National Kidney Month - What It Is Like To Live With End Stage Renal Disease (ESRD)?

Guest Blogger - Colin Caywood

In honor of March's official designation as National Kidney Month, fellow Food Safety News contributing writer Dave Babcock recently published an article, National Kidney Month Kicks Off. In his article, Babcock discusses the connection between long-term kidney health and food safety, a connection which most commonly flows from the development of hemolytic uremic syndrome (HUS) caused by toxins from foodborne bacteria like shiga toxin-producing Escherichia coli (E. coli).

As anyone who has been forced to suffer through ESRD can attest, the physical and mental effects it can cause are devastating.

While it is true that various treatment options presently exist, none of those options are especially desirable. The biggest and most obvious decision for a person diagnosed with ESRD to make is whether to sustain on dialysis for as long as possible, or seek out a kidney transplant, likely enduring dialysis anyway during the waiting period.

If given the choice, most people with ESRD will opt for a kidney transplant. There is evidence that a transplant can increase a person's life expectancy up to three times longer than dialysis alone. It can also have a much less invasive effect on a person's day-to-day life when compared with the requirements of dialysis. Unfortunately, the wait-time for a donor kidney is often a year minimum, but usually longer depending on a variety of factors.

One such wait time factor is blood type. For example, a person with a rare blood type O will have the longest wait period, usually three to four years. Because a patient with blood type O has antibodies against blood types A, B, and AB, it severely limits the donor pool from which a kidney may be harvested. If the patient is fortunate, perhaps a deceased or living close relative, such as a parent or sibling over the age of 18 and who is compatible with the patient, will be able to donate a kidney. Regardless, while awaiting a donor, an ESRD patient must undergo dialysis treatment just to survive until the transplant operation can be performed.

Assuming the patient survives the transplant procedure, they can then look forward to a lifetime of immunosuppressive medications, necessary to prevent their body from rejecting the transplanted kidney. The artificial suppression of the immune system is--as nearly anyone can surmise--fraught with considerable side effects.

Commonly used immunosuppresants include cyclosporine, tacrolimus, meclophenalate, imuran, and corticosteroids. Cyclosporine and tacrolimus have side effects that include increased hair growth and gum hypertrophy, as well as, ironically, damage to the kidney. Meclophenalate and imuran are known to cause low white blood cell count and increased susceptibility to infection. Corticosteroids can produce the undesirable Cushing's syndrome (fatty deposits around the facial cheeks, as well as on the abdomen and back), weight gain, emotional instability, cataracts, decreased growth, softening of the bones and bone pain, hypertension, acne, and difficulty in controlling glucose levels.

Immunosuppressants, like those described above, are necessary for organ transplant recipients. They reduce the body's immune response, thereby preserving the useful life of the transplanted kidney which the body would otherwise recognize as foreign and dangerous. If this occurs, it sets off a chain of events that culminate in the body's rejection of the kidney. But because a healthy and timely immune system response is the body's critical and natural defense against illness, immunosuppression therapy necessarily leads to a lifetime of heightened susceptibility to serious infection, accelerated hardening of the arteries, cancer, and chronic kidney rejection.

Assuming the transplanted kidney is received by the patient without complication, no transplant lasts forever. The patient's transplanted kidney can be expected to last about 15 years if it comes from a living donor, or about 10 years if it comes from a cadaver. Of course, the younger the patient develops ESRD, the higher the probability that a second, or even third, kidney transplant will be required during their lifetime. As each transplant reaches the end of its useful life, the patient will fall back into the cycle of ESRD, dialysis, an increase in kidney-related medical problems and then--assuming another kidney transplant is possible--recovery from transplantation.

Either decision the patient makes--transplant or dialysis--will involve dialysis treatments regardless. As with a transplant, the patient's quality of life is guaranteed to suffer markedly. There are generally two modes of dialysis an ESRD patient may undergo: peritoneal dialysis or hemodialysis.

Peritoneal dialysis has been a major physical therapeutic method of therapy for ESRD for several years. Continuous Ambulatory Peritoneal Dialysis (CAPD) and automated peritoneal dialysis, also called Continuous Cycling Peritoneal Dialysis (CCPD), are the most common form of dialysis therapy used in children. In this form of dialysis, a catheter is placed in the area around the stomach. Dialysate (a chemical bath that draws fluids and toxins out of the bloodstream) is placed into the abdomen and changed four to six times a day. While children must often go to a medical treatment facility, adults can usually perform CAPD/CCPD at home.

The known compilations of peritoneal dialysis include peritonitis (infection of the fluid), which can be a major risk. Symptoms of peritonitis include fever, excruciating abdominal pain with movement, nausea, and vomiting. If left untreated, it usually results in death.

The other common dialysis method to treat ESRD is hemodialysis. During hemodialysis, blood in taken out of the body by a catheter or fistula, and circulated in a machine that simulates the kidney's natural cleansing process, removing harmful toxins and excess fluid from the blood. While the hemodialysis process itself does not physically hurt, patients usually experience nausea and abdominal cramps as excess fluid is pulled from the body, along with fluctuations in blood pressure and heart rate. Hemodialysis is generally performed three times a week, and takes a major time commitment--three to four hours per session is the average.

Beyond the transplant and dialysis complications, bone disease is nearly universal in patients with ESRD. As a result, patients will be prone to develop bone pain, skeletal deformities and abnormal shaped bones, and have a propensity for fractures with minor trauma. Treatment of the bone disease associated with ESRD includes careful control of the patient's serum phosphorous and calcium levels with stringent dietary restrictions, calcium supplements, phosphorus binders, and various other bone disease-fighting medications.

The last major common complication of ESRD worth mentioning is anemia. Anemia can be treated with a shot of erythropoietin given under the skin one to three times a week, or once every few weeks with a longer acting dose. Erythropoietin is a hormone normally produced by the kidney that promotes the formation of red blood cells in the bone marrow. In patients suffering from ESRD, this hormone ceases to be produced, thus anemia results. Left untreated, anemia can cause severe fatigue, nerve damage, mental impairment, heart problems, and death.

Given the gloom and doom of this article, it is important to remember that a person's diagnosis with ESRD is a not a death sentence. But just because a person is fortunate enough to survive a serious shiga toxin-producing E. coli infection and HUS--often the result of foodborne contamination--kidney damage sufficient to result in ESRD will continue to affect their life long after the E. coli infection has passed. The vast complications of ESRD are incredibly serious, often painful, and certain to drastically reduce a person's overall quality of life.

E. coli Litigation Site Updated

Marler Clark’s E. coli lawyers developed this site to keep our clients up-to-date on current litigation being prosecuted by Marler Clark throughout the United States. The site is also a resource for Marler Clark co-counsel in E. coli cases, print and broadcast media who are working on stories about E. coli outbreaks and outbreak-related litigation, and potential clients who are researching Marler Clark in anticipation of filing an E. coli claim.

Presence and Characterization of Shiga Toxin-Producing Escherichia coli and Other Potentially Diarrheagenic E. coli in Retail Meats.

Appl Environ Microbiol. 2010 Jan 15.
Xia X, Meng J, McDermott PF, Ayers S, Blickenstaff K, Tran TT, Abbott J, Zheng J, Zhao S.

Department of Nutrition and Food Science, and Joint Institute for Food Safety and Applied Nutrition, University of Maryland, College Park, Maryland 20742; Center for Veterinary Medicine, Food and Drug Administration, Laurel, MD 20708; Center for Food Safety and Applied Nutrition, Food and Drug Administration, College Park, MD 20740.

To determine the presence of Shiga toxin-producing Escherichia coli (STEC) and other potentially diarrheagenic E. coli in retail meats, 7,258 E. coli isolates collected by the U. S. National Antimicrobial Resistance Monitoring System (NARMS) retail meat program from 2002 to 2007 were screened for Shiga toxin genes. In addition, 1,275 of the E. coli isolates recovered in 2006 were examined for virulence genes specific for other diarrheagenic E. coli. Seventeen isolates (16 from ground beef and 1 from pork chop) were positive for stx genes, including five for both stx1 and stx2, two for stx1 and 10 for stx2. The 17 STEC belonged to 10 serotypes: O83:H8, O8:H16, O15:H16, O15:H17, O88:H38, ONT:H51, ONT:H2, ONT:H10, ONT:H7 and ONT:H46. None of the STEC isolates contained eae, whereas seven carried EHEC-hlyA. All except one STEC isolate exhibited toxic effects on Vero cells. DNA sequence analysis showed that stx2 from five STEC isolates encoded mucus-activatable Stx2d. Subtyping of the 17 STEC isolates by PFGE yielded 14 distinct restriction patterns. Among the 1, 275 isolates from 2006, 11 atypical enteropathogenic E. coli (EPEC) isolates in addition to three STEC were identified. This study demonstrated that retail meats, mainly ground beef, were contaminated with diverse STEC strains. The presence of atypical EPEC strains in retail meat is also of concern due to their potential to cause human infections.

Second Chance by Kip Moore - another E. coli Horror story

Possible Foodborne Illness Link to Urinary Tract Infections?

E. coli bacteria in food -- commonly linked to food poisoning and the stomach pain and diarrhea that result -- might also be the cause of some urinary tract infections. Researchers have found the same strains of the bacteria in chicken from stores and restaurants and in women with the infections. There's no evidence that the germs were transmitted directly to the women through the food they ate, although that's possible.

Still, the findings are the first to suggest a possible link between the food supply and urinary tract infections, said Amee R. Manges, an assistant professor at McGill University in Montreal and lead author of a report on the discovery. It is published in the January issue of Emerging Infectious Diseases.

SOURCES: Amee R. Manges, M.P.H., Ph.D., assistant professor, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal; Pascal James Imperato, M.D., M.P.H.&T.M., dean and professor, School of Public Health, State University of New York Downstate Medical Center, Brooklyn, N.Y.; Marion Nestle, Ph.D., M.P.H., professor, Department of Nutrition, Food Studies and Public Health, New York University, New York City; January 2010, Emerging Infectious Diseases

Parents Food Safety Guide for E. coli

Click on image above to download Safety Guide. E. coli – www.about-ecoli.com

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). More than 700 serotypes of E. coli have been identified. Their “O” and “H” antigens on their bodies and flagella distinguish the different E. coli serotypes, 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. 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). E. coli O157:H7 was first recognized as a foodborne pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis (bloody diarrhea) associated with consumption of contaminated hamburgers (Riley, et al., 1983). The following year, Shiga toxin (Stx), produced by the then little-known E. coli O157:H7 was identified as the real culprit. In the ten years following the 1982 outbreak, approximately thirty E. coli O157:H7 outbreaks were recorded in the United States (Griffin & Tauxe, 1991). The actual number that occurred is probably much higher because E. coli O157:H7 infections did not become a reportable disease (required to be reported to public health authorities) until 1987 (Keene et al., 1991 p. 60, 73). As a result, only the most geographically concentrated outbreaks would have garnered enough attention to prompt further investigation (Keene et al., 1991 p. 583). It is important to note that only about 10% of infections occur in outbreaks, the rest are sporadic. The CDC has estimated that 85% of E. coli O157:H7 infections are foodborne in origin (Mead, et al., 1999). In fact, consumption of any food or beverage that becomes contaminated by animal (especially cattle) manure can result in contracting the disease. Foods that have been sources of contamination include ground beef, venison, sausages, dried (non-cooked) salami, unpasteurized milk and cheese, unpasteurized apple juice and cider (Cody, et al., 1999), orange juice, alfalfa and radish sprouts (Breuer, et al., 2001), lettuce, spinach, and water (Friedman, et al., 1999).

Hemolytic Uremic Syndrome and Death in Persons with Escherichia coli O157:H7 Infection, Foodborne Diseases Active Surveillance Network Sites, 2000-2006

Clinical Infectious Diseases 2009; 49:000–000 - Major Article

L. Hannah Gould, 1, Linda Demma, 1, Timothy F. Jones, 3, Sharon Hurd, 4, Duc J. Vugia, 5, Kirk Smith, 6, Beletshachew Shiferaw, 7, Suzanne Segler, 2, Amanda Palmer, 8, Shelley Zansky, 9, Patricia M. Griffin, 1, and the Emerging Infections Program FoodNet Working Group

Background. Hemolytic uremic syndrome (HUS) is a life‐threatening illness usually caused by infection with Shiga toxin–producing Escherichia coli O157 (STEC O157). We evaluated the age‐specific rate of HUS and death among persons with STEC O157 infection and the risk factors associated with developing HUS.

Methods. STEC O157 infections and HUS cases were reported from 8 sites participating in the Foodborne Diseases Active Surveillance Network during 2000–2006. For each case of STEC O157 infection and HUS, demographic and clinical outcomes were reported. The proportion of STEC O157 infections resulting in HUS was determined.

Results. A total of 3464 STEC O157 infections were ascertained; 218 persons (6.3%) developed HUS. The highest proportion of HUS cases (15.3%) occurred among children aged <5 years. Death occurred in 0.6% of all patients with STEC O157 infection and in 4.6% of those with HUS. With or without HUS, persons aged 60 years had the highest rate of death due to STEC O157 infection. Twelve (3.1%) of 390 persons aged 60 years died, including 5 (33.3%) of 15 persons with HUS and 7 (1.9%) of 375 without. Among children aged <5 years, death occurred in 4 (3.0%) of those with HUS and 2 (0.3%) of those without.

Conclusions. Young children and females had an increased risk of HUS after STEC O157 infection. With or without HUS, elderly persons had the highest proportion of deaths associated with STEC O157 infection. These data support recommendations for aggressive supportive care of young children and the elderly early during illness due to STEC O157.

1 Enteric Diseases Epidemiology Branch, National Center for Zoonotic, Vector‐Borne, and Enteric Diseases, Centers for Disease Control and Prevention, and 2 Georgia Emerging Infections Program, Atlanta, Georgia; 3 Tennessee Department of Health, Nashville; 4 Connecticut Emerging Infections Program, New Haven; 5 California Department of Public Health, Richmond; 6 Minnesota Department of Health, St. Paul; 7 Oregon Department of Human Services, Portland; 8 Maryland Department of Health and Mental Hygiene, Baltimore; and 9 New York State Department of Health, Albany.

Canadian vaccine to combat E. coli and non-E. coli STECs that cause "hamburger disease"

Anne-Marie Hickey of the University of Saskatchewan’s research communications office wrote an interesting article on the work of David Asper, a graduate student at the University of Saskatchewan.

The veterinary microbiology student’s work, soon to be published, is premised on the idea that humans can be protected from harmful bacteria by vaccinating cattle that are the source of the bacteria. Asper’s work builds on groundbreaking research by his supervisor Andrew Potter, director of the Vaccine and Infectious Disease Organization (VIDO) International Vaccine Centre. Potter's work led to the first cattle vaccine against E. coli O157, the leading cause of “hamburger disease.” The vaccine prevents the bacteria from attaching to the animal’s intestines and from colonizing, cutting the disease off at the source.

“The E. coli O157 vaccine is the first of its kind worldwide and is expected to significantly lessen the amount of E. coli O157 present in food products and also in the environment,” said Potter. But while E. coli O157 is the most prevalent type of E. coli in North America, it’s just one of hundreds of E. coli bacteria around the world that cause disease by producing shiga toxin. These shiga toxin-producing E. coli (STEC) produce infections that can range from very mild to severe or even life-threatening. “Right now, STEC bacteria is the number one cause of renal (kidney) failure in children around the world,” said Asper. “It affects adults too, but children are the most susceptible.”

STEC bacteria cause disease in humans if meat becomes contaminated during slaughter or if feces mix with groundwater, polluting drinking or swimming water or food supplies. But the STEC bacteria that cause human illness generally do not make animals sick so healthy cattle often have STEC bacteria living in their intestines.

Due to improved detection methods, cases of non-O157 E. coli infection are on the rise, increasing the importance of having the second-generation vaccine.

“We can protect humans by vaccinating animals before they come in contact with the pathogen. I think that’s very important work that will lead to a lot fewer infections,” Asper said. His work could help prevent tragedies such as the 2000 incident in Walkerton, Ont. when fecal material from cattle seeped into the water system, contaminating drinking water and resulting in thousands of illnesses and seven deaths in the community.

Just as the E. coli O157 cattle vaccine will be a significant tool for use by beef and dairy producers to mitigate human infection risk, Asper’s vaccine could also lessen financial losses to meat producers. When STEC bacteria is found in just one meat sample, beef processors are required to destroy the entire shipment -- a significant cost to farmers.

Lack of Internalization of Escherichia coli O157:H7 in Lettuce (Lactuca sativa L.) after Leaf Surface and Soil Inoculation

Authors: Zhang, Guodong1; Ma, Li2; Beuchat, Larry R.2; Erickson, Marilyn C.2; Phelan, Vanessa H.2; Doyle, Michael P.2

Source: Journal of Food Protection®, Volume 72, Number 10, October 2009 , pp. 2028-2037(10)

Publisher: International Association for Food Protection

Abstract:

Survival and internalization characteristics of Escherichia coli O157:H7 in iceberg, romaine, and leaf lettuce after inoculation of leaf surfaces and soil were determined. A five-strain mixture of E. coli O157:H7 in water and cow manure extract was used as an inoculum for abaxial and adaxial sides of leaves at populations of 6 to 7 log and 4 log CFU per plant. The five strains were individually inoculated into soil at populations of 3 and 6 log CFU/g. Soil, leaves, and roots were analyzed for the presence and population of E. coli O157:H7. Ten (4.7%) of 212 samples of leaves inoculated on the adaxial side were positive for E. coli O157:H7, whereas 38 (17.9%) of 212 samples inoculated on the abaxial side were positive. E. coli O157:H7 survived for at least 25 days on leaf surfaces, with survival greater on the abaxial side of the leaves than on the adaxial side. All 212 rhizosphere samples and 424 surface-sanitized leaf and root samples from plants with inoculated leaves were negative for E. coli O157:H7, regardless of plant age at the time of inoculation or the location on the leaf receiving the inoculum. The pathogen survived in soil for at least 60 days. Five hundred ninety-eight (99.7%) of 600 surface-sanitized leaf and root samples from plants grown in inoculated soil were negative for E. coli O157:H7. Internalization of E. coli O157:H7 in lettuce leaves and roots did not occur, regardless of the type of lettuce, age of plants, or strain of E. coli O157:H7.

Document Type: Research article

Affiliations: 1: Center for Food Safety, University of Georgia, 1109 Experiment Street, Griffin, Georgia 30223-1797, USA; Center for Food Safety and Applied Nutrition, U.S. Food and Drug Administration, 5100 Paint Branch Parkway, College Park, MD 20740, USA 2: Center for Food Safety, University of Georgia, 1109 Experiment Street, Griffin, Georgia 30223-1797, USA

Organics Vrs. Standard Operating Procedure (SOP) Study At Kansas State University Finds No Difference In E. coli Prevalence In Beef Cattle

 We must be pass the time when all the stories seemed to be about how organics would make you able to jump tall buildings in a single bound.

At Kansas State University, researchers have found that "cattle production systems" do not affect E. coli prevalence in beef.  The study looked at organic and "natural production systems" and apparently found that antibiotic susceptibility of Escherichia coli 0157:H7 was unchanged.

We think a better way to communicate what KSU researchers are talking about would be to think of "natural" as standard operating procedure.   The standard method cattle ranchers use to employ some antibiotics and hormones, and use non-organic feeds that are regulated only by the owner of the brand name.

The organic method uses only organic feeds as regulated by the United States Department of Agriculture and do not use antibiotics, hormones or other veterinary products.

"The prevalences of E. coli 0157:H7 that we observed in organically and naturally (SOP) raised cattle were similar in the previously reported prevalence in conventionally raised cattle," the researchers said. "No major differences in antibiotic susceptibility patterns among the isolates were observed."

There more on the KSU study in Foodstuffs, the weekly newspaper of agribusiness.

University of Nebraska-Lincoln Wants To Control E. coli 0157:H7 At The Feedlot

Big Red is out to find a diet that limits E. coli 0157:H7 at the feedlot. Researchers at the University of Nebraska-Lincoln are studying how nutrition of ruminants affects the colonization and growth of E coli 0157:H7.

Nebraska’s Institute of Agriculture and Natural Resources is focusing on how nutrition affects microbiology. It has focused on E. coli research since 1997. Previous research showed E. coli is so common in feedlot cattle it would not be practical to eliminate it.

UNL has worked closely with Canadian researchers on a vaccine. One feed additive was found to reduce fecal shedding of E. coli by about 35 percent, and vaccination reduced shedding by 65 percent.

A company called Bioniche has obtained permission to market the vaccine in Canada. It is awaiting approval for sale in the United States. UNL researchers believe knowing when and where E. coli is being shed in manure is key to controlling it.

UNL is also studying the impact of distiller’s grain on E. coli shedding.

Food Borne Illness Attorney William Marler Says When Its Comes To E. coli Outbreak, Remember What You Ate

The following was an editorial by Youngstown, Ohio television station WYTV-33:

Summertime means firing-up the grill or heading to the county fair, but it also means e-coli dangers.

The US Department of Agriculture says at least three people in Ohio are sick with e-coli after eating meat from Valley Meats in Illinois.  The company is now recalling nearly 96,000 pounds of ground beef.

You can protect yourself from e-coli by washing your hands and food, and fully cooking your meat.  E-coli can cause abdominal pain, and even acute kidney failure.  Health officials say e-coli has a 1 to 10 day incubation period.

William Marler, Food Borne Illness Attorney says, "An e-coli outbreak, it is never the last thing you ate.  It is usually 3 to 4 or 5 days ago that likely made you sick.  So having a pretty good understanding of what your diet has been 3 or 4 or 5 days ago become equivical when the health dept. is investigating."

For more information, you can call the USDA meat and poultry hotline at 1-888-MP-HOTLINE or click here.

Prom Queen Is E. Coli Victim And Cannot Go; So Prom Comes To Her Hospital

Spring break in Mexico has left Fishers High School prom queen in the hospital with E. coli since April 18th, unable to attend the big event.

But thanks to her friends from school and an understanding Indianapolis Hospital staff, the prom came to the queen.

The prom queen and her boyfriend were joined by several friends for a pre-prom dinner Saturday night in a transformed hospital atrium.

Fishers Principal Jason Urban also attended the makeshift prom event to present Westrick and her boyfriend, senior Gabe Hulecki, with their honorary crowns as prom queen and king respectively.

Westrick is said to have excellent prospects for a full recovery.  South Bend's Channel 28 has the the cute story here.

Campaign Underway In UK To Make It Illegal To Provide Advance Warnings Of E. coli Inspections

In the United Kingdom, Professor Hugh Pennington wants all food inspections, primary and secondary, to be unannounced unless “there are specific and justifiable circumstances or reasons why a pre-arranged visit is necessary”.

The Wales News reports that:

In his report into the 2005 epidemic that struck down more than 150 people, most of them children, across the South Wales Valleys and claimed the life of Mason Jones, aged five, Professor Hugh Pennington found that all of the inspections made at the premises of the butcher responsible in the months before people became ill had been pre-arranged.

The largest E. coli outbreak in Wales history has led to a campaign group to lobby for a law that would make it illegal for food hygiene officers to warn the businesses they are about to inspect.
Now unannounced inspections are considered the "best practice," but do not always get carried out that way.  The Wales News has a story on the inspections controversy here.

E coli Showing Up In Too Much Arkansas Private Well Water

 Now the safety of private water wells is being called into question in Arkansas.   

"We don't recommend that people drink water with E. coli in it under any circumstances. There's no safe level of E. coli as far as we're concerned," says Ed Barum.

Barum, with the State Health Department, spoke with KTHV-TV in Little Rock.   The State Health Department tests water samples for  private well owners. 

Results show counties in northwest Arkansas have the highest number of contaminated wells.

Benton County has 85 wells have testing positive for E. coli. Other counties, however, have a higher percentage of contaminated wells. In Conway County, for example, testing of 84 wells came back with 28 positive for one E. Coli strain or another.

Owners of wells with bad water are told to install a chlorination or filtration system. Barum says the Health Department will help " find a solution that will work for them in their particular area with their particular well."

KTHV speculates that the high concentration of contaminated wells in northwest Arkansas could be due to bacteria  the great number of chicken farms in the area.

However Barum told the station that , "There's not a good way to say this is the cause. There's not a good way for us to say in northwest Arkansas the cause for private drinking well water is chicken farming or pig farming or cattle farming. That's just not possible right now with what we know."

For more, check this out.

E. coli O157:H7 Season is Nearly Upon Us - Will it be 2005 and 2006 or 2007 and 2008?

The presence of E. coli O157:H7 in hamburger was defined as an adulterant under the Federal Meat Inspection Act in 1994. However, recalls of E. coli O157:H7 contaminated meat and related illnesses continued over the next decade to grow, as did my law firm. Oddly too, and with near regularity, E. coli O157:H7 recalls and illnesses seemed to begin in the Spring and peak in late Summer and Fall from 1993 through 2002.

After 24 million pounds of contaminated beef were recalled in 34 separate incidents in 2002, recalls dropped off to just over a million pounds a year for the next three years, and then to just 181,900 pounds in 2006. The Centers of Disease Control and Prevention saw E. coli O157:H7 – related illnesses drop 48% between 2000 and 2006.

The reality is that from 1993 through 2002, children sickened with E. coli O157:H7 tainted hamburger made up the bulk of my law practice. However, as E. coli O157:H7 hamburger recalls fell from 2003 through the end of 2006, I wondered if the law firm would survive. Springs just simply were not the same.

But then came Spring 2007. E. coli O157:H7, which begins its life in the hindgut of a cow, mounted a surge on its home court. And, it came back with a vengeance. Since the Spring of 2007, forty-four million pounds of beef have been recalled in 25 incidents due to E. coli O157:H7. And, I am now back in the meat business, and look to Spring not just for the beginning of hay fever season.

Now, Spring 2009 is upon us. In preparing for it, I had some research done on the “seasonality” of E. coli O157:H7 in both humans and cattle and then say what was available in the literature as to the reasons behind it. Perhaps it does not fully explain what I experienced from 1993 though 2008, but it is a start. It is all about being prepared.

Seasonality in humans:

• A review of E. coli O157:H7 diarrhea in the US by Slutsker et al (1997) found that E. coli O157:H7 was isolated most frequently from patients during the summer months.
• Results from an epidemiological review of E. coli O157:H7 outbreaks in the US (1982-2002) showed that outbreaks involving ground beef peaked in summer months (Rangel et al, 2005)
• In a review of non-O157 STEC infections in the US from 1983-2002 revealed that these infections also were most frequent during the summer (Brooks et al, 2005)
• In Scotland, HUS and E. coli O157:H7 infections peaked in patients under 15 years of age in July/August, followed by a plateau from June to September (Douglas et al, 1997). Interestingly, the prevalence in Scottish beef cattle at slaughter was found to be highest during the winter, but the concentration of E. coli O157:H7 (number of bacteria shed in cattle feces) was highest during the warmer months (Ogden et al, 2004).

Seasonality in ruminants:

• Numerous studies in cattle indicate that fecal shedding of E. coli O157:H7 is typically low in the winter, increases in the spring, peaks during the summer and tapers off in the fall (Edrington et al, 2006; Hancock et al, 2001; Hussein et al, 2005, etc.)
• Barkocy-Gallagher et al (2003) found that the prevalence of E. coli O157:H7 in cattle feces peaked in the summer, and prevalence on hides (a known risk factor for beef contamination) was highest from spring through fall.
• A survey of ground beef samples in the US showed that they were 3x more likely to be contaminated with E. coli O157:H7 from June – September (Chapman, et al 2001)
• A survey in the UK found that the majority of retail meats that tested positive for E. coli O157:H7 were collected between May and September.

Hypotheses on why there are seasonal differences in prevalence in both humans and cattle

Human factors:

• Differences in handling and cooking food, or differences in consumption patterns during the summer, especially ground beef (outdoor BBQs, picnics, summer camps)
• Higher prevalence of E. coli O157:H7 in cattle feces and hides entering the slaughterhouse
• More outbreaks linked to swimming pools, recreational water, and agriculture fairs during the summer

Animal factors:

• Speculation that temperature may affect shedding or survival in feces (warmer months promoting survival and/or growth of E. coli O157:H7).
• Studies by Edrington et al (2006 and 2008) suggested that day length and effects on hormones such as melatonin secretion from the gastrointestinal tracts may be the underlying mechanism for seasonality in cattle. The authors hypothesized that the seasonal variation is a result of physiological responses within the host animal to changing day-length. Hormones have been shown to play a role in the regulation of bacterial populations and host immunity.

REFERENCES

1. Barkocy-Gallagher, G. A., T. M. Arthur, M. Rivera-Betancourt, X. Nou, S. D. Shackelford, T. L. Wheeler, and M. Koohmaraie. 2003. Seasonal prevalence of Shiga toxin-producing Escherichia coli, including O157:H7 and non-O157 serotypes, and Salmonella in commercial beef processing plants. J Food Prot 66:1978-86.
2. Besser, R. E., P. M. Griffin, and L. Slutsker. 1999. Escherichia coli O157:H7 gastroenteritis and the hemolytic uremic syndrome, an emerging infectious disease. Annu Rev Med 50:355-67.
3. Brooks, J. T., E. G. Sowers, J. G. Wells, K. D. Greene, P. M. Griffin, R. M. Hoekstra, and N. A. Strockbine. 2005. Non-O157 Shiga toxin-producing Escherichia coli infections in the United States, 1983-2002. J Infect Dis 192:1422-9.
4. Chapman, P. A., C. A. Siddons, A. T. Gerdan Malo, and M. A. Harkin. 1997. A 1-year study of Escherichia coli O157 in cattle, sheep, pigs and poultry. Epidemiol Infect 119:245-50.
5. Douglas, A. S., and A. Kurien. 1997. Seasonality and other epidemiological features of haemolytic uraemic syndrome and E. coli O157 isolates in Scotland. Scott Med J 42:166-71.
6. Dunn, J. R., J. E. Keen, and R. A. Thompson. 2004. Prevalence of Shiga-toxigenic Escherichia coli O157:H7 in adult dairy cattle. J Am Vet Med Assoc 224:1151-8.
7. Edrington, T. S., T. R. Callaway, S. E. Ives, M. J. Engler, M. L. Looper, R. C. Anderson, and D. J. Nisbet. 2006. Seasonal shedding of Escherichia coli O157:H7 in ruminants: a new hypothesis. Foodborne Pathog Dis 3:413-21.
8. Edrington T.S., T. R. Callaway, D. M. Hallford, L. Chen, R. C. Anderson, and D. J. Nisbet. 2008. Effects of exogenous melatonin and tryptophan on fecal shedding of E. coli O157:H7 in cattle. Microb Ecol. 55:553-60.
9. Fernandez, D., E. M. Rodriguez, G. H. Arroyo, N. L. Padola, and A. E. Parma. 2009. Seasonal variation of Shiga toxin-encoding genes (stx) and detection of E. coli O157 in dairy cattle from Argentina. J Appl Microbiol 106:1260-7.
10. Hancock, D., T. Besser, J. Lejeune, M. Davis, and D. Rice. 2001. The control of VTEC in the animal reservoir. Int J Food Microbiol 66:71-8.
11. Hancock, D. D., T. E. Besser, M. L. Kinsel, P. I. Tarr, D. H. Rice, and M. G. Paros. 1994. The prevalence of Escherichia coli O157.H7 in dairy and beef cattle in Washington State. Epidemiol Infect 113:199-207.
12. Hancock, D. D., T. E. Besser, D. H. Rice, D. E. Herriott, and P. I. Tarr. 1997. A longitudinal study of Escherichia coli O157 in fourteen cattle herds. Epidemiol Infect 118:193-5.
13. Hussein, H. S., and L. M. Bollinger. 2005. Prevalence of Shiga toxin-producing Escherichia coli in beef cattle. J Food Prot 68:2224-41.
14. Khaitsa, M. L., M. L. Bauer, G. P. Lardy, D. K. Doetkott, R. B. Kegode, and P. S. Gibbs. 2006. Fecal shedding of Escherichia coli O157:H7 in North Dakota feedlot cattle in the fall and spring. J Food Prot 69:1154-8.
15. LeJeune, J. T., T. E. Besser, D. H. Rice, J. L. Berg, R. P. Stilborn, and D. D. Hancock. 2004. Longitudinal study of fecal shedding of Escherichia coli O157:H7 in feedlot cattle: predominance and persistence of specific clonal types despite massive cattle population turnover. Appl Environ Microbiol 70:377-84.
16. MacDonald, K. L., M. J. O'Leary, M. L. Cohen, P. Norris, J. G. Wells, E. Noll, J. M. Kobayashi, and P. A. Blake. 1988. Escherichia coli O157:H7, an emerging gastrointestinal pathogen. Results of a one-year, prospective, population-based study. JAMA 259:3567-70.
17. Ogden, I. D., M. MacRae, and N. J. Strachan. 2004. Is the prevalence and shedding concentrations of E. coli O157 in beef cattle in Scotland seasonal? FEMS Microbiol Lett 233:297-300.
18. Ostroff, S. M., J. M. Kobayashi, and J. H. Lewis. 1989. Infections with Escherichia coli O157:H7 in Washington State. The first year of statewide disease surveillance. JAMA 262:355-9.
19. Pearl, D. L., M. Louie, L. Chui, K. Dore, K. M. Grimsrud, D. Leedell, S. W. Martin, P. Michel, L. W. Svenson, and S. A. McEwen. 2006. The use of outbreak information in the interpretation of clustering of reported cases of Escherichia coli O157 in space and time in Alberta, Canada, 2000-2002. Epidemiol Infect 134:699-711.
20. Rangel, J. M., P. H. Sparling, C. Crowe, P. M. Griffin, and D. L. Swerdlow. 2005. Epidemiology of Escherichia coli O157:H7 outbreaks, United States, 1982-2002. Emerg Infect Dis 11:603-9.
21. Rasmussen, M. A., and T. A. Casey. 2001. Environmental and food safety aspects of Escherichia coli O157:H7 infections in cattle. Crit Rev Microbiol 27:57-73.
22. Slutsker, L., A. A. Ries, K. D. Greene, J. G. Wells, L. Hutwagner, and P. M. Griffin. 1997. Escherichia coli O157:H7 diarrhea in the United States: clinical and epidemiologic features. Ann Intern Med 126:505-13.
23. Van Donkersgoed, J., T. Graham, and V. Gannon. 1999. The prevalence of verotoxins, Escherichia coli O157:H7, and Salmonella in the feces and rumen of cattle at processing. Can Vet J 40:332-8.

Michigan E. coli O157:H7 Outbreak Linked to Bagged Lettuce, Again. Food Safety Attorney, William Marler, Gives History Lesson.

This is a press release being distributed by Marler Clark:

Seattle--- “E. coli O157:H7 outbreaks associated with lettuce or spinach, specifically the "pre-washed" and "ready-to-eat" varieties sold under various brand and trade names, are by no means a new phenomenon,” according to food-safety attorney, William D. Marler, of Marler Clark.  By way of illustration:

•    in October 2003, thirteen residents of a California retirement home were sickened, and two people died, after eating E. coli-contaminated, pre-washed spinach;

•    in September 2003, nearly forty patrons of a California restaurant chain fell ill after eating salads prepared with bagged, pre-washed lettuce; and

•    in July 2002, over fifty young women fell ill with E. coli O157:H7 at a dance camp after eating “pre-washed” lettuce, leaving several hospitalized and one with life-long kidney damage. 

And this is just a small sampling of the twenty or more E. coli O157:H7 outbreaks since 1995 in which spinach or lettuce was the source.

Several more outbreaks linked to contaminated leafy-produce, including most recently the September 2005 Dole packaged lettuce outbreak, are identified in the chart below, which is based on information gathered by the Center for Science in the Public Interest:

 

DATE VEHICLE Etiology Number of CASES STATES
8/93 Salad E. coli O157:H7 53 WA
7/95 Lettuce (leafy green; red; romaine) E. coli O157:H7 70 MT
9/95 Lettuce (romaine) E. coli O157:H7 20 ID
9/95 Lettuce (iceberg) E. coli O157:H7 39 ME
10/95 Lettuce (iceberg; unconfirmed) E. coli O157:H7 11 OH
5/96-6/96 Lettuce (mesclun; red leaf) E. coli O157:H7 61 CT, IL, NY
5/98 Salad E. coli O157:H7 2 CA
2/99-3/99 Lettuce (iceberg) E. coli O157:H7 72 NE
7/02-8/02 Lettuce (romaine) E. coli O157:H7 29 WA,ID
10/03-5/04 Lettuce (mixed salad) E. coli O157:H7 57 CA
4/04 Spinach E. coli O157:H7 16 CA
9/05 Lettuce (romaine) E. coli O157:H7 32 MN, WI, OR

 

The CSPI data base can be found here.

 

The most recent major E. coli outbreak ties to leafy greens was the Dole Spinach outbreak of 2006.  This included 205 illnesses due to E. coli O157:H7 reported the CDC. This number included 31 cases of HUS, 102 hospitalizations, and 3 deaths. The FDA maintained its conclusion that all the implicated spinach was traced back to Salinas Valley in California.

“We never seem to learn,” said Mr. Marler.  In November 2005, the FDA elucidated its past efforts and present concerns in its "Letter to California Firms that Grow, Pack, Process, or Ship Fresh and Fresh-Cut Lettuce." The letter begins:

“This letter is intended to make you aware of the Food and Drug Administration's (FDA's) serious concern with the continuing outbreaks of food borne illness associated with the consumption of fresh and fresh-cut lettuce and other leafy greens.”

The FDA efforts to lead the lettuce industry to safer practices were nothing new. In 1998, the FDA issued guidance to the industry entitled "Guide to Minimize Microbial Food Safety Hazards for Fruits and Vegetables." The guide is specifically designed to assist growers and packers in the implementation of safer manufacturing practices. On February 5, 2004, the FDA issued a letter to the lettuce and tomato industries to "make them aware of [FDA's] concerns regarding continuing outbreaks associated with these two commodities and to encourage the industries to review their practices."

BACKGROUND: Marler Clark has extensive experience representing victims of E. coli bacterial infections. The firm has represented over 1,000 E. coli victims since 1993, when William Marler represented HUS survivor Brianne Kiner in her $15.6 million E. coli settlement with Jack in the Box. Since that time, Marler Clark has represented victims of E. coli outbreaks traced to ConAgra, AFG, Cub Foods, Supervalu, Carneco, Excel, Topps, Stop & Shop and other ground beef suppliers. 

Contact:  William D. Marler – 1-206-794-5043, bmarler@marlerclark.com.
 

Oklahoma Says Country Cottage Outbreak Is Over

“The spread of E. coli 0111 in this outbreak was directly related to the (Country Cottage) restaurant,” said State Epidemiologist Dr. Kristy Bradley.

And with that statement, Oklahoma health officials declared the E. coli 0111 outbreak over. The Oklahoma State Health Department said:

Although a number of newly reported cases have been identified, the last known outbreak-related case became sick on Sept. 6.

The OSDH has confirmed at least 314 persons became ill as a result of the outbreak. Of that number, 246 were adults, 65 were children, and the ages of three cases have not yet been identified. One person died. At least 72 persons have been hospitalized including 17 who have received dialysis treatment.


Thus far, 1,843 persons have been interviewed as part of the outbreak investigation.


All known cases had association with the Country Cottage restaurant in Locust Grove, OK

Picking Through The Menu At Country Cottage Won't Be Easy

Some restaurants have simple menus and if they have a food poisoning incident it is fairly easy for investigators  to track the sources of the food.   Then, there are restaurants like the Country Cottage in Locust Grove, OK,  which is the center of that area's possible E. coli outbreak.

When it comes to the Country Cottage menu, investigators have their work cut out for them.  Consider what a recent reviewer wrote:

"Country Cottage Restaurant is a buffet style restaurant but they also offer a full menu. They serve breakfast and lunch, 6 days a week. They have all the breakfast items you would expect; for example; scrambled eggs, hash browns, pancakes, sausage, bacon, cinnamon rolls, pastries, biscuits and gravy, and all are extremely delicious.For lunch, they serve fried chicken, stews, soups, fresh homemade rolls and biscuits, mouthwatering gravy, chicken fried steak and numerous vegetables, just to name a few of the items served. Their deserts include homemade pies, cobblers, cakes and cookies as well as pudding and ice cream. There is a enormous selection of food to choose from. There's no possible way to leave hungry.."

For an update, and to see the questions investigators should be answering, check out this on the Marler blog: 40 sickened, 17 hospitalized and 1 death in Oklahoma E. coli Outbreak in Bixby, Broken Arrow, Locust Grove, McAlester, Peggs, Pryor, Sand Springs and Tulsa. Answers are needed.

 

 

USDA Policies Questioned By Attorney Denis W. Stearns

Guest Blog by Denis W. Stearns:

On October 3, 2002 I submitted a petition to the USDA in which I asked the agency to explicitly clarify whether a USDA policy that appeared to allow the deadly pathogen E. coli O157:H7 on so-called “intact meat” applied to meat sold to retail outlets like grocery stores and restaurants. Even now it is a near-universal practice for retail outlets to use this meat—commonly called “boxed beef” because the cuts of meat are individually shrink-wrapped and then boxed—to make ground beef. Sometimes the meat is directly used to make ground beef, and sometimes only trimmings are used—that is, the pieces left over after roasts and steak are cut and trimmed. Either way, there has never been any doubt that tens of thousands of grocery stores and restaurants use tons of intact meat every day to make ground beef. To my mind it makes absolutely no sense that the USDA would allow meat companies to sell intact meat contaminated with E. coli O157:H7. Why allow a loophole so large that it essentially moots USDA policy on this deadly pathogen?

Interestingly, the USDA responded to my petition with a letter from Philip Derfler, Deputy Administrator of the Food Safety and Inspection Service. In the letter, Mr. Derfler acknowledged that USDA policy was unclear, and stated that my petition would be treated as a public comment and referred to the Regulations and Directives Development Staff. That was six years ago, and USDA policy is less clear today than it was back then, and just as indefensible.

We are now in the midst of yet another outbreak of heartbreaking illnesses and likely deaths caused by contaminated meat that the beef industry claims the USDA authorizes it to sell. This claim is hardly new either. In 2004, the American Meat Institute and other meat industry trade groups fought all the way to the United States Supreme Court trying to overturn a Wisconsin Court of Appeals decision. The decision held that USDA policy on intact meat did not immunize meat companies from lawsuits based on allegations that E. coli-contaminated meat was unreasonably dangerous as a matter of state law. In other words, the meat industry was fighting for the right to sell E. coli-contaminated meat, claiming that USDA policy said that it could. It lost, but that did not prompt the USDA to change or clarify its policy.

Putting legal arguments aside, common sense alone clearly demonstrates why an exception for intact meat makes no sense. While the meat industry can cleverly argue that its intact meat is not intended for ground beef, and that cooking always makes it safe, neither statement is true. As the recent Nebraska Beef outbreaks make tragically clear, most intact meat does not reach consumers still intact. Furthermore, if each shrink-wrapped cut of meat had “DO NOT USE FOR GROUND BEEF; E. COLI O157:H7 PRESENT” printed in bold letters on it, there is not a grocery store in the country that would buy it. Indeed, commenting on the current outbreak, a representative of Whole Foods explained that it was using intact meat to make its own ground beef “in an attempt to assure quality and safety.” I guess the joke was on them then.

The current USDA policy on E. coli and intact meat is indefensible because it protects the interests of the meat industry instead of the public health. A policy that is based on the demonstrably false assumption that intact meat is not being used to make ground beef at a retail level is a policy that has no basis in fact or reason. It also entirely ignores the incredible risk of cross-contamination, which is what caused the 2000 outbreak at a Milwaukee-area Sizzler restaurant that killed one child and sickened scores of others. The Sizzler outbreak also recently resulted in a $7.1 million verdict against the same meat company that fought to the Supreme Court (with industry trade groups) for the right to sell the deadly stuff. Meanwhile, all these years later, the USDA says it is continuing to consider its options. Well, I have a suggestion: How about putting the interests of the public first for a change and sticking to a real zero-tolerance policy for this deadly pathogen?

Marler Blog Hot With E. coli News: Here's The Rundown

E coli

E. coli bacteria: what are they, where did they come from, and why are some so dangerous?

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.
Continue Reading...

E. coli O157:H7 is a powerful and deadly bacterium

You cannot see it, taste it, or smell it. 250,000 E. coli O157:H7 (E. coli) bacteria will fit on the head of a pin.  Ten to 50 will kill your child or your grandmother.

More likely due the expertise of Children’s Hospitals, and other top medical centers around the country, deaths at times are avoided, however, often not before Hemolytic Uremic Syndrome (HUS) nearly kills.  HUS, a complication from an E. coli infection, can cause severe damage to kidneys, intestines, and pancreas.  Falling into a coma and suffering further from cognitive impairment are all too common.

I’ve seen the inside of too many of those Intensive Care Units with families who are scared senseless as they watch their children or mother shutdown.  For 15 years, this has been my world.   When I was an undergraduate, I read Upton Sinclair’s, The Jungle.  That book took the American public on a tour of the contaminated underbelly of the meat industry and they were sickened.  It led to the Pure Food & Drug Act and the Federal Meat Inspection Act, versions of which are still in place today.

Until 1993, I thought—because of those laws—that the United States had a safe and secure food supply. But, then came the Jack-in-the-Box E. coli outbreak.  It killed four, and sickened hundreds, including many who were gravely ill with HUS and related complications.  Many of those victims became my clients.

Once again, there was a public outcry for safe meat.  The Food Safety & Inspection Service responded by creating and aggressively enforcing the Mandatory Risk Management System.  Based on research and practices of the U.S. Space Program, the risk management system established checkpoints at every phase of meat processing.

The presence of E. coli was defined as an adulterant under the Federal Meat Inspection Act.  I continued to sue “Big Meat” as most of my clients up to 2002 were children who were made sick by eating E. coli contaminated meat.  I recovered over $350 million during this period from the meat industry and the restaurants they supplied in verdicts and settlements on behalf of those clients.  In 2003 recalls of meat laced with E. coli began to decline.  After 24 million pounds of contaminated beef were recalled in 34 separate incidents in 2002, recalls dropped off to just over a million pounds a year for the next three years, and then to just 181,900 pounds in 2006.  The Centers of Disease Control and Prevention saw E. coli – related illnesses drop 48%.

But then came Spring 2007. E. coli, which begins its life in the hindgut of a cow, mounted a surge on its home court.  And, it came back with a vengeance.  Thirty-three million pounds of beef would be recalled in 22 incidents.  All over the country, slaughterhouses, packing and distribution centers, retail outlets, and restaurants were once again testing positive for E. coli and people-mostly children-were getting seriously sick.

The American meat supply, which had again been touted as safest in the world, tumbled back into disarray.  But, why?

As with any unexplained mystery, theories abound.  Could it really just be meat industry complacency?  Did everyone respond to the good numbers in 2006 by taking a long nap?  Did meat processors slack off—consciously or unconsciously—and relax their testing procedures?

Or could it be better reporting?  Doctors are more aware of E. coli now, and perhaps when patients present symptoms of food poisoning; tests are more likely to be ordered.  When the presence of E coli is found and reported, a recall is triggered.

There’s always global warming.  Seriously though – very smart people have posited that droughts in the southeast and southwest have launched more fecal dust into the air, which then finds its way into beef slaughtering plants.  It has also been suggested that the deluging rainfall in other areas created muddy pens—an ideal environment for E. coli.

While we’re at it, why not blame high oil prices?  High gas prices have fueled (sorry) the growth of ethanol plants.  These plants are often built next to feedlots, and a byproduct of the ethanol production process—distiller’s grains—is considered an excellent (and cheap) alternative to corn for cattle feed.  Unfortunately, research at Kansas State University associates the use of distiller’s grains as feed with an increase in the incidence of E. coli in the hindguts of cattle.

Another controversial issue may affect the meat supply.  The New York Times reported that immigration officials began a crackdown at slaughterhouses across the country in the fall of 2006.  Experienced—albeit undocumented—workers have been cleared out and replaced with unskilled, inexperienced labor.

And then there’s Darwin.  Another theory holds that interventions have caused the wily E. coli microbes to adapt, selecting pathogens that are more resistant to detection or intervention.  E. coli back in our meat cannot be tolerated.  We’ve got a lot of summer of 2008 left. Summer has always been kind to the E. coli bug.  More than 5.6 million pounds of E. coli contaminated beef has been recalled so far in 2008, most supplied by Nebraska Beef Ltd., via the Kroger Grocery chain.  All of which is responsible for a multi-state outbreak of E. coli that again is filling up the ICU’s in Hospitals in the seven states.

What is being done?  Not much.

Congress has held some hearings, but the only new reform is that the names of retail stores that received meat and poultry involved in recalls with high health risk will be made public.  Good as far as it goes.

However, despite 76,000,000 American’s being sickened, 325,000 hospitalized and 5,000 deaths each year, food safety has not made it as a Presidential campaign issue.  Congress, Democrats and Republicans, have about run out its clock.  But E. coli is back in our meat and we better care.

Solutions?

Continue Reading...

USDA Knows Best Cuts of Beef Being Sold With E. coli

If it is the weekend, there is almost always something to read by Phil Brasher in the Des Moines Register.  In "Many beef cuts are never tested for E. coli," Brasher reports that the U.S. Department of Agriculture is about to close the door on the sale of E. coli-tainted cuts of beef.

Brasher writes:

Processors are not allowed to sell ground beef that is tainted by E. coli because the product is considered most likely to carry the bacteria and pose the biggest risk to consumers.
But it's perfectly legal to market whole cuts of beef that might be contaminated by E. coli, and the government doesn't test them for the bacteria, either.
That could be changing. The U.S. Department of Agriculture is considering new regulations for the sale of steaks and other beef cuts, a move that officials in the meatpacking industry say is unjustified and unnecessary.
Richard Raymond, the USDA's undersecretary for food safety, said he was shocked when he found out it was legal to sell E.-coli-contaminated beef. He said he is seeking a "practical solution" to "what I feel to be a gap" in USDA regulations. USDA has not proposed any specific measures.

Donna Rosenbaum, executive director of Safe Tables Our Priority, a consumer advocacy group, said it's "way past time" for the USDA to take steps to prevent the sale of contaminated beef cuts.

"It takes such a small amount of this to make a person sick that putting the burden on consumers for controlling something that is that small to protect their children is just not right," she said.
Go here for the entire Brasher story.

About E. coli O157:H7


See www.about-ecoli.com

E. coli O157:H7 was identified for the first time at the CDC in 1975, but it was not until seven years later, in 1982, that E. coli O157:H7 was conclusively determined to be a cause of enteric disease. Following outbreaks of foodborne illness that involved several cases of bloody diarrhea, E. coli O157:H7 was firmly associated with hemorrhagic colitis.

The Centers for Disease Control and Prevention (CDC) estimated in 1999 that 73,000 cases of E. coli O157:H7 occur each year in the United States. Approximately 2,000 people are hospitalized, and 60 people die as a direct result of E. coli O157:H7 infections and complications. The majority of infections are thought to be foodborne-related, although E.coli O157:H7 accounts for less than 1% of all foodborne illness.

E. coli O157:H7 bacteria are believed to mostly live in the intestines of cattle but have also been found in the intestines of chickens, deer, sheep, goats, and pigs. E. coli O157:H7 does not make the animals that carry it ill; the animals are merely the reservoir for the bacteria.

While the majority of foodborne illness outbreaks associated with E. coli O157:H7 have involved ground beef, such outbreaks have also involved unpasteurized apple and orange juice, unpasteurized milk, alfalfa sprouts, and water. An outbreak can also be caused by person-to-person transmission of the bacteria in homes and in settings like daycare centers, hospitals, and nursing homes.

Symptoms of E. coli O157:H7 infection

E. coli O157:H7 infection is characterized by the sudden onset of abdominal pain and severe cramps, followed within 24 hours by diarrhea. As the disease progresses, the diarrhea becomes watery and then may become grossly bloody - bloody to naked eye. Vomiting can also occur, but there is usually no fever. The incubation period for the disease (the period from ingestion of the bacteria to the start of symptoms) is typically 3 to 9 days, although shorter and longer periods are not that unusual. An incubation period of less than 24 hours would be unusual, however. In most infected individuals, the intestinal illness lasts about a week and resolves without any long-term problems.

Hemolytic Uremic Syndrome (HUS) is a severe, life-threatening complication of an E. coli O157:H7 bacterial infection. Although most people recover from an E. coli O157:H7 infection, about 5-10% of infected individuals goes on to develop HUS. E. coli O157:H7 is responsible for over 90% of the cases of HUS that develop in North America. 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. Visit the Marler Clark sponsored Web site about Hemolytic Uremic Syndrome for more information. www.about-hus.com

Thrombotic Thrombocytopenic Purpura (TTP) is a clinical syndrome defined by the presence of thrombocytopenia (low blood platelet counts) and microangiopathic hemolytic anemia. This has generally been recognized as ìadult HUS.î There are many possible causes, including E. coli O157:H7, all of which act through the common mechanism of inducing endothelial cell damage. The damage triggers a cascade of biochemical events that ultimately leads to the characteristic feature of TTP - widespread dissemination of hyaline thrombi, composed predominantly of platelets and fibrin, which block the terminal arterioles and capillaries (microcirculation) of most of the major body organs, commonly, the heart, brain, kidneys, pancreas and adrenals. Other organs are involved to a lesser degree. The pathophysiology of this disease results in multisystem abnormalities and the clinical manifestations of the syndrome. To learn more about Thrombotic Thrombocytopenic Purpura, visit the Marler Clark sponsored Web site about TTP. www.about-ttp.com

Detection and treatment of E. coli O157:H7

Infection with E. coli O157:H7 is usually confirmed by detecting the bacteria in the stool of the infected individual. Antibiotics do not improve the illness, and some medical researchers believe that medications can increase the risk of complications. Therefore, apart from good supportive care, such as close attention to hydration and nutrition, there is no specific therapy for E. coli O157:H7 infection. The recent finding that a toxin produced by E. coli O157:H7 initially greatly speeds up blood coagulation may lead to medical therapies in the future that could forestall the most serious consequences. Most individuals recover within two weeks.

Preventing E. coli O157: H7 infection

Eating undercooked ground beef is the most important risk factor for acquiring E. coli O157:H7. Cook all ground beef and hamburger thoroughly. Because ground beef can turn brown before disease causing bacteria are killed, use a digital instant read meat thermometer to ensure thorough cooking. Hamburgers should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160∫ 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.

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.

Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf life that is sold at room temperature (such as juice in cardboard boxes or 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.

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. Methods to decontaminate alfalfa seeds and sprouts are being investigated.

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).

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

Avoid petting zoos and other animal exhibits unless there are good hand washing facilities available and other sanitation measures have been taken. Wash your hands and your childrenís hands after handling animals.

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.

Google - E. coli Search

1. E. coli O157:H7 - Escherichia coli O157:H7 - About-Ecoli.com offers a variety of E. coli information: symptoms and risks of infection, detection and diagnosis of E. coli O157:H7, how to prevent E. coli.
www.about-ecoli.com

2. Disease Listing, Escherichia coli O157:H7, Gen Info | CDC.
People can become infected with E. coli O157:H7 in a variety of ways.
www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_g.htm

3. Escherichia coli - Wikipedia
www.wikipedia.org/wiki/Escherichia_coli

4. Bugs in the News - What the Heck is an E. coli? Information about the bacteria and the diseases it causes.
www.people.ku.edu/~jbrown/ecoli.html

5. US FDA/CFSAN - Bad Bug Book - Escherichia coli O157:H7
Morbidity and Mortality Weekly Reports on E. coli O157:H7.
www.cfsan.fda.gov/~mow/chap15.html

6. E. coli Genome Project
www.genome.wisc.edu

7. MedlinePlus: E. Coli Infections - Directory of links to information and news related to the disease.
www.nlm.nih.gov/medlineplus/ecoliinfections.html

8. E. coli is a common type of bacteria that can make you pretty sick. Read more in this kids' article all about E. coli.
www.kidshealth.org/kid/health_problems/stomach/ecoli.html

9. University of Wisconsin Madison Genetics - Features graduate programs, courses, faculty, research, and staff profiles.
www.genetics.wisc.edu

E. coli O157:H7 and Hemolytic Uremic Syndrome

What is E. coli O157:H7?

E. coli is the name of a common family of bacteria, most members of which do not cause human disease. E. coli O157:H7 is a specific member of this family that can cause bloody diarrhea (hemorrhagic colitis) in man. In the eighteen years since E. coli O157:H7 was first identified as a cause of diarrhea, this bacterium has established a reputation as a significant public health hazard.

Overview of Medical Impacts of E. coli O157:H7

After a susceptible individual ingests a sufficient quantity of E. coli O157:H7, the bacteria attach to the inside surface of the large intestine and initiate an inflammatory reaction. This reaction is believed to be due to chemicals secreted by the bacteria, and results in the bloody diarrhea and abdominal cramps characteristic of the intestinal illness. The incubation period is usually about 3 to 8 days, but slightly more or less is common. A wide spectrum of disease is possible from mild diarrhea without blood, to life-threatening and severe bloody diarrhea with excruciating abdominal pain. In most infected individuals the intestinal illness lasts about a week and resolves without any long-term sequelae. Antibiotics do not improve the illness and some believe these medications might even increase the risk of complications. Apart from good supportive care, which should include close attention to hydration and nutrition, there is no specific therapy. About 5 to 10% of individuals go on to develop hemolytic uremic syndrome (HUS), a severe life-threatening complication of the intestinal illness.

HUS was first described in 1955 and is recognized as the most common cause of kidney failure in childhood. E. coli O157:H7 is responsible for over 90% of the cases of HUS that develop in North America. When HUS follows a diarrhea illness the correct terminology is diarrhea-associated HUS (D+HUS) to distinguish the disease from a less common variety of HUS that occurs as a familial, recurrent, or isolated form associated with other clinical situations.

D+HUS is believed to develop when the E. coli O157:H7 enters into the circulation through the inflamed bowel wall and releases a specific chemical known as shiga-like toxin (SLT). SLT, and most likely other chemical mediators, attach to receptors on the inside surface of blood vessel cells (endothelial cells) and initiate an inflammatory reaction that damages the organs supplied by these tiny arteries. Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors (kidney, pancreas, and brain). Red blood cells and platelets are also damaged, either directly by the SLT or secondarily due to the clotting process in damaged blood vessels. By definition, when fully expressed, D+ HUS presents with the triad of hemolytic anemia (red blood cells break down), thrombocytopenia (low platelet count), and acute renal failure (loss of the filter function of the kidney).

There is no known therapy to halt the progression of D+HUS. The active stage of the disease usually lasts one to two weeks during which a variety of complications are possible. D+HUS is a frightening illness that even in the best American centers has a mortality rate of about 5%. By comparison, the mortality rate in the developing world is over 75%. About 50% of patients require dialysis due to kidney failure, 25% develop pancreatitis, 25% experience seizures, and 5% suffer from diabetes mellitus. The majority 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.

Among survivors, about 5% will eventually develop end stage kidney disease with the resultant need for dialysis or transplantation, and another 5 to 10% will develop neurological or pancreatic problems which significantly impair quality of life. Since the longest available follow-up studies of D+HUS are about 20 years, an accurate lifetime prognosis is not available, and as such, lifetime medical follow-up is indicated for even the mildest affected.

Prognosis Features

1.Tonshoff B., Sammet A., Sanden I., Mehls O., Waldherr R., Scharer K., Outcome and prognostic determinants in the hemolytic uremic syndrome of children.

“The rate of recovery correlated with the degree of oligoanuria…. The proportion of patients who recovered was lower in the presence of severe hypertension during the acute phase…. The degree of CNS involvement was a strong predictor of [bad] outcome.”

2.De Jong M., Monnens L. Haemolytic-uremic syndrome: A 10 year follow-up study of 73 patients.

“All six patients belonging to the third group (oliguria for more than 14 days or anuria for more than 7 days) had late sequelae: two started dialysis more than 10 years after the initial phase; three had decreased GFR and concentrating capacity.”

3.Gagnadoux MF., Habib R. Long-term prognosis of childhood HUS.

“after follow up of 15 to 20 years, about 25% of patients affected with typical HUS in their childhood present with some degree of renal impairment. 10% being in advanced renal failure.”

4.Kelles A., VanDyck M., Proesman W. Childhood HUS: long-term outcome and prognostic features.

“severe hypertension, anuria lasting more than 7 days and central nervous system involvment have all been said to be associated with poor outcome that means early death and end-stage renal failure.”

5.Tonshoff B., Sammet A., et al. Outcome and prognostic determinats in the HUS of Children.

“The degree of CNS involvement was a strong predictor of [bad] outcome…. The most important difference in the rate of recovery of our patients was the degree of oligoanuria.”


6.Siegler R., Pavia A., et al. At 20 year population based study of post-diarrheal HUS in Utah.

“severe disease was significantly associated with… prodromal anuria and white blood cell count greater than 20,000…. Seizures or other neurological findings during the acute illness were also strongly associated with bad outcome.”


7.Gianantonio CA., Vitacco M., et al. The hemolytic uremic syndrome.

“One peculiar feature of the HUS is the striking association of severe renal damage and erthrocyte destruction with notable neurologic abnormalities…. Anuria of more than 4 days duration is also a sign of poor prognosis.”

8.Rowe PC. Epidemiology of HUS in Canadian children from 1986 to 1988.

“all patients with oliguria exceeding 15 days or anuria persisting for more than 8 days were left with chronic disease…. None of our patients with oliguria that lasted more than approximately 2 weeks or anuria that persisted more than approximately 1 week escaped chronic disease.”

9.Sprizzirri, Francisco D, Rahman, Ricardo C., Bibiloni, Norma, Ruscasso, Javier D., Amoreo, Oscar R. Childhood hemolytic uremic syndrome in Argentina: long-term follow-up and prognostic features.

“the severity of acute renal failure – as determined by the days of anuria – and the presence of proteinuria one year after the acute phase, were the most useful prognostic indicators [of bad outcome].”


10.Caletti, Maria G., Gallo, Guillermo, and Gianantonio, Carlos. Development of focal segmental sclerosis and hyalinosis in hemolytic uremic syndrome.

“These observations also confirm that prolonged oligoanuria during the acute stage of HUS frequently results in an unfavorable long-term prognosis…. The severe form was defined as anuria more than 7 days…. Proteinuria appeared after a proteinuria-free interval…


11.Schlieper, A., et al. Sequelae of haemolytic uraemic syndrome.

“HUS patients had numerically lower cognitive and achievement scores and higher behavioural problems ratings than their controls on every measure…. The results of this investigation provides preliminary indications of a post-HUS deficit in verbal intelligence and in the verbally based skills of reading comprehension and vocabulary use, as well as behaviour.”


12.Orme, S., Clark, E., Siegler, R.L., Neuropsychological sequele of post-diarrheal hemolytic uremic syndrome encephalopathy.

“HUS subjects consistently scored lower than controls on verbal intelligence, reading comprehension and vocabulary and behavior…. the data suggests that children who suffer from encephalopathy during HUS may have persistent cognitive problems…. The present data show a pattern of relative weakness in problem solving, visual-spatial reasoning, motor speed, memory, mathematical reasoning and spelling.”


13.Robson, Wm. Lane M. M.D., F.R.C.P., Leung, Alexander K.C. M.D., F.R.C.P. Kaplan, Bernard, S. M.B., B.Ch. Hemolytic-Uremic Syndrome.

“The following factors are reported to be associated with a poor prognosis in D+ HUS: Elevated WBC count, Prolonged anuria, Severe prodromal illness, Severe hemorrahagic colitis, Severe multisystem involvement…. The longer the duration of anuria, the less the recovery in GFR that can be expected.”


14.Thomson, Peter D. HUS in Johannesburg, South Africa: Epidemiology and Long-term Follow-up.

“We recommend that all severely affected cases of HUS should be followed for up to 20 years.”

15.Lopez, Eduardo L., Gianantonio, Carlos A., Cleary, Thomas G. The Hemolytic Uremic Syndrome in Argentina.

“A poor prognosis has been associated with oliguria of more than 3 weeks duration and/or anuria of more that 4 days duration.”

About E. coli O157:H7

E. coli O157:H7 was identified for the first time at the CDC in 1975, but it was not until seven years later, in 1982, that E. coli O157:H7 was conclusively determined to be a cause of enteric disease. Following outbreaks of foodborne illness that involved several cases of bloody diarrhea, E. coli O157:H7 was firmly associated with hemorrhagic colitis.

The Centers for Disease Control and Prevention (CDC) estimated in 1999 that 73,000 cases of E. coli O157:H7 occur each year in the United States. Approximately 2,000 people are hospitalized, and 60 people die as a direct result of E. coli O157:H7 infections and complications. The majority of infections are thought to be foodborne-related, although E.coli O157:H7 accounts for less than 1% of all foodborne illness.

Continue Reading...

What causes E. coli outbreaks?

E. coli was officially considered an enteric disease in 1982, when it was determined to be the cause of a foodborne illness outbreak. Since that time, widely publicized E. coli O157:H7 outbreaks have devastated families and communities across the globe.

While the majority of foodborne illness outbreaks associated with E. coli O157:H7 have been linked to ground beef, outbreaks have been linked to produce such as lettuce, spinach, and sprouts. Outbreaks have also been linked to E. coli-contaminated apple and orange juice. Several other instances of E. coli outbreaks have been linked to cross-contamination of food products.

In addition to food products, E. coli outbreaks have been linked to contaminated water in swimming pools and lakes, as well as to dust particles in animal pens and at petting zoos.