The paper, titled "Intraspecies Variation in the Emergence of Hyperinfectious Bacterial Strains in Nature," focuses on the researchers' efforts to seek out and locate hypervirulent strains that present a potential risk to food safety and the livestock industry.

An international team of scientists -- which also included Robert Sinsheimer and William Shimp from UCSB; Yi Xie and Bart Weimer from UC Davis; and John House from University of Sydney, Australia -- conducted a global search for hypervirulent Salmonella strains. They were found among isolates derived from livestock, and rendered current vaccines obsolete.

Bacteria behave like a Trojan Horse, exposing their weapons only after initiating infection. "These strains exhibit this behavior in the extreme -- essentially having a ‘5th gear' they can switch to during infection," said Heithoff, lead author of the paper.

Eventually it is hoped that by identifying these particularly dangerous forms of foodborne bacteria, future outbreaks may be slowed or prevented.

Now that researchers know what to look for, they are developing methods to rapidly detect and discriminate the more harmful strains from their less- virulent cousins. The strategy is aided by a special medium utilized by the researchers that forces the bacteria to reveal their weapons in the laboratory -- the first step in the design of therapeutics to combat them.

1.         Organism

Like generic E. coli, toxin-producing Shiga- toxigenic Escherichia coli (STEC) are Gram- negative, rod-shaped bacteria, but are characterized by the production of Shiga toxins (Stx). Depending on the reference cited, there are 200 to 400 STEC serotypes, many of which have not been implicated in human illness; however, a subset of STEC called enterohemorrhagic Escherichia coli (EHEC), the topic of this chapter, includes only those that cause serious illness. Serotype O157:H7 is the prototypic EHEC strain.

Although O157:H7 is currently the predominant
strain and accounts for ~75% of the EHEC
infections worldwide, other non-O157 EHEC
serotypes are emerging as a cause of foodborne
illnesses. In the United States a group often
referred to as the “big 6” (O111, O26, O121,
O103, O145, and O45) accounts for the
majority of the non-O157:H7 serotypes isolated
from clinical infections and, therefore, is
currently a focus of concern. However, other
EHEC serotypes, such as O113, O91, and others, also can cause severe illness. As a result, the non-O157 EHEC serotypes of public health concern can change quickly, depending on outbreak incidents, and can vary with countries and geographic regions.

A recent example is the large outbreak, in 2011, that was centered in Germany, but also affected various other countries in the European Union. The pathogen was identified as an E. coli strain of serotype O104:H4 that produced Shiga toxin and, therefore, was thought to be an EHEC. However, genetic analysis showed that this pathogen had 93% genetic homology with a strain of Enteroaggregative E. coli (EAEC), which is known for causing persistent diarrhea in under- developed countries, but has seldom been implicated in major foodborne incidents. Hence, the O104:H4 strain that caused the outbreak appears to be an EAEC strain that acquired the ability to produce Shiga toxin.

Currently, it is difficult to determine which serotypes of E. coli are EHEC and equally challenging to predict the emergence of strains that can acquire the genes for Shiga toxin production or other virulence factors and so cause human illness. EHEC are characterized by:

• production of Stx, including Stx1 and/or Stx2. Stx1 is nearly identical to the toxin produced by Shigella dysenteriae Type I. There are many subtypes of both toxins, and some subtypes of Stx2 appear to be implicated in human illness. Stx2 is most often associated with severe sequelae, such as hemolytic uremic syndrome (HUS), which is characterized by acute renal failure.
• presence of LEE (“locus for enterocyte effacement”; pathogenicity island that encodes for intimin, a protein that enables bacterial attachment to epithelial cells).

There are also several other putative virulence factors, including enterohemolysin, but the role of these factors in pathogenesis remains undetermined.

2.         Disease

• Mortality: Patients whose illness progresses to HUS have a mortality rate of 3% to 5%.
• Infective dose: The infective dose of EHEC O157:H7 is estimated to be very low, in the range of 10 to 100 cells. The infective dose of other EHEC serotypes is suspected to be slightly higher.
• Onset: Symptoms usually begin 3 to 4 days after exposure, but the time may range from 1 to 9 days.
• Disease / complications: Infections from EHEC may range from asymptomatic-to-mild diarrhea to severe complications. The acute symptoms are called hemorrhagic colitis (HC), characterized by severe abdominal cramps and bloody diarrhea, which may progress to such life-threatening complications as HUS or thrombotic thrombocytopenia purpura (TTP) – conditions that are most often associated with O157:H7, but that also can occur with other EHEC serotypes. About 3% to 7% of HC cases progress to HUS or TTP. 
Some evidence suggests that Stx2 and intimin are associated with progression to severe disease, such as HUS. Kidney cells have a high concentration of Stx receptors; hence, the kidney is a common site of damage. Some survivors may have permanent disabilities, such as renal insufficiency and neurological deficits. 
Antibiotic therapy for EHEC infection has had mixed results and, in some instances, seems to increase the patient’s risk of HUS. One speculation is that antibiotics lyse EHEC cells, releasing more Stx into the host.
• Symptoms: Hemorrhagic colitis is characterized by severe cramping (abdominal pain), nausea or vomiting, and diarrhea that initially is watery, but becomes grossly bloody. In some cases, the diarrhea may be extreme, appearing to consist entirely of blood and occurring every 15 to 30 minutes. Fever typically is low-grade or absent.
• Duration: In uncomplicated cases, duration of symptoms is 2 to 9 days, with an average of 8 days.
• Route of entry: Oral (e.g., ingestion of contaminated food, water, or fecal particles).
• Pathway: After ingestion, EHEC attaches to intestinal epithelial cells via LEE-encoded factors and produces Stx that are internalized, activated, and can pass into the bloodstream to become systemic.

3.         Frequency

It is estimated that there are about 63,000 cases of EHEC infections in the U.S. yearly. Ground beef and beef products continue to be implicated in most infections; however, contaminated produce increasingly has been implicated as a vehicle. As for STEC non-O157, the CDC estimates that 112,752 cases, per year, are attributed to foodborne illness in the U.S.

EHEC O157:H7 was first identified in an outbreak, in 1982, in which hamburgers from a fast- food restaurant were the vehicle. In 1991 (sic, 1992-1993), hamburgers from fast-food restaurants were implicated in another outbreak, which affected about 700 people in four states. In the mid 1990s, a large outbreak was traced to unpasteurized juices. The largest O157:H7 outbreak on record took place in Japan; radish sprouts were implicated and about 10,000 people were affected. Since then, O157:H7 has been implicated in numerous outbreaks that involved lettuce, salads, various types of sprouts, and, in 2006, bagged spinach. In 2009, an O157:H7 outbreak in the U.S. was traced to frozen, raw cookie dough.

About a dozen non-O157:H7 EHEC outbreaks have been recorded in the U.S., but incidences may be underestimated due to lack of routine testing and appropriate testing methods.

4.         Sources

Raw or undercooked ground beef and beef products are the vehicles most often implicated in O157:H7 outbreaks. Earlier outbreaks also implicated consumption of raw milk. O157:H7 can develop acid tolerance, as evidenced by infections in which acid foods (<pH4.6) were implicated, such as yogurt, mayonnaise, fermented sausages, cheeses, and unpasteurized fruit juices.

Various water sources, including potable, well, and recreational water, also have caused EHEC infections, as has contact with animals at farms or petting zoos.

Produce, including bagged lettuce, spinach, and alfalfa sprouts, increasingly is being implicated in O157:H7 infections.

Interestingly, infections in the U.S. by non-O157:H7 EHEC has been caused by many of these same vehicles, but, as of this writing, beef products have seldom been implicated.

Person-to-person transmission of infection is well documented.

Additional information is available from “Escherichia coli Serotype O157:H7: Novel Vehicles of Infection and Emergence of Phenotypic Variants,” by Dr. Peter Feng, FDA. Emerging Infectious Diseases (1995) 1(2)

5.         Diagnosis

Unlike generic E. coli, EHEC O157:H7 do not ferment the sugar sorbitol, so an effective method is to plate patient’s bloody diarrhea samples onto sorbitol MacConkey medium to screen for sorbitol non-fermenting isolates. These are then typed serologically using antibodies to the O157 and the H7 antigens. However, as other EHEC serotypes are increasingly causing illness, clinical samples are now simultaneously tested for the presence of Stx using commercially-available antibody kits. Any STEC strains found are then serotyped and identified. There are also many PCR assays specific for Stx genes that may be used for screening clinical samples.

6.         Target Populations

All people are believed to be susceptible to hemorrhagic colitis, but young children and the elderly are more susceptible and at higher risk for the illness to progress to more severe complications. Others with weak immune systems also are at risk, such as people with some chronic diseases or AIDS, and people on immunosuppressive medications; for example, some drugs used for arthritis and cancer chemotherapy.

7.         Food Analysis

Presence of EHEC O157:H7 in foods can be determined by plating culture enrichment of food samples onto selective and differential media. Unlike typical E. coli, O157:H7 do not ferment sorbitol and are negative with the MUG assay, so these tests are commonly used to distinguish O157:H7 strains from other E. coli prior to serological testing for the O157 and H7 antigens and also for the presence of Stx genes by PCR. Molecular assays also exist that can specifically detect O157:H7 strains using unique mutational markers.

Detection of non-O157:H7 EHEC, however, is more complex, due to the lack of unique traits. For non-O157 EHEC, food enrichment is first screened for Shiga toxin using an antibody assay or for Stx genes by PCR. Enrichment cultures that are positive for Stx are plated on agar media, and multiple isolates are then tested for Stx genes, in order to obtain a pure culture isolate. These putative STEC isolates are then retested for virulence genes and their serotype determined. This process is both time-consuming and labor-intensive and may require screening hundreds of isolates.

There are numerous commercially-available kits to test for Stx, O157, and a few other EHEC serotypes. However, there are several Stx subtypes and many EHEC serotypes, and not all of these can be detected by commercial test kits. The Escherichia coli link to the FDA Bacteriological Analytical Manual, Chapter 4, provides a description of methods to test for common E. coli. Methods for EHEC and O157:H7 are described in Chapter 4a.

8.         Examples of Outbreaks

For more information about recent outbreaks see the Centers for Disease Control and Prevention (CDC) Morbidity and Mortality Weekly Reports.

9.         Other Resources

More information is available from the following sources.

• USDA (August 11 1998) – USDA Urges Consumers to Use Food Thermometer When Cooking Ground Beef Patties
• CDC – General information about Escherichia coli O157:H7           
• Produce Handling and Processing Practices, from Emerging Infectious Diseases, CDC
• Risk assessment of E. coli O157:H7 in ground beef, from the USDA Food Safety and Inspection Service

In the last week the CDC reported that it in conjunction with state health departments had identified 14 cases of E. coli O157:H7 illness among residents Maryland (3 cases), New Jersey (2 cases), North Carolina (1 case), Ohio (2 cases) and Pennsylvania (6 cases) linked to Sezltzer's Lebanon Beef bologna produced by Palmyra Bolgna Products, Inc.  Hopefully, most will make a complete recorvery.  However, in some cases complications may occur:

Reactive Arthritis is the name used to describe an uncommon, but potentially debilitating group of symptoms that follows a gastrointestinal, genitourinary, or viral infection.

Irritable bowel syndrome (IBS) is one disorder in a spectrum of common functional gastrointestinal disorders. Symptoms of IBS can include constipation, diarrhea, alternating diarrhea and constipation, abdominal pain, urgency, bloating, straining at stools, and a sense of incomplete evacuation.

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.

See all at www.ecolilitigation.com

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

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.

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 "adult HUS." 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.

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 children's 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.

References

Bell BP, Goldoft M, Griffin PM, Davis MA, Gordon DC, Tarr PI, Bartleson CA, Lewis JH, Barrett TJ, Wells JG, et al., (1994). A multistate outbreak of Escherichia coli O157:H7-associated bloody diarrhea and hemolytic uremic syndrome from hamburgers: the Washington experience. JAMA 272:1349-1353.

Boyce TG, Swerdlow DL, and Griffin PM. (1995). Escherichia coli O157:H7 and the hemolytic-uremic syndrome. N. Engl. J. Med. 333:364-368.

Breuer, T, Benkel DH, Shapiro RL, Hall WN, Winnett MM, Linn MJ, Neimann J, Barrett TJ, Dietrich S, Downes FP, Toney DM, Pearson JL, Rolka H, Slutsker L, and Griffin PM. (2001). A multistate outbreak of Escherichia coli O157:H7 infections linked to alfalfa sprouts grown from contaminated seeds. Emerg. Infect. Dis. 7:977-982.

CDC. (n.d.). Food Safety Threats. Retrieved January 2, 2008, from Centers for Disease Control and Prevention Web site.

CDC. (2007, October 9). Multistate Outbreak of E. coli O157 Infections Linked to Topp’s Brand Ground Beef Patties. Updated October 26, 2007. Retrieved January 4, 2008 from Centers for Disease Control and Prevention Web site.

Chandler WL, Jelacic S, Boster DR, Ciol MA, Williams GD, Watkins SL, Igarashi T, and Tarr PI. (2002). Prothrombotic Coagulation Agnormalities Preceding the Hemolytic-Uremic Syndrome. N. Engl. J. Med. 346(1):23-32.

Cody SH, Glynn MK, Farrar JA, Cairns KL, Griffin PM, Kobayashi J, Fyfe M, Hoffman R, King AS, Lewis JH, Swaminathan B, Bryant RG, and Vugia DJ. (1999). An outbreak of Escherichia coli O157:H7 infection from unpasteurized commercial apple juice. Ann-Intern-Med. 130(3): 202-9.

DOH News. (1999, September 16). Capital district E. coli update. State Health Department and CDC epidemiologists complete case-control study of outbreak. Retrieved January 9, 2008, from New York State Department of Health Web site.

Elder RO, Keen JE, Siragusa GR, Barkocy-Gallagher GA, Koohmaraie M, and Laegreid WW. (2000). United States Department of Health and Human Services Web site.

McCarthy TA, Barrett NL, Hadler JL, Salsbury B, Howard RT, Dingman DW, Brinkman CD, Bibb WF, and Cartter ML. (2001). Hemolytic-Uremic Syndrome and Escherichia coli O121 at a Lake in Connecticut, 1999. Pediatrics 108: e59-59

Mead PM, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffin PM, and Tauxe RV. (1999). Food-related Illness and Death in the United States. Emerg. Infect. Dis. 5:607-625.

MMWR Weekly. (1999). Public Health Dispatch: Outbreak of Escherichia coli O157 and Campylobacter among attendees of the Washington County fair- New York, 1999. Sept. 17, 1999 / 48(36);803. Atlanta, GA: Centers for Disease Control and Prevention.

MMWR Weekly. (2005). Outbreaks of Escherichia coli O157:H7 Associated with Petting Zoos—- North Carolina, Florida, and Arizona, 2004 and 2005. December 23, 2005 / 54(50);1277-1280. Atlanta, GA: Centers for Disease Control and Prevention.

New York State Department of Health, and Novello AC. (2000, March). The Washington County fair outbreak report. Albano: New York State Department of Health.

Olsen SJ, Miller G, Breuer T, Kennedy M, Higgins C, Walford J, McKee G, Fox K, Bibb W, and Mead P. (2002). A Waterborne Outbreak of Escherichia coli O157:H7 Infections and Hemolytic Uremic Syndrome: Implications for Rural Water Systems. MMWR. Vol. 8, No. 4 April 2002. Retrieved January 4, 2009 from Centers for Disease Control and Prevention Web site.

Riley LW, Remis RS, Helgerson SD, McGee HB, Wells JG, Davis BR, Hebert RJ, Olcott ES, Johnson LM, Hargrett NT, Blake PA, and Cohen ML. (1983). Hemorrhagic colitis associated with a rare Escherichia coli serotype. N. Eng. J. Med. 308(12): 681, 684-85.

Slutsker L, Ries AA, Maloney K, Wells JG, Greene KD, and Griffin PM. (1998). A nationwide case-control study of Escherichia coli O157:H7 infection in the United States. J. Infect. Dis. 177:962-966.

Tarr PI. (1995). Escherichia coli O157:H7: Clinical, Diagnostic, and Epidemiological Aspects of Human Infection. Clin. Infect. Dis. 20: 1-10.

Weber-Morgan Health Department (August 7, 2006). E. coli News Release. Retrieved January 2, 2008, from Weber-Morgan Health Department Web site.

Wong CS, Jelacic S, and Tarr PI. (2000). The risk of the hemolytic uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N. Engl. J. Med. 342:1930-36.

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).

1. U.S. Department of Agriculture’s (USDA) Food Safety and Inspection Service (FSIS) has the responsibility for ensuring that meat, poultry, and egg products are safe, wholesome, and accurately labeled.

2. Food and Drug Administration (FDA) is charged with protecting consumers against impure, unsafe, and fraudulently labeled food other than in areas regulated by the Food Safety and Inspection Service (FSIS).

3. Centers for Disease Control and Prevention (CDC), is part of the Department of Health and Human Services (DHHS), and has a food safety mission that falls within its surveillance and outbreak response activities, but that is unlike those of USDA and FDA. CDC does not have regulatory authority. Even so, it is the lynch pin of our county’s food safety program. Its pivotal role is exemplified by the following excerpts:

As an agency within the Department of Health and Human Services (HHS), CDC leads federal efforts to gather data on foodborne illnesses, investigate foodborne illnesses and outbreaks, and monitor the effectiveness of prevention and control efforts. CDC is not a food safety regulatory agency but works closely with the food safety regulatory agencies, in particular with HHS’s Food and Drug Administration (FDA) and the Food Safety and Inspection Service (FSIS) within the United States Department of Agriculture (USDA). CDC also plays a key role in identifying prevention strategies and building state and local health department epidemiology, laboratory, and environmental health capacity to support foodborne disease surveillance and outbreak response. Notably, CDC data are used to help document the effectiveness of regulatory interventions.

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?

* Improve surveillance of bacterial and viral diseases. First responders - ER physicians and local doctors - need to be encouraged to test for pathogens and report findings directly to local and state health departments and the CDC promptly. Right now, for every person counted in an outbreak there are some 20 to 40 times those that are sick but never tested. The more we test, the quicker we know we have an outbreak and the quicker it can be stopped.

* These same governmental departments, whether local, state or federal, need to learn to “play well together.” Turf battles need to take a back seat to stopping an outbreak and tracking it to its source. That means resources need to be provided and coordination encouraged so illnesses can be promptly stopped and the offending producer - not an entire industry - are brought to heal.

* Require real training and certification of food handlers at restaurants and grocery stores. There also should be incentives for ill employees not to come to work when ill. We should impose fines and penalties on employers who do not cooperate.

* Stiffen license requirements for large farm, retail and wholesale food outlets, so that nobody gets a license until they and their employees have shown they understand the hazards and how to avoid them.

* Increase food inspections. While domestic production has continued to be a problem, imports pose an increasing risk, especially if terrorists were to get into the act. Points of export and entry are a logical place to step up monitoring. We need more inspectors - domestically and abroad - and we need to require that they receive the training in how to identify and control hazards.

* Reorganize federal, state and local food safety agencies to increase cooperation and reduce wasteful overlap and conflicts. Reform federal, state and local agencies to make them more proactive, and less reactive. This too requires financial resources and accountability. We also need to modernize food safety statutes by replacing the existing collection of often conflicting laws and regulation with one uniform food safety law of the highest standard.

* There are too few legal consequences for sickening or killing customers by selling contaminated food. We should impose stiff fines, and even prison sentences for violators, and even stiffer penalties for repeat violators.

* We need to use our technology to make food more traceable so that when an outbreak occurs authorities can quickly identify the source and limit the spread of the contamination and stop the disruption to the economy. When I buy a book on line I can track it all the way to my mailbox. However, we have yet to find the source of a tomato (or salsa) outbreak after months of sickening hundreds.

* Promote university research to develop better technologies to make food safe and for testing foods for contamination. Provide tax breaks for companies that push food safety research and employee training. Greatly expand irradiation of raw hamburger and other high-risk products.

* Improve consumer understanding of the risks of food-borne illness. Foster a popular campaign similar to Mothers Against Drunk Driving, which uses consumer power to promote a no-tolerance policy toward growers and companies that produce tainted food.

* Provide Presidential leadership on a topic that impacts every single one of us.

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.

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.”

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 "adult HUS." 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 children's 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.

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.