I am always a bit humbled when a victim of food poisoning stands up to the corporations who poisoned them with food – especially food labeled “triple washed” and “ready to eat.”
Jane and Ben Majeska have been married 60 years in August 2009. Their marriage never faced a challenge in those years of the sort that they endured in the fall of 2006. Were it not for her consumption of Dole spinach, September and October of 2006 would have been two more precious months spent active, happy, and together. Instead they were excruciating and terrifying. The impacts of Jane’s HUS involved nearly every body system. The extraordinary efforts of her doctors and Jane’s remarkable strength and will meant the difference between life and death. Jane reflects, and recalls her children consulting the folders where they kept their parent’s funeral plans and end of life wishes. Medical bills to date are nearly $500,000. The Majeskas deserve to be compensated for their deep suffering. To quote, I am sure someone famous, “We will see you in Court!” Here is the Majeska’s story:
JANE MAJESKA’S E. COLI O157:H7 INFECTION
A. The Beginnings of Illness
Jane Majeska is 86 years old and lives in Fond du Lac, Wisconsin with her husband of 60 years, Ben. Together, they are the parents of four grown children. Notwithstanding her age, Jane was very active and healthy. In the weeks to follow, as she fought for her life, many of her physicians reported her excellent prior health. For example, she belonged to the YMCA, and exercised there at least twice weekly.
In late August 2006, Jane consumed Dole baby spinach that she had purchased at the Pick ‘n Save in Fond du Lac. She had, up to that point, enjoyed excellent health. But on September 3, 2006, she developed abdominal cramps and watery diarrhea. The following morning her diarrhea turned bloody, and she also started to feel lightheaded and extremely nauseated. This sudden and unexplained onset of bloody diarrhea, prompted her to go to the ER at St. Agnes Hospital.
B. St. Agnes Hospital: September 4 through September 11, 2006
The Emergency Room
Ben took Jane to the ER at St. Agnes Hospital the morning of September 4. They were accompanied by their son, James. She was initially evaluated by the triage nurse, who noted that Jane had no fever, but was somewhat orthostatic, meaning her heart rate and blood pressure was elevated when standing. She was soon assisted to a bed, where she was then examined by John McCullough, MD. He reported that Jane was suffering from abdominal cramping and bloody diarrhea, along with sweats and generalized weakness.
Dr. McCullough ordered that Jane undergo an EKG and abdominal x-rays. Blood samples were drawn, and she was started on intravenous (IV) fluids. There in the emergency room, she continued to suffer bouts of bloody diarrhea. The blood samples were tested and revealed that her white blood cell count was elevated, indicating an infection.
Admission to the Hospital
While in the emergency room, Jane was seen by gastroenterologist, Gabriel Litman, MD. After advising that Jane needed to be admitted to the hospital, Dr. Litman prescribed continued IV fluids, Protonix and Pepcid to minimize gastric acidity, and Zofran for her nausea. Despite the treatment she was receiving, Jane continued to struggle. Late that night she spiked a fever, and became both hypertensive (high blood-pressure) and tachycardic (rapid heartbeat). The records document that, since admission at 4:00 PM, she had suffered ten bouts of bloody diarrhea.
During her first full day in the hospital, September 5, Jane suffered from persistent rectal bleeding. She was evaluated by another gastroenterologist, Robert Mikkelsen, MD, who decided to prescribe antibiotics. Dr. Mikkelsen also recommended the scheduling of a colonoscopy. Later that day, the results of a stool culture came back negative for Giardia and Cryptosporidium, and the Clostridium difficile toxin assay was negative as well.
The Development of HUS
Over the following three days, Jane’s condition worsened notably. While she continued to suffer from bloody diarrhea, the results of the around the clock testing of her blood and urine began to demonstrate a number of disturbing trends:
• her white blood cell count rose to abnormal levels, indicating infection, and thus prompting Michael Sergi, MD to diagnose Jane as having “infectious diarrhea.”
• her platelet count fell below normal, a condition known as thrombocytopenia.
• Her blood urea nitrogen (BUN) and creatinine levels rose alarmingly, a clear sign of deteriorating kidney (or renal) function.
• Blood and protein were found in her urine, also a sign of kidney failure.
• Her urinary output decreased dramatically, again showing renal decline.
• Her hemoglobin levels and hematocrit declined, reflecting anemia.
• Urinalysis demonstrated trace blood, protein and moderate bacteria.
After the increasing number of doctors involved in Jane’s care learned of these trends, the diagnosis emerged. General medicine specialist, H.K. Saleh, MD reviewed the results and noted the worsening thrombocytopenia and worsening acute renal failure. In light of Jane’s progressive renal failure, Dr. Saleh asked nephrologist Edward Lake, MD to consult. Dr. Lake’s diagnostic impression was “acute, progressive non-oliguric renal failure” and, therefore, likely “HUS/TTP.” Hematologist, Joel Lundberg, MD was subsequently asked to consult, and his impression was thrombocytopenia, hemolytic anemia, and renal insufficiency, all consistent with HUS. Thus, the diagnostic consensus was that Jane was suffering from HUS secondary to infectious diarrhea.
Against the backdrop of this gloomy diagnosis, Jane continued to suffer frequent bouts of diarrhea and severe abdominal cramps. She was treated with hydromorphone for the worsening pain. The nurses described her as appearing shaky and pale, “having difficulty expressing self; unable to finish a sentence and somewhat confused and disoriented…feeling out of it.” The doctors became increasingly concerned with what they termed “mental status changes.” For her part, Jane recalls, “I was losing the ability to communicate with my family. I was frightened.”
As a result of her quickly deteriorating condition, Jane was transferred to the intensive care unit (ICU) on September 10. At this time, she was being treated with Lasix and Diuril in and attempt to assist her failing kidneys in producing urine. She was also still receiving antibiotic treatment, as well as Xopenex to assist her breathing. The placement of a PICC (peripherally inserted central catheter) line was ordered to provide intravenous nutrition. The nurses now described Jane as anxious, wheezing, and disoriented.
Blood tests conducted in the early morning hours on September 11, continued to evidence her worsening condition—nothing was improved, and everything appeared worse. It was clear at this point that Jane’s condition had significantly deteriorated. Dr. Lundberg felt that her clinical picture was consistent with HUS, and that she needed plasmapheresis. Given the progressive decline, Dr. Sergi contacted the intensivists at St. Luke’s Hospital and the decision was made to transfer Jane there to the care of Rakesh Waghray, MD.
C. St. Luke’s Medical Center: September 11 – October 15, 2006
Jane was transported via Brooks Ambulance to St. Luke’s Medical Center, and arrived at 11:55 AM. She was directly admitted to the medical/respiratory intensive care unit (MRICU). The results of tests ordered by Dr. Waghray revealed a continued worsening of HUS, including decreased renal function, worsening anemia, and worsening thrombocytopenia. An EKG showed rapid ventricular response—a type of abnormally fast heart-rate that is quite dangerous.
Joining Dr. Waghray in treating Jane was Rubina Qamar, MD, a hematologist, and Todd Muche, MD, a nephrologist. Each doctor evaluated Jane on her first day at St. Luke’s. Dr. Qamar, who agreed with the HUS diagnosis, thought that Jane was swiftly deteriorating, and that she urgently needed to undergo plasmapheresis and a blood transfusion to treat the anemia. Jane was also exhibited mild tremors, seemed confused, and was unable to follow simple commands. Dr. Qamar expressed concern about new-onset arrhythmia (atrial fibrillation), and low blood pressure, and had an extensive discussion with the family members about all of this. Dr. Muche then completed his evaluation, agreed with the HUS diagnosis, and recommended her immediate preparation for plasmapheresis and dialysis.
To prepare for dialysis and plasmapheresis, the critical care specialist, Krishna Neni, MD, surgically implanted a femoral vascular catheter. Not long after the surgery, Jane underwent plasmapheresis with fresh frozen plasma (FFP). Throughout the procedure, she was described as appearing pale and confused, with rapid breathing.
Jane’s family continued the vigil at her bedside that began with her first hospitalization at St. Agnes. Her husband Ben was 89 years old at the time. Their daughter, Barbara Becker, took Ben to live with her. Every morning Barbara brought Ben to the hospital to sit by Jane’s side, and then she picked him up each night. This went on for week after week. In her moments of lucidity, Jane worried not so much for herself, but for her husband and the stress he was under.
September 12 and 13, 2006
On September 12, Jane received a blood transfusion in the morning that temporarily improved her anemia. By evening, however, the improvement was gone; her hemoglobin and hematocrit had fallen again. This day she also underwent a second plasmapheresis treatment, and her first round of hemodialysis. Throughout these treatments, Jane remained obviously confused. The physicians also continued to investigate the source of Jane’s atrial fibrillation, performing an echocardiogram. Unfortunately, the test results did not provide a clear answer.
Despite a full day of aggressive treatment, Jane’s condition continued to worsen. The test results from early in the morning, September 13, showed persistent anemia, thrombocytopenia and acute, non-oliguric renal insufficiency. Accordingly, Jane underwent both hemodialysis and plasmapheresis—these procedures trying to make up for the fact that her kidneys had failed.
That evening, around nine, Jane was “having a bath and became increasingly confused and agitated, with increasing heart rate and decreasing oxygen saturation levels.” She then suffered a tonic/clonic seizure. The family members at her bedside were terrified. Nurses called critical care specialist, Jeffrey Widell, MD to the bedside. Jane was semi-comatose when he arrived. Dr. Widell treated the seizure with a dose of Phosphenytoin and started an Ativan drip.
In light of the seizure, Dr. Widell determined that Jane was unable to protect her airway and was at risk for aspiration. As a result, the decision was made that it was unsafe to allow Jane to breathe on her own. She was intubated and placed on mechanical ventilation. Because of continuing concerns about her mental status a procedure at the hospital called, “Stroke Team” was activated. A CT scan of the brain and neurology consult were ordered. Jane recalls that: “According to my family, I didn’t know who they were. I couldn’t communicate with them.”
Family members were told that her prognosis was grim. But still they hoped and prayed.
September 14, 2006
At this point, it was hard not to feel like Jane was slipping irretrievably away. But for the plasmapheresis and dialysis, the blood transfusions, and the mechanical ventilation, there was no way that Jane would be alive. The results of morning blood test results showed some fluctuation, but the overall picture was unchanged. She ran a fever that day, and her blood pressure was high as well. Jane got the day off from hemodialysis, but underwent a round of plasmapheresis.
Her physicians spent much of the day attempting to address her neurological difficulties. In the morning, Jane was transported to the radiology department for CT scan of the head. There was evidence of mild atrophy but no acute findings. Following this, a neurological consultation was performed by Nihal Hurath, MD. Jane was noted to be semicomatose, with sustained leg stiffening, and biting of the endotracheal tube. Dr. Hurath conducted a neurological exam that found small, sluggish pupils, twitching of the upper lip, and spontaneous movement of the legs. After then undergoing an EEG, Dr. Hurath summarized his findings: “highly abnormal with diffuse bihemispheric cortical neuronal dysfunction, such as is seen in toxic metabolic hypoxic encephalopathy.” A short time later, Jane was transported to radiology for MRI of the brain. There was no evidence of intracranial hemorrhage or acute ischemia.
Later that evening, Jane began to suffer from increased respiratory distress. Dr. Qamar was notified, and concluded after testing and evaluation that Jane was suffering from respiratory alkalosis. As the day closed, Jane remained unresponsive, breathing via the ventilator, showing no signs of recovery, and few signs of life. Ben told his children that he did not want to live without Jane. They silently wondered if he would have a choice:
We feared for her death. She was on life support. There were considerations about terminating life support. In fact, we had a “death folder” made with regard to her funeral arrangements and we had that available at the hospital at all times.
September 15-17, 2006
Over the next three days hopes dimmed. Despite round-the-clock supportive care, there were no signs of improvement. The best that could be said was that Jane was hanging on, which was to say, that she had not passed away.
Not surprisingly, Jane’s family was praying for some turn in a positive direction. As Jane now recalls: “At this time, the doctors told my children that they couldn’t do anything more for me. My daughter Ann asked the doctors to continue the life support for a while longer.”
And so the treatments continued. She underwent plasmapheresis during these three days, an received dialysis on two of them. In what amounted to the first positive sign in two weeks, Jane seemed to exhibit some responsiveness, and opened her eyes. She was still unable to move her upper extremities, however. By September 17, Jane appeared more alert, and was able to nod appropriately to questions. She remained unable to speak due to the ventilator.
September 18 – 20, 2006
Three more days passed, and Jane took some small steps forward in a few areas, while in others she continued to struggle. She was successfully weaned off the ventilator on September 18, and, on that same day, her platelet count returned to normal. But her urinary output continued to be very low, and she was still confused and disoriented. To offset the ongoing renal failure, Jane received hemodialysis on September 18, and plasmapheresis on September 19 and 20.
On September 20, Jane was evaluated by cardiologist, Atul Bhatia, MD, who determined that Jane’s supraventricular tachycardia had been caused by HUS. Dr. Bhatia recommended that she receive continued treatment with Cardizem, a calcium channel blocker that works by slowing electrical conduction in the heart, and thus slowing the heart rate, and normalizing heart rhythm.
Jane was also evaluated by an infectious disease specialist, Charles Brummitt, MD. Dr. Brummitt concurred with the HIS-diagnosis, and stated that he believed that it had been caused by an E. coli O157:H7 infection. He noted, in particular, that Jane’s daughter had found an open bag of spinach in the refrigerator, and that the spinach had been eaten prior to the onset of illness.
September 21, 2006
Jane had by now been at St. Luke’s for ten days. While she had withstood the potentially fatal first onslaught of HUS, it was daunting to catalog her ongoing problems. She continued to suffer from hemolytic anemia and kidney failure. Chest x-rays showed right-side pneumothorax, and persistent left pleural effusion. Her heart rate was irregular and tachycardic, with moderate elevations of her blood pressure. She was described as being “anxious, nonverbal, following commands, with obvious increased work of breathing.” Dr. Waghray ordered a left lung thoracentesis by the interventional radiologist, for removal of excessive fluid in the lungs, and to obtain a specimen for gram stain and culture. Dr. Qamar ordered another blood transfusion.
Since her admission, Jane had been receiving all of her nutrition intravenously. In order to evaluate the possibility of resuming oral nutrition, a “swallow study” was attempted by speech therapist, Stacy Bennett. But Jane was unable to follow commands, and made no attempts to speak or gesture. The study was thus abandoned and the intravenous nutrition was continued.
Jane underwent the lung thoracentis in the afternoon. Afterward, the placement of a naso-gastric tube caused profuse bleeding. Jane was “aggressively suctioned” and received oxygen until stabilized. Jane states: “My children told me I looked like I had been through a war after that procedure. I bled profusely.”
September 22 – 24, 2006
For three more days, Jane’s condition remained in limbo—neither getting notably better, nor getting notably worse. Even with repeat blood transfusions, anemia remained a problem, and her kidneys were barely functioning. She received plasmapheresis on September 22 and 25.
Jane also continued to suffer from cognitive trouble. She was described as intermittently confused and disoriented. On September 23, critical care specialist Dr. Goldman described Jane as “pale, disoriented and tachypneic at times, with abdominal distension and generalized edema.” His impression was respiratory insufficiency, anemia, renal insufficiency and HUS.
It was hard for Jane’s husband and family to keep up with each new medical challenge. On September 24, a chest x-ray showed evidence that Jane was suffering from a collapsed lung. That day, her blood pressure was also abnormally high. Her levels of LDH, a liver enzyme, had begun again to climb, a sign of increased hemolysis, the destruction of red blood cells.
September 25 – 28, 2006
On her fifteenth day at St. Luke’s Medical Center, there was a disturbing and confusing development. Despite the numerous blood transfusions, and the previous stabilization of her red blood cell counts, suddenly there were signs again of hemolysis—red blood cell destruction. Her hematocrit and hemoglobin had both fallen again. Moreover, her platelet count, which had been normalizing, was once more declining. As a result, Jane received another blood transfusion, and she underwent plasmapheresis.
Unfortunately, despite the transfusion, Jane’s platelet count continued to fall. Her doctors began to suspect that she was suffering from heparin-induced thrombocytopenia (HIT). HIT is essentially a complication that can arise from hemodialysis, and it is life threatening in its own right. It was thus decided that the drug-therapy that accompanied hemodialysis would be altered, and that Jane would be closely close-monitoring for the further development of HIT.
The speech therapist attempted another swallow-test on September 26, but Jane still could not coordinate swallowing with breathing. Sadly, as a result, Jane was forced to remain on intravenous nutrition—eating or drinking by mouth was just too dangerous. Indeed, the very next day Jane was coughing, and blood was noted in her “oral secretions.”
Jane’s abdomen had also become increasingly distended and painful. Nalini Guda, MD, a gastroenterologist, was called in to evaluate this development. After examining Jane, and her by now lengthy medical records, Dr. Guda concluded that the placement of a rectal tube would be necessary to provide “colonic decompression.” The tube was placed on September 28. Jane also received another round of plasmapheresis that day.
September 29 – October 3, 2006
The next five days were a real challenge for Jane and her family. Her red blood cell and platelet counts had continued to decline, despite aggressive treatment for HIT. But in a rare bit of positive news, there were signs that her kidney function was improving. This better news was more than offset, however, by the fact of Jane’s worsening respiratory distress. She had to be sedated, and placed back on mechanical ventilation. It was devastating blow for the family, who well understood that Jane being able to breathe on her own was necessary for her survival. Thus, despite their most fervent hopes, it started to seem like Jane might not survive.
Still on the ventilator the following day, the news for the family got even worse. Chest x-rays revealed that Jane was now also suffering from a pulmonary embolism—one more possibly fatal complication. She was treated with a drip infusion of an anti-coagulant, Argatroban, which her doctors thought should be effective.
On October 2, Jane received plasmapheresis again. Throughout the procedure, her heart-rate was significantly elevated and she was running a fever. She was still not close to producing normal amounts of urine—a sign that her kidneys still were not functioning as needed. Her red blood cell counts had been stable for several days, but once more started to decline. The next day blood tests suggested that her kidney function was declining again. Consequently, she underwent hemodialysis that afternoon, while a blood transfusion was given at the same time.
October 4 – 7, 2006
An awful milestone was reached: Jane had been in the hospital for a month. Thankfully, this day also saw the most significant improvement in her condition so far. Her platelet and red blood cell counts were both up, and her kidney function had improved as well. She was noted by her doctors as “very awake and well-oriented.” Even better, she was deemed stable enough to be removed from the ventilator—a fact that cheered her family incredibly.
The day was not without setbacks, however. Soon after the ventilation tube was removed, Jane became nauseated and vomited. Also, because her LDH was still elevated, she was treated with plasmapheresis again. Nonetheless, both her doctors and her family allowed themselves the hope that perhaps Jane had finally taken a solid turn for the better.
Over the next several days, everyone’s hope was rewarded; slow but steady progress was made. Of course, she still had a long way to go to be anywhere near recovered. On October 5, Jane’s LDH was normal for the first time since admission. Her renal function slipped, however, and she received hemodialysis. She complained of persistent nausea throughout the day. And the ongoing nausea interfered with another round of swallow therapy, meaning that she was forced to remain on intravenous feeding.
As if necessary to rein in otherwise unrealistic hopes of recovery, Jane’s anemia notably worsened on October 7. As a result, she was given yet another blood transfusion that day, again concurrent with another round of hemodialysis. But all in all progress was being made.
October 8 – 9, 2006
The next two days showed continued improvement of both her anemia and renal function. And, finally, for the first time, there was serious talk that she might be able to leave the hospital. Still, there were many things to consider. Jane continued to suffer some persistent nausea, and her abdomen was still much distended. Her heart rate remained irregular, and she was still not producing normal amounts of urine. She underwent hemodialysis again on October 9.
Preparations for Discharge
Steps towards discharge were now being undertaken. The first and most important one was that Scott Hardin, MD performed a rehabilitation consultation. Dr. Hardin noted that Jane had been previously very active, golfing frequently and exercising at the YMCA. At this point in her recovery, she was walking with a wheeled walker but fatigued easily and required minimal to moderate assistance to get out of bed. Dr. Hardin noted moderate muscle atrophy as well. In light his findings, Dr. Hardin recommended aggressive physical, occupational and speech therapy, and rehabilitation nursing. Psychiatric treatment would also likely be necessary. And all of this was to occur at St. Luke’s inpatient rehabilitation unit, and last for at least two weeks.
Amid preparations for discharge, Jane suffered through several setbacks. On October 10, 11, and 12, LDH levels rose again, and her anemia worsened. In addition, urine-production was still abnormally low, and BUN and creatinine remained abnormally elevated. Jane also continued to suffer from nausea. She passed the swallow test though, and was allowed liquid by mouth.
One other big problem was that Jane’s bowels still were not functioning. Dr. Pezanoski explained that weeks without oral intake, along with decreased intestinal motility, had essentially shut the colon down. This was leading to abdominal distention, and a complete lack of bowel movements. Recovering bowel function would become a focus of her rehabilitation stay.
Leaving the Hospital
Jane continued to improve. She received a blood transfusion on October 13, and her red blood cell counts increased as an expected result. Her renal function was improving too. Jane was still having bowel difficulty, however, and she was encouraged to sit on the toilet in fifteen-minute intervals to encourage bowel movements.
Finally, in the early morning hours of October 15, more than one month after admission, Jane was discharged to the rehabilitation center at St. Luke’s.
D. St. Luke’s Inpatient Rehabilitation Center: October 15 – 24, 2006
Dr. Hardin was in charge of Jane’s care at the Rehabilitation Center. During her stay, the issues that that needed to be addressed were numerous and daunting. Among these were:
• Persistent anemia. As late in her stay as October 20, Jane’s red blood cell counts were still both abnormal and decreasing. That same day the results of her LDH test showed evidence of continuing hemolysis.
• Urinary retention. With her kidneys finally producing urine, Jane was unable to void. Nurses had to use a catheter remove the urine. She was instructed how to use the catheter herself, but found the procedure, not surprisingly, uncomfortable.
• Lack of bowel movements. As with the final days at the main hospital, Jane went days without a bowel movement, and became increasingly uncomfortable. With the increase in oral foods, her condition slowly returned to normal.
As soon as the Jane began to improve, her old self started to return. She pursued physical therapy and occupational therapy spiritedly. By the time of discharge, she was able to walk with a cane, and required minimal assistance getting out of bed. Still, there remained some impaired balance and general weakness.
Jane was finally discharged on October 24. Her blood tests at that time still demonstrated mild, persistent anemia. Her BUN and creatinine were normal, but GFR was still low at 56. She was instructed to continue with in-home nursing services and occupational and physical therapy. General follow-up was scheduled with her PCP, Dr. Michael Sergi. She was also told to come to the lab for testing over the next several days as well. Finally, Jane’s discharge medications were Coumadin, Lasix, Potassium supplement, Cardizem, Catapres, Miralax, Senokot, and Flomax.
It is a testament to Jane Majeska’s physical and spiritual strength that she survived her bout with HUS. Still, an illness course as severe as the one that Jane endured carries risks. We asked nephrologist Richard Johnson, MD to address these risks, both generally and with respect to Jane. In discussing HUS survival, Dr. Johnson reports:
In those that do survive, it is common for renal function to resolve, which gives the false allusion that recovery is complete. However, long-term studies suggest that, while overall the situation is favorable, there still is a significant risk for complications… [including]:
• 3% to 16% developing end stage renal disease;
• 1% to 16% developing renal insufficiency;
• 0% to 20% developing hypertension earlier than expected;
• 15% to 31% developing proteinuria;
• 2% to 28% developing mild depression in measured glomerular filtration rate (GFR).
These risks, which are created by HUS, carry their own sequellae as well. For example, Dr. Johnson points out that hypertension is well known to increase the risk factor for stroke and congestive heart failure. In addition, Dr. Johnson states that “the main risk for mildly reduced renal function is not the risk of progressing to end stage renal disease but rather the risk for developing hypertension or cardiovascular events.”
Dr. Johnson then turned to discussing Jane’s own prognosis. As an initial matter, he noted that “The diagnosis of E. coli O157- associated HUS is very likely in this case.” In discussing Jane’s HUS, he termed it “fairly severe” and noted the “many acute complications” she suffered, including volume overload, cardiac arrhythnias, significant acute mental status changes, and oliguric renal failure requiring hemodialysis. Looking forward, Dr. Johnson states:
We know from experimental studies that the renal repair process in HUS is unlikely to be complete, and that some degree of permanent renal injury and scarring likely persists. In a younger person this can translate into increased risk for cardiovascular events, particularly after 10 to 20 years. In her case, the subtle, persistent renal injury is unlikely to affect her longevity due to the fact that she already in her early 80’s…It does make sense to monitor her renal function and blood pressure every 6 months. In the event that she develops low grade proteinuria or hypertension, I would recommend the use of ACE inhibitors.
THE 2006 DOLE E. COLI O157:H7 SPINACH OUTBREAK
A. Ignoring the Risk: Past Spinach Outbreaks
E. coli O157:H7 outbreaks associated with lettuce or spinach, specifically “pre-washed” and “ready-to-eat” varieties, are by no means a new phenomenon. By way of illustration:
• in October 2003, thirteen residents of a California retirement home were sickened, and two people died, after eating E. coli-contaminated, pre-washed spinach;
• in September 2003, nearly forty patrons of a California restaurant chain fell ill after eating salads prepared with bagged, pre-washed lettuce; and
• in July 2002, over fifty young women fell ill with E. coli O157:H7 at a dance camp after eating “pre-washed” lettuce, leaving several hospitalized and one with life-long kidney damage.
And this is just a small sampling of the twenty or more E. coli O157:H7 outbreaks since 1995 in which spinach or lettuce was the source.
Regardless of the fruits of our discovery efforts in this case, the above-described series of outbreaks gave Dole reason to know, prior to last fall’s spinach outbreak, that a problem existed within the leafy-greens industry—a problem that was affecting, sometimes killing, the very people responsible for Dole’s substantial market share in the industry. If track record is any indication, Dole’s response, if it had one, was woefully inadequate. And this is not just a sentiment held by the lawyers at Marler Clark; as Dole and the industry well knows, the same sentiment has been articulated time and again by the Food and Drug Administration. The 2006 spinach outbreak, which ultimately sickened hundreds, if not thousands, was the result of the industry’s lack of action, and conscious disregard of risk.
B. Here We Go Again: Another Dole E. coli O157:H7 Outbreak
Official word of the spinach outbreak broke with the FDA’s announcement, on September 14, 2006, that a number of E. coli O157:H7 illnesses across the country “may be associated with the consumption of produce.” See September 14, 2006 FDA Release, “Preliminary epidemiological evidence suggests,” the statement continued, “that bagged fresh spinach may be a possible cause of this outbreak.” By the date of the announcement, fifty cases had been reported to the CDC, including eight cases of hemolytic uremic syndrome (HUS) and one death. States reporting illness included Connecticut, Idaho, Indiana, Michigan, New Mexico, Oregon, Utah, and Wisconsin.
The much-publicized outbreak grew substantially over the next several days. By September 15, the FDA had confirmed 94 cases of illness, including fourteen cases of HUS and, sadly, one death. Recognizing the lethality of the developing outbreak, the FDA’s September 15 release warned people should “not eat fresh spinach or fresh spinach containing products.”
Press Releases over the ensuing days announced steady growth in the number of people sickened, hospitalized, and with HUS as a result of the outbreak—109 cases from nineteen states by September 17, and 131 cases from twenty-one states just two days later. The latter statistic included 66 hospitalizations and twenty cases of HUS.
Meanwhile, the FDA and CDC, in conjunction with local and state health agencies from across the country, worked feverishly to figure out the brand names associated with illness. Early statistical analysis suggested that many brands were implicated, but the spinach sold under the several brand names had all come from the Natural Selection Foods processing center in San Juan Batista, California. Accordingly, Natural Selection recalled all of its spinach products with “use by” dates from August 17 to October 1, 2006. The recall, of course, included Dole brand spinach. But further data and study ultimately narrowed the possible sources of the outbreak down to one brand of packaged greens: Dole.
Though epidemiological evidence had already strongly linked Dole to the outbreak, the FDA found the proverbial “smoking gun” on September 20. The bag of Dole baby spinach had been purchased and consumed by an Albuquerque, New Mexico woman, and testing by the New Mexico State Health Department had confirmed that the product was contaminated with E. coli O157:H7 bearing the same genetic marker as the outbreak strain. The FDA announced the critical finding on September 21, 2006—also disclosing the “best by” date on the positive Dole bag of August 30—thereby giving a worried public a bit more information on what spinach products to eat, if any, and what to avoid.
By the date of the FDA’s September 21 announcement, the number of confirmed cases had swelled to 157 people from twenty-three states. Ultimately, the FDA confirmed 204 outbreak-related cases, with 102 hospitalizations, thirty-one cases of HUS, and three deaths, though the actual number of people affected by the outbreak was certainly much larger. In addition to the elderly Wisconsin resident, the FDA stated that the outbreak had claimed the lives of two-year-old Kyle Algood, from Chubbuck, Idaho, and also 81-year-old Ruby Trautz, from Bellevue, Nebraska. The tragedy of this outbreak can hardly be overstated.
Epidemiological and laboratory evidence, which had already proved the link to Natural Selection and Dole, soon revealed that the contaminated spinach had been grown at Paicines Ranch in San Benito County, California. More specifically, investigators had traced the source of the contaminated spinach to one field on the ranch that had been leased by Mission Organics.
Once identified as the likely source for the outbreak, Mission Organics became host to health officials looking for the outbreak strain of E. coli O157:H7. State and federal investigators took hundreds of environmental samples and swabs from the vicinity of the implicated spinach field, which was fifty acres in size, including from a nearby cattle pasture and water source. Investigators also sampled the intestinal lining of feral pigs that had been killed as part of the investigation. Samples from a variety of sources, including the pigs, the water, and cattle feces, tested positive for the same strain of E. coli O157:H7 that had now been isolated in over 205 people nationally. Finally, the outbreak strain of E. coli O157:H7 has been isolated in at least thirteen separate bags of Dole baby spinach.
C. The Final Report: Blame Enough For Everyone
Once the investigation was completed, a final report on the outbreak was prepared by the California Food Emergency Response Team (CalFERT), a team comprised of members from the FDA and the California Department of Health Services. The Final Report is replete with facts damning of all those involved in the growing, harvesting, processing, distribution, and sale of the implicated spinach products. For example, speaking of the NSF processing facility, it states:
During the production week from August 14-19, 2006, the NSF South facility had the highest weekly production volume of the month. Between August 13-20, 2006 production email exchanges revealed a string of personnel shortages, including nine absent employees on Sunday, August 13, the date of the weekly-extended sanitation shift. Personnel records reveal that a number of absences were due to illness or illness in the family…NSF did not conduct ATP testing on a daily basis as required by the firm’s SOP. No ATP testing was conducted from August 15-25, 2006. One ATP test collected from a scale vibrator failed on August 10, 2006, and no retest was documented.
The Final Report also faulted NSF’s procedures for monitoring the quality of processing-water, its record-keeping, and its inability to demonstrate that harvesting bins were being washed to prevent cross-contamination.
As for the Mission Organics growing operation, the findings were even more disturbing. The Final Report found that the land on the ranch where the spinach was grown “was primarily utilized for cattle grazing.” Moreover:
Investigators observed evidence of wild pigs in and around the cattle pastures as well as in the row crop growing regions of the ranch…. Potential environmental risk factors for E. coli O157:H7 contamination identified during this investigation included the presence of the wild pigs in and around spinach fields and the proximity of irrigation wells used for ready-to-eat produce to surface waterways exposed to feces from cattle and wildlife.
And despite the right to inspect both NSF’s processing facility, and the Mission Organics fields, the Final Report amply demonstrates that Dole did nothing to protect its customers.
The liability issues in this case are not complex. Under Wisconsin law, anyone who sells a product in a defective condition that is unreasonably dangerous to the user or consumer is subject to strict liability for all harm that proximately results. Green v. Smith & Nephew AHP, Inc., 617 N.W.2d 881 (Wis. 2000) (citing Dippel v. Sciano, 155 NW2d 55, 63 (Wis. 1967) and § 402A Restatement (Second) of Torts (1965)), aff’d, 617 N.W.2d 881 (Wis. 2001). Moreover, “[a] defective product is unreasonably dangerous to the user or consumer when it is dangerous to an extent beyond which would be contemplated by the ordinary user or consumer possessing the knowledge of the product’s characteristics which were common to the community.” Ransome v. WEPCO, 275 N.W.2d 641, 649 (Wis. 1979).
This is true even though the manufacturer has exercised all possible care in the preparation and sale of the product. It is also true that a product may be defective and unreasonably dangerous even though there are no alternative, safer designs available. Additionally, a jury may . . . infer from the fact of damage or injury that a product was defective.
Green, 238 Wis. 2d at 485 (quotations and citations omitted). Finally, under Wisconsin law, “[w]hether a product contains a defect that is unreasonably dangerous is decided on a case-by-case basis.” Keller v. Welles Dep’t Store, 276 NW.2d 319, 322 (Wis. Ct. App. 1979).
Given the facts of the present case, it is beyond dispute that packaged spinach contaminated with E. coli O157:H7—a deadly pathogen—is a defective product dangerous to an extent beyond that which contemplated by an ordinary consumer. In short, the ordinary consumer does not expect to purchase food that, if consumed, may kill them. Dole is strictly liable for all harm caused to Jane as a result of her E. coli O157:H7 infection.
The causal link between Jane’s consumption of Dole baby spinach and her subsequent E. coli O157:H7 infection is beyond dispute. She purchased Dole baby spinach in August, 2006 at the Pick ‘n Save in Fond du Lac, Wisconsin. As you are aware, a significant portion of the outbreak cases in Wisconsin, and in fact, nationally, resulted from purchase of the Dole product from Pick ‘n Save stores.
Jane subsequently developed symptoms consistent with an E. coli O157:H7 infection, including diarrhea that turned bloody, stomach cramps, headaches, muscle aches, and fatigue, within the expected incubation period for E. coli O157:H7. Furthermore, Jane had a confirmed HUS illness, which bears a strong association with E. coli O157:H7. While hospitalized, Jane’s daughter-in-law, Tara Majeska, retrieved an open package of Dole baby spinach from her refrigerator. At that time, she noted the lot code, P227A01, with a “best by” date of August 30, 2006. This too, is consistent with the lot information associated with the outbreak.
Though, in and of themselves, these circumstances support but one conclusion, we have asked medical epidemiologist Edward Belongia, MD, for his opinion on the likely cause of Jane’s illness. Dr. Belongia reported:
There is persuasive evidence that Ms. Majeska’s illness was caused by Shiga toxin-producing E. coli, and that she acquired this infection from consumption of the Dole baby spinach product with product code P227A01. The following evidence supports these conclusions:
1. The characteristics of her illness were typical for postdiarrheal HUS or TTP caused by E. coli O157:H7 infection. These include a severe acute illness with cramps and bloody diarrhea, followed by progressive thrombocytopenia and renal failure developing approximately one week later. Stool culture for E. coli O157:H7 was not performed during the acute illness, and the test for Shiga toxin was unreliable because it was performed late in the course of illness after broad-spectrum antibiotic treatment.
2. The onset of her illness matched the peak occurrence of outbreak-related cases in the US;
3. She purchased and consumed Dole spinach prior to illness onset. The lot number from Dole spinach in her refrigerator matches the implicated lot number that was shown to contain the outbreak strain.
4. A published case-control study of the same outbreak was performed in Utah and New Mexico that confirmed the implicated spinach product as the source of this outbreak (Emerging Infectious Diseases 2008; 14:1633-6). Consumption of fresh brand A (Dole) spinach was strongly associated with E. coli O157:H7 infection by both epidemiologic and laboratory results. The odds ratio for consumption of bagged spinach was 18.7 in cases vs. controls. Food items previously implicated as sources of E. coli O157:H7 were not associated with illness in this outbreak. The outbreak strain of E. coli O157:H7 was isolated from 3 open bags of Dole baby spinach. Lot codes were not reported in the published article, but the authors report that the bags were packed on Aug 15, 2006 at the same plant and on the same shift. This matches the production date for the spinach that was consumed by Mrs. Majeska.
In summary, it is more probable than not that Mrs. Majeska’s illness was caused by E. coli O157:H7 infection that was acquired from consumption of Dole baby spinach.