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Marler Blog Providing Commentary on Food Poisoning Outbreaks & Litigation

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

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

More than 700 serotypes of E. coli have been identified. 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. This section deals specifically with Stx-producing E. coli, including specifically E. coli O157:H7.

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

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

Stx-producing E. coli organisms have several characteristics that make them so dangerous. They are hardy organisms that can survive several weeks on surfaces such as counter tops, and up to a year in some materials like compost. They have a very low infectious dose meaning that only a relatively small number of bacteria (< 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 —a foodborne pathogen

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).

Sources of E. coli Infections

E. coli O157:H7 bacteria and other pathogenic E. coli is believed to mostly live in the intestines of cattle (Elder, et al., 2000) but has also been found in the intestines of chickens, deer, sheep, and pigs. A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coli O157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. Over seven percent of pest fly pools also tested positive for E. coli O157:H7 (Keen et al., 2003). Stx-producing E. coli does not make the animals that carry it ill. The animals are merely the reservoir for the bacteria.

E. coli can be transmitted from several sources:

Foodborne Transmission of Stx-Producing E. coli

E. coli O157:H7 was first recognized as a food borne 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.

Outbreaks

• In the ten years following the 1982 outbreak, approximately thirty E. coli O157:H7 outbreaks were recorded in the United States (Griffin & Tauxe, 1991). It is important to note that only about 10% of infections occur in outbreaks, the rest are sporadic.

• The actual number 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).

• The CDC has estimated that 83% of E. coli O157:H7 infections are food borne in origin (2009 report)). Consumption of any food or beverage that becomes contaminated by animal (especially cattle) manure/feces can result in 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

• Alfalfa, parsley, and radish sprouts

• Lettuce, cabbage, and spinach

• Fruit nuts and berries

• Cookie dough

The Center for Disease Control (CDC), Enteric Disease Branch, released a report dated September 14, 2009 entitled Update on the Epidemiology of Shiga toxin-producing E. coli (STEC) in the United States”. The contents of this timely report have been incorporated into this web piece. CDC’s estimates of the annual number of illnesses caused by Shiga toxin (Stx) producing E. coli (both O157:H7 and non O157:H7) are as follows:

E. coli O157:H7

• 73,000 illnesses

• 2200 hospitalizations

• 61 deaths

Non-O157 STEC

• 113,000 illnesses

• 1100 hospitalizations

• 30 deaths

E. coli infections continue to largely be a foodborne illness.

For the period of 1998-2007 during which there were 334 outbreaks, 7864 illnesses), the vehicles for the infections were as follows:

E. coli O157:H7

• Food borne: 69%

• Waterborne: 18%

• Animals or their environment: 8%

• Person-to-person: 6%

Non-O157:H7

• Food borne: 83%

• Waterborne: 9%

• Animals or their environment: 5%

• Person-to-person: 4%

• According to the cited recent CDC report, the mode (kind of food) causing illness secondary to E. coli O157:H7 outbreaks have changed in the past several years. (Note the emergence of leafy vegetables).

E. coli O157:H7

(1998-2002) (2003-2007)

• Beef 33 42

• Leafy vegetable 11 41

• Dairy 13 13

• Fruits-nuts 41 2

• Sprouts 1 2

• Wild Game 0 1

Poultry 2 0

Non-E. coli O157:H7

(1990-2007)

Fruit (nuts, apple juice and cider, berries) 3

Dairy (cheese, margarine) 2

Leafy vegetables 1

Beef 0

Prevalence of E. coli O157:H7

A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 US County and three large state agricultural fairs found that E. coli O157:H7 could be isolated from:

13.8% of beef cattle,

5.9% of dairy cattle,

3.6% of pigs,

5.2% of sheep,

2.8% of goats.

7.0% of pest fly pools also tested positive for E. coli O157:H7

The Role of Toxin Receptors

Cattle and other animals are merely reservoirs for the bacteria. Shiga toxin (Stx) producing E. coli do not make the animals carriers ill because their bodies do not have receptors for the toxin. Receptors are tiny protein structures that are located on the surface of cells, and are specific for a particular antigen (substance), in this case, Shiga toxin. They provide a “docking station” for the toxin, without which, it cannot injure animals or their organs (e.g., kidneys).

E. coli in Ground Beef

At one time, prior to the widespread dissemination of E. coli throughout the food chain, hemolytic uremic syndrome (HUS) secondary to E. coli O157:H7 infection was known as “Hamburger Disease”. The ground beef connection has not gone away. Numerous outbreaks and massive recalls of “tainted” ground beef continue to plague both the industry and the public.

Meat typically becomes contaminated with E. coli during the slaughtering process, when the contents of an animal’s intestines and feces are allowed to come into contact with the carcass. Unless the carcass is properly sanitized, the E. coli bacteria are mixed into the meat as it is ground.

Because E. coli is mixed throughout the meat during the grinding process, and is not just on the surface, ground beef must be cooked throughout to a temperature of 165° C since only thorough cooking will kill them (see prevention ).

The fall of 2007, was a dreadful season

The Food Safety and Inspection Service (FSIS) of the US Department of Agriculture (USDA) announced the recall of nearly 30 million pounds of ground beef in 20 separate recalls for E. coli contamination. Many of the recalls were announced after illness had been traced to the specific contaminated products.

One of Several September 2007 Ground Beef E. coli Outbreaks

On September 29, 2007, the USDA and FSIS announced that 21.7 million pounds of frozen ground beef patties were being recalled for possible E. coli O157:H7 contamination.

The announcement came after health officials in several states, who were investigating reports of E. coli O157 illnesses, found that many ill persons had consumed the same brand of frozen ground beef patties.

State public health departments and federal laboratories tested patties recovered from patients’ homes; tests conducted by the New York State Wadsworth Center Laboratory and by a FSIS laboratory on opened and unopened packages of the same brand of frozen ground beef patties. They yielded E. coli O157 isolates with several different “DNA fingerprint” patterns, as determined through PFGE.

An October 9, 2007 CDC news release stated that “several state health departments, CDC, and the USDA-FSIS were investigating a multi-state outbreak of Escherichia coli O157:H7 infections” (CDC, October 9, 2007).

Investigators compared the “DNA fingerprint” patterns of E. coli isolated from 35 ill individuals to E. coli strains isolated from the recalled ground beef patties and found that the strain isolated from the ill people matched at least one of the DNA patterns of E. coli strains found in the frozen ground beef patties.

Three cases had confirmed associations with recalled products because the E. coli strain isolated from their stool was also isolated from meat in their home.

The ill persons, ages one to 77 years, resided in eight states: Connecticut (2), Florida (1), Indiana (1), Maine (1), New Jersey (8), New York (11), Ohio (1), and Pennsylvania (10)].

E. coli in Fresh Fruits and Vegetables

Fruit that comes in contact with animal, especially cattle, feces, (as might happen if fruit has fallen and is harvested/picked from/off the ground), can also transmit the illness.

A specific example is the November 1996 unpasteurized apple juice outbreak:

o On November 1, 1996, Odwalla Company recalled all of its products containing unpasteurized apple juice after several children developed HUS.

o It was concluded that contamination occurred when “dropped” apples were harvested from ground that had been contaminated by cow manure; it is important to know that E. coli O157:H7 can survive for long periods of time (e.g., > 1 yr [in compost], for example).

o This tragedy led to the dramatic implementation of juice pasteurization

Fresh vegetables can become contaminated pre- or post-harvest. Contaminated seeds, irrigation water, and flooding have contributed to E. coli outbreaks traced to sprouts, lettuce, spinach, parsley, and other fresh produce. According to the September 2009 CDC report, there were no leafy green vegetables implicated in any E coli O157:H7 outbreak prior to 1995, but since then (1995-2005) there have been 27 such outbreaks:

o Lettuce and lettuce salads: 21 outbreaks

o Cabbage: 3 outbreaks

o Parsley: 2 outbreaks

o Spinach: 1 outbreak

Examples include:

Lettuce E. coli Outbreak, 2006

In early August 2006, public health officials in a mid-sized city in Utah became aware that several people attending a teacher’s conference had contracted E. coli O121:H19 (another Shiga toxin-producing E. coli). The Weber-Morgan Health Department (HD) issued a news release indicating that three people had contracted E. coli O121:H19 from the same source, and that two had developed HUS. Several days later, HD officials revised the number of outbreak victims to four, including three who had developed HUS (Weber-Morgan Health Department, 2006, August 7).

One of the patients with confirmed HUS had not attended the teacher’s conference, but had eaten cheeseburgers with iceberg lettuce prepared at the same restaurant during the outbreak. The second confirmed HUS case was an attendee of the teachers’ conference. A third was determined to be secondary transmission from a person infected at the conference. Samples from three of the HUS patients with E. coli O121:H19 were laboratory-confirmed as genetic matches through DNA sub-typing using Pulsed Field Gel Electrophoresis (PFGE), confirming that their E. coli infections all came from the same source.

Eventually, HD officials concluded that the source of the E. coli outbreak was iceberg lettuce prepared at the same fast-food facility. By the end of the epidemic at least 69 people became ill.

Spinach E. coli Outbreak, 2006

On Friday, September 8, 2006, Wisconsin Department of Health (WDOH) epidemiologists alerted officials at the Centers for Disease Control and Prevention (CDC) that a small cluster of E. coli O157:H7 infections with an unknown source had been identified. Separately, the State of Oregon Public Health Division (ODPH) also noted a small cluster of E. coli infections that same day. Both WDOH and ODPH uploaded the PFGE patterns, (genetic fingerprints), of the E. coli O157:H7 strains that had been isolated from victims of their respective states to PulseNet. This important recent epidemiology tool is an early warning system for outbreaks of food borne disease that is comprised of a national network of public health laboratories that performs DNA “fingerprinting” on bacteria that may be foodborne. PulseNet identifies and labels each “fingerprint” pattern and permits rapid comparison of these patterns through an electronic database at the CDC to identify related strains. Through PulseNet, CDC became aware that the Wisconsin and Oregon outbreaks had been caused by an indistinguishable strain of E. coli, suggesting a common source.

On September 13, 2006, Wisconsin and Oregon health officials reported to CDC that interviews of ill individuals suggested that the consumption of fresh-bagged spinach was common in both clusters, and on September 14, 2006, the Food and Drug Administration (FDA) warned the public not to eat fresh-bagged spinach. By September 15, CDC had received nearly 100 reports of E. coli infection among residents of several states. Epidemiologic investigation indicated that the outbreak had been caused by consumption of bagged spinach produced in a single plant, on a single day, during a single shift. Between August 1 and October 6, 2006, public health officials identified 199 individuals infected with the outbreak strain of E. coli O157:H7 in 26 states; 102 were hospitalized, 31 developed HUS, and 5 died.

Lettuce E. coli Outbreak, 2006

On Jan 12, 2007, the Food and Drug Administration (FDA) announced that it had moved closer to identifying the source of an E. coli O157:H7 outbreak that had sickened approximately 81 individuals in November and December of 2006. Cases were reported in Minnesota (33), Iowa (47), and Wisconsin (1). Twenty-six people were hospitalized, and two developed HUS. The investigation into the outbreak revealed that all ill individuals had contracted E. coli after eating foods at chain Mexican food restaurants in Iowa and Minnesota. Epidemiologic studies by Minnesota and Iowa health officials identified shredded iceberg lettuce served in the restaurants as the likely vehicle of transmission. Minnesota, Iowa, and Wisconsin health officials worked with public health agencies in California in a trace-back effort to determine where the E. coli-contaminated lettuce originated. During the trace-back investigation the strain of E. coli O157:H7 associated with the outbreak was found in two environmental samples gathered from dairy farms near a lettuce field in California’s Central Valley. The FDA was then able to locate the site where the lettuce was grown by reviewing records obtained from the lettuce processor.

Cookie Dough E. coli Outbreak, 2009

On June 18, 2009, the Colorado Department of Public Health and Environment (CDPHE) issued a press release stating that CDPHE, the Centers for Disease Control and Prevention (CDC), and other state health departments were investigating an outbreak of E. coli O157:H7 infections in persons who had eaten raw pre-packaged, refrigerated cookie dough. It sickened 80 in 30 states; 10 progressed to HUS.

Waterborne Transmission of Stx-producing E. coli

Water intended for recreation (e.g., pools, shallow lakes) and for human consumption can also become tainted. When lakes become contaminated, several weeks or months can be required for water quality conditions to improve or return to normal.

1998 E. coli outbreak at a water park

In 1998, an E. coli outbreak occurred among children who had visited a water theme park in the Southeast. Health officials traced the outbreak to an infected toddler who played in a pool while wearing diapers. Even though the pool was chlorinated, its concentration and contact time was presumably insufficient to kill the E. coli resulting from fecal contamination by the toddler, and other children who were in the pool ingested E. coli bacteria while playing in the pool.

1998 E. coli outbreak associated with a municipal water system

Also in 1998, the municipal water system in Alpine, Wyoming, became contaminated with E. coli, resulting in 157 illnesses, with four people developing HUS The outbreak investigation revealed that the town’s water supply, which was supplied by an underground spring and was unchlorinated, became contaminated with surface water prior to the outbreak. A large pool of water was found in the area over the water collection pipes, probably the result of a late snow melt combined with heavy rains and ground water outfalls. In addition, investigators found numerous deer and elk feces were present in the pool area, as animals came to the pool to drink (Olsen, et al., 2002).

1999 E. coli outbreak associated with exposure to recreational water

E. coli contamination at a lake in Connecticut led to an E. coli outbreak in 1999. Eleven people became ill with E. coli infections, and 3 children developed HUS; the attack rate was highest among those who were younger than 10 years who swam and/or swallowed water while swimming (McCarthy, et al., 2001; Tara, et al., 2001).

1999 E. coli outbreak associated with well water

Also in 1999, the New York State Department of Health investigated what is believed to be the largest outbreak of waterborne E. coli O157:H7 illness in United States history. The outbreak occurred at a fair in Washington County, New York, in August of 1999 (New York State Department of Health and Novello, 2000, March). A total of 781 persons were identified with suspected infections of E. coli O157:H7 and/or Campylobacter jejuni. Of these cases 127 persons were culture-confirmed to be ill with E. coli O157:H7, 71 individuals were hospitalized, 14 persons exhibited HUS, and 2 people died.

The environmental and site investigation indicated that unchlorinated water from a well serving the southwestern portion of the fairgrounds was contaminated with E. coli O157:H7 (DOH News, 1999, September 16). Samples of manure collected from a barn located 50 feet from the well and samples from the groundwater flow from the manure storage area located 80 feet from the well tested negative for E. coli O157:H7. However, samples from the septic system tested positive for E. coli O157:H7.

Consumption of only two food or beverage items, soda with ice or ice in any drink, was reported by a majority of the culture-confirmed case patients. MMWR Weekly (1999) reported that the pulsed-field gel electrophoresis testing by the New York state laboratory indicated that the DNA fingerprints of E. coli O157:H7 isolates from the well, the water distribution system, and most confirmed cases were similar.

The epidemiological investigation of this outbreak concluded that a significant relationship was associated with the incidence of the outbreak and the consumption of beverages purchased from vendors supplied with water from the unchlorinated well.

Animal-to-Person Transmission of E. coli

Animal-to-person spread also occurs, and has been identified in several outbreak-situations as well as in isolated settings, such as homes.

E. coli at Fairs and Petting Zoos

The mode of transmission at agricultural fairs, petting zoos, and farm visits was previously thought to be limited to hand-to-mouth transmission following contact with contaminated surfaces or animals. See www.fair-safety.com

Person-to-Person transmission of E. coli

Outbreaks of E. coli O157:H7 can also be caused by person-to-person transmission, which has occurred in daycare centers, hospitals, nursing homes, and private residences. Because the infectious dose is so small it is very easy for the bacteria to be transmitted among people with close physical contact.

2000 E. coli outbreak associated with a daycare

In August of 2000, a daycare in California was traced as the source of an E. coli O157:H7 outbreak. Health department officials who investigated the outbreak determined that the probable “index case”—a child who unknowingly brought the bacteria into the facility—experienced “explosive diarrhea at the daycare on the afternoon of 8-3-00.”

Shortly thereafter, four other children became infected with E. coli O157:H7 on successive days, the 6th, 7th, 8th and 9th of August, 2000. All of the children were in the same day care group. In addition to the illnesses of the children, the mother of one child, and another child’s sibling became ill and tested positive for E. coli. Another toddler also became ill.

According to the Facility Evaluation Report by the Department of Social Services, “[t]he cause of the [E. coli O157:H7] outbreak was due to a sponge being used simultaneously for wiping down a changing table and wiping down a table used for serving meals.”

E. coli case associated with person-to-person contact

A toddler in Idaho who had mild non-bloody diarrhea routinely shared the family’s bathtub with a neighbor’s child. Several days after the two children bathed together, the neighbor child developed bloody diarrhea that progressed to severe HUS. A few days later, the first toddler was also admitted to the same children’s hospital with HUS. Tragically, the neighbor’s child died.

E. coli case associated with person-to-person contact

A father who worked on a dairy farm contracted mild, non-bloody E. coli diarrhea that was transmitted to his son who developed HUS. The same event reoccurred two years later. The son’s second episode was devastating. Although the son survived, he was left with blindness and severe brain damage.

Symptoms of an E. coli Infection

What happens after the Shiga toxin-producing E. coli is ingested?

E. coli infection occurs when a person ingests Shiga toxin (Stx)-producing E. coli (e.g., E. coli O157:H7) after exposure to contaminated food, beverages, water, animals, or other persons. After ingestion, E. coli bacteria rapidly multiply in the large intestine and bind tightly to cells in the intestinal lining. This snug attachment facilitates absorption of the toxin into the small capillaries within the bowel wall where it attaches to globotriaosylceramide (Gb3) receptors.

Inflammation caused by the toxins is believed to be the cause of hemorrhagic colitis, the first symptom of E. coli infection, which is characterized by the sudden onset of abdominal pain and severe cramps, followed within 24 hours by diarrhea (Boyce, Swerdlow, & Griffin, 1995; Tarr, 1995). Hemorrhagic colitis typically occurs within 2 to 5 days of ingestion of E. coli, but the incubation period, or time between the ingestion of E. coli bacteria and the onset of illness, may be as broad as 1 to 10 days.

As the infection progresses, diarrhea becomes watery and then may become grossly bloody, that is, bloody to the naked eye. E. coli symptoms also may include vomiting and fever, although fever is an uncommon symptom.

On rare occasions, E. coli infection can cause bowel necrosis (tissue death) and perforation without progressing to hemolytic uremic syndrome (HUS)—a complication of E. coli infection that is now recognized as the most common cause of acute kidney failure in infants and young children. In about 10 percent of E. coli cases, the Shiga toxin attachment to Gb3 receptors results in HUS.

HUS had been recognized in the medical community since at least the mid-1950’s; however, the syndrome first caught the public’s attention in 1993 following a large E. coli outbreak in Washington State that was linked to the consumption of contaminated hamburgers served at a fast-food chain. A total of 501 E. coli cases were reported; 151 were hospitalized (31%), 45 persons (mostly children) developed HUS (9%), and three died (Bell, et al., 1994).

During HUS, the majority of the toxin gains access to 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 strong Gb3 receptors that grasp and hold on to the toxin.

Organ injury is primarily a function of Gb3 receptor location and density. These receptors are probably always in the gut wall and kidneys, but heterogeneously distributed in the other major body organs. This may be the reason that some patients develop injury in other vital organs (e.g., brain, etc.). Once Stx attaches to receptors, it moves into the cells’ cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury or death, and subsequent damage to vital organs such as the kidney, pancreas, and brain.

How is an E. coli Infection Diagnosed?

Infection with E. coli O157:H7 or other Shiga toxin-producing E. coli is usually confirmed by the detection of the bacteria in a stool specimen from an infected individual. Most hospital labs and physicians know to test for these particular bacteria, especially if the potentially infected individual has bloody diarrhea. Still, it remains a good idea to specifically request that a stool specimen be tested for the presence of shiga toxin-producing E. coli when it is submitted to the lab for testing.

Trace-back and source identification

E. coli O157:H7 is now commonly “fingerprinted.” When a sample is taken from either a piece of meat or poultry that is contaminated with a dangerous form of bacteria, such as E. coli O157:H7, Listeria, Salmonella, or Campylobacter, it can be cultured to obtain and identify the bacterial isolate. If a person consumes some of the contaminated meat or poultry, and becomes infected as a result, a stool sample can then be cultured to obtain and identify the bacterial isolate. These bacterial isolates are then broken down into their various component parts creating a DNA “fingerprint”. The “fingerprint” of the bacteria can then be compared and matched up to the “fingerprint” of isolates from persons who consumed the contaminated product. When DNA “fingerprints” match, they, along with solid epidemiological work, are proof that the contaminated product was the source of the illness.

The process of obtaining the DNA “fingerprint” is called Pulse Field Gel Electrophoresis, or PFGE. This technique is used to separate the DNA of the bacterial isolate into its component parts. It operates by causing alternating electric fields to run the DNA through a flat gel matrix of agarose, a polysaccharide obtained from agar. The pattern of bands of the DNA fragments, or “fingerprints,” in the gel after exposure to the electrical current is unique for each strain and sub-type of bacteria. By performing this procedure, scientists can identify hundreds of strains of E. coli O157:H7 as well as strains of Listeria, Salmonella, and Campylobacter

Treatment for an E. coli Infection

In most infected individuals, symptoms of E. coli infection last about a week and resolve without any long-term problems. Antibiotics do not improve the illness, and some medical researchers believe that these medications can increase the risk of developing HUS (Wong, Jelacic, & Tarr, 2000). Therefore, apart from good supportive care such as close attention to hydration and nutrition, there is no specific therapy to halt E. coli symptoms. The recent finding that E. coli O157:H7 initially greatly speeds up blood coagulation may lead to future medical therapies that could forestall the most serious consequences (Chandler, et al., 2002). Most individuals who do not develop HUS recover within two weeks.

Treatment for those who develop HUS ranges from mild to very intensive. Children are generally in the hospital for about two weeks (range 3 days to 3 months), and adults longer, as their courses tends to be more severe. Since there is no way to end D+HUS, supportive therapy, including meticulous attention to fluid and electrolyte balance, is the cornerstone of survival. For more information about the treatment for HUS, read “What to expect during hospitalization” at www.about-hus.com.

Preventing an E. coli Infection

What can we do to protect our families from E. coli?

Since there is no fail-safe food safety program, consumers need to “drive defensively” as they navigate from the market to the table. It is no longer sufficient to take precautions only with ground beef and hamburgers, anything ingested by family members can be a vehicle for infection. Shiga toxin-producing E. coli are now so widely disseminated that a wide variety of foods can be contaminated. Direct animal-to-person and person-to-person transmission is not uncommon. Following are steps you can take to protect your family from E. coli. See also the section what is our government doing to protect us from E. coli?

1. Practice meticulous personal hygiene. This is true not only for family members (and guests), but for anyone interfacing with the food supply chain. Remember that E. coli bacteria are very hardy (e.g., can survive on surfaces for weeks) and that only a few are sufficient to induce serious illness. Since there is no practical way of policing the hygiene of food service workers, it is important to check with local departments of health in order to identify any restaurants that have been given citations or warnings. The emerging practice of providing sanitation “report cards” for public display is a step in the right direction.

2. Be sure to clean and sanitize all imported and domestic fruits or vegetables. All can be carriers of disease. If possible, fruits should be skinned, or at least vigorously scrubbed and/or washed. Vegetables (and of course meat) should be cooked to a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds. If not cooked, fruits and vegetables should be washed to remove any dirt or other material, and then soaked in chlorinated water (1 teaspoon of household bleach in one quart of water, soaked for at least 15 minutes). They can then be rinsed in clean water to remove the chlorine taste. This will remove most, but not all, bacteria. In the case of leafy vegetables, bacteria may not be limited to the leaf’s surface, but can actually reside within the minute circulatory system of the individual vegetable leaves.

3. Be careful to avoid cross contamination when preparing and cooking food, especially if beef is being served. This requires being very mindful of the surfaces (especially cutting boards) and the utensils used during meal preparation that have come in contact with uncooked beef and other meats. This even means that utensils used to transport raw meat to the cooking surfaces should not be the same that are later used to remove the cooked meat (or other foodstuffs) from the cooking surfaces.

4. Do not allow children to share bath water with anyone who has any signs of diarrhea or “stomach flu”. And keep any toddlers still in diapers out of all bodies of water (especially wading and swimming pools).

5. Do not let any family members touch or pet farm animals. Merely cleaning the hands with germ “killing” wipes may not be adequate!

6. Wear disposable gloves when changing the diapers of any child with any type of diarrhea. Remember that E. coli O157:H7 diarrhea initially is non-bloody, but still very infectious. If gloves are not available, then thorough hand washing is a must.

7. Remember that achieving a brown color when cooking hamburgers does not guarantee that E. coli bacteria have been killed. This is especially true for patties that have been frozen. Verifying a core temperature of at least 160 degrees Fahrenheit for at least 15 seconds is trustworthy. Small, disposable meat thermometers are available, a small investment compared to the medical expense (and grief) of one infected family member.

8. Avoid drinking (and even playing in) any non-chlorinated water. There is an added risk if the water (well, irrigation water or creek/river) is close to, or downstream from any livestock.

Irradiation offers the most practical and effective way of sterilizing foods and protecting the consumer. It is already being used for poultry, and is approved for all other foods. Even though the word “irradiation” conjures up fears of radiation exposure, irradiated food does not become “radioactive”; it is safe, and does not change the taste or texture of food. To insure safety the public needs to be educated and the food industry convinced that this will not only protect the consumer, but also will also favorably affect their bottom line. This should be a “no-brainer” given the fact that tainted foods are costing the food industry hundreds of millions of dollars a year (recently, one beef processing company declared bankruptcy following a massive recall of contaminated hamburgers). If this doesn’t work, the food industry may be required to implement this or other equally effective measures.

What is our government doing to protect us from E. coli?

Congress enacts statutes designed to ensure the safety of the food supply. The U.S. food agencies are accountable to the President, to the Congress, which has oversight authority, to the courts, which review regulations and enforcement actions, and to the public. The principal federal agencies responsible for providing consumer protection are:

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:

On Nov. 15, 2006, a senior official from CDC testified before the Senate Committee on Health, Education, Labor and Pensions, regarding CDC’s food safety activities, with a special emphasis on the recent E. coli spinach outbreak (King, 2006, November 15). He testified, in part, that:

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.

In partnership with state health departments, CDC collects surveillance information on foodborne illness. The states collect data about cases of infections that are of public health importance from doctors and clinical laboratories. CDC helps states investigate outbreaks that are large, severe, or unusual. . . .

CDC specializes in the critically important public health activities of surveillance, epidemiologic response, and investigation of disease. . . .

In 1993, there was a large multi-state outbreak of E. coli O157 infections in the Western United States. In order to prevent future severe outbreaks . . . an effective surveillance network called PulseNet was developed. PulseNet is the national network for molecular sub-typing of foodborne bacteria . . . and is coordinated by CDC. The laboratories participating in PulseNet are in state health departments, some local health departments, USDA, and FDA. PulseNet plays a vital role in surveillance for, and investigation of, foodborne illness outbreaks that were previously difficult to detect. For example, when a clinical laboratory makes a diagnosis of E. coli O157, the bacterial strain is sent to a participating PulseNet laboratory where it is sub-typed, or “DNA fingerprinted” [every E. coli has a unique DNA pattern]. The “fingerprint” is then compared with other patterns in the state, and uploaded electronically to the national PulseNet database maintained at CDC, where it can be compared with the patterns in other states. This gives us the capability to rapidly detect a cluster of infections with the same pattern that is occurring in multiple states. The PulseNet database, which includes approximately 120,000 DNA patterns, is available to participating laboratories and allows them to rapidly compare patterns. Once a cluster of cases with the same DNA pattern is identified, epidemiologists then interview patients to determine whether cases of illness are linked to the same food source or other exposures they have in common. The strength of this system is its ability to identify patterns even if the affected persons are geographically far apart, which is important given the reality of U.S. food distribution systems. If patients have been exposed to a specific food or to another source of infection, and the case count for that illness is larger than one would expect for the time period, the cluster is determined to be an outbreak with a common source.

The group of epidemiologists in the states and at CDC who regularly investigate and report on these outbreaks is called OutbreakNet. The Outbreak Net participants use standardized interview methods and forms and rapidly share the investigation data. With this collaboration, outbreaks can be investigated in a matter of days rather than weeks. As a consequence, CDC [that has no regulatory authority] can more rapidly alert FDA and USDA about implicated food products associated with foodborne illness so that all three agencies can collaboratively take actions to protect public health. Tracing the implicated food back from consumption through preparation, to distributors, and sometimes back to a field or farm can help determine how the contamination occurred, stop distribution of the contaminated product, and prevent further outbreaks from occurring. . . .

Another important surveillance network is CDC’s Foodborne Diseases Active Surveillance Network (FoodNet). This network is collaboration among 10 state health departments, the USDA, and FDA . . . FoodNet conducts active surveillance for foodborne diseases and also conducts related epidemiologic studies that look at both sporadic and outbreak foodborne infections to help public health officials better understand the epidemiology of foodborne diseases in the United States and how to target prevention strategies. We have PulseNet to detect possible outbreaks, OutbreakNet to investigate and report them, and FoodNet to track general trends and define where more effective prevention strategies are needed (emphasis added).

These networks stand prepared to detect a public health event related to the food supply. For example, after investigations of PulseNet-identified clusters of E. coli infection focused attention on the need for specific controls during ground beef processing, regulatory and industry practices changed in 2002, and the incidence of E. coli O157:H7 infections began to decrease sharply. By 2005, the incidence of E. coli O157 infections, as measured in FoodNet, had dropped 29% [Since 2006, however, the incidence appears to be rising, primarily due to outbreaks linked to lettuce and spinach].

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, http://www.bt.cdc.gov/agent/food/.

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, http://www.cdc.gov/ecoli/2007/october/100207.html.

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, http://www.health.state.ny.us/press/releases/1999/ecoli916.htm.

Elder RO, Keen JE, Siragusa GR, Barkocy-Gallagher GA, Koohmaraie M, and Laegreid WW. (2000). Correlation of enterohemorrhagic Escherichia coli O157 prevalence in feces, hides, and carcasses of beef cattle during processing.  Proc. Natl. Acad. Sci. USA 97: 2999-3003.  Retrieved January 7, 2008, from http://www.pnas.org/cgi/reprint/97/7/2999.pdf.

Frenzen, PD, Drake A, and Angulo FJ. (2005). Economic Cost of Illness due to Escherichia coli O157 Infections in the United States, Journal of Food Protection, 68:2623-2630.

Friedman MS, Roels T, Koehler JE, Feldman L, Bibb WF, and Blake P. (1999).  Escherichia coli O157:H7 Outbreak Associated with an Improperly Chlorinated Swimming Pool.  Clin. Infect. Dis. 29(2): 298-303. 

Griffin, PM and Tauxe, RV. (1991).  The Epidemiology of Infections Caused by Escherichia coli O157:H7, Other Enterohemorrhagic E. coli, and the Associated Hemolytic Uremic Syndrome.  Epidemiol Rev. 13: 60-98.

Keene W, McAnulty JM, Hoesly FC, Williams LP, Hedberg K, Oxman GL, Barrett TJ, Pfaller MA, and Fleming DA. (1991).  A Swimming-Associated Outbreak of Hemorrhagic Colitis Caused by Escherichia coli O157:H7 and Shigella Sonnei.  N. Engl. J. Med.  331(9): 579-584

Keen JE, Wittum TE, Dunn JR, Bono JL, and Durso LM. (2003).  Shiga-toxigenic Escherichia coli O157 in agricultural fair livestock, United States. Emerg. Infect. Dis. 12(5):780-786.

King LJ. (2006, November 15).  Testimony on CDC Food Safety Activities and the Recent E. coli Spinach Outbreak:  Hearing Before the Committee on Health, Education, Labor and Pensions, United States Senate.  Retrieved January 2, 2008, from United States Department of Health and Human Services Web site, http://www.hhs.gov/asl/testify/t061115.html

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, http://www.cdc.gov/ncidod/EID/vol8no4/00-0218.htm

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, http://www1.co.weber.ut.us/health/ecoli.php?d=1

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.

About the Author 

William (Bill) Marler is the nation’s leading attorney representing victims of foodborne illness and a stalwart advocate for improved food safety in the United States and abroad. His work began in 1993 when, as a young lawyer, he won record settlements for the families of children made seriously ill in the infamous Jack in the Box E. coli outbreak.  He has since lead his law firm, Marler Clark, to the apex of the legal world by representing thousands of victims of food poisoning. 

Marler has continued to litigate against the food industry and to attract clients who need his services.  In 2007, a 19-year-old dancer, Stephanie Smith, sickened by E. coli-tainted hamburger was left brain damaged and paralyzed.  Her story found its way to the front page of the New York Times in 2009 and landed the paper and its investigative reporter, Michael Moss, a Pulitzer Prize.  Her case against Cargill settled shortly before trial in 2010 for an amount “to care for her for life.” 

In 2009 Linda Rivera, a 57 year old mother of six from Nevada was stricken with what Dr. Siegler described as “the severest multi-organ (bowel, kidney, brain, lung, gall bladder, pancreas) case of E. coli mediated HUS I have seen in my extensive experience.”  Linda’s story hit the front page of the Washington Post and became Senator Harry Reid’s touchstone for moving the Food Safety Bill in 2010.

Working with industry, academia, and government, Marler’s efforts to create a safer food supply have transcended the courtroom. His spends roughly half his time speaking around the world on the need for improved food safety.  To bring discussion to the public, he publishes the acclaimed online newspaper Food Safety News and shares his own opinions and insights on his blog, www.marlerblog.com, which is read by over one million people annually. 

Marler has petitioned the USDA to increase foodborne pathogen regulation and has commissioned private studies to test for unregulated pathogens in the food supply.  In Congressional testimony, he has asked the United States government to “Put me out of business”, calling on it to pass updated, meaningful food safety laws.  In 2011, his work was credited in the passage and signing of the Food Safety Modernization Act, the first major food safety update in decades. 

Though his efforts to reform the food industry have come at the price of long hours and frequent travel, when he is at rest he can be found spending time at his Bainbridge Island home with his wife Julie and three daughters, Morgan, Olivia, and Sydney.

Marler Clark Resources

Botulism Blog

Botulism Blog

Campylobacter

About Campylobacter

Campylobacter Blog

E. coli

E. coli

About Hemolytic Uremic Syndrome

E. coli Blog

E. coli Lawsuits & Litigation

Hepatitis A

About Hepatitis A

Hepatitis A Lawsuits & Litigation

Hepatitis A Blog

Listeria

About Listeria

Listeria Blog

Norovirus

About Norovirus

Norovirus Blog

Salmonella

About Salmonella

Salmonella Lawsuits & Litigation

Salmonella Blog

Shigella

About Shigella

Shigella Lawsuits & Litigation

Shigella Blog

Complications of Foodborne Illness

Guillain-Barre Syndrome

Hemolytic Uremic Syndrome

Irritable Bowel Syndrome

Reactive Arthritis

General Foodborne Illness Information

Foodborneillness

Outbreak Database

See Also 

Marler Clark

Bill Marler’s Blog

Food Safety News

Food Poison Journal

Real Raw Milk Facts

Fair Safety

Marler Clark Copyright 2011

  • Doc Mudd

    Coliform bacteria, including E. coli, are ubiquitous in animals and humans. Always have been, always will be. It’s a packaged deal.
    That fact was the fundamental reason for early public health initiatives: sanitary sewers; water treatment facilities; ordinances regulating the keeping of farm animals in urban areas; health inspection of farms, processors and food establishments; also the good old standard “employees must wash hands before returning to work” signs prominently adorning every restroom in America.
    A century and a half of progress in human sanitation can temporarily be undone in an instant by one thoughtless operator anywhere along the food chain. Germs never sleep! People require constant reminding…some more than others.