A sample platter of bacterial and viral outbreaks linked to cantaloupe

More than you ever wanted to know about cantaloupes from www.outbreakdatabase.com:

No.

Year

State(s)

Confirmed Illnesses

Pathogen

Description

1.

1985

Wisconsin

16

Campylobacter

Melon or cantaloupe

2.

1990

30 States

245

Salmonella

Cut cantaloupe at salad bars

3.

1991

International, including U.S.

400

Salmonella

Mexican cantaloupe

4.

1997

California

24

Salmonella

Mexican cantaloupe

5.

1998

Ontario, Canada

22

Salmonella

Cantaloupe

6.

1999

Iowa

61

Norovirus

Restaurant, cantaloupe or melon

7.

2000

California, Oregon, Colorado, Washington, New Mexico, Nevada

47

Salmonella

Mexican cantaloupe

8.

2001

California, Arizona, New York, Minnesota, Oregon, Washington, Hawaii, Georgia, Nevada

50

Salmonella

Viva Brand cantaloupe

9.

2002

California, Minnesota, Missouri, Oregon, Arkansas, Vermont, Washington, Nevada, Texas

58

Salmonella

Susie Brand cantaloupe

10.

2003

New York, Ohio, New Mexico, Massachusetts, Connecticut, Missouri

58

Salmonella

Day care center and private homes, cantaloupe/honeydew melon

11.

2006

Multi-State and International

41

Salmonella

Cantaloupe cut at processing facility in Canada

12.

2007

California

11

Salmonella

Private home cantaloupe

13.

2008

15 States

53

Salmonella

Agropecuraria Mobtelibano cantaloupe, from Honduras

14.

2008

California

23

Norovirus

Restaurant, melon and cantaloupe

15.

2011

11 States

20

Salmonella

Del Monte cantaloupe

16.

2011

28 States

147

Listeria

Jensen Farms cantaloupe

17.

2012

21 States

178

Salmonella

Indiana Farm cantaloupe

Outbreak Database Tracks Salmonella Cantaloupe Outbreaks

After almost 20 years – yes, it has been that long since the Jack in the Box E. coli O157:H7 outbreak – a few years ago I started loosing track of the number of foodborne illness outbreaks.  That is why we developed the Foodborne Illness Outbreak Database.

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The database has come in handy to track just how often cantaloupes – and other foods – have caused problems.  Here is a sample platter of outbreaks linked to cantaloupe with links to citations (Download as PDF):

No.

Year

State(s)

Confirmed Illnesses

Pathogen

Description

1.

1985

Wisconsin

16

Campylobacter

Melon or cantaloupe

2.

1990

30 States

245

Salmonella

Cut cantaloupe at salad bars

3.

1991

International, including U.S.

400

Salmonella

Mexican cantaloupe

4.

1997

California

24

Salmonella

Mexican cantaloupe

5.

1998

Ontario, Canada

22

Salmonella

Cantaloupe

6.

1999

Iowa

61

Norovirus

Restaurant, cantaloupe or melon

7.

2000

California, Oregon, Colorado, Washington, New Mexico, Nevada

47

Salmonella

Mexican cantaloupe

8.

2001

California, Arizona, New York, Minnesota, Oregon, Washington, Hawaii, Georgia, Nevada

50

Salmonella

Viva Brand cantaloupe

9.

2002

California, Minnesota, Missouri, Oregon, Arkansas, Vermont, Washington, Nevada, Texas

58

Salmonella

Susie Brand cantaloupe

10.

2003

New York, Ohio, New Mexico, Massachusetts, Connecticut, Missouri

58

Salmonella

Day care center and private homes, cantaloupe/honeydew melon

11.

2006

Multi-State and International

41

Salmonella

Cantaloupe cut at processing facility in Canada

12.

2007

California

11

Salmonella

Private home cantaloupe

13.

2008

15 States

53

Salmonella

Agropecuraria Mobtelibano cantaloupe, from Honduras

14.

2008

California

23

Norovirus

Restaurant, melon and cantaloupe

15.

2011

11 States

20

Salmonella

Del Monte cantaloupe

16.

2011

28 States

147

Listeria

Jensen Farms cantaloupe

17.

2012

20 States

141

Salmonella

Indiana Farm cantaloupe

 

 

 

 

 

 

 

 

 

 

 

Ohio, a Hotbed of E. coli Cases

As a result of eating food at a picnic at Neff’s Lawn Care in Germantown, at least 75 individuals became ill with E. coli O157:H7 from as yet an unknown vector. Of those, 14 were hospitalized. Marler Clark has been retained by three of those families to investigate the cause of the outbreak.

Public Health – Dayton & Montgomery County is continuing an investigation into the cause of the foodborne outbreak. Over 300 people may have attended an annual customer appreciation picnic held by Neff’s Lawn Care, 9400 Ekhart Road, on July 3. Of the ill, 18 have been confirmed as being infected by E. coli O157. A 73-year old male died on July 24, and a 14-year old male who was in serious condition has been released from the hospital. A 4-year old girl, experiencing hemolytic uremic syndrome (HUS), remains hospitalized in serious condition.

Over the last decade there have been these Ohio-related E. coli cases:

ConAgra Ground Beef E. coli Outbreak Lawsuits - Nationwide (2002)

Cuyahoga County E. coli outbreak - Ohio (2009)

Dole Spinach E. coli Outbreak Lawsuits - Nationwide (2006)

Freshway Lettuce E. coli Outbreak Lawsuits - Multistate (2010)

JBS Swift E. coli Outbreak Lawsuits - Nationwide (2009)

Jimmy John’s Clover Sprouts E. coli O26 Outbreak Lawsuits - Multistate (2012)

KFC E. coli Outbreak Lawsuit - Ohio (1999)

Nebraska Beef E. coli Outbreak - Nationwide (2008)

Nestle Toll House Cookie Dough E. coli Outbreak Lawsuits - Nationwide (2009)

Tyson Fresh Meats E. coli Lawsuit - Ohio (2011)

Valley Meats E. coli Outbreak Lawsuits - Ohio, Illinois, Pennsylvania (2009)

For more information on E. coli, see www.about-ecoli.com and for hemolytic uremic syndrome, see www.about-hus.com.

Some Nasty Facts about E. coli caused HUS

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.

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.

Its three central features describe the essence of Hemolytic Uremic Syndrome: 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.

Seneca Lake Spraypark Cryptosporidium Class Action

Welcome to the official website for information regarding the Seneca Lake Spraypark Cryptosporidium Class Action. Timothy Springer, et al. v. The State of New York, Claim No. 111361. This site is the proper location for periodic updates on the litigation. In addition, potential class members can retrieve the forms necessary for application to become members of the class.

Membership in the Class is now closed. There are nearly 2,500 people who have sought to join the Class. We are currently in active discovery with the State of New York to prove its responsibility for the outbreak. We have mailed all those who sought membership a Questionnaire (pdf) that we need to prove damage claims. While many of you have previously submitted much of this information, The Questionnaire (pdf) contains additional requests and is in a form that we can use to establish proof of claim. Therefore you need to complete and return This Questionnaire (pdf) with information for each claimant. A copy of The Questionnaire (pdf) can be printed from this page. The DEADLINE for returning The Questionnaire (pdf) has been extended to SEMPTEMBER 30, 2008. All Questionnaires (pdf) should be mailed to the following address:

SENECA LAKE CLAIMS ADMINISTRATOR
c/o THE NOTICE COMPANY
P.O. BOX 455
HINGHAM, MA 02043

For additional information on the status of the litigation visit the Update page.

Common myths about food safety at home

Myth #1: Food poisoning isn’t that big of a deal. I just have to tough it out for a day or two and then it’s over.

Fact: Many people don’t know it, but some foodborne illnesses can actually lead to long-term health conditions, and 3,000 Americans a year die from foodborne illness. Get the facts on long-term effects of food poisoning.

Myth #2: It’s OK to thaw meat on the counter. Since it starts out frozen, bacteria isn’t really a problem.

Fact: Actually, bacteria grow surprisingly rapidly at room temperatures, so the counter is never a place you should thaw foods. Instead, thaw foods the right way.

Myth #3: When cleaning my kitchen, the more bleach I use, the better. More bleach kills more bacteria, so it’s safer for my family.

Fact: There is actually no advantage to using more bleach than needed. To clean kitchen surfaces effectively, use just one teaspoon of liquid, unscented bleach to one quart of water. 

Myth #4: I don’t need to wash fruits or vegetables if I’m going to peel them.

Fact: Because it’s easy to transfer bacteria from the peel or rind you’re cutting to the inside of your fruits and veggies, it’s important to wash all produce, even if you plan to peel it.

Myth #5: To get rid of any bacteria on my meat, poultry, or seafood, I should rinse off the juices with water first.

Fact: Actually, rinsing meat, poultry, or seafood with water can increase your chance of food poisoning by splashing juices (and any bacteria they might contain) onto your sink and counters. The best way to cook meat, poultry, or seafood safely is to make sure you cook it to the right temperature.

Myth #6: The only reason to let food sit after it’s been microwaved is to make sure you don’t burn yourself on food that’s too hot.

Fact: In fact, letting microwaved food sit for a few minutes (“standing time”)helps your food cook more completely by allowing colder areas of food time to absorb heat from hotter areas of food. 

Myth #7: Leftovers are safe to eat until they smell bad.

Fact: The kinds of bacteria that cause food poisoning do not affect the look, smell, or taste of food. To be safe, use our Safe Storage Times chart to make sure you know the right time to throw food out.

Myth #8: Once food has been cooked, all the bacteria have been killed, so I don’t need to worry once it’s “done.”

Fact: Actually, the possibility of bacterial growth actually increases after cooking, because the drop in temperature allows bacteria to thrive. This is why keeping cooked food warmed to the right temperature is critical for food safety.

Myth #9: Marinades are acidic, which kills bacteria—so it’s OK to marinate foods on the counter.

Fact: Even in the presence of acidic marinade, bacteria can grow very rapidly at room temperatures. To marinate foods safely, it’s important to marinate them in the refrigerator.

Myth #10: If I really want my produce to be safe, I should wash fruits and veggies with soap or detergent before I use them.

Fact: In fact, it’s best not to use soaps or detergents on produce, since these products can linger on foods and are not safe for consumption.  Using clean running water is actually the best way to remove bacteria and wash produce safely.

Thanks to www.foodsafety.gov

Trouble with Imports: Why the Salmonella Tempeh, Tuna and Pine Nut Outbreaks are a larger Problem

When Smiling Hara Tempeh Managing Executive Chad Oliphant began buying starter culture used to make the popular bean product tempeh from Maryland-based Tempeh Online, he surely did not expect it to be contaminated with Salmonella (or anything else, for that matter). And, why should he? Like most people in his position, I imagine Mr. Oliphant was acting under the belief that the products purchased from overseas exporters have been vetted for safety issues. Of course, this outbreak has shown that Smiling Hara Tempeh should have tested its product prior to sending it out for consumption, but it is also serves as an example of a burgeoning trend of foodborne illness outbreaks linked to imported food.

Food products now come from over 250,000 foreign establishments in 200 countries. Indeed, 15 percent of fruits, 20 percent of vegetables, and 80 percent of seafood comes from overseas. And, with the consumption of imported foods growing, we have seen an increase in foodborne illness outbreaks linked to them.

In just the past year consumers felt the pain of multiple import-related outbreaks: Turkish pine nuts, Mexican papayas, and Guatemalan cantaloupe were a few products linked to Salmonella outbreaks in 2011. Contaminated sprout seeds imported to Germany from Egypt caused the disastrous E. coli outbreak that sickened thousands and killed 50 in Europe, including some Americans in Spring 2011. Most recently, alongside the tempeh outbreak, a nationwide Salmonella outbreak was traced to sushi made from imported Nakaochi scrape (aka tuna Scrape), ground tuna meat scraped from the ribs and backbones on tuna. The contaminated tuna scrape was imported from India and distributed by a California company to supermarkets and restaurants all over the country. Despite labels indicating the product should be cooked, it was used in sushi rolls and ceviche—dishes served raw. Over 300 Americans who ate the raw imported tuna scrape became ill with Salmonella infections.

Perhaps it should not be altogether unsurprising that we are experiencing foodborne illness outbreaks tied to imported foods, given the lack of oversight afforded to imports.

While forty-five percent of import-related foodborne illnesses are tied to seafood, the U.S. Food and Drug Administration (FDA) only inspects 1 percent of seafood that enters the country. Of the seafood inspected, 51 percent gets rejected due to spoilage, physical abnormalities, or pathogen contamination. All other imported food fares only slightly better, with 2 percent becoming subject to inspection.

So while thousands of people were likely sickened by imported food last year, my dire prediction is that we’ll continue to see a rise in import-related foodborne illness outbreaks. That is, unless there are upgrades to current FDA import policies.

Fortunately, I’m not alone in this thinking.

In 2010, President Obama signed into law the US FDA Food Safety Modernization Act (FSMA), which included a substantial revamp of food safety procedures required for domestic food production and imports. If Funded the FMSA will increase the number of import inspections; importers will be specifically required to have a program to verify that the food products they are bringing into this country are safe as well as verify that their suppliers are in compliance with reasonably appropriate risk-based preventive controls.

Unfortunately, there are some very real hurdles to clear before FSMA can take effect.

A critical defect in FSMA is the absence a funding mandate. This means that while FDA may be required by law to implement improved food safety procedures, there will not be enough money to put those policies into action. Currently, the funding for FSMA lies in the hands of Congress, though as FDA Commissioner Margaret Hamburg has pointed out: so far Congress has been unwilling to allocate FDA the funds necessary to validate the legislation.

Of course there is another roadblock that preempts even the likes of Congress. The Whitehouse Office of Management and Budget (OMB) is responsible for approving draft rules such as the provisions established in FSMA. The FSMA rules pertaining to imports were supposed to be finalized by January 4, 2012, but five months later they remain in OMB, apparently stalled.

Where does this leave us?

We will continue to see a rise in the number of imports.

Americans will continue to eat more imports

Without funding and enacting FSMA import rules, we will continue to see more outbreaks associated with imports.

As for Smiling Hara Tempeh, perhaps if OMB had been on schedule and Congress had appropriated sufficient funding, over 80 people would not have become victims of Salmonella poisoning. In the meantime it will be up to American importers to ensure the foods they are bringing in from other countries are safe.

E. coli Outbreaks and HUS: The acute and long-term consequences

Acute hemolytic uremic syndrome (HUS)

Post-diarrheal hemolytic uremic syndrome (D+HUS) is a severe, life-threatening complication that occurs in about 10 percent of those infected with E. coli O157:H7 or other Shiga toxin- (Stx-) producing E. coli.

The chain of events leading to HUS begins with ingestion of Stx-producing E. coli (e.g., E. coli O157: H7) in contaminated food, beverages, animal to person, or person-to-person transmission.

These E. coli rapidly multiply in the intestine causing colitis (diarrhea), and tightly bind to cells that line the large intestine. This snug attachment facilitates absorption of the toxin into the intestinal capillaries and into the systemic circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin.

Organ injury is primarily a function of Gb3 receptor location and density. Receptors are probably heterogeneously distributed in the major body organs, and this may explain why some patients develop injury in other organs (e.g., brain, pancreas).

Once Stx attaches to receptors, it moves into the cell’s cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury and/or death. This cellular injury activates blood platelets and the coagulation cascade, which results in the formation of clots in the very small vessels of the kidney, resulting in acute kidney injury and failure.

The red blood cells undergo hemolytic destruction by Stx and/or damage as they attempt to pass through partially obstructed microvessels. Blood platelets (required for normal blood clotting), are trapped in the tiny blood clots or are damaged and destroyed by the spleen.

Each kidney has between 700,000 and 1,000,000 filtering units, called “nephrons.” The heart of each filter is a microscopic bundle of blood vessels called glomeruli. Blood goes into each glomerulus and waste products pass through a membrane into tubules, which connect together and ultimately collect the urine and pass it out of the kidney.

The glomerulus is the main filter of the nephron and is located within the Bowman's capsule. The glomerulus resembles a twisted mass of tiny tubes through which the blood passes. The glomerulus is semipermeable, allowing water and soluble wastes to pass through and be excreted out of the Bowman's capsule as urine. The filtered blood passes out of the glomerulus into the efferent arteriole to be returned through the medullary plexus to the intralobular vein. Meanwhile, the filtered water and aqueous wastes are passed out of the Bowman's capsule into the proximal convoluted tubule.

In HUS, a certain number of glomeruli are permanently damaged due to loss of blood flow as tiny thrombi occlude those blood vessels. The toxins from E. coli O157:H7 also have a direct effect on the cells lining the blood vessels and tubules and can cause cell death. Once a filter is gone, it is gone forever. When a lot of filters are gone, the remaining ones work harder because there are fewer of them. If enough filters are lost, the remaining filters experience “hyperfiltration,” which leads to enlargement, and over time, scarring, which in turn leads to the loss of more filters.

Serious kidney injury usually manifests through reduced filter function, hypertension, and/or proteinuria. It is easy to get a rough estimate of kidney filter function by looking at the level of waste products, especially creatinine in the blood over time. There are also formulas to estimate filter function once you have a creatinine value. The key is whether filter function changes over time. Since the kidneys primarily regulate blood pressure, the development of hypertension after HUS also signals serious kidney injury and is considered a bad prognostic sign. So too is proteinuria—the passage of protein molecules in the urine—which is a sign that the glomeruli have been damaged, and the remaining filters are hyperfiltrating—i.e. they are being overworked due to the loss of filtering capacity of other dead or damaged filters.

If enough filters are lost either due to injuries suffered during the acute HUS illness, or later in life due to the process of hyperfiltration, a patient will reach end stage renal disease (“ESRD”). ESRD, truly a worst-case scenario for someone who has survived the acute HUS illness, is a very painful process that can take decades to play out. The demands on the kidneys increase through puberty and, for women, especially during pregnancy, adding another variable to issues of future renal health for girls who have suffered severe HUS.

Long-term consequences of hemolytic uremic syndrome (HUS)

Multiple 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. One of the best predictors is the duration of anuria and/or oliguria.

Milford, et al, (J Pediatrics, 1991) studied the importance of proteinuria at one year following the acute episode of HUS in 40 children. They found that a poor prognosis defined as hypertension, decreased renal function or end stage renal disease was strongly associated with proteinuria at the one year follow up.

Perlstein et al, (Arch Dis Child, 1991) reported results of oral protein loading in 17 children with a past history of HUS; they demonstrated that functional renal reserve was reduced in children with a past history of HUS who had normal renal function and normal blood pressure as compared to normal children. This study suggests that functional renal reserve in children with HUS is reduced although renal function and blood pressure are normal. The authors point out that the long-term significance of this finding is unknown and needs to be determined but the study suggests that functional renal reserve may be reduced in spite of normal recovery and that children with HUS need long term follow-up.

In the article by Gagnadouz, et al, (Clinical Nephrology, 1996) 29 children were evaluated 15-25 years after the acute phase of HUS. Only 10 of the 29 children were normal, 12 had hypertension, 3 had chronic renal failure and 4 had end stage renal disease (65.5%). Severe sequelae occurred in children with oligo/anuria for more than or equal to 7 days.

Other studies (Caletti, et al, Pediatric Nephrology, 1996) have demonstrated that histological finding of focal and segmental sclerosis and hyalinosis are observed several years following HUS. In that article, only 25% of the children had normal renal function during long-term follow-up.

Similarly, Moghal, et al. (Journal of Pediatrics, 1998) performed kidney biopsies in children with persistent proteinuria three to seven years following the acute episode of HUS. Global glomerulosclerosis was noted in six of the seven patients and two had segmental sclerosis as well. In addition, tubular atrophy and interstitial fibrosis was seen in all but one. Finally, the glomeruli in the children with HUS were significantly larger than those in normal children. These are finding that are typically found in individual with reduced nephron number and are consistent with changes of hyperperfusion and hyperfiltration is surviving nephrons. Hyperfiltration is a process that frequently leads to progressive renal damage and the development of end stage renal failure.

In 1997 Spizzirri, et al, (Pediatr Nephrol, 1997), reported that 69.2% of children with 11 or more days of anuria and 38.4% of children with 1-10 days of anuria had chronic sequelae. In addition, of patients with proteinuria at the 1-year follow-up, 86% had renal abnormalities at the end of the follow-up. The authors suggested that children with residual proteinuria with or without hypertension would probably develop progressive chronic renal failure.

In 2002, Blahova, et al, reported that long term follow up of 18 children who had HUS 10 or more years previously, only 6 children were normal while the other 12 children had either residual renal symptoms, chronic renal insufficiency or renal failure (66.6%). Many of the children with residual renal symptoms or chronic renal insufficiency/renal failure had appeared to have recovered normally at earlier check ups.

Recently, Lou-Meda, et al, reported that 14 patients with microabluminuria and no overt proteinuria at 6 to 18 months after the acute phase of HUS, on long term follow up three had a decreased glomerular filtration (GFR), one had overt proteinuria, and four had hypertension. Eight of the 14 patients had at least one sequelae for an incidence of 57.1%. Six children had overt proteinuria and at the most recent follow up, two had hypertension, four and a low renal function and two had continued proteinuria; four (66.6%) had at least one renal sequale.

Recently, Oakes, et al, determined the risk of later complications in children who had HUS several years earlier; they found that the incidence of late complications increased markedly in those with more than 5 days of anuria or 10 days of oliguria. Among children with greater than 10 days of oliguria 63.3% had a low glomerular filtration rate, 33.3% had hypertension and 88.7% had at least one long term complication.

In summary, many children who have recovered normal renal function following the acute episode of HUS have a high risk for the development of late complications from their acute episode of HUS. The risk is substantially lower in children who did not require dialysis and in children who were not oliguria or anuric while the risk is the highest in children who had oligo/anuria for more than 7 days. In one study, all children with oligo/anuria for 14 days had residual renal disease (100%).

It is important to note that the risks of long-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.

Long-term side effects of hemolytic uremic syndrome (HUS)

Adolescents and young adults with chronic kidney disease face a number of complications from their chronic kidney disease (Andreoli SP, Acute and Chronic Renal Failure in Children, 2009) including alterations in calcium and phosphate balance and renal osteodystrophy (softening of the bones, weak bones and bone pain), anemia (low blood count and lack of energy), hypertension (high blood pressure) as well as 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 patients 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 (low blood cell count that leads to a lack of energy) 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).

Renal replacement therapy can be in the form of dialysis (peritoneal dialysis or hemodialysis) or renal transplantation. The average waiting time for a deceased donor kidney for children age 0-17 years is approximately 275-300 days while the average waiting time for patient’s age 18-44 years is approximately 700 days (United States Renal Data Systems, Table 7.8, 2005).

Following transplantation, a patient will need to take immunosuppressive medications for the remainder of his/her 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.

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 postoperative period.

Lifelong 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) and increased incidence of malignancy (cancer) and chronic rejection of the kidney.

A patient may need more than one kidney transplant during his/her life. 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 age when the patient receives his/her first transplant he/she may need 1-2 transplants. The life expectancy of a person with a kidney transplant is significantly less than the general population and the life expectancy of person on dialysis a markedly less than the general population.

If and when a child needs a second kidney transplant after loss of his/her first transplant, he/she will need dialysis until a subsequent transplant can be performed. He/She 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 form 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 major complication of peritoneal dialysis.

E. coli O157:H7 and other shiga-toxin producing E. coli are very dangerous bacteria – especially to children. The acute phase – even for those who do not progress to hemolytic uremic syndrome (HUS) – can be a painful and frightening experience. For those who progress to HUS, the risk of death is real. And, even if the child survives, it may well be left with chronic health problems for the remainder of its life.

Questions and Answers: Raw Milk E. coli Outbreaks in Missouri and Oregon

The Boone County (Missouri) Health Department and Oregon State Department of Health have announced E. coli outbreaks that has sickened nearly two dozen people linked to the consumption of raw (unpasteurized) milk.

In the wake of these outbreaks, the food safety experts and E. coli attorneys at Marler Clark are sharing the answers to frequently asked questions to those who may have been exposed in the outbreak.

Missouri and Oregon Raw Milk E. coli Outbreak: FAQs

Q: I drank raw milk and believe I may have an E. coli infection. How do I know whether it’s E. coli or not? What are the symptoms of E. coli?

A: If you believe you may have an E. coli infection, the E. coli attorneys at Marler Clark recommend that you seek medical attention. E. coli infections are characterized by acute gastroenteritis.E. coli infection symptoms include abdominal pain and severe stomach cramps, followed within 24 hours by diarrhea. The diarrhea caused by E. coli is often bloody. The incubation period, or the time from ingestion of E. coli bacteria until the symptoms start, is generally 2-4 days.

Hemolytic uremic syndrome is a severe and sometimes deadly complication of E. coli infection that can result in acute kidney failure. A small percentage of E. coli outbreak victims – mostly young children and elderly people – suffer this complication. At least two young children have been hospitalized with HUS since this Missouri raw milk E. coli outbreak began.

Q: What should I do if I think I’m part of the raw milk E. coli outbreak?

A: The Marler Clark E. coli attorneys recommend contacting your local health department to report your illness. Again, if you believe you need medical assistance for your E. coli infection, contact your healthcare provide and submit a stool sample for testing. An E. coli diagnosis involves culturing E. coli bacteria from an ill individual’s stool.

Q: How will I know if I’m part of the Missouri or Oregon raw milk E. coli outbreak?

A: E. coli bacteria can be detected in stool. A fecal sample provided to a healthcare provider or health department is placed in nutrient broth or on agar and incubated for 2-3 days. After that time, a trained microbiologist can identify E. coli bacteria and confirm its identity by looking at biochemical reactions.

Treatment with antibiotics before collecting a specimen for testing can affect bacterial growth in culture, and lead to a negative test result even when E. coli causes the infection. If E. coli is isolated from an ill person’s stool, a bacterial isolate can be compared to isolates from other ill individuals – and possibly from raw milk samples. Bacterial isolates that have matching “DNA Fingerprints” indicate a potential common source of E. coli infection. Epidemiologists work to determine whether two people with positive bacterial isolates with indistinguishable DNA fingerprints are part of a common outbreak – in this case, one tied to E. coli-contaminated raw milk.

Q: I drank raw milk and got E. coli. I’m thinking about hiring a law firm to represent me, but am concerned about the cost of legal representation for my E. coli case. What are the costs of hiring a lawyer for an E. coli case? How do I find the most experienced E. coli attorney?

A: The lawyers at Marler Clark have been representing E. coli victims since 1993 and have recovered over $600,000,000 for clients. The Marler Clark E. coli attorneys provide free case evaluations for all potential raw milk E. coli outbreak victims, and victims of other foodborne illness outbreaks. Our E. coli lawyers do not charge an hourly fee. Our firm works on behalf of clients and only collects fee on a contingent basis. That means we collect our fees for E. coli cases as a percentage of the recovery obtained on our clients’ behalf after the case has been resolved. You can contact Marler Clark for a free E. coli case evaluation and further explanation of fees through our free case evaluation form or by calling us toll-free at (866) 770-2032.

Questions and Answers: Salmonella Tuna Sushi Outbreak

In the wake of an April, 2012 Centers for Disease Control and Prevention (CDC) announcement that at least 116 people have become ill in a Salmonella outbreak linked to Sushi, the attorneys at Marler Clark are distributing a FAQ list for consumers who may have been exposed in the outbreak.

A total of 116 persons infected with the outbreak strain of Salmonella Bareilly have been reported from 20 states and the District of Columbia. The number of ill persons identified in each state is as follows: Alabama (2), Arkansas (1), Connecticut (5), District of Columbia (2), Florida (1), Georgia (5), Illinois (10), Louisiana (2), Maryland (11), Massachusetts (8), Mississippi (1), Missouri (2), New Jersey (7), New York (24), North Carolina (2), Pennsylvania (5), Rhode Island (5), South Carolina (3), Texas (3), Virginia (5), and Wisconsin (12).  12 ill persons have been hospitalized, and no deaths have been reported.

Collaborative investigation efforts of state, local, and federal public health agencies indicate that a frozen raw yellowfin tuna product, known as Nakaochi Scrape, from Moon Marine USA Corporation is the likely source of this outbreak of Salmonella Bareilly infections. Nakaochi Scrape is tuna backmeat that is scraped from the bones of tuna and may be used in sushi, sashimi, ceviche, and similar dishes. Moon Marine USA Corporation (also known as MMI) of Cupertino, Calif. is voluntarily recalling 58,828 lbs of a frozen raw yellowfin tuna product, labeled as Nakaochi Scrape AA or AAA. Nakaochi Scrape is tuna backmeat, which is specifically scraped off from the bones, and looks like a ground product.

 What do consumers need to know in a Sushi Salmonella Outbreak?

Q: I ate sushi and think I may have Salmonella. What are the symptoms of Salmonella infection?

A: Salmonella infections can have a broad range of illness, from no symptoms to severe illness. The most common clinical presentation is acute gastroenteritis. Salmonella symptoms include diarrhea, and abdominal cramps, often accompanied by fever of 100°F to 102°F (38°C to 39°C). Other symptoms of Salmonella infection may include bloody diarrhea, vomiting, headache and body aches. The incubation period, or the time from ingestion of the bacteria until the symptoms start, is generally 6 to 72 hours; however, there is evidence that in some situations the incubation can be longer than 10 days.

Q: What should I do if I think I’m part of the sushi Salmonella outbreak?

A: The Marler Clark Salmonella attorneys advise that you contact your local health department to report your illness. Again, if you believe you need medical assistance for your Salmonella infection, contact your healthcare provider. The Centers for Disease Control and Prevention (CDC) estimates that for every reported case of Salmonella, an additional 29.3 infections go undiagnosed and unreported. Undiagnosed Salmonella victims are never counted in official Salmonella outbreak case-counts. There may well be nearly 3,000 sickened.

Q: How will I know if I’m part of the sushi Salmonella outbreak?

A: Salmonella bacteria can be detected in stool. A fecal sample provided to a healthcare provider or health department is placed in nutrient broth or on agar and incubated for 2-3 days. After that time, a trained microbiologist can identify Salmonella bacteria, if present, and confirm its identity by looking at biochemical reactions. Treatment with antibiotics before collecting a specimen for testing can affect bacterial growth in culture, and lead to a negative test result even when Salmonella causes the infection. If Salmonella is isolated from an ill person’s stool, a bacterial isolate can be compared to isolates from other ill individuals – and possibly from food samples. Bacterial isolates that have matching “DNA Fingerprints” indicate a potential common source of Salmonella infection. Epidemiologists work to determine whether two people with positive bacterial isolates with indistinguishable DNA fingerprints are part of a common outbreak – in this case, one tied to Salmonella-contaminated sushi.

Q: I ate sushi and got Salmonella. I’m thinking about hiring a law firm to represent me, but am concerned about the cost of legal representation for my Salmonella case. What are the costs of hiring a lawyer for a Salmonella case? How do I find the most experienced Salmonella attorney?

A: The lawyers at Marler Clark have been representing Salmonella victims since 1998 and have recovered over $600,000,000 for clients. The Marler Clark attorneys provide free case evaluations for all potential sushi Salmonella outbreak victims, and victims of other foodborne illness outbreaks. Our Salmonella lawyers do not charge an hourly fee. Our firm works on behalf of clients and only collects fee on a contingent basis. That means we collect our fees for Salmonella cases as a percentage of the recovery obtained on our clients’ behalf after the case has been resolved. You can contact Marler Clark for a free case evaluation and further explanation of fees through our free case evaluation form or by calling us toll-free at (866) 770-2032.