E Coli Lawyer & Attorney : Marler Clark Law Firm : E. coli Blog

This week's Food Safety Infosheet from the International Food Safety Network (iFSN) out of Kansas State University and the University of Guelph addresses concerns about E. coli O157:H7 - a potentially deadly foodborne pathogen.  From the infosheet:

E. coli O157:H7 can cause vomiting, diarrhea and can lead to kidney damage and is most dangerous for children and the elderly.

Foods that have been associated with E. coli O157:H7 include ground beef, fruits and vegetables, sprouts and unpasteurized juices.

When meat is ground, E. coli O157:H7 can be mixed from the surface into the middle of a patty or meatball. The only way to ensure that the dangerous
bacterium is killed is to use a digital tip-sensitive thermometer.

All three E. coli victims in the infosheet were hospitalized with Hemolytic Uremic Syndrome (HUS), a severe, life-threatening complication of an E. coli O157:H7 infection. Although most people recover from the symptoms of E. coli O157:H7 infection, about 5-10% of infected individuals develop (HUS).  The essence of the syndrome is described by its three central features: destruction of red blood cells (hemolytic anemia), destruction of platelets (those blood cells responsible for clotting, resulting in low platelet counts, or thrombocytopenia), and acute renal failure.

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A five-year-old from Hutchinson, Kansas, was released from Wesley Medical Center after being hospitalized for a month with hemolytic uremic syndrome.  Aubrey Anderson's kidneys failed after she became ill with an E. coli infection in October. 

According to the Hutchinson News, Aubrey was released from the hospital to recover at home because her mother is a registered nurse.  Public health officials have yet to identify the source of Aubrey's illness, and she will continue medical follow-up for months to years.  As the Hutchinson News reported:

It will be weeks, and perhaps months, before the family knows how much the illness damaged her kidneys, and whether she'll face a lifetime of treatment or be in the clear, said her father, Bill Anderson.

"We won't know until we get at least six or seven weeks out if there's any residual scarring as a result of the E. coli," Anderson said. "If there is scarring, it may mean anywhere from a range of a kidney transplant to her maybe having to take oral medication for the rest of her life to keep her body in balance."

Initial indications were that her kidneys were functioning, so the family is optimistic she'll make a full recovery.

All persons who have experienced HUS should be formally evaluated by a nephrologist—a kidney specialist—at a year following their acute illness. Kidneys injured by HUS may slowly recover function over at least a six month period following the acute episode and perhaps longer. Even persons with “mild” HUS who did not require dialysis should be formally evaluated. Such an evaluation should include a routine physical, blood pressure measurement, and blood and urine analyses from which kidney filtration rate can be calculated.

Physicians doing follow-up on HUS patients will carefully look for indications of kidney injury. These will include whether there is an abnormal amount of protein in the urine that may signal a significant injury to the kidneys or blood in the urine which also can reflect kidney injury. As assessment of the HUS patient’s glomerular filtration rate—“GFR”—is essential to determining whether the kidneys are functioning in the range of normal for that person age, sex, and size. It is also important to establish a baseline GFR so that future assessment of kidney function can reflect any potential loss of filtering capacity over time.

Studies done to date on HUS outcomes have largely confirmed a positive correlation between more severe kidney involvement acutely, particularly the need for extended dialysis, an increased incidence of future renal complications. However, it has been shown in multiple studies that even moderate kidney compromise in the acute phase of HUS can result in long-term complications due to damage to the filtering units in the kidneys.

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Sharon Smith, the mother of Stephanie Smith, a Minnesota resident who has been hospitalized for months after eating a hamburger and becoming ill with E. coli poisoning, spoke with Kirsti Marohn of the St. Cloud Times for an article that appeared in today's paper.  She shared the story of the few days before Stephanie became ill with symptoms of E. coli infection, and of her hospitalization. 

The 20-year-old dance instructor has undergone intensive medical treatment while doctors work to support her body.  Five days after becoming ill, Stephanie was hospitalized with hemolytic uremic syndrome and was placed in a coma when she began having seizures.  As Kristi Marohn wrote:

Two months later, she remains in critical condition at St. Marys Hospital in Rochester, fighting for her life against a severe case of E. coli poisoning.

Doctors have told Sharon that Stephanie remains extremely critical. She was diagnosed with hemolytic uremic syndrome, caused when E. coli toxins enter the bloodstream.

The severity of her case is very rare, similar to only a handful of others worldwide. Still, Sharon hasn’t given up hope that her only daughter, with her wide smile and warm personality, will pull through.

There are hopeful signs. Stephanie’s kidneys have started functioning again, and she no longer needs dialysis. But there are setbacks, too. Her tongue has swelled so doctors have had to prop her mouth open and put an oxygen mask on her. So far, attempts to lower the coma-inducing drugs have resulted in more seizures. She continues to breathe with the help of a respirator.

Stephanie's is one of the most severe E. coli cases reported on in recent years, but she is not alone.  Other E. coli victims from outbreaks this fall have also been hospitalized for lengthy periods - at least one other in a coma. 

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In September, an E. coli outbreak among students at Galena Elementary School perplexed health officials.  Several children became ill with E. coli and a source of the outbreak was elusive.  The sibling of two students at Galena Elementary battled an E. coli infection during the outbreak, and continues to recover after being on dialysis.  His mother has been hospitalized since she became ill with E. coli over 52 days ago. 

WAVE3 TV out of St. Louis, Missouri, reported the story of Amelia Seraiah's E. coli illness and hospitalization last night:

A Floyd County woman watched her son battle a deadly strain of E. coli back in September. Now she's hospitalized with the same illness. But her health isn't the only problem the single mother of five is facing.

It was 52 days ago -- on September 30th -- when Amelia Seraiah came down with the deadly bacteria. Her children are now staying with family members, who say they just pray she makes a full recovery.

Sharon Peltier has a lot to be thankful for this week. Her 3-year-old grandson, William, is off dialysis and doing better. He spent 17 days last month in Kosair Children's Hospital. Now Peltier's daughter (William's mother) is in Norton Hospital, fighting the same illness: E. coli.

Amelia isn't the only person battling an E. coli infection who will spend Thanksgiving in the hospital.  7-year-old Jayden Moss, of Willard, Utah, is expected to remain hospitalized until February.  He became ill with an E. coli infection earlier this fall and has suffered brain damage due to neurological involvement of HUS.  According to KSL.com:

Jayden is now at the learning level of an infant after developing Hemalitic Uremic Syndrome (HUS) from E. coli.

"He started throwing up and diarrhea," his mother, Rachael, said.

It eventually shut down his kidneys, and blood vessels in his body began bursting, causing severe brain damage. "Right now he doesn't walk, doesn't talk, he doesn't eat on his own, he's fed by a machine," Jayden's father, Jeremiah, explained.

According to the KSL story, Jayden's first-grade classmates have raised $6,500 to help his family pay their medical bills.

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A Mattoon High School senior from Mattoon, Illinois, who became ill with an E. coli infection last September shared his story with the Herald & Review. 

Matt Roberts became ill with an E. coli infection last September - just before an E. coli outbreak was traced to El Rancherito restaurant in Effingham.  His E. coli infection progressed to hemolytic uremic syndrome (HUS) and he was hospitalized for over a month.  While hospitalized, Matt was placed in a medically-induced coma for ten days, and underwent dialysis and blood and plasma transfusions.  Even after he was released from the hospital, Matt continued to receive plasma transfusions.

While Matt was ill, the Coles County Health Department worked to identify the source of his E. coli infection but has thus far been unable to determine the source of his illness.  According to the Herald & Review:

Coles County Health Department officials confirmed in early October they did not suspect any area restaurants as the source of Matt's infection or the E. coli contracted by another unidentified Coles County resident, who recovered from the illness relatively quickly.

Nor was Matt anywhere near the Effingham El Vaquero restaurant, to which seven E. coli cases were linked in late September.

And Matt was showing symptoms well before the Effingham outbreak.

A 20-year-old woman from Wisconsin was also hospitalized and in a drug-induced coma.  Stephanie Smith became ill this fall after eating ground beef contaminated with E. coli and developed HUS.

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The Hutchinson News from Hutchinson, Kansas, reported today that five-year-old Aubrey Anderson is undergoing dialysis treatments at a Wichita hospital to combat the effects of hemolytic uremic syndrome (HUS) secondary to E. coli infection.  The child has been hospitalized for 18 days. 

From About-HUS.com:

The essence of Hemolytic Uremic Syndrome is described by its three central features: destruction of red blood cells (hemolytic anemia), destruction of platelets (those blood cells responsible for clotting, resulting in low platelet counts, or thrombocytopenia), and acute renal failure. In HUS, renal failure is caused when the nephrons, or filtering units, become occluded (blocked) by micro-thrombi, which are tiny blood clots. In almost all cases, the filtering ability of the kidneys recovers as the body of the patient slowly dissolves the micro-thrombi within the microvessels.

A typical person is born with about one million filtering units, called nephrons, in each kidney. The core of the nephron is a bundle of tiny blood vessels, called a glomerulus, where osmotic exchange allows for the filtration of wastes that eventually collect in the urine and are excreted. During Hemolytic Uremic Syndrome, the lack of blood flow to the nephrons can cause them to die or be damaged, just as heart muscle can die as the result of coronary vessel occlusion during a heart attack. Dead nephrons do not regenerate.

In general, the longer a patient suffers kidney failure, the greater the loss of filtering units as a result. At some point, the damage to the kidneys’ filtering units can be so severe that the patient will, over a period of years, lose kidney function and suffer end-stage renal disease (ESRD), which requires chronic dialysis or transplantation.

HUS can also cause transient or permanent damage to other organs, which include the pancreas, liver, brain, and heart. The essential pathogenic process is the same regardless of the organ affected: microthrombi inhibit necessary blood flow and cause tissue death or damage. During the acute stage of Hemolytic Uremic Syndrome, patients must be carefully monitored for these extra-renal complications. It is very difficult to predict the severity and course of HUS once it initiates.

The active stage of Hemolytic Uremic Syndrome may be defined as that period of time during which there is evidence of hemolysis and the platelet count is less than 100,000. In HUS, the active stage usually lasts an average of six days (range, 2-16 days). It is during the active stage that the complications of HUS per se usually occur.

In the Hutchinson News article, Aubrey's father discussed her condition:

"Aubrey's hemoglobin was down a little today, which is not good," Anderson said in an e-mail. "Her platelets, however, have reached a 'normal' level and the doctor feels that they will not decrease again, and that is encouraging. Her toxicity level is down from yesterday, but they would like to see it come down farther."

Aubrey remains on a feeding tube, which goes down through her nose and bypasses her stomach into her intestines. She continues to frequently vomit, however, which displaces the feeding tube.

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Aubrey Anderson, a five-year-old from Sterling, Kansas, has been hospitalized with hemolytic uremic syndrome (HUS) secondary to E. coli infection, according to several media reports.  She is currently being treated at Wesley Medical Center in Wichita, and doctors believe she could remain hospitalized for 3-6 weeks. 

KSN TV's website featured a story on the child's illness, and interviewed her parents.  From the story:

Aubrey's kidneys have shut down, but the Anderson's are confident she will recover.

"I think there is more than a 95 percent chance that she will come out of this without any residual affects," Bill said.

Aubrey does have a long road ahead.

Public health officials have not yet been able to determine the source of Aubrey's illness, unlike in the case of Courtney Hansen, an eight-year-old from Ellsworth, Wisconsin, who was recently released from the hospital after a five-week stay while she was treated for HUS.  In Courtney's case, the Pierce County Herald reported that she and her younger twin sisters all became ill with E. coli infections after eating wind-fall apples. 

Two benefits are planned to raise money for medical expenses.  Details of the benefits were provided in the Herald:

The family and Our Savior’s Lutheran Church invite the public to attend the two benefits in Courtney’s honor.

The first is a luncheon 11 a.m. to 2 p.m. Saturday, Nov. 10, at Our Savior’s Lutheran Church, N6450 530th St., Beldenville.

Lunch will consist of soup, sandwichs and salads. Homemade pies will be available for sale.

There will be silent auction as well. To donate an item for the auction, contact Audrey Severson at 273-5019 or mail items directly to: Auction Item, c/o Severson, N6059 530th St., Ellsworth, WI 54011.

The second benefit will be a Hunters’ and Shoppers’ Breakfast 4 a.m. to 9 a.m. Saturday, Nov. 17, also at Our Savior’s Lutheran Church.

The breakfast menu will include egg bakes and rolls.

Free will donations will be accepted at both events.

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WAVE TV reported Saturday that Sidney Jacobi, a 6-year-old child who is part of the E. coli outbreak among Galena Elementary School students, is home from the hospital.  Sidney sustained the most serious injures of any child hospitalized during the outbreak, suffering hemolytic uremic syndrome, which caused kidney failure.  WAVE interviewed Sidney's mother about her illness and return home:

"She was so fluid and puffy that she didn't look like herself," Marcia said.

During the time she was in the hospital, Sidney received cards from hundreds of people. Some that knew her and many that didn't.

Sidney is still recovering. High blood pressure is still a concern.

"We still have to watch her kidneys and our numbers still need to come down," said Marcia.

Follow-up treatment for victims of E. coli and hemolytic uremic syndrome is very important, and all persons who have experienced HUS should be formally evaluated by a nephrologist—a kidney specialist—at a year following their acute illness. Kidneys injured by HUS may slowly recover function over at least a six month period following the acute episode and perhaps longer. Even persons with “mild” HUS who did not require dialysis should be formally evaluated. Such an evaluation should include a routine physical, blood pressure measurement, and blood and urine analyses from which kidney filtration rate can be calculated.

Physicians doing follow-up on HUS patients will carefully look for indications of kidney injury. These will include whether there is an abnormal amount of protein in the urine that may signal a significant injury to the kidneys or blood in the urine which also can reflect kidney injury. As assessment of the HUS patient’s glomerular filtration rate—“GFR”—is essential to determining whether the kidneys are functioning in the range of normal for that person age, sex, and size. It is also important to establish a baseline GFR so that future assessment of kidney function can reflect any potential loss of filtering capacity over time.

Studies done to date on HUS outcomes have largely confirmed a positive correlation between more severe kidney involvement acutely, particularly the need for extended dialysis, an increased incidence of future renal complications. However, it has been shown in multiple studies that even moderate kidney compromise in the acute phase of HUS can result in long-term complications due to damage to the filtering units in the kidneys.

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WATE.com reported yesterday that a Cocke County, Tennessee child died after fighting an E. coli infection.  According to the story, the girl, who was 20-months-old and was diagnosed with E. coli on October 9, was determined to be brain-dead on Monday and her heart stopped functioning late Tuesday night.  As to the source of her illness, WATE reported:

Officials with the East Tennessee Regional Health Department said Wednesday the source of Jaycee's infection has not been confirmed.

However, her family says Jaycee had a little bit of hamburger meat the Saturday before she got sick but they don't know if that was the cause of her infection.

Since no other E. coli infections have been reported recently in Cocke County, health officials say they think the cases will be limited to Burgin's.

Young children who become infected with E. coli O157:H7 and other strains of E. coli are susceptible to a complication of E. coli infection called hemolytic uremic syndrome (HUS).  HUS develops when the toxin from E. coli bacteria, known as Shiga-like toxin (SLT), enters the circulation by binding to special receptors. These Shiga-toxin receptors, known as Gb3 receptors, are probably heterogeneously distributed in the major body organs allowing disparate thrombotic (blood clotting) impacts in different HUS victims, although the greatest receptor concentration appears to be in the kidneys, especially in children. As the inflammatory reaction process accelerates, red blood cells are destroyed and cellular debris aggregates within the microvasculature while the body’s inherent clot breaking mechanisms are disrupted. The result is formation of microthrombi within particularly susceptible organs such as the kidneys and brain. Because there exists no way to halt the progression of HUS, doctors are left to support the HUS victim while the acute process runs its course.

Some organs appear more susceptible than others to the damage caused by these toxins, possibly due to the presence of increased numbers of toxin-receptors. These organs include the kidney, pancreas, and brain.

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A six-year-old first grade student at Galena Elemenary School in Indiana has been hospitalized with kidney failure after she developed hemolytic uremic syndrome following an E. coli infection, according to WLKY news.  The child is one of six students at the school who have been confirmed as suffering E. coli infections, with five cases unconfirmed but possibly linked to the outbreak.  WLKY reported that the state health department has joined the outbreak investigation, and is sending three additional investigators to help determine the source of the outbreak.  According to the news report:

The school has been thoroughly cleaned, officials said, but parents are still concerned about the safety of their kids.

State Health Officials said they are sending three more specialists to Floyd County to help track down the source of an E. Coli infection.

Two food specialists and a second epidemiologist are scheduled to inspect the school Tuesday.

In 1998, a seemingly similar E. coli outbreak-situation occurred in Washington state. 

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The Troy Messenger published a follow-up story on Mallory Chandler, a Troy, Alabama, toddler who became ill with an E. coli infection and HUS while she was on vacation with her family in late June.  Mallory was recently released from the hospital, and The Messenger spoke with her grandmother, Linda Chandler, about her illness and hospitalization.

Where Mallory contracted E.coli, Chandler said probably no one will ever know.

“They thought it might have been from the pool, but I don't really think that,” she said. “It could have come from anywhere. She could have touched something and then put her hand in her mouth. We just don't know.”

Exposure to E. coli can occur in any of a number of different ways.  The following is a list of ways to avoid exposure to E. coli O157:H7:

1. Cook all ground beef thoroughly.

Eating undercooked ground beef is the most important risk factor for acquiring E. coli O157:H7.[1] Because ground beef can turn brown before disease causing bacteria are killed, use a digital instant read meat thermometer to ensure thorough cooking. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160º F. Persons who cook ground beef without using a thermometer can decrease their risk of illness by not eating ground beef patties that are still pink in the middle. If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking.[2]

Avoid spreading harmful bacteria in your kitchen. Keep raw meat separate from ready-to-eat foods. Wash hands, counters, and utensils with hot soapy water after they touch raw meat. Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties.

Wash meat thermometers in between tests of patties that require further cooking.

2. Drink only pasteurized milk, juice, or cider.

Commercial juice with an extended shelf life that is sold at room temperature (e.g. juice in cardboard boxes, vacuum-sealed juice in glass containers) has been pasteurized, although this is generally not indicated on the label. Most juice concentrates are also heated sufficiently to kill pathogens.

3. Wash fruits and vegetables thoroughly, especially those that will not be cooked.

Children younger than 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured.[3] Methods to decontaminate alfalfa seeds and sprouts are being investigated.

4. Drink municipal water that has been treated with chlorine or other effective disinfectants, or bottled water that has be sterilized with ozone or reverse osmosis (almost all major brands use one or the other method).

5. Avoid swallowing lake or pool water while swimming, especially pool water in public swimming facilities.

6. Avoid Petting Zoos and other animal exhibits.

7. Make sure that persons with diarrhea, especially children, wash their hands carefully with soap after bowel movements to reduce the risk of spreading infection, and that persons wash hands after changing soiled diapers.

Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.

[1.] Slutsker L, Ries AA, Maloney K, Wells JG, Greene KD, Griffin PM. A nationwide case-control study of Escherichia coli O157:H7 infection in the United States. Journal of Infectious Diseases 1998;177:962-926.
[2.] http://vm.cfsan.fda.gov and http://www.cfsan.fda.gov/~dms/fc01-toc.html give the Food and Drug Administration advice and Food Code, respectively, about food cooking temperatures and other prevention techniques.
[3.] Breuer T, Benkel DH, et al. A Multistate outbreak of Escherichia coli O157:H7 infections linked to alfalfa sprouts grown from contaminated seeds. Emerg Infect Dis, 2001; 7:977-82.

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The Huntsville Times reported today on an outlying case of E. coli that was investigated as potentially linked to the E. coli outbreak linked to lettuce consumed at Little Rosie's restaurant in Huntsville.  While that case was ultimately determined to be unrelated to the Little Rosie's E. coli outbreak, the Times updated its report on three victims of the outbreak who were hospitalized.  The three remain hospitalized with hemolytic uremic syndrome (HUS).  A recap on the outbreak from today's article:

Health officials say the Huntsville outbreak most likely was caused by contaminated lettuce served at Little Rosie's between June 27 and June 30. Eighteen of the 19 known victims ate at the popular Mexican restaurant on Whitesburg Drive on those dates; the other infected person did not eat at Little Rosie's and caught the bacteria another way.

Three Little Rosie's customers have been in the hospital since about July 4 undergoing dialysis for kidney damage.

Treatment for HUS is minimal, with doctors providing mostly supportive care for individuals who develop the syndrome.  Dialysis and plasmapheresis are two treatments physicians can use to help victims battle HUS.  From the About-HUS website:

There is no known therapy to halt the progression of Hemolytic Uremic Syndrome. The active stage of the disease usually lasts one to two weeks, during which a variety of complications are possible. HUS is a frightening illness that even in the best American medical facilities has a mortality rate of about 5%. By comparison, the mortality rate in the developing world is much higher. About 50% of patients require dialysis due to kidney failure, 25% develop pancreatitis, 25% experience seizures, and 5% suffer from diabetes mellitus. The majority of Hemolytic Uremic Syndrome patients requires transfusion of blood products and develops complications common to the critically ill. The illness is a living nightmare for the patients and families, and leaves a painful memory that lingers long after the acute illness had passed.

Among survivors of HUS, about five percent will eventually develop end stage kidney disease, with the resultant need for dialysis or transplantation, and another five to ten percent experience neurological or pancreatic problems which significantly impair quality of life. Since the longest available follow-up studies of HUS are about twenty (20) years, an accurate lifetime prognosis is not available, and as such, medical follow-up is indicated for even the mildest affected cases.

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The Bracken County, Kentucky, health department is investigating how three children became ill with E. coli infections.  According to an article posted at wlwt.com, two siblings and another child fell ill with E. coli nearly a month ago.  Two of the children were hospitalized for several weeks with hemolytic uremic syndrome. 

WLWT interviewed Nicole Logan, the mother of two of the children who were ill - one, her son, Zachary, has been receiving treatment for HUS for over 3 weeks.

"Sometimes the children are not very sick and just have abnormalities in their blood tests. Other times they become very ill and require dialysis or even [have] permanent kidney failure," said Dr. Mitchell Cohen of Children's Hospital.

The Health Department is investigating what could have caused the three cases.

"They're for some reason leaning toward hamburger or spaghetti sauce," said Logan. "I just hope they can find it. I hope it's not still out there. I don't want more people to get sick."

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The Troy Messenger reported that a 22-month-old child has been hospitalized with hemolytic uremic syndrome in the Birmingham, Alabama, Children's Hospital.  Her grandfather, Dr. Malone Chandler, was interviewed for the story, and discussed her illness and possible exposures she could have had to E. coli, the most common cause of HUS.

“The concern for Mallory is that her kidney function began to decline in the past 24 hours. She is on dialysis, temporarily, and she has had a blood transfusion. She is not in great shape, but the news that we got today is encouraging.”

Chandler said the source of Mallory's illness is not known and may never be.

“At the beach, Mallory played in the pool,” he said. “She had not eaten anything much since last Wednesday or Thursday, so we really don't know of any food that she might have eaten that could have made her sick. We are wondering if it could have been something in the pool water.”

Chandler said in the past week four children have been admitted to Children's Hospital suffering from the same symptoms as Mallory.

Past outbreaks have been traced to contaminated water sources, such as pools, water parks, and spray parks.  In the summer of 1998, 26 children became ill from E. coli O157:H7 contracted while playing in the kiddie pool at White Water Park, a commercial water park in suburban Atlanta. Seven of those children were hospitalized and a 2-year-old boy died after suffering HUS.

Operators of the pool initially denied responsibility for the E. coli outbreak, but investigators determined that the chlorine level in the pool was well below the local health standard on the days when the water was contaminated, greatly increasing the risk of infection.

Marler Clark represented most of the victims and their families, eventually obtaining millions of dollars in settlements. The incident also increased national awareness of the hazards of water contamination, prompting the industry to pay closer attention to pool cleaning and chlorine.

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According to an article posted on the Times Argus Web site, two Vermont children have been hospitalized in Boston with hemolytic uremic syndrome secondary to E. coli infection.  The health officials investigating the two cases at this point do not believe that the cases are related, but are continuing to look into the source of both children's E. coli infections.

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Today's Daily Record, a newspaper out of Morris County, New Jersey, featured an article on former Marler Clark client Barbara Kowalcyk.  Barbara served on the Board of Directors for S.T.O.P. (Safe Tables Our Priority) for several years, and recently formed the Center for Foodborne Illness Research and Prevention (CFI). 

Barbara and her husband, Michael, were propelled into food safety advocacy in 2001, when their two-year-old son, Kevin, died after suffering an E. coli O157:H7 infection and hemolytic uremic syndrome.  In the article, Barbara was quoted on what led her to become an activist:

"Our public health department didn't have the resources or, frankly, the desire to spend a lot of time investigating our case because it wasn't part of an outbreak," Kowalcyk said. "They did very little to help us. We only found out what we did because we contacted an attorney and he worked on our case."

The Kowalcyks had limited knowledge of foodborne illness before their son got sick. The family lived in Wisconsin at the time. They now live in Loveland, Ohio, near Cincinnati.

"We knew a lot more than most people do. We didn't eat out very often, yet we really didn't know enough," Kowalcyk said. "We both are highly educated; we both have master's degrees. I am a biostatistician by training and spent my entire career working in clinical research, so I am publicly health-minded anyway. We were well aware that food could kill."

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The story of Ashley and Isabella Armstrong's E. coli illnesses was told in a Monticello, Indiana, Herald Journal article today.  Reporter Doug Howard interviewed the girls' grandparents, Randy and Robin Armstrong, and told of their experience with watching Ashley suffer for months while battling for her life with hemolytic uremic syndrome and kidney failure.  The story concluded  with a few paragraphs on the Armstrongs' food safety advocacy efforts:

The Armstrongs said that one thing they would like to see come out of their ordeal and those of anyone affected by foodborne illness from contaminated food is more stringent government regulations on food safety.

In response to the spate of recalls over the past year - from spinach to peanut butter to pet food - the House Committee on Energy and Commerce last month addressed food safety at its Oversight and Investigations subcommittee hearing entitled, "A Diminished Capacity: Can the FDA Assure the Safety and Security of the Nation's Food Supply?"
Ashley and her family - father Michael, mother Elizabeth, and older sister Isabella - were among representative from three families whose members suffered food poisoning after eating contaminated food and who sent representatives to testify in front of the committee, as did companies whose products were found to be responsible for large scale foodborne illness outbreaks.

Ashley and her family are also are part of a documentary on food safety and foodborne illness, scheduled to air on the CNN network on May 19 and 20.

The Armstrong family also spoke with the New York Times for an upcoming article about food contamination this week.

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The following is a comprehensive description of hemolytic uremic syndrome, its symptoms, and the complications and long-term risks associated with HUS.

*** A glossary of terms can be found at the bottom of this entry. ***

Hemolytic uremic syndrome is a severe, life-threatening complication of an E. coli bacterial infection that was first described in 1955, and is now recognized as the most common cause of acute kidney failure in childhood. E. coli O157:H7 is responsible for over 90% of the cases of HUS that develop in North America. In fact, some researchers now believe that E. coli O157:H7 is the only cause of HUS in children.

HUS develops when the toxin from E. coli bacteria, known as Shiga-like toxin (SLT) [1,2], enters cells lining the large intestine. The Shiga-toxin triggers a complex cascade of changes in the blood. Cellular debris accumulates within the body’s tiny blood vessels and there is a disruption of the inherent clot-breaking mechanisms. The formation of micro-clots in the blood vessel-rich kidneys leads to impaired kidney function and can cause damage to other major organs.

What are the Symptoms associated with Hemolytic Uremic Syndrome?

About ten percent of individuals with E. coli O157:H7 infections (mostly young children) goes on to develop Hemolytic Uremic Syndrome, a severe, potentially life-threatening complication. HUS is an extremely complex process that researchers are still trying to fully explain.

The essence of Hemolytic Uremic Syndrome is described by its three central features: destruction of red blood cells (hemolytic anemia), destruction of platelets (those blood cells responsible for clotting, resulting in low platelet counts, or thrombocytopenia), and acute renal failure. In HUS, renal failure is caused when the nephrons, or filtering units, become occluded (blocked) by micro-thrombi, which are tiny blood clots. In almost all cases, the filtering ability of the kidneys recovers as the body of the patient slowly dissolves the micro-thrombi within the microvessels.

A typical person is born with about one million filtering units, called nephrons, in each kidney. The core of the nephron is a bundle of tiny blood vessels, called a glomerulus, where osmotic exchange allows for the filtration of wastes that eventually collect in the urine and are excreted. During Hemolytic Uremic Syndrome, the lack of blood flow to the nephrons can cause them to die or be damaged, just as heart muscle can die as the result of coronary vessel occlusion during a heart attack. Dead nephrons do not regenerate.

In general, the longer a patient suffers kidney failure, the greater the loss of filtering units as a result. At some point, the damage to the kidneys’ filtering units can be so severe that the patient will, over a period of years, lose kidney function and suffer end-stage renal disease (ESRD), which requires chronic dialysis or transplantation.

HUS can also cause transient or permanent damage to other organs, which include the pancreas, liver, brain, and heart. The essential pathogenic process is the same regardless of the organ affected: microthrombi inhibit necessary blood flow and cause tissue death or damage. During the acute stage of Hemolytic Uremic Syndrome, patients must be carefully monitored for these extra-renal complications. It is very difficult to predict the severity and course of HUS once it initiates.

The active stage of Hemolytic Uremic Syndrome may be defined as that period of time during which there is evidence of hemolysis and the platelet count is less than 100,000. In HUS, the active stage usually lasts an average of six days (range, 2-16 days). It is during the active stage that the complications of HUS per se usually occur.

What are the complications and long-term risks associated with Hemolytic Uremic Syndrome?

Several studies have demonstrated that children with HUS who have apparently recovered will develop hypertension, urinary abnormalities and/or renal insufficiency during long-term follow-up.

End Stage Renal Disease, Dialysis and Kidney Transplantation

End Stage Renal Disease

Children and adolescents with chronic renal failure face a number of complications from the condition, including alterations in calcium and phosphate balance and renal osteodystrophy (softening of the bones, weak bones and bone pain), anemia (low blood cell count that leads to a lack of energy), growth failure (final height as an adult substantially below normal), hypertension (high blood pressure), and other complications.

Renal osteodystrophy (softening of the bones) is an important complication of chronic renal failure. Bone disease is nearly universal in patients with chronic renal failure; in some children, symptoms are minor to absent while others may develop bone pain, skeletal deformities and slipped epiphyses (abnormal shaped bones and abnormal hip bones) and have a propensity for fractures with minor trauma. Treatment of the bone disease associated with chronic renal failure includes control of serum phosphorus and calcium levels with restriction of phosphorus in the diet, supplementation of calcium, the need to take phosphorus binders, and the need to take medications for bone disease.

Anemia is a very common complication of chronic renal failure. The kidneys make a hormone that tells the bone marrow to make red blood cells and this hormone is not produced in sufficient amounts in children with chronic renal failure. Thus, children with chronic renal failure gradually become anemic while their chronic renal failure is slowly progressing. The anemia of chronic renal failure is treated with human recombinant erythropoietin (a shot given under the skin one to three times a week or once every few weeks with a longer acting human recombinant erythropoietin).

Growth failure ultimately leading to short height as an adult is a very common complication of chronic renal failure in children. The mechanisms of growth failure are complex and due to multiple causes. Poorly controlled renal osteodystrophy (bone disease), inadequate nutrition (insufficient intake of adequate calories), chronic acidosis (blood system too acid) and abnormalities of the growth hormone axis (growth hormone deficiency) are each major contributors to poor growth in the child with chronic renal failure. Growth hormone therapy with human recombinant growth hormone has been approved for use in children with chronic renal failure and such therapy has been shown to accelerate growth, induce persistent catch up growth and lead to normal adult height in children with chronic renal failure. Growth hormone therapy requires giving a shot under the skin once a day. Complications of growth hormone therapy are rare but may include glucose intolerance and exacerbation of poorly controlled renal osteodystrophy.

Dialysis and Kidney Transplantation

Renal replacement therapy can be in the form of dialysis (peritoneal dialysis or hemodialysis) or renal transplantation.

If the patient does not have a living related donor for their first kidney transplant and when they need a second kidney transplant after loss of the first transplant, they will need dialysis until a subsequent transplant can be performed. The patient can be on peritoneal dialysis or on hemodialysis.

Peritoneal dialysis has been a major modality of therapy for chronic renal failure for several years. Continuous Ambulatory Peritoneal Dialysis (CAPD) and automated peritoneal dialysis also called Continuous Cycling Peritoneal Dialysis (CCPD) are the most common forms of dialysis therapy used in children with chronic renal failure. In this form of dialysis, a catheter is placed in the peritoneal cavity (area around the stomach); dialysate (fluid to clean the blood) is placed into the abdomen and changed 4 to 6 times a day. Parents and adolescents are able to perform CAPD/CCPD at home. Peritonitis (infection of the fluid) is a major complication of peritoneal dialysis.

Hemodialysis has also been used for several years for the treatment of chronic renal failure during childhood. During hemodialysis, blood is taken out of the body by a catheter or fistula and circulated in an artificial kidney to clean the blood. Hemodialysis is usually performed three times a week for 3-4 hours each time in a dialysis unit.

Renal transplantation can be from a deceased or a living related donor (parent or sibling who is over the age of 18 who is compatible). Should the patient have a living related donor available to donate a kidney, they can undergo transplantation without the need for dialysis (preemptive transplantation). Should they not have a living related donor, they will likely need to undergo dialysis while on the waiting list for a deceased donor transplant. Fortunately, children have the shortest waiting time on the deceased donor transplant list. The average waiting time for children age 0-17 years is approximately 275-300 days while the average waiting time for patients age 18-44 years is approximately 700 days.

Following transplantation, the patient will need to take immunosuppressive medications for the remainder of their life to prevent rejection of the transplanted kidney. Medications used to prevent rejection have considerable side effects. Corticosteroids are commonly used following transplantation. The side effects of corticosteroids are Cushingnoid features (fat deposition around the cheeks and abdomen and back), weight gain, emotional liability, cataracts, decreased growth, osteomalacia and osteonecrosis (softening of the bones and bone pain), hypertension, acne and difficulty in controlling glucose levels. The steroid side effects, particularly the effects on appearance, are difficult for children, especially teenagers, and non compliance do to the side effects of medications is a risk in children; again, particularly teenagers.

Cyclosporine and/or tacrolimus are also commonly used as immunosuppressive medications following transplantation. Side effects of these drugs include hirsutism (increased hair growth), gum hypertrophy, interstitial fibrosis in the kidney (damage to the kidney), as well as other complications. Meclophenalate is also commonly used after transplantation (sometimes imuran is used); each of these drugs can cause a low white blood cell count and increased susceptibility to infection. Many other immunosuppressive medications and other medications (anti-hypertensive agents, anti-acids, etc) are prescribed in the post operative period.

Life long immunosuppression, as used in patients with kidney transplants, is associated with several complications including an increased susceptibility to infection, accelerated atherosclerosis (hardening of the arteries), increased incidence of malignancy (cancer) and chronic rejection of the kidney.

United States Renal Data Systems (USRDS) report that the half-life (time at which 50% of the kidneys are still functioning and 50% have stopped functioning) is 10.5 years for a deceased transplant in children age 0-17 years and 15.5 years for a living related transplant in children 0-17 years. Similar data for a transplant at age 18 to 44 years is 10.1 years and 16.0 years for a deceased donor and a living related donor, respectively. Thus, depending upon the age when the patient receives their first transplant they may need 2-3 transplants over the course of their life.

Thus, the life expectancy of a person with a kidney transplant is significantly less than the general population and the life expectancy of a person on dialysis is markedly less than the general population.

Hemolytic uremic syndrome patient follow-up.

Children who appear to have recovered from HUS may develop late complications. A precise determination of the risk of late complications is not likely. It is important to note that the risks of longer term (more than 20 years) complications are unknown and are likely to be higher than risks at 10 years, as many of the above studies describe.

All persons who have experienced HUS should be formally evaluated by a nephrologist—a kidney specialist—at a year following their acute illness. Kidneys injured by HUS may slowly recover function over at least a six month period following the acute episode and perhaps longer. Even persons with “mild” HUS who did not require dialysis should be formally evaluated. Such an evaluation should include a routine physical, blood pressure measurement, and blood and urine analyses from which kidney filtration rate can be calculated.

Studies done to date on HUS outcomes have largely confirmed a positive correlation between more severe kidney involvement acutely, particularly the need for extended dialysis, and increased incidence of future renal complications. However, it has been shown in multiple studies that even moderate kidney compromise in the acute phase of HUS can result in long-term complications due to damage to the filtering units in the kidneys.

Among survivors of HUS, estimates are that about five percent will eventually develop end stage kidney disease, with the resultant need for dialysis or transplantation, and another five to ten percent experience neurological or pancreatic problems which significantly impair quality of life. Since the longest available follow-up studies of HUS are about twenty (20) years, an accurate lifetime prognosis is not available, and as such, medical follow-up is indicated for even the mildest affected cases.

[1] Recent research suggests that E. coli O157:H7 acquired its pathological character when a bacteriophage (virus that infects bacteria) transmitted genetic material for the creation of the toxin from a closely related Shigella bacterial species (hence the epithet, Shiga-like toxin) to a formerly benign species of E. coli.

[2] Verotoxin-globotriaosyl ceramide binding receptors.

Glossary of terms

1. allograft: a graft derived from an individual of the same species that is sufficiently unlike genetically to interact antigenically
2. antagonist: in biochemistry, an antagonist acts against and blocks an action.
3. anticoagulant: any agent used to prevent the formation of blood clots.
4. antigen: a protein or carbohydrate substance (as a toxin or enzyme) capable of stimulating an immune response
5. antibody titers: a measure of proteins of high molecular weight that are produced normally after stimulation by an antigen and act specifically against the antigen in an immune response
6. anuria: absence of urine excretion
7. case fatality rate: the proportion of deaths among a group of persons with a particular condition or disease
8. basal ganglia: a region consisting of 3 clusters of neurons located at the base of the brain that are responsible for involuntary movements
9. C-reactive protein: a special type of protein produced by the liver that is only present during episodes of acute inflammation
10. CT scan: A computerized axial tomography scan is more commonly known by its abbreviated name, CAT scan or CT scan; an x-ray procedure which combines many x-ray images with the aid of a computer to generate cross-sectional views and, if needed, three-dimensional images of the internal organs and structures of the body
11. cortical necrosis: tissue death of the outer layer of the kidney
12. creatinine: a chemical waste molecule that is generated from muscle metabolism and transported through the bloodstream to the kidneys. The kidneys filter out most of the creatinine and dispose of it in the urine. As the kidneys become impaired, the creatinine will rise.
13. dialysis/hemodialysis: process of removing blood from an artery to purify it (remove wastes or toxins from the blood) and adjust fluid and electrolyte imbalances, adding vital substances, and returning it to a vein (see also peritoneal dialysis)
14. double-blinded study: A study in which neither the study groups nor the evaluator are aware of who receives the experimental treatment or procedure versus the placebo or comparison treatment
15. dysphasia: difficulty in swallowing
16. effective renal plasma flow (ERPF): the amount of plasma flowing through the kidney tubules per unit time; differentiated from renal plasma flow which is approximately 10% greater than ERPF
17. electroencephalograph (EEG): an apparatus for detecting and recording brain waves
18. end-stage renal disease (ESRD): the final stages of a terminal kidney disease or condition when there is complete or near complete failure of the kidneys to function
19. etiology: the cause of a disease
20. fibrinolytics: clot-dissolving drugs
21. gastric: relating to the stomach
22. genotype: the genetic constitution (the genome) of a cell, an individual or an organism.
23. glomerular: pertaining to the glomerulus, a tiny structure in the kidney that filters the blood to form urine.
24. glomerular filtration rate (GFR): the rate at which blood is filtered through tufts of capillaries in the kidney
25. glomerulonephritis: a disorder that causes inflammation of the internal kidney structures (specifically, the glomeruli); it may be a temporary and reversible condition, or it may be progressive.
26. graft: placing tissue or organs from one area on the body or from another person or an animal into the patient’s body; in this case transferring a kidney from one person to another
27. hemiparesis: muscular weakness or partial paralysis restricted to one side of the body
28. hemolytic anemia: anemia caused by excessive destruction (as in chemical poisoning, infection, or sickle-cell anemia) of red blood cells
29. hemorrhagic colitis: bloody infection/inflammation of the colon (bowel)
30. histological: in reference to the minute structure of tissues discernible with the microscope
31. hyperfiltration: abnormal increase in the filtration rate of the renal glomeruli
32. hypertension: high blood pressure
33. hyponatremia: deficiency of sodium (salt) in the blood
34. infarct/infarction: an area of necrosis (death) in a tissue or organ resulting from obstruction of the local circulation by a thrombus or embolus
35. internal/external capsule: fibrous express ways that contain nerves to transmit information within certain parts of the brain
36. in vitro: outside the living body and in an artificial environment
37. intravenous (IV): within a vein
38. ischemia: localized tissue anemia due to obstruction of the inflow of arterial blood (as by the narrowing of arteries by spasm or disease)
39. leukocyte: white blood cell
40. leukocytosis: increase in the number of white blood cells
41. microangiopathy: a disease of very fine blood vessels
42. microvascular: of, relating to, or constituting the part of the circulatory system made up of minute vessels (as venules or capillaries) that average less than 0.3 millimeters in diameter
43. monoclonal antibody: an antibody derived from a single cell in large quantities for use against a specific antigen
44. morbidity: the incidence of disease; the rate of sickness (as in a specified community or group)
45. morphologic: of, relating to, or concerned with form or structure
46. mortality: the number of deaths in a given time or place; the proportion of deaths in a given population
47. MRI/magnetic resonance imaging: a radiology technique using magnetism, radio waves, and a computer to produce images of body structures
48. nephrotic syndrome: a constellation of signs and symptoms including protein in the urine, low blood protein levels, high cholesterol levels, and swelling; results in damage to the kidneys, particularly the basement membrane of the glomerulus
49. neutrophil: type of white blood cell, filled with neutrally-staining granules, tiny sacs of enzymes that help the cell to kill and digest microorganisms it has engulfed
50. oliguria: reduced excretion of urine
51. parenteral: drug or substance, like supplementary nutrition, administration by intravenous, intramuscular, or subcutaneous injection; especially introduced other than by way of the intestines
52. paresis: paralysis
53. pathogenesis: the origin of a disease and the chain of events leading to that disease.
54. peritoneal dialysis: technique that uses the patient's own body tissues inside of the belly (abdominal cavity) to act as a filter to remove waste products and excess water from the body
55. placebo: an inert or harmless substance used especially in controlled experiments testing the efficacy of another substance (as a drug)
56. plasmapheresis: separating out the plasma from the whole blood, replacing the plasma, and returning plasma and original blood cells to the patient
57. platelet: An irregular, disc-shaped element in the blood that assists in blood clotting. During normal blood clotting, the platelets clump together.
58. primary: first in order of time or development
59. prodromal: a symptom or set of symptoms that occur before the onset of a disease or condition
60. proteinuria: protein in the urine
61. prothrombotic: a substance which encourages the production of blood clots
62. randomized: things or persons put in a random order so that every thing or person is equally likely to be selected; study subjects are randomly distributed into groups which are either subjected to the experimental procedure (or use of a drug) or which serve as controls.
63. receptor: a structure on the surface of a cell (or inside a cell) that selectively receives and binds a specific substance.
64. rectal prolapse: the falling down or slipping of a the rectum (the terminal part of the intestine) from its usual position
65. renal: kidney
66. retina: the sensory membrane that lines most of the large posterior chamber of the eye; functions as the immediate instrument of vision by receiving the image formed by the lens and converting it into chemical and nervous signals which reach the brain by way of the optic nerve
67. sequelae: an after effect of disease, injury, procedure, or treatment
68. serotype/group: a group of intimately related microorganisms distinguished by a common set of antigens
69. Shiga toxin/Stx: a poisonous product of the E. coli organism; toxins are usually very unstable and can cause damage to cells. Toxins typically induce antibody formation.
70. sodium: the major positive ion (cation) in fluid outside of cells. When combined with chloride, the resulting substance is table salt. Excess sodium is excreted in the urine. Too much or too little sodium can cause cells to malfunction.
71. stupor: decreased mental status or consciousness; loss of alertness
72. tetraspastic: a state of hypertonicity or increase over the normal tone of a muscle, with heightened deep tendon reflexes, affecting all four extremities
73. thalamus/thalami: the part of the brain that serves to relay impulses and especially sensory impulses to and from the cerebral cortex (the gray matter of the cerebrum that functions chiefly in coordination of sensory and motor information)
74. thrombocytopenia: persistent decrease in the number of blood platelets that is often associated with hemorrhagic conditions -- called also thrombopenia
75. thrombogenic: tending to produce a thrombus (a clot of blood formed within a blood vessel and remaining attached to its place of origin)
76. thrombosis: the formation or presence of a blood clot within a blood vessel
77. thrombotic thrombocytopenic purpura (TTP): a blood disorder characterized by low platelets, low red blood cell count (caused by premature breakdown of the cells), abnormalities in kidney function, and neurological abnormalities; caused by a deficiency in the von Willebrand Factor cleaving protease, known as ADAMTS13. The loss of this enzyme results in large complexes of von Willbrand factor circulating in the blood, which in turn causes platelet clumping and red blood cell destruction.
78. vascular endothelial growth factor: substance made by cells that stimulates new blood vessel formation
79. white matter: neural tissue that consists largely of myelinated (sheathed) nerve fibers, has a whitish color, and underlies the gray matter of the brain and spinal cord or is gathered into nerves

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