers or abdominal pain, or bloody or dark stools, she advised him to return immediately or go to the ER. Jordan went home and tried to follow the instructions given him by the nurse practitioner, but he only got worse and worse.

St. Luke’s Meridian Medical Center

On March 30, 2018 at 2:45 AM, Jordan presented to St. Luke’s Meridian Medical Center, where Konrad Kessler, MD evaluated him in the emergency department for his worsening abdominal pain, nausea, vomiting, and diarrhea. After vomiting for hours without any intake, Jordan was now experiencing retching and dry heaves, which felt much worse to him than if he had something to throw up. He told the doctor about the clinic visit where he was diagnosed with a virus, but since then he began experiencing abdominal pain “before, after and during” bowel movements. His stool had also turned bloody for the three hours preceding his coming to the ER. Currently, Jordan rated his pain as 10/10 in severity, with was non-radiating and did not get better or worse with anything he tried. He was still urinating normally, as far as he could tell.

On exam, Dr. Kessler found Jordan dehydrated with tacky mucous membranes, and dry and cracked lips. His vital signs were in normal range, and his lungs were clear. Jordan’s abdomen was diffusely tender to even light palpation, and it was especially severe in his left side with rebound tenderness, and tenderness to percussion. His right abdomen was also tender, but less so.

Among the disorders Dr. Kessler thought might be causing Jordan’s symptoms, he considered toxic megacolon,[2]colitis, gastroenteritis, bowel obstruction, among others. He planned to obtain diagnostic laboratory studies and imaging while they attempted to treat him symptomatically with pain and nausea medications. He started Jordan on intravenous fluids and sent blood, urine, and stool to the lab for analysis.

The lab soon reported a number of abnormalities, including an elevated white blood cell count of 14.59, which contained a predominance of neutrophils.[3] He also had a slightly elevated hemoglobin of 18.1, reflecting his severe dehydration. His kidney function was currently in normal range, with a BUN and creatinine of 18 and 0.91, and his liver function was similarly normal.[4]His lipase was in normal range. His serum electrolytes were slightly abnormal, with his bicarbonate just out of normal range.

At 3:18 AM, radiologist Brian McMahan, MD performed an IV-contrast-enhanced CT of Jordan’s abdomen and pelvis, during which he found no signs of obstruction. Jordan’s appendix was surgically absent, an expected finding as he had it removed in 2013. Dr. McMahan observed thickening of the descending and transverse colon, “likely due to underdistention.” The ascending colon was also inflamed, and there was a trace of free fluid surrounding it. Dr. McMahan thought Jordan’s CT was consistent with mild colitis, although the changes he saw were largely nonspecific.

Dr. McMahan kept Jordan under observation in the ER for an hour and a half, after which he reported that his symptoms were much improved. He declined any pain or nausea medications, feeling that the reversal of his dehydration with IV fluids was helping him enough. The doctor discussed the diagnostic findings from Jordan’s labs and CT scan with him and his mother, and he reassured them that he appeared to have a gastrointestinal illness that should be self-limited. Dr. McMahan deemed Jordan safe for outpatient management and discharged him home from the ER with a prescription for Zofran in case he needed it. He encouraged him to stay as well hydrated as possible and to return if he noticed any blood in his emesis, or he had persistent vomiting, dehydration, or uncontrolled abdominal pain. Jordan left the ER at around 4:30 AM.

Getting worse at home…

Unfortunately, Jordan went home and grew steadily worse. After his initial improvement with IV hydration in the ER, he was unable to keep up with oral fluids, and his diarrhea increased in frequency. Even worse was the rectal bleeding—Jordan’s bloody diarrhea began to contain less stool and more blood, and by 11 PM on the 30th, it appeared to be only bright red blood. His lightheadedness returned, and he began feeling very dizzy, which alarmed his family.

St. Luke’s Meridian Medical Center – ER – sent home again

On Saturday, March 31, 2018 at 1:02 AM, Jordan returned to the Meridian ER, where Steven N. Wyman, MD evaluated him and sent repeat blood work to the lab. Jordan’s white blood cell count had increased to 22.76 and his platelets began to fall, now measuring 138K. A stool test for toxigenic C. difficilewas negative. Dr. Wyman restarted Jordan on IV fluids and gave him a dose of IV antibiotics (ciprofloxacin). At 3 AM sent Jordan home with a prescription to take oral ciprofloxacin 500 mg twice daily for a week and to see gastroenterologist Mark Mallory, MD on Monday if his symptoms persisted.

Confirmation of Shiga toxinin stool

At 4 AM, the hospital laboratory reported at critical value to the ER that Jordan’s stool had returned positive results for Shiga toxin. Dr. Wyman called Jordan at home and was told that he was still having bloody diarrhea. “I requested that he return to the Emergency Department for reevaluation.”

Return to Meridian ER diagnosed with STEC infection – antibiotics stopped

Jordan arrived back at the ER at 8 PM on April 1, 2018. Dr. Wyman was on duty when he arrived, and he told the doctor that he continued to have bloody diarrhea every 5-30 minutes. Dr. Wyman ordered intravenous fluids and reassessment of his blood work. The lab soon returned results showing an elevated white count of 28.83, and low platelets of 60K. His BUN and creatinine were 25 and 1.32. Dr. Wyman commented that Jordan had now developed “some minor renal insufficiency with a creatinine of 1.32 and thrombocytopenia with a platelet count of 60,000. Bilirubin is also elevated at 4.4.” His transaminases were in normal range. Dr. Wyman again consulted with gastroenterology and the consensus was to discontinue all antibiotics and admit Jordan for supportive care. Jordan’s diagnoses upon leaving the ER were: “Shiga toxin-producing Escherichia coliinfection” (STEC), “Renal insufficiency,” and “Thrombocytopenia.”

Admission under contact isolation – Meridian Hospital Day 1

On April 1, 2018 at 10:41 PM, hospitalist Mary Ann Huntington, MD formally admitted Jordan to the hospital as an inpatient under contact isolation, diagnosing him with “sepsis,” “STEC,” and “AKI.” Dr. Huntington reviewed Jordan’s history of his present bloody diarrhea, which had now been going on for four days, including his two ER visits and now return to the hospital for admission. He continued to complain of diffuse crampy abdominal pain, some nausea, but no current vomiting. Despite not having eaten for four days, he stated he was not hungry. Dr. Huntington noted that the antibiotics that were started had since been discontinued with this admit, since his stool studies returned positive results for Shiga toxin. She addressed his diagnosis of “sepsis,” commenting that it was related to the Shiga toxin producing E. coli— “Shigella, Salmonella, Campylobacterwere negative. C. difficilewas negative.” Dr. Huntington thought Jordan’s acute kidney injury was likely secondary to volume depletion from recurrent diarrhea; however, she thought it was possible that Jordan was developing hemolytic uremic syndrome.

Meridian Hospital Day 2-3 – evolving HUS, oliguria

Hospitalist Meaghen Friel, MD came in to see Jordan during morning rounds on April 2, 2018. He continued to have bloody diarrhea, and his exam was significant for “profound rebound pain.” She checked his morning labs, which showed an improved WBC of 23.57, but a worsening of his acute kidney injury (BUN 32, creatinine 1.42). She noted that he had not had any urinary output in the prior 24 hours. His platelets had dropped to 26K, which increased her concern for HUS, so she ordered an LDH and haptoglobin.[5]

On April 3, 2018, at 1:43 PM, Aaron A. Fearday, MD came in for a nephrology consultation to evaluate Jordan’s acute kidney injury, reviewing his worsening renal function labs. Jordan reported that he was in his usual state of good health until 6 days before, at which time he developed abdominal pain and diarrhea so severe, it caused him to seek care twice in the ER. Jordan stated that he was initially taking Imodium for the diarrhea. Dr. Fearday noted that Jordan’s father was concerned about his son’s nutrition, but Jordan had declined a feeding tube. Dr. Fearday discussed with Jordan and his dad in detail that parenteral nutrition was not a good idea at that time. He agreed with Jordan’s other providers that he had HUS. Dr. Fearday commented in his chart note:

The patient’s labs are all consistent [with] thrombotic microangiopathy given his hemolysis, thrombocytopenia, and acute kidney injury. In the setting of diffused diarrhea and stool culture, Williams will also be seeing the patient later today. His father was concerned that we were ‘not doing anything.’ I explained that we are giving him fluids and we are also closely watching his clinical status. I reiterated that antibiotics and anti-motility agents can often prolong the infection and the symptoms and are not recommended at this time.

Dr. Fearday also discussed with Jordan and his dad that it was going to “… take time for his body to fight this infection. I explained that if the kidney function worsens, we could do dialysis, but I don’t think that there is an indication at this time.” His father wanted to know if they could do dialysis to “ease the burden on the kidney,” and Dr. Fearday explained that dialysis would not achieve that goal: “I explained that dialysis cleans the blood when the kidneys are not working. His mother and father are very anxious about the illness of Jordan. I explained that we are watching his clinical course closely.”

Hematology consultation – platelet transfusion

Travis Williams DO came in for a hematology consultation when it became clear that Jordan was developing hemolytic uremic syndrome. His BUN and creatinine were now 57 and 3.22, and his platelets dropped further to just 13K. His LDH was elevated at 2705. He noted that Jordan was given IV ciprofloxacin in the ER and since taken two days of the oral medication before it was stopped at the beginning of this admit. Jordan stated that he was actually feeling better, although he was having difficulty urinating.

Dr. Williams concurred with Jordan’s diagnoses of  “Shiga Toxin E. coliwith HUS (STEC-HUS) with progressive thrombocytopenia, renal failure, hyperbilirubinemia, elevated LDH.” He noted that Jordan was still having bloody stools, but no fevers, altered mental status or confusion. He saw no current indication for total plasma exchange (TPE) or fresh frozen plasma (FFP) infusions; however, since Jordan was significantly thrombocytopenic, he recommended a platelet transfusion to keep his counts above 20K while currently bleeding.

Jordan received a platelet transfusion that afternoon. Dr. Williams ordered a transfusion of packed red blood cells (pRBCs) if Jordan’s hemoglobin fell below 8 g/dL, and he wanted some other labs checked, commenting: “To be complete I would ensure coags, fibrinogen, and ADAMTS13[6]have been checked. Typically, HUS is more platelet consumptive as opposed to coagulation factors consumption.” Meanwhile, he advised supportive measures with intravenous hydration and continued renal support by nephrology.

Meridian Hospital Day 4 – continued oliguria

On April 4, 2018, hospitalist Shanna Case, MD evaluated Jordan during morning rounds. He complained of continued incessant bloody diarrhea, describing some 30 episodes during the prior 24 hours, which actually represented a decrease in number. His pain was under control, but he required frequent dosing of narcotic pain medications (Dilaudid). He was unable to tolerate anything orally except for a small amount of water. Jordan was barely producing any urine and was effectively anuric. His mental status appeared intact and he denied confusion, about which his mother agreed.

Jordan was visited by hematology and nephrology. Jordan reported frequent bowel movements that still contained some blood. Dr. Fearday noted that his renal function had worsened overnight (BUN 79, creatinine 4.79). Jordan thought he was producing some urine, but the doctor observed that it was actually very little. He explained that they would assess him daily for the need for dialysis. “There is a chance he may benefit from dialysis in the next day or two if there is no clinical improvement.” Jordan was becoming volume overloaded, and he was hyponatremic as well as oliguric. Dr. Fearday recommended they stop his IV fluids the next day if that did not change. Jordan’s mother was present at his bedside discussed the care plan.

Meridian Hospital Day 5 – marginal urine increase

On April 5, 2018, Dr. Case reviewed Jordan’s morning labs, which continued to reflect sepsis, hemolytic anemia, thrombocytopenia, and worsening renal function, as well as marginal liver dysfunction (WBC 39.94, hemoglobin 9.2, hematocrit 26.1, platelets 21K, BUN 94, creatinine 5.42, AST 61). While his leukocytosis was worse, his tachycardia had improved, and his serum lactate normalized. His diarrhea was also improving, although still frequent, and his stools less bloody. Dr. Case commented that Jordan’s HUS was reported to the Department of Health on the 5thby nephrology. She noted his platelets were stable overnight, and his hemoglobin was just high enough to avoid a blood transfusion. She commented that nephrology was following his renal function, which continued to worsen secondary to the toxic effect of Shiga toxin Escherichia coli. Improving urine output. Jordan’s urinary output increased somewhat, and she saw no current indication for hemodialysis at that time. He was still hyponatremic and hypervolemic and remained on reduced fluids per nephrology recommendations to address those things.

At 10 PM, Sandra Van Hooser, RN summoned the hospitalist when Jordan began complaining of crushing chest pain to the left side of his chest. The pain did not radiate or get worse with deep inspirations and Jordan did not require supplemental oxygen. He continued to make frequent trips to the bathroom for diarrhea. He had not been measuring his urine output, stating it was too difficult with the diarrhea. Jordan had been suffering with hiccups all day, which was thought to have something to do with the chest pain episode, and the physician did not think he needed to be placed on cardiac monitoring with an EKG.

Meridian Hospital Day 6-7 – blood transfusion pRBCs – improving urinary output

On April 6, 2018, Robert Davidson, MD came in for nephrology, finding Jordan much the same as the day before, including the unrelenting hiccups. He made no changes to his diagnoses or care plan.

Dr. Case came in a little later and evaluated Jordan, who told her that his diarrhea had become bloody again overnight and his abdominal pain was not well controlled, even on the narcotics being given “as needed.” He was feeling very fatigued and lightheaded that day with ambulation. His morning labs showed a WBC 41.57, hemoglobin 7.4, hematocrit 21.1, platelets 24K, BUN 93, creatinine 4.44, and LDH 2776. Dr. Case ordered a blood transfusion of two units pRBC’s (packed red blood cells). She made some adjustments to Jordan’s narcotic pain medication orders, hoping to get his pain under better control. Jordan’s urine output was improving slightly that day.

At 5:47 PM, Dr. Williams came in for hematology/oncology and went over Jordan’s lab results. His mother was at the bedside, and the doctor explained that his extremely elevated white blood cell count was reflective of ongoing bone marrow issues related to hemolytic uremic syndrome, with its associated hemolytic anemic and thrombocytopenia. He observed that Jordan’s elevated LDH and serum ferritin were consistent with hemolysis from Shiga toxin. If Jordan developed fevers, then he would be more concerned and would order blood cultures to rule out a systemic infection. He explained that antibiotics were contraindicated with HUS because they could actually make his condition worse.

Dr. Case came in to see Jordan on April 7, 2018, observing that his urinary output was improving daily. His diarrhea was no longer bloody, and the frequency was down to hourly. He was able to tolerate small amounts of fruit and juice. He stated his pain was better controlled. His lab improved that morning since yesterday’s blood transfusion (WBC 37.07, hemoglobin 8.1, hematocrit 23.0, platelets 28K, BUN 83, creatinine 3.46, AST 215, ALT 56, total bili 3.1, LDH 3168).

Dr. Davidson came in for nephrology, and Jordan expressed a desire to go home. He stated his diarrhea had improved and he was urinating more, hoping that would convince the doctor. Dr. Davidson did not think Jordan’s HUS was getting worse at this point, but his LDH was still very high and probably reflected ongoing hemolysis. He explained to Jordan and his mom that he was too ill to be discharged any time soon.

Meridian Hospital Day 8 – development of neurologic symptoms (myoclonus)

When Dr. Case evaluated Jordan around 8 AM on April 8, 2018, she was happy to see that he was having even less frequent diarrhea (every 2 hours) that continued to be nonbloody, but he still had a very poor appetite and was taking in only a little fruit and juice. He appeared exhausted, and he stated he was not sleeping much. His labs were still markedly abnormal, albeit improving (WBC 31.00, hemoglobin 7.3, hematocrit 21.6, platelets 41K, BUN 69, creatinine 2.65, LDH 2556).

Of greater concern was that Jordan had developed a new neurologic symptom, exhibiting episodes of jerking when he drifted off to sleep. In addition, he had two episodes of nosebleeds overnight; however, his coagulation panel was reassuring. He was still afebrile and denied any confusion or other mental status changes. Dr. Case conferred with neurology, who thought the jerking episodes were probably myoclonus from uremia, although Jordan’s BUN was gradually improving.

Neurology Consultation

At 1:12 PM, neurologist Daniel Abenroth, MD came in to evaluate Jordan. Upon reviewing the history of his symptoms and talking to Jordan and his mom, he learned that he had been having the jerking movements for 2-3 days. Dr. Abenroth did a neuro assessment commented in his chart note:

23-year male who has developed acute myoclonus in the setting of hemolytic uremic syndrome. Uremia itself is a known cause of myoclonus. Though he is producing urine, he’s been clearly dealing with acute kidney injury and HUS, which has also resulted in a number of metabolic abnormalities. His acute myoclonus is likely the result of his HUS, AKI, and metabolic disturbances. My concern for underlying seizures or other causes of myoclonus is low at this time. This myoclonus is typically a self-limited phenomenon that improves as the renal and metabolic disturbances improve. This is unlikely to represent the onset of new chronic condition. Typical symptomatic treatment modalities include Keppra[7]and [benzodiazepines]. Treatment for the myoclonus in his case is not essential (his myoclonus is relatively rare during the day; 3-4 reported episodes today), though treatment could provide symptomatic relief. This was explained to the patient. At this time, he prefers to defer more meds unless his condition fails to improve or worsens.

Seizures – Rapid Response Team (RRT) response

The St. Luke’s Internal Medicine (SLIM) service paged Dr. Abenroth around 8:45 PM in the evening on April 8, 2018, after Jordan had an episode of reported arm twitching while on the toilet. The staff found Jordan on the bathroom floor with twitching arms and legs. Afterward, he appeared to be agitated. The nursing staff and family felt this episode was different and looked more like a seizure instead of myoclonus.

The Rapid Response Team documented Jordan’s seizure episode:


Ryan Fox, RN 8:05 PM. I heard a call for “help” from the pt’s room. I was preparing to gown-up where I observed the pt seated on the toilet with his legs extended and leaning his torso and head back while his shoulders and head were being supported by his significant other. The pt appeared to be seizing at that time. I immediately entered the room and took over for the pt’s [significant other] in protecting his head. The pt was having what appeared to be a tonic clonic seizure; his legs and arms were fully extended and the pt was convulsing. The pt had bloody frothy saliva coming from his mouth. Kelly Wolfe, RN, entered the room and I requested that she call a rapid response and get staff assistance.

The seizure lasted approximately 28 seconds from the time I entered the room. I instructed the family to lay down some blankets and a pillow on the ground next to the toilet and the pt was transferred from the toilet to the ground. The pt appeared to be in a post-ictal state after being positioned on the ground; the pt was non-verbal, inactive, and had a distant gaze in his eyes with nystagmus that would not focus on me. Vital signs were obtained and were found to be stable.


Lisa Stimpson, RN 8:30 PM. Rapid response called for this patient who had seizure-like activity while on the toilet. Event witnessed by staff and family. Arrived to find patient awake and lying on bathroom floor. Pt had been placed on oxygen and carefully assisted to floor for safety w/o fall or injury except for small bite to lower lip with scant bleeding. Pt appears to be postictal. Not able to maintain eye contact or follow commands, incomprehensible speech, moving all extremities spontaneously. GCS 11. PERRL. Placed green sheet under pt and used lift to return to bed. Seizure pads placed on bed. Family at bedside, however pt remains altered, agitated and tachycardic. Hospitalist came promptly to bedside to assess. Orders for Keppra and brain MRI scheduled for morning. BG 167. Pt now calm. Still not speaking to family but maintaining eye contact. HR trending down to baseline. Keppra infusing.


Daniel Orchard, MD. My colleague Sam Gallo PA was paged that the patient may have had a seizure. In brief Jordan Anglen is a 23 yo man here with E. Coli causing HUS, AKI, thrombocytopenia and anemia. He developed myoclonic jerks as a result of the uremia and was evaluated by neurologist. Dr. Abenroth earlier today. The patient chose to defer meds at that time. A full workup for seizure including MRI/EEG was not recommended given the natural course of myoclonic jerks and the likelihood of seizure was low.

When I arrive at the room, the patient’s girlfriend, mother, and father are gowning up to go in and tell me that I’m needed right away because he is having a seizure. The girlfriend tells me he was on the toilet when he started to have jerking movements like earlier today, he also reached out suddenly with both arms grabbing the toilet. There was no head trauma, but he was not responding to questions. On exam, his eyes are not dilated, he is moving all extremities spontaneously, he is purposefully moving his hands in front of his face and seems to be looking at them, he sometimes groans/moans. He had no evidence of head trauma. He doesn’t seem sluggish as is typically found during a post-ictal state. He is tachycardic.

Dr. Abenroth diagnosed Jordan with “probable acute seizure” and started him on Keppra 500 mg twice daily (renal dosing for seizure) and ordered an MRI for the following day. He deferred an EEG for now, commenting, “Whether myoclonus or seizures, we will treat with Keppra. Furthermore, whether myoclonus or seizure, either is likely due to his HUS and several metabolic disturbances. This is unlikely to represent the new onset of a chronic seizure disorder.” If needed for breakthrough seizures, Dr. Abenroth ordered Ativan 1-2 mg intravenously. He planned to see Jordan for a reassessment in the morning.

Jordan not improving after seizure – incontinent of bowel and bladder

After Jordan’s seizure, his family was understandably extremely upset and worried about their son. They soon summoned the nursing staff that Jordan seemed to be getting much worse. At 10:30 PM, Lisa Stimpson, RN called the SLIM service to communicate her concern that, 2.5 hours after the seizure, Jordan remained non-communicative and unable to maintain eye contact or follow commands, and he was now incontinent of bowel and bladder. He would moan rather than speak his answers.

The nurse spoke with both Sam Gallo, PA and Daniel Orchard, MD. The family requested that an MRI be done immediately and not wait for morning. She conveyed a message to the doctors: “Family is very concerned and dissatisfied.” Despite the family’s request, the doctors were not convinced of the need to return to the unit—both felt it appropriate to continue with observation and proceeding with the MRI in the morning as ordered.

Meridian Hospital Day 9 – more seizure activity, incontinence

Shortly after midnight on April 9, 2018, the nursing staff urgently paged hospitalist Mousumi Nandy, MD for another “event” that was still ongoing. Jordan’s mental status appeared to be worsening, with three additional episodes of incontinence of bowel and bladder. His parents were at the bedside and extremely anxious and upset and demanded that Jordan to be seen by a doctor.

Dr. Nandy soon arrived on the unit and spoke with Jordan’s nurse and his family, who told him that Jordan had an observed 28-seconds-long generalized tonic-clonic seizure, in the presence of nursing staff, and following that he was not following any commands, which was a definite change from the time of his first seizure. Prior to the seizure, “… patient was alert awake doing fine.” “Family both parents are very concerned. Mom is wanting to get something done now to find answers regarding his changes.”

Dr. Nandy observed that Jordan was awake but not responding to any verbal or tactile commands. His pupils were reactive and equal. He was unable to cooperate for a neurological exam; however, he moved all four extremities on his own. During Dr. Nandy’s first examination, he observed some “posturing” with Jordan’s right elbow flexed and his hand curled inside, as well as the left hand straight but fist curled inside towards the body. He continued to moan intermittently. During Dr. Nandy’s second examination, Jordan did not exhibit posturing but “… was flinging his hands in the air and then held it over his forehead, resting to move.”

Moved to ICU for seizure watch

Dr. Nandy ordered Jordan moved to the ICU to for seizure monitoring, and he wanted a stat CT of his head to rule out a bleed. He ordered stat labs to include a complete blood count, metabolic panel, and LDH. At 2:32 AM, radiologist John Waltz, MD performed an unenhanced CT of Jordan’s head, which he read as normal.

Dr. Nandy paged neurologist Dr. Abenroth to inform him that he had moved Jordan to the ICU. He explained that Jordan had been persistently encephalopathic since the seizure at 8 PM a few hours earlier, with reported episodes of flexion of his arms (predominantly one arm). He stated that Jordan had remained non-communicative and was receiving renal dosing of Keppra through his IV. “This remains as a significant neurologic change as compared to when I last saw him [yesterday] afternoon, when he was neurologically normal.”

TTP versus HUS – recommendation for plasmapheresis[8]

Dr. Nandy remained concerned for the possibility of TTP[9]as the cause of Jordan’s neurologic change. Dr. Abenroth addressed this possibility but deferred to hematology and the SLIM team:

TTP can certainly cause a variety of neurologic symptoms, including seizure, encephalopathy, or stroke. Similar changes can also be found in HUS, though significant acute neurologic change remains one of the hallmarks of TTP. The diagnosis of TIP, especially as it relates to the subtle differences between TTP and HUS is beyond the expertise of neurology. As such, I defer ultimate diagnosis of TTP vs. HUS to experts of that disease. However, Neurology recognizes the importance of prompt treatment for TTP with plasmapheresis in cases of suspected disease. As such, if the SLIM and Hematology services have a significantly high suspicion of TTP, then Neurology recommends treatment with plasmapheresis. Plasmapheresis has also been used in cases of atypical HUS. If the SLIM and hematology services feel that patient has atypical HUS, plasmapheresis is also a consideration. Ultimately, the diagnosis of TTP (and whether plasmapheresis is ultimately used) will be deferred to the experts of that condition (hematology and SLIM).

Dr. Abenroth pointed out that a stat head CT was read as normal. He thought it unlikely that Jordan was suffering a stroke, commenting: “In the chance it is stroke, no typical acute stroke treatment is recommended (tPA and aspirin are contraindicated on account of thrombocytopenia) …” In the setting of Jordan’s recent seizure, Dr. Abenroth thought his current condition might simply be post-ictal, but an ongoing seizure was also possible. He recommended that SLIM give Jordan another 2 mg of Ativan now to assess for neurologic change. If he continued to have persistent neurologic symptoms despite the dosing of benzodiazepines, along with additional time to recover from a possible post-ictal state, then Dr. Abenroth recommended that Jordan be transferred to Boise early in the morning (about 8 AM) so that continuous EEG monitoring could be initiated immediately.

After speaking with Dr. Abenroth, Dr. Nandy discussed Jordan’s clinical presentation with the hematologist on call, Dr. Alluri. He expressed his concerns about Jordan’s sudden change of mental status in a patient with HUS and whether he needed to be started on plasmapheresis. “At this point her recommendation was to continue to watch him, since his labs are improving, she will talk to Dr. Williams from hematology who had seen the patient earlier to follow up and decide whether patient would benefit from plasmapheresis or watchful waiting.”

Jordan’s parents were present for the consultations, and Dr. Nandy talked with them at length about their son’s care plan. He ordered the placement of a Foley catheter at 4:39 AM to deal with Jordan’s continued incontinence.

In ICU and not improving – tachycardic and febrile to 101.7ºF

At 8 AM on April 9, 2018, Shanna Case, MD and nephrologist Robert Davidson, MD came in to evaluate Jordan in the ICU, noting that he had been transferred there during the night because of seizure activity. The nursing staff indicated that he had been febrile that morning. His morning labs were in and continued to reflect sepsis, renal dysfunction associated with HUS, and some degree of liver dysfunction (WBC 30.55, hemoglobin 8.8, hematocrit 25.1, platelets 62, BUN 62, creatinine 2.26, AST 132, ALT 79, LDH 2405). Jordan was tachycardic with heart rates ranging from 117-128, with at least one oxygen desaturation down to 88%. The doctors reassessed Jordan’s differential diagnoses, which now included “HUS-TTP versus status epilepticus[10]versus less likely stroke.” They continued his seizure treatment with Keppra, adding Vimpat[11]pending implementation of continuous EEG monitoring.

Neurology consulting recommended a trial of plasmapheresis “… due to clinical decline per discussions with hematology, nephrology.” Upon review of Jordan’s labs, the doctors noted that that his ADAMST13 had come back normal and his complement levels were low, making atypical HUS unlikely. His renal function, while still significantly impaired, was improving steadily and he continued to produce greater amounts of urine. He was currently running a fever of 101.7ºF, but the doctors continued to avoid giving him any antibiotics. They continued his narcotic pain medications and anti-emetics.

Transfer to St. Luke’s Boise for cEEG and plasmapheresis

Travis Williams, DO came in for hematology at 8:14 AM, noting Jordan’s seizure activity, high fevers, and confusion. Given Jordan’s increasingly critical status and move to the ICU, his care team was of the consensus that he should be transferred to Boise for a higher level of care, where he could receive continuous EEG monitoring and be started on plasmapheresis, although Jordan was considered to have typical D+HUS and not atypical HUS.[12]Rather, Dr. Williams’ recommendation to start plasmapheresis was based on Jordan’s change in mental status, which he felt was directly related to Shiga toxins. “Schistocytes seen on peripheral smear. Elevated LDH and a ferritin consistent with hemolysis from Shiga toxin.” He discussed this with nephrologist Dr. Davidson, who concurred, and they contacted the critical care team in Boise with a plan to begin plasmapheresis as soon as he got there.

St. Luke’s Boise Medical Center – Hospital Day 9 – ICU Day 1 – TPE 1

On April 9, 2018, Jordan was transferred to St. Luke’s Boise Medical Center some 10 miles away by ambulance. The interfacility transport was initiated at 8:57 AM and the ambulance crew arrived at his bedside shortly thereafter. Just prior to moving Jordan, he became extremely agitated and began pulling at his IV lines and Foley catheter, requiring him to be sedated for the ride with Dilaudid. His care was turned over to the ICU team in Boise at 10:25 AM.

Dr. Abenroth met Jordan in the Boise ICU after he was transferred, along with nephrologist Tyler Harris, MD. He was still poorly responsive; his eyes were open, but he was unable to follow any commands or speak. His admission diagnoses included “acute myoclonus, secondary to HUS,” “possible seizures, secondary to HUS,” “hemolytic uremic syndrome,” “encephalopathy, septic-metabolic,” and “possible non-convulsive status epilepticus.” The ICU team conferred over the question as to whether Jordan had TTP:

The SLIM and hematology services maintain that this is most consistent with HUS. Patient will still undergo [therapeutic plasma exchange] in the small chance this is TTP.[Regarding] his encephalopathy, my highest suspicion is that he either has a severe septic metabolic encephalopathy or having seizures. If in fact he has TTP, stroke is a possibility. However, with his thrombocytopenia, neither aspirin or TPA is appropriate. Thus, MRI brain is not essential at this time. I have a low suspicion of CNS infection at this time. He already has a known reason for a fever, and his WBC count continues to improve daily without antibiotics.

Dr. Abenroth continued Jordan on Keppra 500 mg IV every 12 hours, Vimpat 200 mg IV every 12 hours, and deferred a brain MRI for the time being. They also deferred a lumbar puncture at that time. Of note, Jordan’s blood cultures obtained at Meridian were negative for growth of any bacteria.

Insertion of dialysis catheter in preparation for TPE

Later that afternoon, Dr. Harris performed the insertion of a temporary hemodialysis (“trialysis”) catheter under sedation by interventional radiology, in order to accommodate therapeutic plasmapheresis. The catheter was placed into Jordan’s right internal jugular vein, with the tip terminating in the inferior vena cava.

Jordan underwent his first plasmapheresis later that day.

Hospital Day 10 – Boise ICU Day 2 – TPE 2 – another blood transfusion

On April 10, 2018, Robert Davidson, MD came in for nephrology at 8:06 AM, noting that Jordan had undergone a therapeutic plasma exchange (TPE) with fresh frozen plasma (FFP) the day before. He was still running a fever of 101.5ºF that morning, but his labs were improving, including his leukocytosis and renal function, but he continued to exhibit severe hemolytic anemia (WBC 18.43, hgb 6.9, hematocrit 20.9, platelets 99K, BUN 48, creatinine 1.78.). Dr. Davidson planned daily [TPE] for at least five days. He commented that “the literature suggests use of eculizumab[13]in this setting,” indicating that he had spoken with hematologist Dan Zuckerman, MD about that and would revisit the issue at some point.

Critical care intensivist Scott Link, MD came in at 8:46 AM, observing that Jordan’s mental status was unchanged overnight. He was hoping to see some improvement after the first plasma exchange. Dr. Link reviewed Jordan’s labs and commented that most values were improving, with the exception of continued severe anemia, for which he was to receive a blood transfusion of pRBCs that day. A continuous EEG was in process and they were awaiting an assessment of that by neurology. Meanwhile, Jordan continued to receive regular doses of Keppra and Vimpat as ordered.

Improvement in mental status

Dr. Zuckerman visited Jordan for hematology just before noon, finding him awake and making purposeful movements, including tracking with his eyes intermittently. He and Dr. Link had just made the decision to proceed with eculizumab but, given Jordan’s slight signs of neurologic improvement, his mother wanted to hold off on the drug for another 24 hours. Meanwhile, the doctors confirmed Jordan’s immunization status since eculizumab would increase his risk of acquiring an infection. If Jordan showed no further neurologic improvement or worsened by the next morning, they planned to initiate the infusion.

Dr. Abenroth came in to see Jordan at 12:22 PM and reviewed the continuous video EEG started the day before. He was happy to see the improvement in his mental status, which included the ability to follow simple commands that morning. He was also less agitated. Dr. Abenroth discussed the EEG with the epileptologist, who identified no seizures, “only encephalopathic pattern.” Jordan’s encephalopathy also looked somewhat improved on the tracing, and so Dr. Abenroth decreased his seizure medications that day (Vimpat to 100 mg twice daily, Keppra unchanged at 400 mg twice daily) and monitor him for seizure activity. Pharmacy notified the doctors that Jordan’s eculizumab was ordered and was expected to arrive in the next 24-48 hours; however, Jordan never required the administration of the medication.

Hospital Day 11 – Boise ICU Day 3 – TPE 3 – more seizure activity

On April 11, 2018 at 2 AM, the nursing staff paged the critical care to Jordan’s bedside when his mother noticed him with increased twitching and feared he was about to have another seizure. However, his neurologic exam was stable with no new changes other than the twitching. Unfortunately, by 4 AM, Jordan was clearly exhibiting seizure activity, with an observed episode of stiffening of his extremities and unresponsiveness to stimuli. The nurse administered IV Ativan as ordered prior to contacting the ICU attending.

Sogol Nowbar, MD responded to the page and observed the video recording of Jordan, confirming the nurse’s observations at 4:08 AM. Jordan was currently “somnolent and “likely post-ictal.” There were no obvious EEG changes, however, and there had been no respiratory compromise. Dr. Nowbar asked the nurse to update neurologist Dr. Kashirny in order to determine whether any additional anti-seizure therapy was needed or repeat imaging advised. She did so, and received no new orders.

Another seizure

At 3:51 AM, when the nursing staff entered Jordan’s room to draw his morning labs, they approached his bedside and attempted to orient him to time and place. She asked Jordan if he was in pain, to which he nodded “no,” but while she was checking his urinary output, Jordan quickly moved his left arm above his head and started grunting. The nurse described that Jordan’s jaw became rigid and blood tinged sputum started coming from his mouth. She rapidly summoned the Rapid Response Team.

Multiple personnel soon arrived in Jordan’s room, who observed him with mild body rigidity. He then became unresponsive and began high pitched grunting. His heart rate increased to the 140’s, but his blood pressure remained in normal range, as did his oxygen saturations, throughout the episode. Jordan was administered additional IV Ativan during the episode. Within 30 minutes of the seizure, Jordan opened his eyes in response to his name, but his affect was flat. He was moving all extremities voluntarily.

Dr. Davidson came in for nephrology at 7:31 AM and learned of Jordan’s apparent seizure a few hours earlier. He thought Jordan’s mental status was improving, despite the seizure. Hospitalist Michael D. Madison, DO arrived shortly thereafter and determined that the red frothy sputum observed by the nurse was caused by Jordan’s biting down on his lip during the seizure.

Improving mental status

Dr. Zuckerman came in for hematology/oncology at 10 AM and also observed that Jordan appeared to be doing better, “… although had another seizure.” He wondered about “primary epilepsy.” At 1:55 PM, Dr Abenroth arrived to see Jordan for neurology and reviewed the details of his morning seizure activity and, upon looking at the cEEG tracing, confirmed that Jordan had indeed suffered an actual seizure. He, too, wondered whether Jordan had an underlying seizure disorder, “probable epilepsy,” besides the encephalopathy related to his HUS. He thought Jordan’s encephalopathy was “septic-metabolic” and improving. He commented in his chart note:

He has been severely encephalopathic; differential diagnosis includes septic-metabolic encephalopathy vs seizures. Less likely consideration stroke. In discussion with the epileptologist about the EEG pattern, there is legitimate concern that patient actually has an underlying seizure disorder beyond acute symptomatic seizures from his condition. Though his HUS can certainly be a precipitant (and likely is for patient) of acute seizures and still likely is for Jordan, his EEG has features concerning for concomitant epilepsy.

Though the emergence of his seizures only at the time of his critical medical condition (with no prior medical history of seizures) raises the question of whether this truly represents epilepsy, the EEG was concerning enough where it is most prudent to treat for now as though this is a primary generalized epilepsy. In the future, long-term outpatient evaluation will be necessary to further clarify this diagnosis and treatment. This was explained in detail to the patient and family.

Dr. Abenroth increased Jordan’s anti-seizure medications to Keppra 1000 mg every 12 hours and ordered a brain MRI after the current EEG was complete. He continued his Vimpat 100 mg twice daily.

Later in the afternoon, Jordan failed a swallow test when speech/language therapist Jennifer Wood, SLP came in to evaluate him. The ICU team felt Jordan needed to be started on total parental nutrition (TPN[14]); however, his family objected and refused the initiation of TPN that night. They expressed a concern about his infectious and volume overload risks and felt their son was improving and hoped he would pass the swallow test the next day. The nurse conveyed the family’s concerns to the ICU staff and held Jordan’s TPN until they could meet with the family. Jordan continued with daily therapeutic plasma exchanges without difficulty.

Hospital Day 12 – Boise ICU Day 4 – TPE 4

On April 12, 2018, Dr. Davidson came in for nephrology in the morning, finding Jordan alert and vocalizing his responses to questions. He was no longer having loose stools. His morning labs reflected improvement (WBC 16.72, hemoglobin 7.8, hematocrit 23.2, BUN 35, creatinine 2.17). Dr. Davidson continued Jordan’s orders for TPE that day and the next with fresh frozen plasma, then he wanted to discontinue the treatments. Jordan’s mom noticed some twitching during the night, which were relieved with Ativan. She indicated that he had been talking and was more interactive since the night before, and he was asking for something to eat and drink. Unfortunately, when Dr. Madison came in for the hospitalist service, he observed that Jordan was unable to pass a swallow evaluation with SLP the day before. Pending today’s evaluation, he approved Jordan to advance his diet to oral fluids and soft solids. If neurology were to discontinue his cEEG, Dr. Madison thought Jordan could be transferred out of the ICU.

Mari Beth Stein, NP came in for oncology/hematology at 9 AM and reviewed Jordan’s labs, noting that his platelet count was now in normal range and his creatinine was almost back to normal. Jordan’s dad asked her about shortening the plasmapheresis, but she told him she was committed to the five days as laid out by nephrology. She did state that Jordan was not going to need the eculizumab.

At 9:38 AM, Jordan passed a swallow evaluation and was approved for full liquids and thin solids, as long as aspiration precautions were followed (“sit upright, 1:1 assist, single sips”) and they were attempted slowly.

Dr. Abenroth came in for neurology during the afternoon and reviewed Jordan’s seizure activity from the day before with Dr. Kashirny. “It was a clear seizure. There were also interictal features in a pattern that is classic for generalized epilepsy disorders. He has continued to have epileptiform activity intermittently that is responsive to benzodiazepines.”

Dr. Abenroth continued to opine that Jordan’s acute myoclonus was secondary to HUS, but he probably had an underlying seizure disorder. Because he continued to have intermittent myoclonic activity with associated EEG abnormalities on the cEEG tracing, and because he was responsive to benzodiazepines, Dr. Abenroth ordered regular dosing with clonazepam; 1 mg that afternoon and 1 mg at bedtime. He wanted to continue with the EEG tracing, and his Keppra and Vimpat as ordered. He continued to order Ativan for breakthrough myoclonic or seizure activity, and his Vimpat could be increased to 200 mg twice daily if that occurred. He continued Jordan’s orders for daily plasmapheresis for at least that day and one more.

Hospital Day 13 – Boise ICU Day 5 – TPE 5

On April 13, 2018, Christopher Keller, MD came in for nephrology at 8:32 AM and observed that today would be Jordan’s fifth day of five days of therapeutic plasma exchange therapy. He was happy with Jordan’s morning labs, which showed significant improvement in his Shiga toxin HUS, with a lower LDH, improved kidney function, and normal platelet count. He did not cancel today’s TPE but thought it should be the last one needed. Hematology/oncology signed off the case that morning.

No more cEEG monitoring – moved out of the ICU

Dr. Abenroth came in for neurology and reviewed Jordan’s cEEG tracings for all five days he had been in the ICU. By day 5, he observed that Jordan’s EEG continued to show improvement over 24-48 hours and was dramatically improved by the end of Day 4. On Day 5, he identified an “essentially unremarkable background presented as posterior alpha activity with a large amount of normal sleep background.” There was no epileptiform activity noted on the last day of the EEG. Dr. Abenroth was satisfied that this improvement was a pattern and that the continuous monitoring could be discontinued. He cautioned Jordan and his parents that, as he was clinically sick in the ICU with what was potentially juvenile myoclonic epilepsy, this abnormality needed to be re-evaluated when Jordan had completely recovered from his acute illness in order to make a final diagnosis of potential epilepsy.

At 11:22 AM, Jordan was moved out of the ICU after his EEG was disconnected and moved to a regular medicine bed.

At 5 PM, Jordan underwent an MRI of his brain, both IV contrast enhanced and unenhanced, during which radiologist Steven Marx, MD identified a normal appearing brain and dura, with no hemorrhage, edema, or mass effect, and normal vascularity.

Boise Hospital Day 14 – removal of dialysis catheter

On April 14, 2018, Sergei Kashirny, MD came in for neurology, finding Jordan awake and alert. He was observed to be following commands reliably and was fully conversant and speaking coherently. Jordan had experienced no seizure activity in the prior 24 hours, and Dr. Kashirny decreased his Vimpat to 50 mg twice daily for two days, with orders to discontinue the medication at that time. He continued Jordan’s Keppra 1000 mg twice daily, as well as his Ativan to be used as needed, and clonazepam at bedtime.

Dr. Keller came in for nephrology and ordered the discontinuation of Jordan’s temporary dialysis catheter, as he would no longer be needing therapeutic plasma exchange therapy. He reviewed his lab work and observed that his renal function panel was all in normal range and he was urinating well. Dr. Keller signed off Jordan’s case for nephrology.

PT, OT, ambulating the halls…

Michael Madison, DO came in for the hospitalist service during the afternoon, and Jordan told him he was feeling “really good” that day. He was awake and alert and very talkative, and asking if he could go home. He was eating and wanted to walk, although he admitted to feeling unsteady on his feet. Jordan was having some headaches that were thought to be medication overuse vs. withdrawal headaches. Neurology was working on weaning him off the benzodiazepines, and also moving away from narcotic medications for pain relief. He was advised to use acetaminophen IV if he needed something for his headaches. Although Jordan’s renal function had rebounded, he was still severely anemic and required another transfusion of pRBCs that day for a hemoglobin of 7.2. His electrolytes were in balance.

Physical and occupational therapy visited Jordan that evening and recommended that he be discharged to inpatient rehabilitation when medically appropriate to leave standard hospital care. He demonstrated decreased upper extremity strength and activity tolerance and was working with both PT and OT to address those deficits. PT noted that he was overall slow-moving and easily distracted, requiring cues to stay on topic and task. “Initially with walking he was scissoring and stumbling. With a walker he was the same but not understanding why he was having a hard time walking a straight line. With cues, he still struggled and, if he was distracted, he could not get right back on task.”

Boise Hospital Day 15-19 – preparing for discharge to rehab

On Sunday, April 15, 2018, Dr. Madison came in for the hospitalist service and continued transitioning Jordan to oral medications, which included Keppra and Vimpat, the latter of which was about to be discontinued in two days. He was advanced to a regular diet. Natasha Pappas came in for case management to discuss with Jordan and his mom his discharge to rehab, which could occur as soon as the next day. They discussed preferred rehab facilities, settling on St. Luke’s Rehab as their first choice. If Jordan had his way, he would just head home in his seriously deconditioned state, but his mom and the therapists convinced him of the utility of building his strength and stamina before doing that. His mom wanted to make sure that, wherever Jordan went, they could monitor his blood in case he needed more transfusions.

Dr. Madison resumed discharge discussions with Jordan and his parents the next day, and his dad was concerned about how somnolent the anti-seizure medications made him. However, he understood the important of seizure prevention at least for the time being. Jordan still exhibited generalized weakness, but he was ambulating the halls and working hard at PT and OT.

On April 17, 2018, Dr. Madison observed that Jordan was very drowsy, which he attributed to a recent Keppra dose. He continued to be weak and unsteady on his feet, but he was not having any seizures. His labs continued to exhibit improvement (WBC 8.08, hemoglobin 8.2, hematocrit 25.0, platelets 238K, BUN 28, creatinine 0.98) and his blood cultures had not grown any bacteria. He was eating and drinking without difficulty, and he was having normal urinary output and bowel movements.

Jordan was growing very bored and wanted to get out of the hospital. He worked daily with PT, OT, and SLP, the latter of which was focusing on memory strategies, attention tasks, and safety awareness, among other cognitive issues that had suffered from his long critical illness. By the 19th, Jordan was progressing towards his self-care goals, although he was still limited by decreased insight and occasional safety awareness. He exhibited occasional impulsiveness but was able to self-correct without cues (“this may be pt’s baseline due to being young and active”). He was able to perform grooming at the sink with close supervision. His swallow function was near baseline, and SLP was able to discontinue therapy at that time. PT worked with him on higher balance exercises and cognition for safe transition to home.

Boise Hospital Day 20 – getting ready to leave for rehab

On April 20, 2018, hospitalist Allyson Komori, DO evaluated Jordan for discharge from the hospital to sub-acute inpatient rehabilitation. She thought he was ready for transfer to St. Luke’s Rehabilitation Hospital, where they would continue working with him on ongoing strengthening and improvement in his stamina for a safe transition to home. Dr. Komori discharged Jordan from the hospital with the following diagnoses:

Principle Final Discharge Diagnosis:

  1. STEC (Shiga toxin-producing Escherichia coli) infection

Secondary Discharge Diagnoses:

  1. Hemolytic uremic syndrome
  2. Seizure disorder with myoclonus
  3. Acute renal injury
  4. Metabolic encephalopathy
  5. Dysphagia
  6. Protein calorie malnutrition
  7. Hemolytic anemia
  8. Thrombocytopenia
  9. Hypokalemia
  10. Hypernatremia
  11. Generalized weakness

Transferred to St. Luke’s Rehabilitation Hospital

Clifford L. Tenley, MD received Jordan into inpatient rehabilitation on April 20, 2018 at 1:07 PM, for “ongoing restorative care,” after his recent diagnosis of Shiga toxin producing Escherichia coli(STEC) infection.Jordan and his family were by now well aware and shared with Dr. Tenley that his STEC HUS illness began with the consumption of contaminated romaine lettuce. Dr. Tenley thoroughly reviewed the onset and progression of Jordan’s illness and hospital course before he was discharged. Jordan was currently taking Keppra 1000 mg three times daily, as well as clonazepam 1 mg at bedtime for seizure prophylaxis.

St. Luke’s Rehab Day 2-3

On April 21, 2018, Jordan started physical therapy, and he was alert and oriented and independent of transfers in his room. He had a “ground pass,” but his family had to be with him to use it. Jordan was ambulatory throughout the unit without the use of an assistive device, with his nurse as standby assist only. The nurse noted that Jordan had a steady, balanced gait.

Dr. Tenley came in to see Jordan on April 22, 2018 and was happy to see him doing extremely well. He had no nausea, vomiting, diarrhea, or constipation. He was eating lunch and consuming his entire tray. He was able to take a shower on his own that morning, but he commented that his left leg felt “drunk.” He told the doctor he was hoping to be discharged the next day. Dr. Tenley observed “marked improvement overall in the patient’s condition and status at this time. He likely could be discharged in the very near future if not tomorrow.” Jordan was still anemic on the 20thwith a hemoglobin of 8.7 and hematocrit of 26%. Dr. Tenley wanted to make sure that he would not be returning to work for at least another week once he was discharged home.

St. Luke’s Rehab Day 4 – going home

On April 23, 2018, case manager Amy Alderman was notified by Dr. Tenley that Jordan was ready for discharge from rehab. She talked with Jordan and learned that he lived in a duplex with his girlfriend and two roommates. Although both she and the roommates would be able to assist him, Jordan was planning to go to his parent’s home when no one was available to be with him the first few days. He stated that he worked at Costco and they were going to put him on light duty until he was ready to get back to his normal, heavier work.

Shannon C. Boyer, NP came in to discharge Jordan from the rehab unit at 3:08 PM. She went over his discharge medications with him and instructions for outpatient follow-up with his physicians, starting with hematologist Dr. Williams on May 1. Jordan’s vital signs were normal and stable, and he was exhibiting no severe symptoms from his ongoing anemia. He was discharged that afternoon.

St. Luke’s Hematology Outpatient Clinic

On May 1, 2018, Jordan presented for an outpatient visit with Travis Williams, DO.  Dr. Williams wanted to see him in follow-up of his thrombocytopenia. Jordan had blood work done that day, which showed a WBC 5.26, hemoglobin 10.0, hematocrit 30.0, and platelet count 182K. Jordan’s main complaint was the side effects of his anti-seizure medications, especially the clonazepam at night, which made him feel very sedated and “quasi out of body experience.” Otherwise, he felt he was regaining his strength after his acute illness. Dr. Williams was happy with Jordan’s hematologic recovery and did not think he needed any other follow-up than a recheck of his CBC in a month.

St. Luke’s Family Health Clinic – Meridian – establishing PCP care

Jordan established care with PCP Rebecca Locke, DO on May 10, 2018. Jordan was interested in getting back to normal, and he explained that he could not drive or drink because of the medication he was on. He hoped to get off the medication.

Dr. Locke reviewed Jordan’s records and observed that he had been placed on Keppra and clonazepam following seizures while hospitalized with E. coli. She went over his hospital course with him, discussing everything that had happened to him. He told her that he had a neurology appointment scheduled for the 23rd. Dr. Locke documented all of Jordan’s hospital diagnoses and his current state of recovery from each. She wanted to make sure he knew he needed another CBC in about a month, as recommended by the hematologist.

Dr. Locke discussed seizure follow-up recommendations with Jordan and that he needed to follow state laws about a return to driving, which set guidelines for how long he had to wait after a seizure. She was not sure about Idaho’s law, so she advised Jordan to avoid driving until his neurologist gave him the okay. She also deferred to neurology about continuing his anti-seizure medications until they advised it was okay to discontinue them. Meanwhile, she discussed the importance of yearly physicals and to do the follow-up with specialists as recommended when he was discharged from the hospital.

St. Luke’s Neurology – sobering precautions

On May 23, 2018, Jordan went to see Sergei Kashirny, MD for his first neurology follow-up since discharge. Jordan was still on clonazepam at night, and Keppra twice daily. Dr. Kashirny wanted Jordan to continue on his current doses of those medications. If he remained seizure-free for the next 2-3 months, then the doctor was willing to discontinue the clonazepam and continue Jordan on Keppra only. At that point, he planned to repeat an EEG in about 3-6 months to evaluate for any signs of primary generalized epilepsy. Jordan’s mother was with him at this visit, and Dr. Kashirny spent time with both of them to answer their questions and talk about seizure precautions. He did not want Jordan to drive for three months after his last seizure, and he advised him against working on heights/ladders, swimming unsupervised, taking baths (take showers instead)—i.e., to avoid any situation where, should he lose consciousness, either he or someone else could be injured. Dr. Kashirny reviewed “SUDEP” (sudden unexplained death in epilepsy) and emphasized the importance of staying compliant with his anti-epileptic medications. He advised Jordan that, if he had a seizure lasting 5 minutes or more, had back-to-back seizures, or seizures without a prompt return to baseline level of consciousness, 911 should be summoned to take him to the nearest emergency room.

Jordan returned to see Dr. Kashirny on August 2, 2018 for a follow-up visit. He denied any seizure activity or myoclonic jerks. He stated he was currently taking Keppra twice daily (1000 mg each time) and clonazepam 0.5 mg at night. He admitted to some chronic anxiety. Dr. Kirshirny continued with the same plan as delineated at Jordan’s May visit, planning to repeat an EEG to make sure no further seizure activity was present. He advised him to continue taking the Keppra at the current dose but to stop the clonazepam. If he noted any myoclonic activity, he wanted to restart it at the same once daily dose as before. Jordan had his “adult awake/drowsy/sleep” testing done on August 28, 2018 at the EEG laboratory, which Dr. Kashirny interpreted as a normal exam by Dr. Kashirny. His report read: “There are no focal lateralizing or epileptiform features.” In a final comment, he cautioned: “Normal EEG does not exclude a diagnosis of epilepsy. Please correlate clinically with EEG findings.” Dr. Kashirny wanted to see Jordan again in six months.

2019 Neurology Outpatient Visit

On January 22, 2019, Dr. Kashirny saw Jordan in his office for a follow-up visit. Jordan reported no seizure activity or myoclonic jerks, currently on a dose of Keppra short acting 1000 mg twice daily. Jordan was diligent about taking his medication but reported an occasional lapse in dosage. Dr. Kashirny recommended that he continue on the Keppra for at least the next 12-18 months. If he stayed seizure-free during that time, he wanted to repeat an EEG and then slowly discontinue the medication if the test picked up no epileptiform activity. At this point, Dr. Kashirny could not clearly rule out a seizure disorder, potentially “juvenile myoclonic epilepsy.” Dr. Kashirny started him on a slightly increased dose of Keppra, utilizing the extended release form (Keppra XR) of 750 mg to take three times daily (2,250 mg total) instead of the short acting 1 gm tablets twice daily (2,000 mg total). He offered Jordan the option of a one-time nightly dose to improve compliance.


Jordan’s girlfriend Josie reflects on his E. coliO157:H7 HUS illness:

I feel like more than anyone I’ve had to see how much this has affected Jordan, how many aspects of his life have changed, or been lost. Anyone who knows Jordan knows he’s an overthinker, doesn’t just jump into a situation but analyzes every aspect of what could go wrong. He’s good at making sure a situation doesn’t turn bad, if he has a say in it.

Ever since he got sick, he’s had no control in his life. From his job, to coming home, to even mentally and physically, I can see how much this is draining from him. The one place he has the most control is work, but how in control and productive can you be when you’re working around possible epilepsy. His own work duties are handed off to someone else until he’s cleared to perform them. So he’s stuck having to deal and rely on others and put the control in their hands.

He comes home from work exhausted cause his body isn’t used to 40-hour work weeks after lying in a hospital bed for a month without food.

And when he does come home to rest, it’s not home because we’re living in the middle of construction. We didn’t have the time to see all our options, to make sure we were getting into a good living situation. We were trying to avoid being homeless.

I could go on and on. He lost 20 pounds coming out of the hospital but hasn’t had a kitchen to be able to eat a good home cooked meal since he got out. He had to get a new car battery because he wasn’t able to drive his car, so the battery died. He hasn’t been able to drink beer because of the seizure meds he has to take.

Because of those seizures, I’ve watched my boyfriend forget Christmas, I’ve watched him forget time with his family, I’ve watched this man I love forget our anniversary. Because of those seizures, I’ve watched [him] forget his proposal to me twice.And have had to watched how devasted and scared he was that he couldn’t remember. Losing your memory isn’t something small. You’re losing a part of you every time you try to remember. And he has no control in getting those parts of him back.For someone who tries so hard to make sure things go right, to do the right thing, his life shouldn’t look so out of his control.


[1}        Normal vital sign ranges for the average healthy adult while resting are:

  • Blood pressure: 90/60 mm Hg to 120/80 mm Hg.
  • Breathing: 12 to 18 breaths per minute.
  • Pulse: 60 to 100 beats per minute.
  • Temperature: 8°Fto 99.1°F (36.5°C to 37.3°C)/average 98.6°F (37°C)

[2]          Toxic megacolonis a marked enlargement of the colon, esp. the transverse colon. Clinically, tachycardia, and leukocytosis occur. There may be abdominal tenderness, a palpable abdominal mass, confusion, cramping, and change in number of bowel movements per day. Venes, Donald. Taber’s Cyclopedic Medical Dictionary (Taber’s Cyclopedic Medical Dictionary (Thumb Index Version)) (Page 1480). F.A. Davis Company. Kindle Edition

[3]          Neutrophiliarefers to an increase in the number of neutrophils in the blood (e.g., as a result of inflammation, infection, corticosteroid drugs, or malignancies). Ibidat 1620.

[4]          Reference ranges for this lab: WBC 3.80-11K, hemoglobin 13.7-17.5 g/dL, hematocrit 39-55%, platelets 150-420K, BUN 9-20 mg/dL, creatinine 0.66-1.25 mg/dL, AST 17-59 U/L, ALT <50 U/L.

[5]          Jordan’s haptoglobin was reported as low at <10 mg/dL and his LDH elevated at 2776 U/L. The hemolytic-uremic syndrome (HUS) is defined by the association of hemolytic anemia (low haptoglobin levels, high lactate dehydrogenase levels, and schistocytes), thrombocytopenia, and acute renal failure. Olivia Boyer and Patrick Niaudet, “Hemolytic Uremic Syndrome: New Developments in Pathogenesis and Treatment,” International Journal of Nephrology, vol. 2011, Article ID 908407, 10 pages, 2011. doi:10.4061/2011/908407

[6]          ADAMTS13 deficiency =<10%. Jordan’s level was 78%. In nearly all patients, aHUS can be distinguished from TTP on the basis of an ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) enzyme activity measurement. It is essential that aHUS and TTP be differentiated quickly, as they require markedly divergent treatments. The standard treatment for TTP is plasma exchange, a therapy that has no role for patients with a diagnosis of aHUS established by ADAMTS13 activity levels. http://www.hematologyandoncology.net/files/2013/02/ho1012_sup171.pdf

[7]          LEV (aka levetiracetam, brand name Keppra) is used in the treatment of seizures; epilepsy; bipolar disorder; neuralgia; new daily persistent headache, and belongs to the drug class pyrrolidine anticonvulsants.”LEV 500 Pill – levetiracetam 500 mg.” LEV 500 Pill – levetiracetam 500 mg. Drugs.com, n.d. Web. 31 Jan. 2017.

[8]          Plasmapheresisis a process that filters the blood and removes harmful antibodies.  It is a procedure done similarly to dialysis; however, it specifically removes antibodies from the plasma portion of the blood.  Antibodies are part of the body’s natural defense system which help destroy things that are not a natural part of our own bodies, like germs or bacteria. In therapeutic plasma exchange, using an automated centrifuge, filtered plasma is discarded and RBCs along with replacement colloid (eg, donor plasma or albumin) are returned to the patient.Kaplan, Bernard S et al. “Current treatment of atypical hemolytic uremic syndrome” Intractable & rare diseases research vol. 3,2 (2014): 34-45

[9]          Hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) share the morphologic lesion of thrombotic microangiopathy (TMA), characterized by thrombi occluding the microvasculature. The HUS and TTP syndromes overlap clinically; however, certain features have been relied on to distinguish most cases labeled HUS, which is predominantly a disease of children younger than 5 years, from most cases labeled TTP, which is predominantly a disease of adults. Renal manifestations are more prominent than neurologic ones in HUS, whereas neurologic findings are more prominent than renal findings in TTP. Fogo, Agnes B., et al. “Thrombotic microangiopathies.” Fundamentals of Renal Pathology. Springer Berlin Heidelberg, 2014. 135-142.

[10]        Status epilepticus(SE) is a medical emergency associated with significant morbidity and mortality. SE is defined as a continuous seizure lasting more than 30 min, or two or more seizures without full recovery of consciousness between any of them. Cherian, A., & Thomas, S. V. (2009). Status epilepticus. Annals of Indian Academy of Neurology, 12(3), 140–153.

[11]        Vimpat (Lacosamide) is used either alone or in combination with other medications to prevent partial epileptic seizures. https://www.pdr.net/drug-summary/Vimpat-lacosamide-580

[12]         HUS is classified in 2 subgroups: HUS associated with a foodborne infection with Shiga toxin-producing Escherichia coli(STEC+) and atypical HUS (aHUS), or STEC-HUS. McCoy, Nicole, and Donald J Weaver. “Hemolytic Uremic Syndrome with Simultaneous Shiga Toxin Producing Escherichia Coli and Complement Abnormalities.” BMC Pediatrics 14 (2014): 278. PMC. Web. 31 Jan. 2017.

[13]        Eculizumab (Soliris) is the only agent approved for the treatment of non–Stx-HUS. The FDA approved eculizumab for the treatment of non–Stx-HUS in 2011. Eculizumab is a humanized monoclonal antibody against C5 that inhibits the activation of terminal components of complement.Volokhina, E., et al. “Pharmacokinetics and pharmacodynamics of eculizumab in individualized treatment of atypical HUS.” Pediatric Nephrology. Vol. 31. No. 10. 233. Springer, 2016

[14]        TPN by definition is nutrition given intravenously. It typically consists of dextrose, amino acids, emulsified fats, trace elements, vitamins, and minerals to patients who are unable to assimilate adequate nutrition by mouth.Because TPN solutions are concentrated and can cause thrombosis of peripheral veins, a central venous catheter is usually required. Venes, Donald. Taber’s Cyclopedic Medical Dictionary (Taber’s Cyclopedic Medical Dictionary (Thumb Index Version)) (Page 1650). F.A. Davis Company. Kindle Edition.

The State of Arkansas is stepping up as a leader and pushing responsible retailers to stop selling a defective and potentially deadly product. Hopefully the FDA will act as well as the DEA.

Manufacturers and retailers be forewarned; if you sell this product and it causes harm, you will be held to account.  Insurers of these manufacturers and retailers, ask yourself is this a good insurance risk?

Senator Cotton Warns of Opioid Overdoses from Unwashed Poppy Seeds

An opioid epidemic is sweeping the country. More than sixty thousand Americans are dying from opioid overdoses each year-more than the number of Americans who died in all twenty years of the Vietnam War. What a staggering fact that is. But behind each number is a tragedy for a family who loses its loved one. Today, I want to tell the story of the Hacala family from Rogers, Arkansas. It’s a story of love, persistence, courage. And, I hope, a story that will save other families from the tragedy they felt.

Betty and Steve Hacala are joining us in the gallery today. I met Betty and Steve three weeks ago at a roundtable on the opioid epidemic in Little Rock with Attorney General Leslie Rutledge, state and local law enforcement, and the families of opioid victims. The news is full of tragic deaths from heroin, fentanyl, and prescription drugs. I met families that day whose children died from those well-known drugs. But I learned from the Hacalas about another killer: unwashed poppy seeds.

Their son, Stephen Jr., died in his sleep from an overdose two years ago. Stephen was only 24 years old, a recent graduate of the University of Arkansas. He loved to play guitar, and he was very accomplished at it. He was the joy of his parents’ life; he was the joy of his sisters Christina and Lauren’s lives. His sudden death came as a shock to them. But they got another shock when an autopsy determined that Stephen died of morphine intoxication. There were no drugs in his apartment-no pill bottles, no needles, nothing. What had been found was a five-pound bag of unwashed poppy seeds; Stephen had ordered the seeds on Amazon. The Arkansas Crime Lab soon determined that the poppy seeds were the source of the morphine that killed Stephen.

Stephen’s death resulted in part because of a dangerous gap in our nation’s drug laws. It’s been well known for ages that poppies are dangerous, both addictive and toxic. That’s why it’s illegal to grow or own almost any part of the poppy-the straw, the pod, the latex. But there’s an exception, of course, for poppy seeds, which many people enjoy on bagels, muffins, cakes, and other pastries. The seed itself isn’t addictive, but unwashed seeds tend to still have bits of the plant on them, which can be washed off and used to create a powerful narcotic. To give you a sense of just how deadly poppy-seed tea can be, a lethal dose of morphine is about 200 milligrams, but researchers at Sam Houston State University, commissioned by the Hacalas, concluded that there were about 6,000 milligrams of morphine in that five-pound bag of seeds that Stephen bought. That’s over 30 times the lethal dose. Stephen had no way of knowing just how toxic these seeds were.

While there are plenty of legitimate uses for washed poppy seeds, there are no legitimate uses for unwashed seeds. Yet drug dealers and unscrupulous merchants are abusing the legal status of washed seeds to profit and to push unwashed seeds, which are widely available through online retailers. And when you read the user comments, you can easily find instructions for how to brew poppy-seed tea and a description of its narcotic effects. So there’s no question of these unwashed seeds being used for grandma’s poppy-seed cake-it’s plain they’re being used to smuggle the banned drug into our homes, and the manufacturers and distributors should know that.

And Betty and Steve made sure they did. It’s hard to imagine the grief they feel. It would’ve been easy to despair. But they did not. They wanted to save other families from their fate, to be sure Stephen’s death would have meaning. They researched the issue, commissioning that report at Sam Houston State and studying the market for unwashed poppy seeds. And they became advocates, meeting with community leaders and elected officials. As I said, I only learned about the danger of unwashed poppy seeds by meeting the Hacalas.

After that meeting, I put in a call to the leadership of Walmart and Amazon, which at the time both allowed unwashed poppy seeds to be sold on their websites. They listened to our case and quickly agreed to stop selling poppy seeds that are labeled as unwashed. This is important. The two behemoths of online commerce agreeing to take down those seeds was a victory and a testament to what normal citizens like Steve and Betty can accomplish.

But this is more than a labeling problem. In fact, some of the most potent and deadly seeds, which we know about thanks to the work of Steve and Betty, are not labeled as unwashed and are still available for purchase. Therefore, I will work in the Senate and with the Drug Enforcement Agency to ban unwashed seeds entirely, but today I do want to take a moment to thank Amazon and Walmart for taking an important first step-for our country, for our state, and for the Hacalas and families like theirs.

It’s always hard to lose a loved one, and a child is the hardest loss of all. I suspect that nothing can assuage that kind of grief. But because of the Hacalas’ courage and determination, we can hope that a few more families will be spared it. That’s an act of true love, for Stephen and for their fellow Americans.

218 sick

28 with hemolytic uremic syndrome

5 deaths

In 2018 in the United Sates, 210 people infected with the outbreak strain of E. coli O157 were reported from 36 states. 96 people were hospitalized, including 27 people who developed a type of kidney failure called hemolytic uremic syndrome (HUS). 5 deaths were reported from Arkansas, California, Minnesota (2), and New York. In Canada, 8 cases of E. coli O157 that were genetically similar to the U.S. outbreak linked to romaine lettuce coming from the Yuma growing region in the U.S. The 8 Canadian illnesses were reported in 5 provinces: British Columbia, Alberta, Saskatchewan, Ontario and Quebec. 1 of the Canadian cases was hospitalized with HUS and no deaths were reported in Canada.

Health officials in both Canada and the U.S. have worked hard to do the hard epidemiological and environmental investigations that lead to traceback and root cause analysis that lead to new ways of preventing these tragedies for the consumers and the producers.  However, the hard work is essentially done in obscurity with little or no transparency.  Through the litigation process we are cracking open the door so the public can see both where product was grown (more to come on that in the coming weeks) and were the product was sold.

Because of the lack of transparency on behalf of investigators we have to do it through litigation.  Here is where the FDA is to date:

Here is where we are to date:

Here are some helpful documents from the FDA and CDC – romaine2 – romaine5 – Ecoli O157 1804MLEXH-1 06272018-2

And, the CAFO is still in Yuma:

No amount of money can compensate for the loss of a child or another family member.  I recall the Jensen Farms Listeria outbreak in 2011 that sickened 147, killing over 33 and the impact on the families.  All the deaths were horribly memorable, but I recall two WWII vets who survived years of war only to be killed by a cantaloupe.  Being involved in a lawsuit nearly 10 times the size is sobering.

  • For the 204 dead $265 to $525 Million US – Mortality cases were assigned compensation values of US$1,244,747 and US$2,524,312 per fatality for minimum and maximum human life valuation adjusted for South Africa which was 15% to 80% of U.S. values. The total valuation of mortalities over the 16 months of the outbreak ranged from US$265 million using the low valuation for a fatality to US$525 million using the high valuation.
  • For those who survived – Hospitalization costs associated with one-month recovery from listeriosis were estimated at US$10.4 million.  Note, however, the direct costs that were not estimated consisted of: current and future value of outpatient care and medication costs to treat chronic and acute cases, future cost of human suffering and lost productivity.

Here is my summarization of a well-done article:

According to a recent article in Food Control, in 2017-2018, Listeria was reported on polony (processed deli meat) and listeriosis was observed in South Africa (L. monocytogenes sequence type 6 (ST-6) was identified as the causal agent for listeriosis). Due to its potential effects, we conducted cost estimates to assess the implications of listeriosis outbreak with respect to illnesses, hospitalizations and deaths, and productivity losses. Cost estimates were computed on publicly available data by using USDA-ERS cost computation model for Listeria. Listeriosis had significant impacts, as mortality of 204 individuals with confirmed listeriosis cases was reported, with infants having the highest percent of fatalities (42%). The cost valuation of fatality cases was over US$ 260 million. Hospitalization costs associated with one-month recovery from listeriosis were estimated at US$ 10.4 million[1]. According to the authors, the objective of this research was to determine the cost implications of the 2017 listeriosis outbreaks in South Africa on morbidity and hospitalization costs, mortality, and productivity losses to affected individuals.

The cost calculator of Listeria foodborne illness produced by the USDA Economic Research Service was used to compute costs associated with listeriosis outbreaks in South Africa. The computation had low, average, and high cost listeriosis-case outbreak scenarios. The components of listeriosis losses were estimated as direct and indirect costs. The direct costs were computed from valuation of human life (value of statistical life ($/person) × deaths from outbreak), hospitalization costs (mean cost of regular or internal care unit ($/person) × number of hospital cases), work losses from Listeria affected individuals was computed as mean productivity loss ($/person × number of cases missing work).[2]

The human impacts and health outcomes associated with listeriosis outbreak were derived from the listeriosis situation report. These included sick individuals but those who did not go to the doctor (costs can’t be quantified), sick and went to the doctor, and hospitalized with final outcomes within time periods (costs measured), sick and hospitalized without a final outcome (costs could not be measured). Data for hospitalization consisted of adolescent, mothers, children, infants (newborn to <28 days). The hospitalized outcomes for infants, children, and adolescents were based on age groups with morbidity and mortality records for cost analyses.

In order to calibrate the ERS model for South African conditions, we evaluated mortality compensation values from Miller which were estimated for all countries in the world through meta-analysis of available global data to derive ranges of multipliers (global average ~120) required to convert per capita GDP to the estimated value of a human life. These multipliers estimated for South Africa were used to derive the minimum to maximum range of life valuation for the analysis. Therefore, mortality cases were assigned compensation values of US$ 1,244,747 and US$ 2,524,312 per fatality for minimum and maximum human life valuation adjusted for South Africa which was 15% to 80% of U.S. values. Compensation values for mortality were derived by adjusting current South African per capita GDP by estimated multipliers. These values were then multiplied by the average percent (64.94%) of South African life expectancy remaining for all age-classes specific to the 204 outbreak fatalities.

In this computation, the South African hospital costs per patient were assumed to be 12.1% of U.S. hospital costs. The medical cost estimates included the average costs per care of regular hospitalization due to listeriosis for intensive care units (ICU) based on South African conditions. We excluded the cost computations for chronic cases of listeriosis, as data on disability attributed to listeriosis were not readily available and chronic conditions have yet to manifest themselves. In some instances, the outcomes of hospitalization were still pending (have not yet been determined).

Productivity losses (the average number of work days) due to listeriosis outbreak was assessed, on the assumption that able-bodied working age (15 to 64 years old) individuals were gainfully employed. The productivity losses per case were computed for a duration of one month, as this was the estimated duration of hospitalization and medical recovery from listeriosis for acute or non-fatal cases and pending in which case outcomes have not yet been determined (185 cases of 15-49 years old and 34 cases of 50-64 years old) as well as 89 (15-49 years old) and 26 (50-64 years old) cases discharged from hospitalization. Lost income during hospitalization was computed using the average monthly income in South Africa.

The outbreak of listeriosis contamination of polony and associated deli meat products led to serious health consequences for consumers in South Africa. Listeriosis occurrences were recorded in all nine provinces in South Africa. Among the provinces, confirmed listeriosis ranged from 6 to 606 cases with mortality of 3 to 106 cases. Overall, there were 1,034 total confirmed listeriosis cases with 204 fatalities. Listeriosis was recorded on babies (≤ 28 days old) to adults over 65 years old. The total cases varied among age groups as 441 cases were babies and 83 cases were > 65 years old. The number of fatalities was lowest for those > 65 years old, and highest for infants. No data were available on the exact ages of listeriosis-affected individuals due to confidentiality regulations. Reports indicated that all individuals diagnosed with listeriosis had consumed polony or deli meat contaminated with L. monocytogenes.

The total valuation of mortalities over the 16 months of the outbreak ranged from US$ 265 million using the low valuation for a fatality to US$ 525 million using the high valuation. At both one year (52 weeks) and at the recall for contaminated product at 62 weeks of listeriosis, the cumulative costs of listeriosis were already approaching values similar to the total estimated cost for listeriosis for both minimum and maximum estimates. The South African Rand (ZAR) equivalent cost estimates are also presented.

There was a total of 544 adults, where hospitalized cases consisted of 338 adults and 92 mothers, while mortality totaled 114 cases. Hospitalized newborn recovery from listeriosis totaled 400 cases with 90 mortalities. For adolescents and adults greater than 15 years of age or those in unknown age groups, there were 285 cases. The hospitalized adolescents and adults over 15 years old or those with unknown ages and with pending outcome of hospitalization from foodborne listeriosis had 145 cases. There were 255 hospitalized newborns that recovered, while newborns with pending outcome comprised 145 listeriosis cases. The total mortality costs for 204 individuals was at least US$ 265 million. The hospitalization costs for babies born with listeriosis were estimated at US$ 15,840 per case with a total estimated cost of over US$ 6 million. The mortality cases of babies born with listeriosis computed based on standards amounted to US$ 1.28 million/case for a total cost of US$ 115 million. For the adults, the medical costs for maternal hospitalization cases amounted to over US$ 364,000, while for other adults and deceased adults, hospitalization costs were over US$ 1.3 million and US$ 902,000, respectively. The costs associated with the mortality of 114 adults attributed to listeriosis amounted to over US$ 145 million. The total costs associated with the projected hospitalization were US$ 10,367,280. Hospitalization costs per case varied at US$ 15,840/case for babies, US$ 7,920/case for hospitalized older individuals that died, and US$ 3,960/case for being hospitalized.[3]

The total losses in one month of lost productivity for maternal, adult cases was computed as US$ 184,276 at US$ 2,003 per case. For other adults with moderate cases (no mortality recorded) of listeriosis, loss productivity was computed at US$ 1,230 per case totaling US$ 415,740. Productivity losses were only 0.22% of listeria outbreak costs.[4]

And, if anyone ever questions why surveillance and prevention of foodborne illness makes economic sense:


[1] According to the authors, in Sub-Saharan Africa (South Africa inclusive), costs associated with foodborne pathogens and illnesses are not precisely known, as many cases go unreported or have incomplete diagnosis (De Noordhout et al., 2014).

[2] The direct costs that were not estimated consisted of: current and future value of outpatient care and medication costs to treat chronic and acute cases, future cost of human suffering and lost productivity.

[3] The drawbacks for this study are that there were some direct and indirect costs that could not be quantified due to medical confidentiality issues that were excluded from the analyses. These include medication costs, sampling, laboratory/diagnosis costs, administrative costs, surveillance costs, the long-term effects of listeriosis on affected individuals in South Africa and possibly other countries.

[4] According to the authors, no attempt was made to quantify disability-adjusted life years (DALY, where one DALY equals one year of healthy life lost, that was attributed to listeriosis), due to lack of specific data (exact ages, case severity, and duration) of affected individuals. Therefore, hospitalization costs were assumed to be the same for all cases.

Following the declaration of the Listeria outbreak in December 2017, a multi-sectoral outbreak response was initiated. Findings were shared by the Minister of Health, Dr. Aaron Motsoaledi at a public media briefing on 4 March 2018 (statement available at www.nicd.ac.za), and are summarized below. In addition, the National Department of Health requested a full recall of implicated processed meat products.  According to Dr. Aaron Motsoaledi:

In our constant search for the source of the outbreak and the treatment of people who are affected, a team from the NICD has interviewed 109 ill people to obtain details about foods they had eaten in the month before falling ill. Ninety-three (85%) people reported eating ready-to-eat (RTE) processed meat products, of which polony was the most common followed by viennas/sausages and then other ‘cold meats’.

On Friday 12th January, nine children under the age of 5 years presented to Chris Hani Baragwanath Hospital with febrile gastro-enteritis. The paediatrician suspected foodborne disease, including listeriosis, as a possible cause. The environmental health practitioners (EHPs) were informed and on the same day visited the crèche, and obtained samples from two unrelated polony brands (manufactured by Enterprise and Rainbow Chicken Limited (RCL) respectively) and submitted these to the laboratory for testing.

Listeria monocytogenes was isolated from stool collected from one of the ill children, and from both of the polony specimens collected from the crèche. These isolates were sent to the NICD Centre for Enteric Diseases, and underwent whole genome sequencing and genomic analysis. The ST6 sequence type was confirmed on all three isolates on Saturday 27th January. Remember that in the last press conference I informed you that from clinical isolates obtained from patients (patient blood), 9 sequence types of Listeria monocytogenes were isolated and 91% were of sequence type 6 (ST6). We had then concluded that time that this outbreak is driven by ST6.

Following the lead from the tests performed on these children from Soweto and the food they had ingested, the EHPs (Environmental Health Practitioners), together with the NICD and DAFF representatives, accompanied by 3 technical advisors from the World Health Organisation in Geneva, visited a food- production site in Polokwane and conducted an extensive food product and environmental sampling.

Listeria monocytogenes was isolated from over 30% of the environmental samples collected from this site, which happens to be the Enterprise factory in Polokwane.

To conclude the investigation, whole genome sequencing analysis was performed from this Enterprise factory and the results became available midnight or last night. The outbreak strain, ST6, was confirmed in at least 16 environmental samples collected from this Enterprise facility. 


According to the Centre for Enteric Diseases (CED) and Division of Public Health Surveillance and Response, Outbreak Response Unit (ORU), National Institute for Communicable Diseases (NICD)/ National Health Laboratory Service (NHLS) the current number of ill and deceased are as follows:

As of 26 July 2018, 1060 laboratory-confirmed listeriosis cases have been reported to NICD from all provinces since 01 January 2017.

To date, 749 cases were reported in 2017, and 311 cases in 2018. Females account for 56% (549/979) cases where gender is reported. Neonates ≤28 days of age are the most affected age group, followed by adults aged 15 – 49 years of age. Most cases have been reported from Gauteng Province (58%, 614/1060) followed by Western Cape (13%, 136/1060) and KwaZulu-Natal (8%, 83/1060) provinces. Final outcome data is available for 76% (806/1060) of cases, of which 27% (216/806) died.

218 sick

28 with hemolytic uremic syndrome

5 deaths

In 2018 in the United Sates, 210 people infected with the outbreak strain of E. coli O157 were reported from 36 states. 96 people were hospitalized, including 27 people who developed a type of kidney failure called hemolytic uremic syndrome (HUS). 5 deaths were reported from Arkansas, California, Minnesota (2), and New York. In Canada, 8 cases of E. coli O157 that were genetically similar to the U.S. outbreak linked to romaine lettuce coming from the Yuma growing region in the U.S. The 8 Canadian illnesses were reported in 5 provinces: British Columbia, Alberta, Saskatchewan, Ontario and Quebec. 1 of the Canadian cases was hospitalized with HUS and no deaths were reported in Canada.

Health officials in both Canada and the U.S. have worked hard to do the hard epidemiological and environmental investigations that lead to traceback and root cause analysis that lead to new ways of preventing these tragedies for the consumers and the producers.  However, the hard work is essentially done in obscurity with little or no transparency.  Through the litigation process we are cracking open the door so the public can see both where product was grown (more to come on that in the coming weeks) and were the product was sold.



We have a romaine E. coli case in Idaho of a young man who suffered a severe case of hemolytic uremic syndrome (HUS), was hospitalized for a month and incurred nearly $250,000 in medical expenses and lost wages.  He has a risk of future kidney complications (including a transplant), but not likely to meet the legal standard of more likely than not – greater than 50%.  He did suffer seizures because of the HUS, but it is well maintained on medications, and it is hopeful, over time, that he may well be weaned off the medications and be able to drive again.  Under Idaho law he will be able to recover wage loss and medical expenses (economic damages) and a capped amount for nonmonetary losses (pain and suffering) – Well, unless a court and a jury determines that it is “reckless misconduct” to grow, process and sell romaine lettuce.

Sometimes bad facts make good law – recall the lawsuit against the auditor in the Jensen Farms Listeria cantaloupe case?

Idaho Code § 6-1603 established in 2003 a cap of $250,000.00 for noneconomic damages, damages that are subjective, nonmonetary losses including, but not limited to, pain, suffering, inconvenience, mental anguish, disability or disfigurement incurred by the injured party; emotional distress; loss of society and companionship; loss of consortium; or destruction or impairment of the parent-child relationship. Idaho Code § 6-1603(1) also provides for an annual adjustment tied to the increase or decrease of the annual wage; for 2018, the effective cap was established at $357,210.62.

The full text of the statute reads as follows:

6-1603.  LIMITATION ON NONECONOMIC DAMAGES. (1) In no action seeking damages for personal injury, including death, shall a judgment for noneconomic damages be entered for a claimant exceeding the maximum amount of two hundred fifty thousand dollars ($250,000); provided, however, that beginning on July 1, 2004, and each July 1 thereafter, the cap on noneconomic damages established in this section shall increase or decrease in accordance with the percentage amount of increase or decrease by which the Idaho industrial commission adjusts the average annual wage as computed pursuant to section 72-409(2), Idaho Code.

(2)  The limitation contained in this section applies to the sum of: (a) noneconomic damages sustained by a claimant who incurred personal injury or who is asserting a wrongful death; (b) noneconomic damages sustained by a claimant, regardless of the number of persons responsible for the damages or the number of actions filed.

(3)  If a case is tried to a jury, the jury shall not be informed of the limitation contained in subsection (1) of this section.

(4)  The limitation of awards of noneconomic damages shall not apply to:

(a)  Causes of action arising out of willful or reckless misconduct.

(b)  Causes of action arising out of an act or acts which the trier of fact finds beyond a reasonable doubt would constitute a felony under state or federal law.

Setting aside the fairness of capping noneconomic damages at $357,210.62 for a case as serious as this one, the real issue is whether the cap applies at all under section (4)(a) above?  In 2018 was it “reckless misconduct” to grow, process, source and sell romaine lettuce from Yuma?

Certainly, as well cited above, leafy greens have been a source of E. coli-related illnesses for decades, and there have been concerns raised about lettuce grown in the Yuma region.  The CDC reports as of May 20, 2010, a total of 26 confirmed and 7 probable cases related to an E. coli O145 outbreak have been reported from 5 states since March 1, 2010 linked to shredded romaine grown in Yuma.[1] In the FDA’s “Environmental Assessment Report in December 2010,” the authors determined:

that the R.V. park is a reasonably likely potential source of the outbreak pathogen based upon the evidence of direct drainage into the lateral irrigation canal; the moist soil in this drainage area; the multiple sewage leach systems on the property; the presence of other STEC found in the lateral irrigation canal and in the growing fields of the suspect farm; and the fact that the section of the lateral canal downstream from the R.V. park supplies water to only one other farm in addition to the suspect farm.

Two pumps are located on the main Wellton canal near the lateral canal split that supplies water to fields of the suspect farm; one gasoline powered pump on a trailer and one permanent electric pump with an attached hose. The electric pump supplies canal water to an attached open-end hose. The site is not secured from vehicles and the hose pump is also unsecured. At the time of this investigation there were people living in recreational vehicles on undeveloped land within one mile of the hose pump. The fact that this area is open to vehicles and the pump and hose are unsecured make it possible for an R.V. owner to dump and rinse out their R.V. septic system into the main Wellton canal at the lateral canal split that supplies the farm. The ground near the hose pump shows erosion evidence of drainage into the Wellton canal. Soil collected from this erosion site tested positive for other Stx2-producing STEC but did not match the outbreak strain.

In a 2009 “Survey of Selected Bacteria in Irrigation Canal Water – Third Year” written by Jorge M. Fonseca, he correctly predicted the human and industry problems that were likely to plague the Yuma lettuce growers:

Despite the fact that no Arizona lettuce grower has been involved in any contaminated-lettuce outbreak, it is of paramount importance to determine the reasons why Arizona lettuce is regarded as safe. This can help lower possibilities of any emerging problem and prevent a catastrophic damage to the industry, as it has occurred in other regions when no control was taken to reduce risks of contaminated product.

A PowerPoint done by Dr. Fonseca again illustrated the varying risks of lettuce production in Yuma.  An example of a few of his points of concern:

And, then the 2018 romaine lettuce E. coli outbreak struck, sickening hundreds in the United States and Canada with dozens suffering from acute kidney failure with five reported deaths.  Once again, the Wellton Irrigation Canal was the focus of attention in the “Memorandum to File on the 2018 Environmental Assessment”:

During this EA, three samples of irrigation canal water collected by the team were found to contain E coli O157:H7 with the same rare molecular fingerprint (using whole genome sequencing (WGS)) as the strain that produced human illnesses (the outbreak strain). These samples were collected from an approximate 3.5-mile stretch of an irrigation canal in the Wellton area of Yuma County that delivers water to several of the farms identified in the traceback investigation as shipping romaine lettuce that was potentially contaminated with the outbreak strain. The outbreak strain was not identified in any of the other samples collected during this EA, although other pathogens of public health significance were detected.


Not surprisingly, the FDA in its full “Environmental Assessment of Factors Potentially Contributing to the Contamination of Romaine Lettuce Implicated in a Multi-State Outbreak of E. coli O157:H7,”[2] concluded that the risk of environmental contamination was in fact a well-know and long-standing risk:

Food safety problems related to raw whole and fresh-cut (e.g., bagged salad) leafy greens are a longstanding issue. As far back as 2004, FDA issued letters to the leafy greens industry to express concerns about continuing outbreaks associated with these commodities. FDA and our partners at CDC identified 28 foodborne illness outbreaks of Shiga-toxin producing E. coli (STEC) with a confirmed or suspected link to leafy greens in the United States between 2009 and 2017. This is a time frame that followed industry implementation of measures to address safety concerns after a large 2006 outbreak of E. coli O157:H7 caused by bagged spinach. STEC contamination of leafy greens has been identified by traceback to most likely occur in the farm environment.

Contamination occurring in the farm environment may be amplified during fresh-cut produce manufacturing/processing if appropriate preventive controls are not in place. Unlike other foodborne pathogens, STEC, including E. coli O157:H7, is not considered to be an environmental contaminant in fresh-cut produce manufacturing/processing plants.

Well-established reservoirs for E. coli O157:H7 are the intestinal tract of ruminant animals (e.g., cattle, goats, and deer) that are colonized with STEC and shed the organism in manure. Ruminant animals colonized with STEC typically have no symptoms. In contrast, human infection with E. coli O157:H7 usually produces symptomatic illness often marked by severe, often bloody, diarrhea; severe adverse health outcomes or even death can result. Humans shed E. coli O157:H7 in the stool while ill and sometimes for short periods after symptoms have gone away, but humans are not chronic carriers. Various fresh water sources, including municipal well, and recreational water, have been the source of E. coli O157:H7 infections in humans, as has contact with colonized animals at farms or petting zoos. However, most E. coli O157:H7 infections in humans occur from consuming contaminated food.

In its summary of its environmental findings (also summarized in a November 1, 2018 to public officials) the “FDA [in part] identified the following factors and findings as those that most likely contributed to the contamination of romaine lettuce from the Yuma growing region with E. coli O157:H7 that caused this outbreak”:

  • FDA has concluded that the water from the irrigation canal where the outbreak strain was found most likely led to contamination of the romaine lettuce consumed during this outbreak.
  • There are several ways that irrigation canal water may have come in contact with the implicated romaine lettuce including direct application to the crop and/or use of irrigation canal water to dilute crop protection chemicals applied to the lettuce crop, either through aerial or ground-based spray applications.
  • How and when the irrigation canal became contaminated with the outbreak strain is unknown. A large animal feeding operation is nearby but no obvious route for contamination from this facility to the irrigation canal was identified. Other explanations are possible although the EA team found no evidence to support them.

Idaho Code Section 6-1603(4)(a) states that the statutory limit on non-economic damages in tort actions seeking damages for personal injury or death does not apply in cases where the cause of action arises “out of willful or reckless misconduct.” Idaho Pattern Civil Jury Instruction 2.25 provides the definition of “willful and wanton,” and notes that there is no distinction between “reckless” and “willful and wanton.” Hennefer v. Blaine County Sch. Dist. 61 158 Idaho 242, 248 (2015). According to the IDJI, “[t]he words ‘willful and wanton’…mean more than ordinary negligence. The words mean intentional or reckless actions, taken under circumstances where the actor knew or should have known that the actions not only created an unreasonable risk of harm to another, but involved a high degree of probability that such harm would actually result.” IDJI 2.25

While Idaho considers reckless or willful misconduct “simply a degree of negligence…that involves both intentional conduct and knowledge of a substantial risk of harm,” its courts have further elaborated that while “use of the words ‘intentional’ and ‘knowledge’ might indicate a purely subjective standard for recklessness…there is an objective element to the recklessness standard.” Hennefer 158 Idaho at 248.  Thus, while reckless misconduct can consist of a conscious choice of a course of action with knowledge of the serious danger to others, (subjective), it can also consist of a conscious choice of a course of action with knowledge of facts that would disclose the danger to any reasonable man (objective). Id. The serious danger mentioned in the standard is one that “involves a risk substantially greater in amount than that which is necessary to make the conduct negligent.” Id. Accordingly, a jury need only find that a defendant should have known that his actions created a high probability that harm would actually result; such a finding is considered sufficient to meet the standard espoused by Idaho Code section 6-1603. Id. at 249.

Using this standard, there is substantial evidence supporting the conclusion that growing, processing, sourcing, and selling romaine lettuce from Yuma constituted reckless misconduct. It is widely known that STEC infections are life-threatening to humans and the most common cause of infection is consumption of contaminated food. Additionally, STEC outbreaks associated with leafy greens are unsettlingly common occurrences as evidenced by the 28 identified outbreaks occurring between 2009 and 2017. The FDA, CDC, and other governmental agencies have sought to combat the frequency of these occurrences by issuing various communications with state officials, publishing the results of its investigations into the outbreaks, and advising on best practices to avoid such outbreaks.

Among the FDA’s many suggestions, it recommended that the leafy green industry should assess the need for and develop commodity-specific procedures, policies, and best practices to enhance the safety of leafy greens, including, at a minimum, address (1) how agricultural water directly contacting harvestable portions of the crop can be guaranteed safe and adequate for its intended use; (2) how risks related to land uses near or adjacent to growing fields that may contaminate agricultural water or leafy green crops directly (e.g., nearby cattle operations or dairy farms, manure, or composting facilities) can be assessed and mitigated; (3) how food safety procedures, policies, and practices are developed and consistently implemented on farms as well as regularly verified to minimize the potential for contamination and/or spread of human pathogens; and (4) how a root cause analysis should be performed to determine the likely source of any contamination by a foodborne pathogen identified in the agricultural environment, agricultural water, or in the fresh-cut ready-to-eat produce.

Given the available knowledge regarding STEC, its transmission to and effect on humans, as well as the nature—and demonstrated prior history— of STEC transmission from ruminant animal operations to leafy greens and the repeated government advisory and caution of that danger, the undeterred insistence of growing, processing, sourcing, and selling romaine lettuce from a region repeatedly plagued by STEC contamination and subsequent outbreaks is a considerably reckless activity. The findings from the 2018 romaine lettuce outbreak considerably enhance the veracity of that conclusion. Despite all the aforementioned knowledge, the source of the 2018 outbreak that affected hundreds and killed five was found to be a contaminated irrigation canal that supplied water to several farms identified in the traceback investigation who were downstream from a sizeable cattle operation. Such undeterred action in spite of the substantial available knowledge on the risks developed and disseminated over the years fits squarely within Idaho’s characterization of reckless misconduct and should accordingly be treated as such.


[1] https://www.cdc.gov/ecoli/2010/shredded-romaine-5-21-10.html

[2] https://www.fda.gov/Food/RecallsOutbreaksEmergencies/Outbreaks/ucm624546.htm

I have been talking about food safety and litigation for the last few decades.  The groups I have spoken to have been all types in the food industry – from beef to leafy greens – as well as the heroes of public and environmental health.  I had a chance today  to talk to leaders in the insurance industry about how they can save money by encouraging their insureds to put food safety first.

According to the CDC, since the last update on December 21, 2018, 63 ill people from 24 states, and the District of Columbia, have been added to this investigation.

As of February 13, 2019, 279 people infected with the outbreak strain of Salmonella Reading have been reported from 41 states and the District of Columbia. 107 people have been hospitalized. One death has been reported from California.

Epidemiologic and laboratory evidence indicates that raw turkey products from a variety of sources are contaminated with Salmonella Reading and are making people sick. In interviews, ill people report eating different types and brands of turkey products purchased from many different locations. Four ill people lived in households where raw turkey pet food was fed to pets. The outbreak strain has been identified in samples taken from raw turkey pet food, raw turkey products, and live turkeys.

Several turkey products have been recalled because they might have been contaminated with Salmonella. Please see the list of recalled items below. A single, common supplier of raw turkey products or of live turkeys has not been identified that could account for the whole outbreak.

The Public Health Agency of Canada has identified ill people in Canada infected with Salmonella Reading bacteria with the same DNA fingerprint.  As of January 31, 2019, there have been 72 confirmed cases of Salmonella Reading illness investigated in the following provinces and territories: British Columbia (20), Alberta (24), Saskatchewan (6), Manitoba (13), Ontario (6), New Brunswick (1), Northwest Territories (1), and Nunavut (1). Individuals became sick between April 2017 and early January 2019. Eighteen individuals have been hospitalized. One individual has died. Individuals who became ill are between 0 and 96 years of age. The majority of cases (55%) are female.

The outbreak strain of Salmonella Reading is present in live turkeys and in many types of raw turkey products, indicating it might be widespread in the turkey industry. CDC and USDA-FSIS have shared this information with representatives from the turkey industry and requested that they take steps to reduce Salmonella contamination.