Food Poisoning Lawyer & Attorney : Marler Clark : Food Poison Journal

Hemolytic uremic syndrome (HUS) is a potentially fatal complication of E. coli O157:H7 infection, most common in children. At Marler Clark, we too often have to explain HUS to the lawyers and insurers for companies that have sold contaminated food.

Acute renal failure is one of the signature elements of HUS. Many of those who develop HUS must receive dialysis to survive. Most of those that survive the acute phase of HUS regain enough renal function to abandon dialysis, at least for a time.

One of the most disheartening aspects of the syndrome, however, is the irreversible damage done to the kidneys during the acute stage. The damage sustained in the short term then places the patient at risk for long term renal complications, including end stage renal disease (ESRD). That damage to the kidney is referred to as a "hyperfiltration injury."

Hyperfiltration injury is a term used to describe chronic, progressive damage in kidneys that have already sustained a severe acute injury (such as in HUS) that results in the destruction of a substantial percentage of nephrons.   Nephrons are the functional units of the kidney and are comprised of glomeruli connected to renal tubules.

The remaining functional glomeruli attempt to adapt to their reduced number by enlarging (hypertrophy) and by hyper- filtrating (i.e., the remaining glomeruli work extra hard) in an attempt to meet the needs of the body. For a time, they are usually able to compensate, but they are being “over worked”, and their “cry for help” is manifested by the spillage of protein (albumin) in the urine (proteinuria).

As time passes, the hyperfiltration injury causes progressive loss of the remaining glomeruli due to fibrosis (scar tissue formation). And, in time, once the remaining functional nephron population drops below 10 percent, the person’s survival requires initiation of “renal replacement therapy”.

The use of an angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) is usually helpful in slowing the fibrotic process, but no known treatment can stop it. ESRD, also known as stage 5 kidney disease, eventually occurs.

Once ESRD is reached there are two survival options, neither enticing. The patient must then receive long-term dialysis treatment or a renal transplant.

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West Missouri Beef, LLC has voluntarily recalled 14,000 pounds of boneless beef products due to potential contamination by E. coli O157:H7.  USDA's Food Safety and Inspection Service (FSIS) announced the Class I recall in a press release last night.  It is the third Class I recall this year, and the fifth since November, adding up to 1,636,000 pounds of beef products that have been recalled due to potential E. coli O157:H7 contamination in the last 3+ months.

What is a Class I recall?

A Class I recall, according to FDA definitions, should occur when "there is a reasonable probability that the use of or exposure to a violative product will cause serious adverse health consequences or death."  Class II and III recalls are appropriate only when there is a significantly lesser, or remote, risk of adverse health consequences, or when the health consequences are minor.  Due to its lethal capacity, E. coli O157:H7 is a bacteria that always requires a Class I recall.

What is E. coli O157:H7?

Escherichia coli (E. coli) are members of a large group of bacterial germs that inhabit the intestinal tract of humans and other warm blooded animals (mammals, birds). Newborns have a sterile alimentary tract which within two days becomes colonized with E. coli.

More than 700 serotypes of E. coli have been identified. The different E. coli serotypes are distinguished by their “O” and “H” antigens on their bodies and flagella, respectively. The E. coli serotypes that are responsible for the numerous reports of contaminated foods and beverages are those that produce Shiga toxin (Stx), so called because the toxin is virtually identical to that produced by another bacteria known as Shigella dysenteria type 1 (that also causes bloody diarrhea and hemolytic uremic syndrome [HUS] in emerging countries like Bangladesh) (Griffin & Tauxe, 1991, p. 60, 73). The best known and most notorious Stx-producing E. coli is E. coli O157:H7. It is important to remember that most kinds of E. coli bacteria do not cause disease in humans, indeed, some are beneficial, and some cause infections other than gastrointestinal infections, such urinary tract infections. This section deals specifically with Stx-producing E. coli, including specifically E. coli O157:H7.

Shiga toxin is one of the most potent toxins known to man, so much so that the Centers for Disease Control and Prevention (CDC) lists it as a potential bioterrorist agent (CDC, n.d.). It seems likely that DNA from Shiga toxin-producing Shigella bacteria was transferred by a bacteriophage (a virus that infects bacteria) to otherwise harmless E. coli bacteria, thereby providing them with the genetic material to produce Shiga toxin.

Although E. coli O157:H7 is responsible for the majority of human illnesses attributed to E. coli, there are additional Stx-producing E. coli (e.g., E. coli O121:H19) that can also cause hemorrhagic colitis and post-diarrheal hemolytic uremic syndrome (D+HUS). HUS is a syndrome that is defined by the trilogy of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and acute kidney failure.

Stx-producing E. coli organisms have several characteristics that make them so dangerous. They are hardy organisms that can survive several weeks on surfaces such as counter tops, and up to a year in some materials like compost. They have a very low infectious dose meaning that only a relatively small number of bacteria, less than 50, are needed “to set-up housekeeping” in a victim’s intestinal tract and cause infection.

The Centers for Disease Control and Prevention (CDC) estimates that every year at least 2000 Americans are hospitalized, and about 60 die as a direct result of E. coli infections and its complications. A recent study estimated the annual cost of E. coli O157:H7 illnesses to be $405 million (in 2003 dollars) which included $370 million for premature deaths, $30 million for medical care, and $5 million for lost productivity (Frenzen, Drake, and Angulo, 2005).
 

What is Hemolytic Uremic Syndrome?

Post-diarrheal Hemolytic Uremic Syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10% of those infected with E. coli O157:H7 or other Shiga toxin (Stx) producing E. coli. D+HUS was first described in 1955, but was not known to be secondary to E. coli infections until 1982. It is now recognized as the most common cause of acute kidney failure in infants and young children. Adolescents and adults are also susceptible, as are the elderly who often succumb to the disease.

How did these otherwise harmless E. coli become such killers? It seems likely that DNA from a Shiga toxin producing bacterium known as Shigella dysenteriae type 1 was transferred by a bacteriophage (bacteria infected with a virus) to harmless E. coli bacteria, thereby providing them with the genes to produce one of the most potent toxins known to man. So potent, that the Department of Homeland Security lists it as a potential bioterrorist agent. Although E. coli O157:H7 are responsible for the majority of cases in America, there are many additional Stx producing E. coli that can cause D+ HUS.

The chain of events leading to HUS begins with ingestion of Stx producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages or through person to person transmission. These E. coli rapidly multiply in the intestines causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once Stx attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade which results in the formation of clots in the very small vessels of the kidney resulting in acute kidney injury and failure. The red blood cells are hemolyized (destroyed) by Stx and/or damaged as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.
 

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Virtually every time an E. coli O157:H7 outbreak occurs, the most severely injured people develop a condition called hemolytic uremic syndrome (HUS).  The cluster being investigated by health officials in Belgium, Wisconsin is no exception.  At least one of the cases, believed to be a child, developed HUS and spent multiple weeks hospitalized at Children's Hospital of Wisconsin.

What is HUS?

Post-diarrheal Hemolytic Uremic Syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10% of those infected with E. coli O157:H7 or other Shiga toxin (Stx) producing E. coli. D+HUS was first described in 1955, but was not known to be secondary to E. coli infections until 1982. It is now recognized as the most common cause of acute kidney failure in infants and young children. Adolescents and adults are also susceptible, as are the elderly who often succumb to the disease.

How did these otherwise harmless E. coli become such killers?

It seems likely that DNA from a Shiga toxin producing bacterium known as Shigella dysenteriae type 1 was transferred by a bacteriophage (bacteria infected with a virus) to harmless E. coli bacteria, thereby providing them with the genes to produce one of the most potent toxins known to man. So potent, that the Department of Homeland Security lists it as a potential bioterrorist agent. Although E. coli O157:H7 are responsible for the majority of cases in America, there are many additional Stx producing E. coli that can cause D+ HUS.

From Diarrhea to Dialysis

The chain of events leading to HUS begins with ingestion of Stx producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages or through person to person transmission. These E. coli rapidly multiply in the intestines causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once Stx attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade which results in the formation of clots in the very small vessels of the kidney resulting in acute kidney injury and failure. The red blood cells are hemolyized (destroyed) by Stx and/or damaged as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.

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Every time an E. coli O157:H7 outbreak occurs, we get yet another reminder how devastating the bacteria can be, particularly when it causes hemolytic uremic syndrome (HUS).  See www.about-hus.com..  And every time we represent a young child with HUS, I am reminded of the story of Regan Erickson, who was sickened in the spinach E. coli outbreak in September 2006 (We represented over 100 victims, including nearly 30 who suffered kidney failure and hemolytic uremic syndrome). 

Tiffany and Russ Erickson were just like most Americans until September 2006. Their four-year-old son Regan (pronounced "Ree-gun") was one of many young kids whose future was unalterably and forever changed by spinach. What appears below is Regan's story. It is a little long, but that must be forgiven. Regan's illness very nearly cost him his life.

ONSET OF ILLNESS:

Regan's mother, Tiffany, and his sister, Emma, were both sickened during the Spinach outbreak as well. Tiffany actually fell ill first, on August 28. It felt like cruel timing, given that it was only three days before Emma’s birthday and little more than a week since discovering that she was pregnant with her third child, Maggie, but Tiffany took everything in stride. She had no reason to suspect that she was dealing with anything more than a run-of-the-mill flu, and her primary concern was with the health of her unborn child.

After twenty-four hours or so, however, thoughts began to change about the nature of Tiffany’s illness. Her bouts of diarrhea had grown more frequent and severe, and her abdomen was beset by cramps more severe than labor pains. Then, the evening of August 29, after a particularly painful bout of diarrhea, Tiffany noticed that the toilet bowl was streaked with blood. Up until this point, Tiffany had endured everything with resolute confidence, but this symptom suggested something that she had never before reckoned with.

Tiffany soon underwent a diagnostic procedure called an endoscopy to shed light on what was wrong. Of his wife’s illness, before his thoughts turned to Regan alone, Russ recalls:

We left the urgent care facility and gave the drugs some time to work, but the pain continued to be unbearable. As my concern shifted from the baby to Tiffany I couldn’t stand seeing her in that much pain, tired from lack of sleep, and not able to get comfortable.

Meanwhile, Regan had begun to develop symptoms, and Emma soon would. “We didn’t realize that the illnesses could be related,” Russ recalls, “since Regan couldn’t express his pain as well as Tiffany. He just knew his ‘tummy’ hurt and he began having diarrhea.” Emma’s symptoms began the very next day, September 1.

Russ recalls:

Everyone in the family was sick, tired, and the children being so young, not knowing how to tell or deal with the symptoms like diarrhea, I was continually cleaning, comforting, and helping where I could, all without Tiffany’s help who is usually the stalwart caregiver. We knew that we had some kind of ‘bug’ but not how severe yet. It presented a lot like flu symptoms, but we began to know it was more serious as the kids, just as Tiffany, began to have blood in their stool, and then blood instead of stool. That is a scary, unnerving experience to see blood when your 3 and 4 year olds are using the bathroom.

Compared to four year-old Regan, the illnesses that Tiffany and Emma Erickson suffered were nothing more than a small current in a raging sea. Nevertheless, to hear Russ describe what his wife and daughter endured is to fully comprehend the aggressive nature of this virulent pathogen. Emma endured many days of an illness more acutely painful than anything her parents had ever seen. But as sick as she was, her older brother was fast-becoming critically ill, and her parents thoughts and attention soon went solely and exclusively to Regan.

REGAN'S ILLNESS:

During an appointment with his pediatrician on September 4, Tiffany reported that Regan had had twenty bouts of bloody diarrhea that day, prompting endless complaints of a sore stomach. Regan been unable to eat or drink for days, and had developed redness and inflammation in the rectal area due to the frequency and severity of the diarrhea. These seemingly benign signs were immediately concerning to the pediatrician, who immediately sent Regan and his parents to Mckay Dee Hospital's emergency department. Tiffany and Russ rushed to the ER and carried their son in, having no concept of the road that lay ahead.

Regan remained hospitalized at Mckay Dee for the next two days. Gradually, blood tests showed that he was becoming anemic and losing platelets, and he was also not urinating normally. Soon, stool tests showed exactly why. Regan had been infected by E. coli O157:H7, and he was developing HUS. Doctors at Mckay Dee knew that Regan was critically ill, and they transferred him by Ambulance to Primary Children's Medical Center (PCMC) in Salt Lake City on September 6.

Meanwhile, Tiffany and Russ had begun the painful process of contacting friends and relatives. Russ’s mother dropped everything and, leaving at 4:00 AM, drove to Salt Lake City from Las Vegas. She recalls:

I arrived at Primary Children’s just after the ambulance arrived. They had just gotten Regan in his room. It was a flurry of activity, doctors and nurses in and out of the room. I was taken aback by his appearance. The last time I had seen him was on the 4th of July. He was playing with all his cousins, excited with all the fireworks, eating bar-b-que, and being a normal kid. Today he was pretty much unresponsive; he didn’t even know I was there. So pale and vulnerable, it broke my heart to see him in that condition. I was also taken aback by the appearance of Russell and Tiffany. It was obvious that Tiffany was still not well. She looked pale and tired. As if she was just barely making sense of the whole bizarre turn of events. Russell looked like he hadn’t slept in days . . . come to find out he hadn’t. He had been holding his little family together for over a week now. The only one of them not affected, the burden of care had been fully placed upon his shoulders. And they sagged at the weight of it all. He was tired; with worry in his eyes, fear in his voice and faith in his heart he told me that they were in the best hospital, with the best doctors and that Regan would be okay.

Regan had a difficult night his first night at PCMC. He had run a fever consistently; he had been nauseated despite Zofran; and he had vomited and suffered from painful abdominal distention all night long. Perhaps more significantly, he had had little to no urinary output all night, his face was swollen, and there were signs that his pancreas had already been affected, in addition to his kidneys, by the shiga-toxins released by the E. coli O157:H7 bacteria in his gastrointestinal tract. Regan's nephrologist planned to begin dialysis immediately if the Lasix, a diuretic, did not stimulate more urine production.

Tiffany placed a call to her mother, Tonya Peterson, the afternoon of September 7. Tonya remembers:

Tiffany told me that his pancreas and kidneys had shut down. I couldn’t believe it. I sat at work at my desk, crying for several hours, unable to concentrate on my work. I thought that Regan might not make it. I called my dad and asked him to take me to see Regan. I knew I wouldn’t be able to drive to the hospital in my condition. I was too distraught at the thought of losing Regan. He was such a sweet, innocent little boy. He called me “Ma-mah,” his version of “grandma.”

Regan continued his descent toward total kidney failure that night. He had stopped producing urine completely, and his nephrologist ordered that Regan be prepped for peritoneal dialysis. Accordingly, Regan was transported to the operating room on Friday morning, September 8, where doctors placed a spiral peritoneal catheter for dialysis. He also placed a PICC (peripherally inserted central catheter) line in Regan’s right arm to facilitate infusion of blood products, medicine, and IV nutrition. Then dialysis began.

September 9-13

Regan ran a fever all night on September 8 and vomited five times. He produced no urine and continued to suffer bouts of bloody diarrhea, producing 76 ml of mostly blood before 11:00 AM on September 9. Attendants administered morphine to ease the little boy’s immense discomfort. And because he continued to suffer from nausea and vomiting, doctors began Regan on total parenteral nutrition. Dialysis continued with hourly exchanges.

Over the next two days, Regan remained critically ill. He continued to have no renal function, and his hematocrit continued to drop, which indicated progressive anemia. In addition, Regan had consistently elevated blood pressure readings and was overloaded, in fact bloated, from fluid retention because he was unable to urinate.

Russ recently recalled his sense of devastation and total helplessness during this time:

Together with the surgeries, dialysis, and transfusions was a lot of heartache and a lot of pain. As I watched Regan suffering, I felt helpless. He wasn’t comforted by me and there wasn’t anything I could do to fix the situation. I could just watch, wait, and hope that he would pull through this illness.
***
I also had Emma and Tiffany to worry about. Emma was still having trouble adjusting to what was going on, and she was still regaining strength from her own illness. She couldn’t understand why Regan had to stay at the hospital and have tubes coming out of him all over the place when she had been sick and gotten better without any of that. Tiffany was still recovering, ragged from stress, and she was in a difficult first trimester with all the ailments that come along with that. I was very worried about what I could do to help my family, and it didn’t feel like much.

Regan’s hematocrit continued to drop on September 12, indicating progressing anemia. Doctors ordered that a transfusion of leukocyte filtered packed red blood cells be administered as soon as possible. Regan’s bloody diarrhea continued, but seemed to be improving, and his WBC count dropped as well. Nonetheless, Regan continued to be anuric, leaving his nephrologists little choice but to continue peritoneal dialysis.

September 14-16

By Thursday, September 14, Regan’s medical picture continued to be dire. He continued to be medicated for nausea, hypertension, fevers, to stimulate red blood cell production, and he continued to receive a bronchodilator. He also remained positive, by stool culture, for E. coli O157:H7, and consequently remained under strict quarantine.

Russ’s mother stayed at the hospital, alternating with Tiffany and Russ, at least one of whom was always at Regan’s bedside. She says of Regan’s first week:

The chair made into a bed of sorts and the nurses brought me blankets and pillows. We realized very quickly that the hour drive to PCMC every day was not only costly for the kids but most inconvenient. One of Russell’s cousins lived in the area of the hospital and invited Russell and Tiffany to stay at their house. The Ronald McDonald House had a distance rule that they missed qualification for by just 7 miles. They decided that as long as I could stay with Regan at night, they would go home to sleep in their own bed and then when I had to leave they would go to Russell’s cousin’s house and take turns staying at the hospital at night with their boy.

Throughout the week Regan was so sick that I still wondered if he even knew who I was. He progressed somewhat with the dialysis and his lab tests improved at a snail’s pace. Toward the end of the week they declared him E. coli free and he was allowed to ride in the little red wagon and get out of that tiny room for a minute. Up until that time not only was he confined to the room but his sister, Emma, wasn’t allowed in the play room and his family had strong precautions they were to take to insure that the E. coli would stay contained.

Regan remained very irritable and uncommunicative on Saturday, September 16, prompting an examining physician to describe him as an irritable young lad who had pulled the blanket over his head and his knees up to his abdomen during the examination attempt. Nevertheless, no new symptoms had arisen, and Regan’s hemolytic anemia and thrombocytopenia had begun to improve. Peritoneal dialysis, however, continued just as before.

September 18-23

By September 18, Regan had begun to pass a small amount of urine, and his stools had firmed up. He nevertheless remained extremely irritable and very uncooperative, evidently suffering significant discomfort from his ongoing symptoms. He had begun to moan during the drainage cycle of his ongoing peritoneal dialysis, which had been further reduced to twelve hours per day. But despite the encouraging sign of modest urine production, Regan’s kidney labs had not improved; BUN and creatinine levels remained very high at 62 and 6.1.

Over the next several days, Regan’s kidney lab values continued to fluctuate, so doctors ordered an increase to seventeen hours per day on September 20 due to an unexpected increase in creatinine to 6.7. And on September 22, in fact, Regan again could muster no urine at all. He was anemic and symptomatic with weakness, fatigue, and shortness of breath—all of which convinced his medical team that another transfusion was in order. Dialysis continued as well.

Dr. Sherbotie evaluated Regan the morning of September 23, noting that Regan’s appetite was “clearly” improving with only occasional vomiting. Regan was also able to produce a “substantial amount” of urine that morning. Nevertheless, his lab values indicated ongoing renal dysfunction, and peritoneal dialysis continued with a decrease in the number of hours.

September 25-26

Regan's nephrologist noted significant improvements during his initial assessment on September 26. Generally speaking, Regan appeared well and “was quiet but interactive.” He had lost weight—significant to the clinical picture because it suggested a reduction in fluid retention—and he continued to produce more urine. Nevertheless, he remained on dialysis.

September 27-28

On Wednesday, Regan’s urinary output continued to increase. He produced 641 ml (3 ml/kg/hr) with 550 ml intake. His appetite also continued to improve and, though still cranky, he was more playful than he had been previously. Additionally, his hematocrit, WBC, platelets, sodium, potassium, and glucose were all within normal range, and his BUN and creatinine were trending down with values of 56 and 5.4. With this positive news, Regan’s nephrology team ordered that peritoneal dialysis be stopped for the first time since September 8.

The order to stop dialysis did not, however, mean that the dialysis catheter could be removed. Labs on September 28 indicated another increase in BUN and creatinine, to 60 and 5.9, which values had remained elevated since dialysis was discontinued the day before. Regan’s blood pressure was stable but high at 118-122 over 70-90. Accordingly, Amlodipine continued for Regan’s hypertension.

September 29

On Friday morning, Regan was doing well overall. He continued to be anxious, but seemed to be less cranky, and he was able to eat and drink more and had further increase in urinary output. His facial edema had also improved, but Regan was considered to be generally mildly edematous. He also continued to have elevated but stable blood pressures.

Later in the day, Regan again went to the operating room—this time, however, to have his dialysis catheter removed. Tiffany recalls:

This was a surgery that wasn’t quite as scary to send him in to. He’s laughing because the anesthesiologist put some type of goofy medicine in his PICC line that just made him into a hoot and a half. I was still quite nervous but it felt better to send a laughing child into surgery than a sickly one.

September 30—Discharge from PCMC

On Saturday, September 30, 2006, after four weeks in the hospital and countless dialysis treatments, Regan Erickson was discharged home. His discharge diagnoses included HUS; pancreatitis; acute renal failure requiring peritoneal dialysis from September 8 to 26; placement of PICC on September 8 and removal on September 26; placement of peritoneal dialysis catheter on September 8 and removal on September 29; anemia requiring blood transfusions and ongoing Darbopoetin infusion; emesis requiring Prevacid and Erythromycin Ethylsuccinate (anti-infective); hyperphosphatemia requiring calcium carbonate with meals and phosphate restriction; hypocalcemia status post calcium supplements between meals and IV Calcium chloride x 2; and reactive airway disease.

REGAN'S PRESENT CONDITION AND PROGNOSIS:

Sadly, a child's HUS illness doesn't really end when he is discharged from the hospital. Regan is a perfect example of this. He remained on blood pressure medications after discharge, and he continued to suffer physical and emotional problems related to his prolapsed rectum and the trauma of going through an illness as severe as his was.

Tiffany recalls:

A couple of months after Regan's hospitalization, we made a decision, which hindsight tells us was a bad one, to go to Las Vegas with my husband for a conference he had. His parents live there so we thought it would be a nice cheap vacation. We drove down. The morning after we arrived Regan's prolapse came back out but this time we couldn't get it back in the entire day. I had been speaking over the phone to a pediatrician throughout the day. By the time the prolapse had been out for 12 hours we were advised to take him to the ER in Las Vegas. He was hospitalized.

When we got home I took Regan to a local surgeon and then to a pediatric GI doctor. We decided to allow Regan to use a pullup and stay off the toilet for several months. Regan had a hard time with the toilet because it really scared him when the prolapse would appear. We bought a box of rubber gloves and made sure we had plenty packets of lubricating gel.

Regan is one of many people, mostly children, sickened in the Spinach outbreak whose lives have permanently changed as a result of their illnesses. He is forecast by several of the country's leading pediatric nephrologists to require multiple kidney transplants due to the severity of the kidney injury that he suffered in the Spinach outbreak. Lifetime medical costs will run into the millions of dollars.

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 Tuesday morning, we will be filing lawsuits on behalf of the families of two children sickened in the ongoing, likely developing, outbreaks of E. coli O157:H7 linked to ground beef.  The lawsuits will be filed in Plymouth County Superior Court for the Commonwealth of Massachussetts against Brockton, Mass.-based Crocetti-Oakdale Packing, Inc., doing business as South Shore Meats Inc., and Ashville, NY-based Fairbank Farms, Inc. Both companies recalled meat last week after their products were identified as the source of a national E. coli outbreak.

The medical complications associated with E. coli O157:H7 infection are many.  Most infections are characterized by 7-10 days of diarrhea, frequently bloody, severe abdominal cramps, and a host of other painful symptoms.  Infection by this dangerous pathogen frequently results in hospitalization, and kills with frightening efficiency and regularity.  Those who are acutely susceptible to severe infection whether by age or immuno-compromisation frequently have dangerously severe medical courses.  

Far and away the most frightening medical complication associated with infection by E. coli O157:H7, however, is hemolytic uremic syndrome, or HUS.  The chain of events leading to HUS begins with ingestion of Stx producing E. coli (e.g., E. coli 0157: H7) in contaminated food, beverages or through person to person transmission. These E. coli rapidly multiply in the intestines causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once Stx attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade which results in the formation of clots in the very small vessels of the kidney resulting in acute kidney injury and failure. The red blood cells are hemolyized (destroyed) by Stx and/or damaged as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.

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BBC news is reporting that a 32 year old woman who suffered an E. coli O157:H7 infection is "improving."  Still, her current condition is testimony to the level of risk associated with the bacteria.  The woman's mother provided this update:

"They have lightened the sedation and are hoping to bring her off the ventilator.  She's now able to nod and shake her head but I don't think she's fully aware of what's happened to her.  She's off the dialysis now but she may need further dialysis in future. The doctors say it's two steps forward, one step backwards."

The 32 year-old woman has an 11 week old son, and is one of four people connected to the outbreak according to Wales health officials.

The investigation is focusing on a "chip shop," the Llay Fish Bar in Wrexham, Wales.

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The news media has been full of reports concerning the arrests of more than 40 people folllowing  a corruption investigation in New Jersey.  Among the more startling aspects of the story are the allegations that those arrested were involved in the trafficking of human kidneys.   An op-ed by Sally Satel in yesterday's Wall Street Journal, provided an interesting take on the story.  Satel argued that the extreme lack of available kidneys for those on transplant lists make this type of black market all but inevitable.  She wrote:

When I needed a kidney several years ago and had no donor in sight, I would have considered doing business with someone like Mr. Rosenbaum. The current law—the National Organ Transplant Act of 1984—gave me little choice. I would be a felon if I compensated a donor who was willing to spare me years of life-draining dialysis and premature death.

The illicit organ trade is booming across the globe. It will only recede when the critical shortage of organs for transplants disappears. The best way to make that happen is to give legitimate incentives to people who might be willing to donate. Instead, I fear that Congress will merely raise the penalties for underground organ sales without simultaneously establishing a legal mechanism to incentivize donors.

Satel concludes by arguing that any new legislation to crack down on organ trafficking should include incentives to increase the availability of organs for transplant recipients.

The point here is not to join the policy debate on organ donor regulation, but rather to recognize the depth of the risks faced by HUS survivors.  HUS is a somewhat rare, but devastating complication of E. coli O157:H7 infection.  Renal failure is a primary element of the acute stage of HUS.   Most of those who develop HUS recover renal function, at least temporarily.   Many, however, are left with permanent damage that can eventually necessitate placement on the long transplant lists that Satel describes.

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KSFY in Sioux Falls, South Dakota, reports that a one-year-old boy from Sioux Center, Iowa is currently hospitalized with hemolytic uremic syndrome at a Sioux Falls area hospital.  There are no reported "confirmed" cases in the JBS outbreak from Iowa . . . Yet.  But these outbreaks tend to evolve.  After all, we're talking about a product that many people buy and simply throw into their freezers until they're ready to consume it.  That means that these products can last months.  All the more reason for concerted public health efforts to spread the word about developing outbreaks and assist retailers in getting recalled products off their shelves . . . and out of consumers houses.

We've seen hundreds of kids in Isaiah Romero's exact medical circumstances.   I hope to see a news report soon saying that his illness was not as bad as it could have been.  Too many have gone the other way over the last few years.  In the meantime, we'll keep moving in discovery against JBS Swift in the New Mexico case that we filed yesterday (filed in Colorado). 

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We have already heard from several families whose children have developed hemolytic uremic syndrome (HUS) after contracting E. coli O157:H7 from Nestle cookie dough.  Most often, though we certainly see cases where the pathalogic process described below affects other organs, HUS affects the kidneys.  Here is a short explanation of what HUS is, and why it is so lethal. 

The toxins that are released by E. coli O157:H7 bacteria (called shiga-toxins) are so potent, in fact lethal, that the Department of Homeland Security lists it as a potential bioterrorist agent. (Although E. coli O157:H7 are responsible for the majority of cases in America, there are many additional shiga-toxin producing E. coli that can cause HUS. 

The chain of events leading to HUS begins with ingestion of E. coli 0157: H7 bacteria in contaminated food. These E. coli rapidly multiply in the intestines causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys, or other organs, where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once shiga-toxin attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade which results in the formation of clots in the very small vessels of the kidney resulting in acute kidney injury and failure. The red blood cells are hemolyized (destroyed) by shiga-toxins and/or damaged as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.
 

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With reports of 66 cases of E. coli O157:H7 across 28 states, Nestle has announced a recall of its Cookie Dough Products.  The illnesses include 25 hospitalizations, and 7 cases of hemolytic uremic syndrome (HUS).  HUS is a life-threatening complication of E. coli O157:H7 infection, that recently was reported as the cause of death in two young children in the U.S not appearing to be related to this outbreak.

On its website, Nestle apologizes, sort of, for the "inconvenience" it has caused.   Inconvenience?  Being late to work is inconvenient.   Fighting for your life on dialysis is something else. That "apology" doesn't come until after Nestle has taken the time for blaming the victims:  "Nestlé Toll House cookies made from refrigerated and frozen dough are perfectly safe for consumption when prepared according to the instructions on the label. These clearly state that the raw dough must be baked before consumption."

Here is the actual information on the label: 

Cookie Dough is Filled by Weight.   Use or Freeze by Date Indicated on the Package.  Cookie Dough Contains Raw Ingredients.  Bake Before Consuming.

None of this excuses Nestle from having a product on the shelves with E. coli O157:H7 in it.   As an initial matter, baking of the dough comes AFTER handling of the product, and therefore after exposure of the bakers (likely including families with children) to E. coli O157:H7.  More importantly, there are many products on the market right now, labeling themselves as cookie dough products, that are ready to eat, including ice cream, and breakfast pastries.  

This "Yahoo Answers" page, from before today's recall, shows a majority of respondents indicating that consuming raw cookie dough is just fine.   

All of this, and we are expected to believe that Nestle had no idea that people might be eating the dough raw?  And that Nestle was doing everything it could to discourage such a practice?

C'mon.

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In April, The Oklahoma State Health Department (OHD) published its final report on a massive outbreak of E. coli 0111 linked to the Country Cottage restaurant in Locust Grove, Oklahoma.    E. coli O111, one of the family of E. coli bacteria, is classified as an STEC, a shiga toxin producing escherichia coli.  In other words, it is, like E. coli O157:H7, pathogenic to humans and carries the potential to cause hemolytic uremic syndrome (HUS). 

The findings of the report also help illustrate an important legal point about the work we do at Marler Clark.   Despite a thorough investigation, OHD was not able to pinpoint the particular food source or sources that caused the 341 documented cases of E. coli O111.   "It could not be conclusively determined how E. coli O111 was introduced into the restaurant."   The OHD looked at a number of possibilities for the "original" source of the contamination - tainted well water; an infected food worker; contaminated food. 

From a legal standpoint, not being able to identify the "original" source of the infection is irrelevant to the customers claims against the restaurant.  Following a doctrine called "strict liabilty"  an injured customer simply has to prove that a restaurant meal caused his or her illness.  It is not necessary that the claimant be able to trace an illness to the mashed potatoes as opposed to the gravy.  In Oklahoma, the rule of "strict liability" is laid out in the case of Kirkland v. Gen. Motors, Corp (1974), but for all intents and purposes, the rule would apply anywhere in the U.S. 

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Andrew Martin of the New York Times wrote a nice article this morning on the safety of our food supply.  We represent all three individuals profiled in his article:  Heather Whybrew, Carl Ours, and Mary Tardiff.  All suffered devastating illnesses in separate outbreaks and from different pathogens.  All have unbelievable stories of suffering. 

Heather's story is unique, perhaps because she had lived through so much pain in her life even before her severe E. coli O157:H7 illness.  In November 2004, after two years of headaches, she was diagnosed with a brain tumor. Treatment for her relatively rare condition—giant cell glioblastoma—included a full craniotomy to remove the tumor from the left frontal lobe of Heather’s brain. The procedure left her partially paralyzed. She remained hospitalized at Seattle Children’s Hospital and in intensive rehabilitation from November 16 until December 24, 2004.

During her rehabilitation, Heather had to relearn many basic motor functions, including how to walk.  Relearn these skills she did, and despite her brain tumor, Heather eventually went on to college at Pacific Lutheran University.

Heather was infected by E. coli O157:H7 in the midst of finals her freshman year from contaminated lettuce served in a University Cafeteria. She would ultimately be hospitalized at St. Francis Hospital and Seattle Children's Hospital for three weeks.  During her hospitalization, Heather battled endless nausea, vomiting, and diarrhea, a bad pneumonia illness, and severe blood clots in the superficial veins of her arms.  The combined medical treatment would cost almost $114,000.  She would have to make up her final exams during the next school year.

By the time Heather had recovered to the point that she could return to school at Pacific Lutheran University, class was already well into the first semester.  Thus, as a result of her E. coli O157H7 illness, not only did Heather miss final exams her freshman year, but also she had to drop certain courses from her schedule during fall semester of her sophomore year.  She will be forced to take another year of class at Pacific Lutheran University as a result of the delays caused by her E. coli O157:H7 illness.  The cost of this additional year will be at least $36,000. 

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Amy Bowen of the St. Cloud Times has written about Stephanie Smith, 20, (Just for Kix instructor) who is struggling for her life after contracting what appears to be a critical case of E. coli poisoning. She was on life support Friday in the intensive care unit at St. Marys Hospital, Rochester. Doctors are treating her for a severe case of E. coli poisoning that they believe came from ground beef she ate, said Smith's mother, Sharon Smith of Cold Spring. Doctors have yet to confirm the strain of infection through lab tests. Doctors diagnosed Stephanie Smith with hemolytic uremic syndrome. The condition is caused when E. coli toxins enter the bloodstream. It causes kidney failure and low blood-cell counts, Dr. Kirk Smith said.

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