AN INTRODUCTION TO E. COLI BACTERIA
Escherichia coli (or E. coli) is the most prevalent infecting organism in the family of gram-negative bacteria known as enterobacteriaceae.  E. coli bacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich.  Dr. Escherich also showed that certain strains of the bacterium were responsible for infant diarrhea and gastroenteritis, an important public health discovery. Although E. coli bacteria were initially called Bacterium coli, the name was later changed to Escherichia coli to honor its discoverer. 
E. coli is often referred to as the best or most-studied free-living organism. [1, 3] More than 700 serotypes of E. coli have been identified. [1,4] The “O” and “H” antigens on the bacteria and their flagella distinguish the different serotypes.  It is important to remember that most kinds of E. coli bacteria do not cause disease in humans. [1, 2] Indeed, some E. coliare beneficial, while some cause infections other than gastrointestinal infections, such as urinary tract infections. 
The E. coli that are responsible for the numerous reports of contaminated foods and beverages are those that produce Shiga toxin, so called because the toxin is virtually identical to that produced by Shigella dysenteria type 1.  The best-known and also most notorious E. coli bacteria that produce Shiga toxin is E. coli O157:H7. [1, 4] The Centers for Disease Control and Prevention (CDC) has estimated that every year at least 2,000 Americans are hospitalized, and about 60 die as a result of E. coli infection and its complications. [4, 5] A study published in 2005 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. 
E. COLI O157:H7
E. coli O157:H7—a foodborne pathogen
E. coli O157:H7 is one of thousands of serotypes of Escherichia coli. The testing done to distinguish E. coli O157:H7 from its other E. coli counterparts is called serotyping. 
Pulsed-field gel electrophoresis (PFGE), sometimes also referred to as genetic fingerprinting, is used to compare E. coliO157:H7 isolates to determine if the strains are distinguishable. [3, 7] A technique called multilocus variable number of tandem repeats analysis (MLVA) is used to determine precise classification when it is difficult to differentiate between isolates with indistinguishable or very similar PFGE patterns. 
E. coli O157:H7 was first recognized as a pathogen in 1982 during an investigation into an outbreak of hemorrhagic colitis associated with consumption of hamburgers from a fast-food chain restaurant.  Retrospective examination of more than three thousand E. coli cultures obtained between 1973 and 1982 found only one isolate with serotype O157:H7, and that was a case in 1975.[4, 9] In the ten years that followed, there were approximately thirty outbreaks recorded in the United States.  This number is likely misleading, however, because E. coli O157:H7 infections did not become a reportable disease in any state until 1987, when Washington became the first state to mandate its reporting to public health authorities. [11, 12] Consequently, an outbreak would not be detected if it was not large enough to prompt investigation.[11, 13]
E. coli O157:H7’s ability to induce injury in humans is a result of its ability to produce numerous virulence factors, most notably Shiga toxin (Stx), which is one of the most potent toxins known to man. [4, 14, 15] Shiga toxin has multiple variants (e.g., Stx1, Stx2, Stx2c), and acts like the plant toxin ricin by inhibiting protein synthesis in endothelial and other cells.  Endothelial cells line the interior surface of blood vessels and are known to be extremely sensitive to E. coliO157:H7, which is cytotoxigenic to these cells. 
In addition to Shiga toxin, E. coli O157:H7 produces numerous other putative virulence factors, including proteins which aid in the attachment and colonization of the bacteria in the intestinal wall, and which can lyse red blood cells and liberate iron to help support E. coli metabolism. 
E. coli O157:H7 evolved from enteropathogenic E. coli serotype O55:H7, a cause of non-bloody diarrhea, through the sequential acquisition of phage encoded Stx2, a large virulence plasmid, and additional chromosomal mutations. [18, 19] The rate of genetic mutation indicates that the common ancestor of current E. coli O157:H7 clades likely existed some 20,000 years ago.  E. coli O157:H7 is a relentlessly evolving organism, constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat. [21, 22] The prospect of emerging pathogens as a significant public health threat has been emphasized by the CDC for some time. As Robert Tauxe of the CDC notes:
After 15 years of research, we know a great deal about infections with E. coli O157:H7, but we still do not know how best to treat the infection, nor how the cattle (the principal source of infection for humans) themselves become infected. 
Although foods of a bovine origin are the most common cause of both outbreaks and sporadic cases of E. coli O157:H7 infections, outbreaks of illnesses have been linked to a wide variety of food items. For example, produce has been the source of substantial numbers of outbreak-related E. coli O157:H7 infections since at least 1991. [13, 24] Outbreaks have been linked to alfalfa, clover and radish sprouts, lettuce, and spinach. [31, 32]Other vehicles for outbreaks include unpasteurized juices, yogurt, dried salami, mayonnaise, raw milk, game meats, hazelnuts, and raw cookie dough. [10, 13, 30]
Non-O157 Shiga Toxin-Producing E. coli
E. coli are classified by their O and H antigens (e.g., E. coli O157:H7, E. coli O26:H11) and broadly categorized as Shiga toxin-producing E. coli (STEC) O157 or non-O157 STEC. For many years, most recognized STEC outbreaks were associated with STEC O157. Despite the dominance of STEC O157, at least 150 non-O157 strains of E. coli are known to cause human illness and have been associated with outbreaks.
In the US, documented outbreaks of non-O157 E. coli include 10 involving O111; 6 involving O26; 3 involving O45; 2 involving O145, O104, and O6; and one each involving O51; O103; O27; and, O84. Non-O157 STEC outbreaks are rare but tend to primarily be due to contaminated food and person-to-person transmission.
Non-O157 STEC infections are under-recognized and under-reported due to inadequate epidemiological and laboratory surveillance. In the United States, E. coli O157:H7 became nationally notifiable in 1994, whereas non-O157 STEC infections were not reportable until 2000.  Screening for non-O157 STEC remains rare. This is no surprise since by 2007 only 66% of clinical labs screened all stool samples for E. coli O157:H7 and fewer than 10% of labs ever conducted on-site testing for non-O157 STEC. As with E. coli O157:H7, non-O157 STEC cases tend to occur during the summer months.
Non-O157 STEC can be difficult to identify in laboratory screening for E. coli O157 because they do not ferment sorbitol. Most stool cultures suspected to contain STEC are first screened for Shiga toxin; a positive test could be either E. coli O157:H7 or non-O157 STEC. Unfortunately, some labs will discard Shiga toxin-positive cultures after reporting to the referring doctor without identifying the strain. State laboratories can send STEC cultures to the CDC to determine the serotype. Some states, such as Minnesota and Connecticut have begun studies of their own to identify non-O157 STEC.
In recent years, improved diagnostic assays for non-O157 STEC have contributed to an increased appreciation of the severity of disease caused by these strains, including hemolytic uremic syndrome (HUS). Notably, the number of non-O157 STEC cases reported to CDC’s FoodNet has risen steadily each year; from 2000-2006, there was an overall 4-fold increase in incidence (0.12 cases per 100,000 to 0.42 cases per 100,000 population) at FoodNet sites. The most common serogroups reported to cause foodborne illness in the United States are O26, O111, O103, O121, O45, and O145.  These six serotypes account for 75% of human infections.
Worldwide, non-O157 STEC outbreaks emerged in the 1980s, and the first reported outbreaks in the United States occurred in the 1990s. [57, 55] The number of reported outbreaks due to non-O157 STECs remains relatively low in the United States, but experts agree that documented outbreaks probably represent the “tip of the iceberg.” From 1983-2002, seven non-O157 STEC outbreaks were reported in the United States.  During the following five-year period from 2003-2007, CDC documented an additional five non-O157 STEC outbreaks (CDC Outbreak Surveillance Data, http://www.cdc.gov/foodborneoutbreaks/outbreak_data.htm).
An extraordinary non-O157 outbreak occurred in Germany beginning in May 2011. The STEC involved was extremely rare: E. coli O104:H4. It was also extremely virulent. Ultimately, the outbreak sickened nearly 4,000 people and killed more than 50. This strain was not only resistant to many antibiotics, but it also possessed a novel mechanism for sticking to intestinal cells. Other unusual aspects of this outbreak were that it affected a disproportionately large percentage of women. Further, nearly a quarter of those infected developed HUS and of those the vast majority was women. It appears that this non-O157 STEC acquired its virulence factors and antibiotic resistance through horizontal gene acquisition rather than point mutations or descent from prior generations of bacteria.  The outbreak was ultimately traced to contaminated seeds of fenugreek from Egypt, sold as sprouts by an organic farm in Germany.
A study of non-O157 STEC concluded that these strains may account for up to 20 to 50% of all STEC infections in the United States.  The prevalence of non-O157 STEC infections is placing an increasing burden on society and the health care system in the United States.
E. coli O157:H7 bacteria and other pathogenic E. coli mostly live in the intestines of cattle, but E. coli bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. [1, 35] 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 7% of pest fly pools also tested positive for E. coli O157:H7.  Shiga toxin-producing E. coli does not make the animals that carry it ill.  The animals are merely the reservoir for the bacteria. 
According to a study published in 2011, an estimated 93,094 illnesses are due to domestically acquired E. coli O157:H7 each year in the United States.  Estimates of foodborne-acquired O157:H7 cases result in 2,138 hospitalizations and 20 deaths annually. 
What makes E. coli O157:H7 remarkably dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. [4, 27] “E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.”  As few as 20 organisms may be sufficient to infect a person and, as a result, possibly kill them.  And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44° Fahrenheit, survives freezing and thawing, is heat-resistant, grows at temperatures up to 111 F, resists drying, and can survive exposure to acidic environments. [27, 28] And, finally, to make it even more of a threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact. [4, 13]
Trace-back and source identification
E. coli O157:H7 and other non-O157 STECs are now routinely “fingerprinted” as part of surveillance of foodborne disease.  This surveillance was first initiated in response to the major outbreak of E. coli O157:H7 infections in 1993. As described by the CDC on the PulseNet website:
In 1993, a large outbreak of foodborne illness caused by the bacterium Escherichia coli O157:H7 occurred in the western United States. In this outbreak, scientists at CDC performed DNA “fingerprinting” by pulsed-field gel electrophoresis (PFGE) and determined that the strain of E. coli O157:H7 found in patients had the same PFGE pattern as the strain found in hamburger patties served at a large chain of regional fast-food restaurants. Prompt recognition of this outbreak and its cause may have prevented an estimated 800 illnesses. As a result, CDC developed standardized PFGE methods and in collaboration with the Association of Public Health Laboratories (APHL), created PulseNet so that scientists at public health laboratories throughout the country could rapidly compare the PFGE patterns of bacteria isolated from ill persons and determine whether they are similar.
(For more information, go here: http://www.cdc.gov/pulsenet/whatis.htm#role)
When a sample is taken from food that is contaminated with bacteria, such as E. coli O157:H7, Listeria, Salmonella, or Campylobacter, the sample is tested (or cultured) to obtain and identify the bacterial isolate.  Similarly, if a person consumes contaminated food, and becomes infected as a result, a stool sample can be cultured to obtain and identify the bacterial isolate. These bacterial isolates are then broken down into component parts to create a DNA “fingerprint.” [52, 53] The “fingerprint” can then be compared and matched up to the “fingerprint” of isolates from other persons who consumed the contaminated food.  When “fingerprints” match, the match is proof that the contaminated food was the source of the illness.
The process of obtaining the DNA “fingerprint” is called Pulse Field Gel Electrophoresis (PFGE).  The PFGE technique is used to separate the DNA of the bacterial isolate into smaller pieces. The DNA is placed in a flat gel matrix of agarose, a polysaccharide obtained from agar, and exposed to an alternating electric field. [52, 53] Individual pieces of DNA, or bands, will migrate across the gel, creating a bar code-like pattern unique to each strain.  By performing the procedure, scientists can identify hundreds of strains of E. coli O157:H7 as well as strains of Listeria, Salmonella, and Campylobacter. 
Cattle as Reservoirs
Beef and dairy cattle are known reservoirs of E. coli O157:H7 and non-O157 STEC strains. [58, 59] In reviews of STEC occurrence in cattle worldwide, the prevalence of non-O157 STECs ranged from 4.6 to 55.9% in feedlot cattle, 4.7 to 44.8% in grazing cattle, and 0.4 to 74% in dairy cattle feces. The prevalence in beef cattle going to slaughter ranged from 2.1 to 70.1%. While most dairy cattle-associated foodborne disease outbreaks are linked to milk products, dairy cattle still represent a potential source of contamination of beef products when they are sent to slaughter at the end of their useful production life (termed “cull” or “spent” dairy cows); this “dairy beef” is often ground and sold as hamburger.
The high prevalence of E. coli O157 and non-O157 STEC in some cattle populations, combined with the lack of effective on-farm control strategies to reduce carriage, represents a significant risk of contamination of the food supply and the environment. Non-O157 STEC are also harbored in other ruminants, including swine. 
Numerous Shiga toxin-producing E. coli serotypes known to cause human illness are of bovine origin, thus putting the beef supply at-risk. Both E. coli O157:H7 and non-O157 STEC may colonize the gastrointestinal tract of cattle, and potentially contaminate beef carcasses during processing. Although not as well studied, the risk factors for contamination of beef products from cattle colonized with non-O157 STECs are probably the same or very similar to E. coli O157:H7. For example, cattle hides contaminated with E. coli O157:H7 during slaughter and processing are a known risk factor for subsequent E. coli O157:H7 contamination of beef products. One study showed that the prevalence of non-O157 STEC (56.6%) on hides is nearly as high as that found for E. coli O157:H7 (60.6%). 
A review of published reports from over three decades found that non-O157 STEC were more prevalent in beef products compared with E. coli O157.  In this study, the prevalence of non-O157 STEC ranged from 1.7 to 58% in packing plants, from 3 to 62.5% in supermarkets, and an average of 3% in fast food restaurants. In a recent survey of retail ground beef products in the United States, 23 (1.9%) of 1,216 samples were contaminated with non-O157 STEC.  In another study, researchers found a 10 to 30% prevalence of non-O157 STEC in imported and domestic boneless beef trim used for ground beef. 
Environmental Sources of E. coli
E. coli O157:H7 bacteria and other pathogenic E. coli are believed to mostly live in the intestines of cattle, but these bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. [1, 35] 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. coliO157: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.  Shiga toxin-producing E. coli does not make the animals that carry it ill, the animals are merely the reservoir for the bacteria.  
Products Implicated in Previous Non-O157 STEC Outbreaks
There is a paucity of information on the vehicles of transmission for human non-O157 STEC infections, but contaminated raw dairy products, produce, and water have been implicated in the United States.  A review of non-O157 STEC in Connecticut showed that exposures, including ground beef, were similar in both non-O157 STEC and E. coli O157:H7 cases, suggesting that the routes of transmission are similar (CDC 2007). Considering the relatively high prevalence of both E. coli O157:H7 and non-O157 STEC in cattle populations and their products, it is not surprising that ground beef and other beef products could be a common food vehicle.
Non-O157 STEC outbreaks attributed to ground beef and its sausage products have been documented outside the United States including Argentina, Australia, Germany, and Italy. These beef-related outbreaks involved 8 STEC serogroups (O1, O2, O15, O25, O75, O86, O111, and O160). HUS cases were reported in five of the six outbreaks, mostly striking children, and the elderly.
What happens after the Shiga toxin-producing E. coli are ingested?
The colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within 24 hours, and sometimes fever.  The incubation period—that is, the time from exposure to the onset of symptoms—in outbreaks is usually reported as 3 to 4 days but may be as short as 1 day or as long as 10 days. [4, 13, 26] Infection can occur in people of all ages but is most common in children. 
Unlike other E. coli pathogens, which remain on intestinal surfaces, Shiga toxin-producing bacteria, like O157:H7, are invasive.  After ingestion, E. coli bacteria rapidly multiply in the large intestine and then bind tightly to cells in the intestinal lining. [1, 26] This snug attachment facilitates absorption of the toxins into the small capillaries within the bowel wall. [1, 33, 45] Once in the systemic circulation, Shiga toxin becomes attached to weak receptors on white blood cells, thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin. 
Inflammation caused by the toxins is believed to be the cause of hemorrhagic colitis, the first symptom of E. coliinfection, which is characterized by the sudden onset of abdominal pain and severe cramps. [29, 42] Such symptoms are typically followed within 24 hours by diarrhea, sometimes fever. [1, 4]
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.
The duration of an uncomplicated illness can range from one to twelve days. [4, 23] In reported outbreaks, the rate of death is 0-2%, with rates running as high as 16-35% in outbreaks involving the elderly, like those that have occurred at nursing homes. 
Shiga toxin–producing E. coli (STEC) cause approximately 100,000 illnesses, 3,000 hospitalizations, and 90 deaths annually in the United States. [39, 54] As noted, most reported STEC infections in the United States are caused by E. coliO157:H7, with an estimated 73,000 cases occurring each year.  According to the CDC:
Non-O157 STEC bacteria also are important causes of diarrheal illness in the United States; at least 150 STEC serotypes have been associated with outbreaks and sporadic illness. In the United States, six non-O157 serogroups (O26, O45, O103, O111, O121, and O145) account for the majority of reported non-O157 STEC infections. 
Persons with non-O157 STEC tend to have less severe illness, but some non-O157 STEC members can cause very severe infections, including those that result in HUS and death. Non-O157 STEC that cause HUS overwhelmingly produce Shiga toxin 2 with or without Shiga toxin 1. As with E. coli O157:H7, more severe disease results from Shiga toxin 2 production by non-O157 STEC.
A Life-Threatening Complication—Hemolytic Uremic Syndrome
E. coli O157:H7 infections can lead to a severe, life-threatening complication called the hemolytic uremic syndrome (HUS). [4, 13] HUS accounts for most of the acute deaths and chronic injuries caused by the bacteria.  HUS occurs in 2-7% of victims, primarily children, with onset five to ten days after diarrhea begins. [23, 44] “E. coli serotype O157:H7 infection has been recognized as the most common cause of HUS in the United States, with 6% of patients developing HUS within 2 to 14 days of onset of diarrhea.” [44, 45] And it is the most common cause of renal failure in children. [26, 45, 48]
Approximately half of the children who suffer HUS require dialysis, and at least 5% of those who survive have long term renal impairment.  The same number suffers severe brain damage.  While somewhat rare, serious injury to the pancreas, resulting in death or the development of diabetes, also occurs.  There is no cure or effective treatment for HUS.  And, tragically, children with HUS too often die, with a mortality rate of five to ten percent. 
Once Shiga toxins attach to receptors on the inside surface of blood vessel cells (endothelial cells), a chemical cascade begins that results in the formation of tiny thrombi (blood clots) within these vessels. [33, 45] Some organs seem more susceptible, perhaps due to the presence of increased numbers of receptors, and include the kidney, pancreas, and brain. [26, 33] Consequently, organ injury is primarily a function of receptor location and density. [33, 54]
Once they move into the interior of the cell (cytoplasm), Shiga toxins shut down protein machinery, causing cellular injury or death. [33, 46] This cellular injury activates blood platelets too, and the resulting “coagulation cascade” causes the formation of clots in the very small vessels of the kidney, leading to acute kidney failure.
The red blood cells are either directly destroyed by Shiga toxin (hemolytic destruction), or are damaged as cells attempt to pass through partially obstructed micro-vessels. [33, 46] Blood platelets become trapped in the tiny blood clots, or they are damaged and destroyed by the spleen. 
When fully expressed, HUS presents with the triad of hemolytic anemia (destruction of red blood cells), thrombocytopenia (low platelet count), and renal failure (loss of kidney function). [33, 45] Although recognized in the medical community since at least the mid-1950s, HUS first captured the public’s widespread 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. [6, 28] Over 500 cases of E. coli were reported; 151 were hospitalized (31%), 45 persons (mostly children) developed HUS (9%), and three died. [6, 28]
Of those who survive HUS, at least five percent will suffer end stage renal disease (ESRD) with the resultant need for dialysis or transplantation.  But, “[b]ecause renal failure can progress slowly over decades, the eventual incidence of ESRD cannot yet be determined.”  Other long-term problems include the risk for hypertension, proteinuria (abnormal amounts of protein in the urine that can portend a decline in renal function), and reduced kidney filtration rate. [33, 47] Since the longest available follow-up studies of HUS victims are 25 years, an accurate lifetime prognosis is not available and remains controversial. 
Other Complications from Infection
IBS is a chronic disorder characterized by alternating bouts of constipation and diarrhea, both of which are generally accompanied by abdominal cramping and pain.  Suffering an E. coli O157:H7 infection has been linked to the development of post-infectious irritable bowel syndrome (IBS). This link was demonstrated by the Walkerton Health Study (WHS), which followed one of the largest O157:H7 outbreaks in the history of North America.  In this outbreak, contaminated drinking water caused over 2,300 people to be infected, resulting in 27 recognized cases of HUS, and 7 deaths. The WHS followed 2,069 eligible study participants. Among its findings, WHS noted that, “Between 5% and 30% of patients who suffer an acute episode of infectious gastroenteritis develop chronic gastrointestinal symptoms despite clearance of the inciting pathogens.” 
Not surprisingly, E. coli O157:H7 infection is associated with long-term emotional disruption as well, not just for the victim, but for entire families.  A recent study reported that “parents experienced long-term emotional distress and substantive disruption to family and daily life” following an E. coli O157:H7 infection in the family. 
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. [1, 54] Most hospitals labs and physicians know to test for these bacteria, especially if the potentially infected person 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. 
Treatment for an E. coli Infection
In most infected individuals, symptoms of a Shiga toxin-producing E. coli infection last about a week and resolve without any long-term problems. [1, 42] Antibiotics do not improve the illness, and some medical researchers believe that these medications can increase the risk of developing HUS.  Therefore, apart from 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. coliO157:H7 initially speeds up blood coagulation may lead to future medical therapies that could forestall the most serious consequences.  Most individuals who do not develop HUS recover within two weeks. [33, 42]
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 enough 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 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.
- 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 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.
- 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 reside within the minute circulatory system of the individual vegetable leaves.
- 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 meet 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.
- 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).
- Do not let any family members touch or pet farm animals. Merely cleaning the hands with germ “killing” wipes may not be adequate!
- Wear disposable gloves when changing the diapers of any child with any type of diarrhea. Remember that E. coliO157:H7 diarrhea initially is non-bloody, but still very infectious. If gloves are not available, then thorough hand washing is a must.
- 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.
- 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.
1. Eisenstein, Barry and Zaleznik, Dori, “Enterobacteriiaceae,” in Mandell, Douglas, & Bennett’s PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES, Fifth Edition, Chap. 206, pp. 2294-2310 (2000).
2 Feng, Peter, et al., “Enumeration of Escherichia coli and the Coliform Bacteria,” in BACTERIOLOGICAL ANALYTICAL MANUAL (8th Ed. 2002), available online at http://www.cfsan.fda.gov/~ebam/bam-4.html.
3. James M. Jay, MODERN FOOD MICROBIOLOGY at 21 (6th ed. 2000).
4. Griffin, Patricia and Tauxe, Robert, “The Epidemiology of Infections Caused by Escherichia coli O157:H7, Other Enterohemorrhagic E. coli, and the Associated Hemolytic Uremic Syndrome,” EPIDEMIOLOGICAL REVIEW, Vol. 13, pp. 60-98 (1991).
5. Frenzen, Paul D., et al., “Economic Cost of Illness due to Escherichia coli O157 Infections in the United States,” JOURNAL OF FOOD PROTECTION, Vol. 68, pp. 2623-2630 (2005).
6. Bell, B.P., et al., “A multistate outbreak of Escherichia coli O157:H7-associated bloody diarrhea and hemolytic uremic syndrome from hamburgers: the Washington experience.” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 272, pp. 1349-1353 (1994).
7. Bala Swaminathan, et al., “PulseNet: Molecular Subtyping Network for Foodborne Bacterial Disease Surveillance, United States,” EMERGING INFECTIOUS DISEASES Vol. 7, No. 3, pp. 382-89 (May-June 2001).
8. Konno T. et al., “Application of a multilocus variable number of tandem repeats analysis to regional outbreak surveillance of Enterohemorrhagic Escherichia coli O157:H7 infections,” JAPANESE JOURNAL OF INFECTIOUS DISEASE, Vol. 64, No. 1, pp. 63-5 (January 2011).
9. Riley, LW, et al., “Hemorrhagic colitis associated with a rare Escherichia coli serotype,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 308, No. 12, pp. 681, 684-85 (1983).
10. Feng, Peter, “ Escherichia coli Serotype O157:H7: Novel Vehicles of Infection and Emergence of Phenotypic Variants,” EMERGING INFECTIOUS DISEASES, Vol. 1, No. 2, at 47 (April-June 1995).
11. Keene, William E., et al., “A Swimming-Associated Outbreak of Hemorrhagic Colitis Caused by Escherichia coli O157:H7 and Shigella Sonnei,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 331, at 579 (Sept. 1, 1994).
12. Ostroff, Stephen M., et al., “Infections with Escherichia coli O157:H7 in Washington State: The First Year of Statewide Disease Surveillance,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 262, No. 3, at 355 (July 21, 1989).
13. Rangel, Josefa M., et al., “Epidemiology of Escherichia coli O157:H7 Outbreaks, United States, 1982-2002,” EMERGING INFECTIOUS DISEASES, Vol. 11, No. 4, 603 (April 2005).
14. Johannes, L, “Shiga toxins, from cell biology to biomedical applications,” NATIONAL REVIEW OF MICROBIOLOGY, Vol. 8, pp. 105-16 (2010).
15. Suh, J.K., et al., “Shiga Toxin Attacks Bacterial Ribosomes as Effectively as Eucaryotic Ribosomes,” BIOCHEMISTRY, Vol. 37, No. 26, pp. 9394–398 (1998).
16. Sandvig, K, “Pathways followed by ricin and Shiga toxin into cells,” HISTOCHEMISTRY AND CELL BIOLOGY, vol. 117, no. 2, pp. 131-141 (2002).
17. Welinder-Olsson, C and Kaijser, B, “Enterohemorrhagic Escherichia coli (EHEC),” SCANDINAVIAN JOURNAL OF INFECTIOUS DISEASE, Vol. 37, pp. 405-16 (2005).
18. Kaper, J.B. and Karmali, M.A., “The Continuing Evolution of a Bacterial Pathogen,” PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE, Vol. 105, No. 12, pp. 4535-4536 (March 2008).
19. Wick, L.M., et al., “Evolution of genomic content in the stepwise emergence of Escherichia coli O157:H7,” JOURNAL OF BACTERIOLOGY, Vol. 187, pp. 1783–1791 (2005).
20. Zhang, W, et al., “Probing genomic diversity and evolution of Escherichia coli O157 by single nucleotide polymorphisms,” GENOME RESEARCH, Vol. 16, pp. 757–67 (2006). The full-text of this article is available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473186/pdf/757.pdf
21. Robins-Browne, R.M., “The relentless evolution of pathogenic Escherichia coli,” CLINICAL INFECTIOUS DISEASES, Vol. 41, pp. 793–94 (2005).
22. Manning S.D., et al., “Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCE, Vol. 105, No. 12, pp. 4868-73 (2008).
23. Tauxe, Robert A., “Emerging Foodborne Diseases: An Evolving Public Health Challenge, “ EMERGING INFECTIOUS DISEASES, Vol. 3, No. 4, pp. 425-427 (Oct.-Dec. 1997).
24. CDC, “Multistate Outbreak of Escherichia coli O157:H7 Infections Associated with Eating Ground Beef—United States, June-July 2002,” MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 51, at 638 (2002) reprinted in JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 288, No. 6, 690 (Aug. 14, 2002).
25. Scallan, E, et al., “Foodborne illness acquired in the United States –major pathogens, EMERGING INFECTIOUS DISEASES, Vol. 17, No. 1, (Jan. 2011), available at: http://www.cdc.gov/EID/content/17/1/7.htm.
26. Su, Chinyu Su &Brandt, Lawrence “Escherichia coli O157:H7 Infection in Humans,” ANNALS OF INTERNAL MEDICINCE, Vol.123, Issue 9, pp. 698-707 (1995).
27. Juneja, V.K., et al., “Thermal Destruction of Escherichia coli O157:H7 in Hamburger,” JOURNAL OF FOOD PROTECTION, Vol. 60, No. 10, pp. 1163-1166 (1997).
28. Griffin, Patricia M., et al., “Large Outbreak of Escherichia coli O157:H7 Infections in the Western United States: The Big Picture,” in RECENT ADVANCES IN VEROCYTOTOXIN-PRODUCING ESCHERICHIA COLI INFECTIONS, at 7 (M.A. Karmali & A. G. Goglio eds. 1994).
29. Boyce, T.G., et al., “Escherichia coli O157:H7 and the hemolytic-uremic syndrome,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 333, pp. 364-368 (1995).
30. Breuer, T, et al., “A multistate outbreak of Escherichia coli O157:H7 infections linked to alfalfa sprouts grown from contaminated seeds,” EMERGING INFECTIOUS DISEASES, Vol. 7, pp. 977-982 (2001).
31. Friedman, M.S., et al., “Escherichia coli O157:H7 Outbreak Associated with an Improperly Chlorinated Swimming Pool,” CLINICAL INFECTIOUS DISEASE, Vol. 29, No. 2, pp. 298-303 (1999).
32. Cody, S.H., et al., “An outbreak of Escherichia coli O157:H7 infection from unpasteurized commercial apple juice,” ANNALS OF INTERNAL MEDICINE, Vol. 130, No. 3, pp. 202-9 (1999).
33. Siegler, Richard, “The Hemolytic Uremic Syndrome,” PEDIATRIC NEPHROLOGY, Vol. 42, p. 1505 (Dec. 1995)
34. Chandler, W.L., et al., “Prothrombotic Coagulation Abnormalities Preceding the Hemolytic-Uremic Syndrome,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 346, No. 1, pp. 23-32 (2002).
35. Elder, R.O., et al., “Correlation of enterohemorrhagic Escherichia coli O157 prevalence in feces, hides, and carcasses of beef cattle during processing,” USDA Agricultural Research Service, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (2000). http://www.pnas.org/content/97/7/2999.long
36. Keen, J.E., et al., “Shiga-toxigenic Escherichia coli O157 in agricultural fair livestock, United States,” EMERGING INFECTIOUS DISEASES, Vol. 12, No. 5, pp. 780-86 (2003).
37. King, L.J., 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, Nov. 15, 2006, available online at http://www.hhs.gov/asl/testify/t061115.html.
38. McCarthy, T.A., et al., “Hemolytic-Uremic Syndrome and Escherichia coli O121 at a Lake in Connecticut, 1999,” PEDIATRICS, vol. 108, pp. e59-59 (2001).
39. Mead, Paul M., et al., “Food-related Illness and Death in the United States,” EMERGING INFECTIOUS DISEASES, Vol. 5, pp. 607-625 (1999).
40. Olsen, S.J., et al., “A Waterborne Outbreak of Escherichia coli O157:H7 Infections and Hemolytic Uremic Syndrome: Implications for Rural Water Systems,” MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 8, No. 4 (April 2002). The full text of article is available online at http://www.cdc.gov/ncidod/EID/vol8no4/00-0218.htm.
41. Slutsker, L, et al., “A nationwide case-control study of Escherichia coli O157:H7 infection in the United States,” JOURNAL OF INFECTIOUS DISEASE, Vol. 177, pp. 962-966 (1998).
42. Tarr, Philip, “Escherichia coli O157:H7: Clinical, Diagnostic, and Epidemiological Aspects of Human Infection,” CLINICAL INFECTIOUS DISEASE, Vol. 20, pp. 1-10 (1995).
43. Wong, C.S., et al., “The risk of the hemolytic uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 342, pp.1930-36 (2000).
44. Safdar, Nasia, et al., “Risk of Hemolytic Uremic Syndrome After Treatment of Escherichia coli O157:H7 Enteritis: A Meta-analysis,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 288, No. 8, pp. 996 (Aug. 28, 2002).
45. Garg, Amit X, et al., “Long-term Renal Prognosis of Diarrhea-Associated Hemolytic Uremic Syndrome: A Systematic Review, Meta-Analysis, and Meta-regression, “ JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. 290, No. 10, p. 1360 (Sept. 10, 2003).
46. Siegler, Richard, “Postdiarrheal Shiga Toxin-Mediated Hemolytic Uremic Syndrome,” JOURNAL OF AMERICAN MEDICAL ASSOCIATION, Vol. No. 10, p. 1379 (Sept. 10, 2003).
47. Robitaille, Pierre, et al., “Pancreatic Injury in the Hemolytic Uremic Syndrome, PEDIATRIC NEPHROLOGY, Vol. 11, pp. 631-32 (1997).
48. Bell, Beth, et al., “Predictors of Hemolytic Uremic Syndrome in Children During a Large Outbreak of Escherichia coli O157:H7 Infections,” PEDIATRICS, Vol. 100, No. 1, p. 1 (July 1, 1997), full text available online at http://www.pediatrics.org/cgi/content/full/100/1/e12.
49. Marshall, J., et al., “Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery,” GASTROENTEROLOGY, Vol. 131, pp. 445-50 (2006).
50. Hungin, A., et al., “Irritable Bowel Syndrome in the United States: Prevalence, Symptom Patterns and Impact,” ALIMENTARY PHARMACOLOGY AND THERAPEUTICS, Vol. 21, No. 11, pp. 1365-75, (2005). Online at http://www.ncbi.nlm.nih.gov/pubmed/15932367
51. Pollock, KG, et al., “Emotional and behavioral changes in parents of children affected by hemolytic-uremic syndrome associated with verocytotoxin-producing Escherichia coli: a qualitative analysis,” PYSCHOSOMATICS, Vol. 50, No. 3, pp. 263-9 (May-June 2009).
52. Boxrud, D., “Genetic Testing,” Food Safety News, August 31, 2006, online at http://www.foodsafetynews.com/2009/08/genetic-testing-1/
53. Boxrud D, et al., “Comparison of multiple-locus variable-number tandem repeat analysis, pulsed-field gel electrophoresis, and phage typing for subtype analysis of Salmonella enterica serotype Enteritidis,” JOURNAL OF CLINICAL MICROBIOLOGY, Vol. 45, No. 2, pp. 536-43 (Feb. 2007).
54. CDC, “Recommendations for Diagnosis of Shiga Toxin–Producing Escherichia coli Infections by Clinical Laboratories,” MORBIDITY AND MORTALITY WEEKLY REVIEW, Vol. 88, No. RR-12 (Oct. 16, 2009), available online at http://www.cdc.gov/mmwr/PDF/rr/rr5812.pdf
55. CDC,“Shiga toxin-producing Escherichia coli: burden and trends.” FOODNET NEWS, Winter 2008. Available at: http://www.cdc.gov/FoodNet/news/2008/January_FoodNet_News.pdf
56. Brooks, J. T., E. G. Sowers, J. G. Wells, K. D. Greene, P. M. Griffin, R. M. Hoekstra, and N. A. Strockbine.,“Non-O157 Shiga Toxin-Producing Escherichia coli Infections in the United States, 1983-2002.” J. INFECT DIS. 192:1422-9 (2005) available online at http://www.foodpoisonjournal.com/uploads/file/466536_web%5B1%5D.pdf
57. Johnson, K. E., C. M. Thorpe, and C. L. Sears. “The Emerging Clinical Importance of Non-O157 Shiga Toxin-Producing Escherichia coli” CLIN INFECT DIS. 43:1587-95 (2006) available online at http://cid.oxfordjournals.org/content/43/12/1587.full.pdf+html
58. Hussein, H. S. “Prevalence and pathogenicity of shiga toxin-producing Escherichia coli in beef cattle and their products.” J ANIM SCI. 85:E63-72 (2007) available online at http://jas.fass.org/content/85/13_suppl/E63.full.pdf
59. Hussein, H. S. and T. Sakuma, “Prevalence of shiga toxin-producing Escherichia coli in dairy cattle and their products.” J DAIRY SCI. 88:450-65 (2005) abstract available online at http://www.ncbi.nlm.nih.gov/pubmed/15653509
60. Fratamico, P. “Non-O157 Shiga Toxin-Producing E. coli Associated with Muscle Foods. Meeting abstract.” P.195.02. (2007) available online at http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=210878
61. Barkocy-Gallagher, G. A., T. M. Arthur, M. Rivera-Betancourt, X. Nou, S. D. Shackelford, T. L. Wheeler, and M. Koohmaraie. “Seasonal prevalence of Shiga toxin-producing Escherichia coli, including O157:H7 and non-O157:H7 serotypes, and Salmonella in commercial beef processing plants.” J FOOD PROT. 66:1978-86 (2003) available online at http://www.ars.usda.gov/SP2UserFiles/Place/54380530/2003661978.pdf
62. Hussein, H. S. and L. M. Bollinger. “Prevalence of Shiga toxin-producing Escherichia coli in beef.” MEAT SCI. 71:676-89 (2005) available for purchase online at http://www.sciencedirect.com/science/article/pii/S0309174005002032
63. Samadpour, M., V. Beskhlebnaya, and W. Marler. “Prevalence of non-O157 enterohaemmorrhagic Escherichia coli in retail ground beef in the United States.” 7th International Symposium on Shiga Toxin (Verocytoxin)-producing Escherichia coli Infections. Buenos Aires, Argentina. (2009) available at https://www.marlerblog.com/uploads/file/PREVALENCE%20OF%20NON.pdf
64. Bosilevac J. M., M. N. Guerini, D. M. Brichta-Harhay, T. M. Arthur, and M. Koohmaraie. “Microbiological characterization of imported and domestic boneless beef trim used for ground beef.” J FOOD PROT. 70:440-9 (2007) available online at http://www.ars.usda.gov/SP2UserFiles/Place/54380530/2007700440.pdf
65. Rasko, D.A. et al. “ Origins of the E. coli Strain Causing an Outbreak of Hemolytic-Uremic Syndrome in Germany.” N ENGL J MED 365:709-717 (2011) available online at http://www.nejm.org/doi/full/10.1056/NEJMoa1106920