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E. coli

E. coli Facts

Escherichia coli (abbreviated as E. coli) are a very large and diverse group of bacteria that live in the intestinal tracts of warm blooded animals (predominantly cattle, pigs, goats, sheep, deer, and elk) and humans.  The E. coli bacteria do not affect the animals – the animals are merely a carrier for the bacteria.  Most E. coli bacteria reside in the lumen of the colon and do not cause human illness in generally healthy individuals; however, some select types are known to cause disease (Donnenberg, 2010; Centers for Disease Control and Prevention (CDC), November 2009).

The disease-causing E. coli strains are categorized according to the method by which they produce illness, also known as a virulence mechanism (CDC, November 2009).  The CDC groups virulent E. Coli into five different groups: Shiga toxin-producing (STEC), enteroinvasive (EIEC), enterotoxigenic (ETEC), enteropathogenic (EPEC), and enteroaggregative (EAEC) (CDC, November 2009).  Although the CDC cites diffusely adherent E. coli (DAEC) as having less well-established pathogenic properties (CDC, November 2009), this sixth category is becoming increasingly accepted in the medical community, and is often listed along with the traditional five categories in medical texts (Donnenberg, 2010; Giannella, 2010; Ochoa and Cleary, 2007).

Enteroaggregative E. coli (EAEC)

Enteroaggregative E. coli (EAEC), the most recently added group to the CDC’s list of pathogenic types of E. coli, was first identified as a cause of diarrhea in 1987.  EAEC has increased in importance in select settings, and is detected with increasing frequency (Donnenberg, 2010).  Despite its increased importance, comparatively little is known about EAEC, a group of organisms characterized by the aggregative pattern in which they adhere to laryngeal epithelial cells (Kumar, 2009; Adachi et al., 2007).

Symptoms of EAEC infection include watery, mucoid diarrhea and low-grade fever, typically accompanied by little or no vomiting. Watery diarrhea may persist for a number of weeks before resolving (Ochoa and Cleary, 2007).

Some clinical studies indicate that EAEC causes acute and persistent diarrhea in children living in developing countries; however, other clinical studies have concluded that there is no meaningful or significant link between EAEC and diarrhea.  This variation in study results suggests the possibility that certain EAEC strains are simply more virulent than others.  Supporting this conclusion is the fact that some EAEC serotypes – O44:H18, for example – are more pathogenic than others (Giannella, 2010).  Additionally, EAEC serotypes belong to a wide range and combination of O and H serotypes (Ochoa and Cleary, 2007).

EAEC numbers among the many causes of travelers’ diarrhea (TD), and has been associated with the condition at frequencies rivaling those of ETEC (Donnenberg, 2010; Giannella, 2010).  EAEC has also been linked to persistent diarrhea in HIV-positive patients (Donnenberg, 2010).

E. coli strains that adhere in an aggregative pattern have been isolated more frequently from children suffering with acute diarrhea, and have been isolated in such cases both in the developing and the developed world (Donnenberg, 2010; Giannella, 2010).  Further, up to one of every three children infected with EAEC presents with grossly bloody diarrhea (stools in which blood is visible to the naked eye) (Giannella, 2010).

Enteroinvasive E. coli (EIEC)

Originally described in Asia, the enteroinvasive E. coli (EIEC) group contains a relatively small number of E. coli serogroups (O28ac, O29, O124, O136, O143, O144, O152, O164, O167, and a few nontypable strains) that all have certain properties closely related to the Shigella bacteria (Giannella, 2010; Ochoa and Cleary, 2007).

EIEC infections occur most commonly in the context of an outbreak; an EIEC outbreak caused by imported cheese occurred in the United States in 1971 (Giannella, 2010; Ochoa and Cleary, 2007).  However, infection is endemic in developing countries and regions where it is possible to frequently isolate this type of bacterium (Ochoa and Cleary, 2007).

Transmission occurs via food, water, or person-to-person contact (Kumar, 2010).  EIEC strains have been identified worldwide and have caused foodborne outbreaks, particularly in regions of eastern Europe and South America (Adachi et al., 2007).

Illness is characterized by watery diarrhea.  Some patients experience a dysenteric syndrome that includes bloody mucoid diarrhea, intestinal cramping, fever, and tenesmus (a feeling of incomplete evacuation after a bowel movement) (Giannella, 2010).

Enteropathogenic E. coli (EPEC)

Beginning in the 1920s and through the 1940s, severe diarrheal epidemics ravaged neonatal nurseries.  These outbreaks, associated with very high rates of mortality, were traced to a single cause: enteropathogenic E. coli(EPEC) strains (Giannella, 2010; Adachi et al., 2007).  The first of the diarrhea-causing E. coli strains to be discovered and described, EPEC strains are characterized by a local pattern of adherence to HEp-2 cells (a specialized cell line).  EPEC strains may differ substantially, and thus are usually further identified by their serotype (Adachi et al., 2007).

EPEC outbreaks occasionally occur in neonatal wards and daycare centers in the developed world, and are usually linked to one of the approximately 14 EPEC serotypes associated with neonatal diarrhea (including well-known serotypes O55, O111, and O119) (Giannella, 2010).  The mortality rate seen in such outbreaks has dropped dramatically and such outbreaks occur with much less frequency (Giannella, 2010; Ochoa and Cleary, 2007).

Today, infants and children living in developing countries constitute the main concern in the context of EPEC infection.  EPEC bacteria are a major cause of both persistent and acute diarrhea in developing countries, mostly in children under the age of two (Giannella, 2010; Ochoa and Cleary, 2007).  Persistent diarrhea (diarrhea lasting more than 14 days) is of particular concern in developing countries due to the high risk that potentially lethal malnutrition will result (Ochoa and Cleary, 2007).

Symptoms of EPEC infection include profuse non-bloody, watery diarrhea with mucus present.  Additionally, infections caused by this class of bacteria may also cause vomiting and low-grade fever (Ochoa and Cleary, 2007).  In severe infections, extensive vomiting may occur, making oral rehydration difficult.  Such infections present a risk of life-threatening dehydration (Donnenberg, 2010).

Studies have shown that breast milk protects against EPEC infection.  Lactoferrin, a globular glycoprotein found in breast milk, degrades the mechanism that EPEC bacteria use to cause illness (Adachi et al., 2007).

Enterotoxigenic E. coli (ETEC)

Enterotoxigenic E. coli (ETEC) describes the group of E. coli bacteria that, though production of special toxins, stimulate the intestinal lining and cause secretion of excess fluid; in humans, this excess fluid subsequently causes diarrhea (CDC, November 2009).  Researchers in India first discovered these strains of E. coli when, driven by their recent discoveries in studying cholera, they focused on E. coli bacteria as a potential cause of acute toxigenic diarrheal disease (Giannella, 2010).

ETEC transmission generally occurs when an individual consumes infected food or beverage. Person-to-person transmission, while possible, occurs rarely because of the high number of ETEC organisms required for infection (Adachi et al., 2007).  Studies indicate that in order to cause illness, somewhere between 10and 1010 organisms must exist in the individual (Adachi et al., 2007).

ETEC bacteria make people ill through the production of either or both of two types of enterotoxins – heat-labile (LT) and heat-stable (ST) – that cause diarrhea in humans (Giannella, 2010; CDC, November 2009).  Both LT and ST ultimately cause diarrhea by making cells excrete chloride and water into the intestines while at the same time inhibiting intestinal fluid absorption, although they do so by activating different cellular mechanisms (Donnenberg, 2010; Kumar, 2009).

Since the 1960s, when the scientific community discovered that ETEC causes diarrhea in humans, the disease has been recognized as a major bacterial cause of diarrhea among children in the developing world and among travelers, with the tropics experiencing the highest incidence of infection (Giannella, 2010; CDC, November 2009).  ETEC strains are increasingly recognized by researchers and the medical community as a cause of foodborne illness in developed countries, including the U.S., although the majority of U.S. ETEC outbreaks to date have been waterborne (Craig and Zich, 2010; Adachi et al., 2007).

ETEC bacteria cause more cases of diarrhea in travelers from North America and Northern Europe to developing countries than any other bacteria.  The bacteria constitute the most common cause of gastroenteritis outbreaks on cruise ships; such outbreaks most likely result from ship water stored at overseas ports (Giannella, 2010).  ETEC affects children at a higher rate than any other population group, and is responsible for between 15 and 50% of all diarrheal episodes in children living in developing countries.

Symptoms and Diagnosis

24-72 hours after ingesting ETEC bacteria, the infected individual begins to experience upper intestinal distress, followed shortly by watery diarrhea (Craig and Zich, 2010; Giannella, 2010).  Fever is rare, and vomiting occurs in fewer than one-half of adult cases (Craig and Zich, 2010).  Headache, muscle aches, and bloating may also occur, but are less common (CDC, November 2009).  Most individuals with an ETEC E. coliinfection experience only mild dehydration; however, children and the elderly may experience severe complications from even relatively mild amounts of intestinal purging (Giannella, 2010).

The infection so mild as to only produce a few loose bowel movements, or so severe that it mimics cholera and leads to severe dehydration rice-water stools (clear, watery stools with flecks of mucus that may have a slightly “fishy” odor) (Giannella, 2010).  In more severe cases, diarrhea rarely lasts longer than 48-72 hours; however, in milder cases, disease subsides more gradually, and diarrheal symptoms may last up to a week after onset (Craig and Zich, 2010).

Generally, patients infected with an ETEC strain that produces only ST enterotoxins experience an overall milder diarrheal attack than those infected with a strain that produces only LT or both ST and LT enterotoxins.  ST only strains do, however, tend to cause more vomiting, and patients infected with an ST-only strain also have more constitutional complaints (Giannella, 2010).

There exists no readily-available method of laboratory diagnosis for ETEC strains.  Identification of LT and ST enterotoxins is feasible using real-time polymerase chain reaction (PCR) assay (Craig and Zich, 2010).  PCR is a complex process that creates thousands or millions of copies of a single piece of DNA.  Unfortunately, this method is not clinically available, making detection of ETEC bacteria generally impractical, if not impossible (Craig and Zich, 2010).  As a result, doctors base most ETEC diagnoses on an evaluation of the patient’s history and symptoms (CDC, November 2009).

Treatment

ETEC infections should be treated with fluid replacement and general supportive care.  Generally, these infections do not require treatment with antibiotics because most episodes of ETEC diarrhea are self-limited, and the diarrhea rids the body of the infectious agent (Giannella, 2010).

In more severe cases of traveler’s diarrhea, antibiotics may shorten the duration of diarrhea if antibiotic treatment begins early in the course of infection.  Labs are detecting ETEC strains resistant to historically effective antibiotics (including quinolones and TMP-SMX) with increasing frequency (Giannella, 2010).

Antimotility agents, such as Imodium and Lomotil, should generally be avoided if possible.  Although they do help relieve the diarrhea and cramping associated with ETEC, they also make it more difficult for the body to expel the toxin.  The CDC recommends not to take such medications if experiencing bloody diarrhea or high fever.  Finally, if antimotility drugs are taken, the CDC recommends discontinuing these medications if symptoms continue for more than 48 hours (CDC, November 2009).

Prevention

You can reduce the risk of traveler’s diarrhea caused by an ETEC infection by:

  1. Avoiding ice;
  2. Drinking only bottled beverages;
  3. When brushing teeth and washing fruits and vegetables, using water that has been bottled, boiled, or chemically treated with iodine or chlorine;
  4. Not eating meat and vegetables unless they are served steaming hot;
  5. Eating raw fruits and vegetables only when you peel them yourself; and
  6. Regularly washing hands with soap and water.

(Donnenberg, 2010; CDC, November 2009)

Shiga Toxin-Producing E. coli (STEC)

The most virulent strains of E. coli produce shiga toxins and are called “shiga toxin-producing” E. coli, or STEC.  Among diarrhea-causing E. coli, STEC bacteria alone express the gene for Shiga toxins type 1 (Stx1) and 2 (Stx2) (Hunt, 2010).  Shiga toxins are so named because they are virtually identical to those produced by another well-known bacterium, Shigella dysenteriae; both Shiga toxins and Shigella dysenteriae are named for Japanese microbiologist Kiyoshi Shiga (Hunt, 2011).

Due to their cytotoxic effect on the Vero monkey kidney cell line, STEC strains are also sometimes referred to as verocytotoxic or verocytotoxin-producing E. coli (VTEC) (Hunt, 2010).  In reference to the bloody stools that often accompany STEC infection, older literature often called STEC bacterica “enterohemorrhagic E. coli” (EHEC); even today, some continue to use this term (CDC, June 2011; Hunt, 2010).

Documented STEC infections have occurred in over 30 countries located across 6 continents (Craig and Zich, 2010).  The most commonly identified STEC in North America is E. coli O157:H7 (often shortened to E. coliO157 or even just “O157”).  When you hear news reports about outbreaks of “E. coli” infections, they are usually referring to E. coli O157 (CDC, June 2011).  Though E. coli O157 is the predominate strain identified in outbreaks and sporadic cases in the United States and many other locations worldwide, there are a few areas where another E. coli strain is responsible for the largest number of cases.  For example, STEC O91 is the serotype most frequently isolated from adult patients in Germany (Hunt, 2010; Bielaszewska et al, 2008).

In addition to E. coli O157, many other kinds (called serogroups) of STEC cause hemorrhagic colitis (bloody diarrhea).  These other kinds are sometimes called “non-O157 STEC.” E. coli serogroups O26, O111, and O103 are the non-O157 serogroups that most often cause illness in the United States (CDC, June 2011).  The non-O157 STEC are not nearly as well understood, partly because current protocols do not test for them.  The failure to test for non-O157 STEC is due in large part to the fact that such serotypes are difficult to detect (CDC, May 2010).  Additionally, the CDC acknowledges that there is limited public health surveillance data on the occurrence of non-O157 STEC infections (CDC, May 2010).  Thus, outbreaks of these non-O157 serogroups are rarely identified.

As a whole, the non-O157 serogroups are less likely to cause severe illness than E. coli O157.  Some non-O157 STEC serogroups, however, cause the most severe illnesses (CDC, June 2011).  These non-O157 serogroups are normally found in the fecal flora of animals including cattle, sheep, chickens, goats, elk, dogs, and cats (CDC, June 2011; Giannella, 2010).  Pigs and birds, along with some other kinds of animals, may pick up the STEC bacteria from the environment and spread it, even though this kind of bacteria does not usually reside in their digestive tracts. G enerally, STEC bacteria that make humans sick do not cause illness in animals (CDC, June 2011).

STEC organisms are extremely virile: they can survive for weeks on surfaces such as kitchen counters and food preparation surfaces, and over a year within other materials.  Unfortunately, a very small amount of E. coli in one’s system can be deadly, and the infectious dose of E. coli has been reported to be approximately 100 bacteria (Hunt, 2010).  Such a low infectious dose enables person-to-person transmission of STEC, which leads to secondary cases in which individuals who have physical contact with an infected person become ill (Hunt, 2010).

E. coli O157:H7

The Center for Disease Control first discovered E. coli O157:H7 in 1975, although the bacteria was not implicated in food-borne illnesses until 1982 during an investigation into an outbreak of hemorrhagic colitis associated with contaminated hamburger. Though outbreaks were initially tied to consumption of undercooked ground beef, recent outbreaks have been traced to other foods. These sources of contamination include a wide variety of foods, including lettuce, leafy greens, venison, apple cider, alfalfa sprouts, raw milk, and salami (Sodha et al., 2010).

E. coli O157:H7 bacteria reside in the gastrointestinal tracts of healthy cattle.  The cattle excrete some of the bacteria in manure, and produce may become infected when grown in contaminated manured soil or washed with contaminated water during processing (Hunt, 2010; Sodha et al., 2010).  Swimming in contaminated bodies of water and person-to-person transmission have also resulted in O157:H7 outbreaks (CDC, June 2011; Sodha et al., 2010).

Since 1982, when acute hemorrhagic colitis was first recognized in two different outbreaks that occurred in Michigan and Ohio, more than 100 E. coli O157:H7 outbreaks have been detected in the United States (Giannella, 2010; CDC, June 2011).  In actuality, the number is probably much higher because E. coli O157:H7 did not become a reportable disease (one that, upon detection by a lab, doctor, or hospital – must be reported by law to local health officials) until 1987.

The CDC estimates that every year over 73,000 are sickened, 2000 are hospitalized, and 60 die as a result of E. coli O157:H7 poisoning (Giannella, 2010).  O157:H7 is estimated to be the cause of between 0.6% and 2.4% of all cases of diarrhea.  Further, studies estimate that this serotype causes between 15 and 36% of all cases of hemorrhagic colitis in the United Kingdom, Canada, and the United States (Giannella, 2010).

How is STEC transmitted?

STEC bacteria may be transmitted to humans by

  • eating undercooked contaminated ground beef;
  • eating raw foods including contaminated spinach, sprouts, and lettuce;
  • drinking contaminated unpasteurized juices or milk;
  • drinking contaminated water;
  • direct animal-to-human contact; or
  • direct human-to-human contact.

The vast majority (reported 85%) of all E. coli illnesses are foodborne related.  Inevitably, infections start when you swallow STEC; in other words, infection begins when you get tiny (usually invisible) amounts of human or animal feces in your mouth. Unfortunately, this happens more often than we would like to believe.

Although most E. coli illnesses are foodborne related, a small percentage of cases have been tied to other transmission vehicles such as water, animals, ads person-to-person contact.  People have become infected by swallowing lake water while swimming, touching the environment in petting zoos and other animal exhibits, and by eating food prepared by people who did not wash their hands well after using the toilet. Some examples are outlined below.

a) Foodborne transmission

The majority of foodborne STEC outbreaks in the past 25 years were related to the consumption of undercooked ground beef. (Giannella, 2010). Several recent outbreaks, however, have been linked to precooked meat patties, roast beef, salami, spinach, lettuce, alfalfa sprouts, parsley, unpasteurized milk, yogurt, fresh-pressed apple cider, and unpasteurized apple juice (Giannella, 2010).

2011 European Seed / Sprout Outbreak

The Robert Koch Institute (RKI), Germany’s national-level public health authority, was notified about a cluster of three pediatric cases of hemolytic uremic syndrome (HUS) (Frank et al., 2011).  All three children were admitted to the university hospital in the city of Hamburg on the same day (Frank et al., 2011).  The next day, a team from RKI arrived to assist in the public health investigation. The team quickly realized that case numbers were continuing to rise, that the disease affected adults as well as children, and that there were cases in other parts of the country, particularly northern Germany (Frank et al., 2011).

After initially blaming the outbreak on consumption of raw cucumbers contaminated with E. coli, RKI announced on June 10, 2011 that contaminated sprouts from one farm in Germany were the likely source of the outbreak (CDC, July 2011).  However, on June 24, 2011, France reported another cluster of E. coli O104:H4 infections (CDC, July 2011).  Those infected were people who had attended an event held in Bordeaux, France, and eaten sprouts served at the event (CDC, July 2011).  These sprouts were not from Germany, but had been privately produced in small quantities by the event organizer, who had purchased the seeds locally in Bordeaux (CDC, July 2011).

Thus, on July 5, 2011, the European Food Safety Authority (EFSA) issued a report identifying a single lot of fenugreek seeds from an Egyptian exporter as the most likely source of the sprouts linked with both the German and French outbreaks (CDC, July 2011).

As of July 7, 2011, the World Health Organization (WHO) reported 3,941 cases of E. coli O104:H4 infection, including 52 fatalities, spread across 16 European countries and North America (WHO, 2011).  In 909 of those cases, the individual developed HUS, a potentially fatal type of kidney failure often associated with STEC (WHO, 2011; CDC, July 2011).

There have been six confirmed cases of STEC O104:H4 in the United States (CDC, July 2011).  Five of the six infected individuals had recently traveled to Germany, which is where they were likely exposed; the sixth person likely contracted the infection through close contact with one of the other infected individuals (CDC, July 2011).  The cases, which were confirmed to genetically match the outbreak strain, came from five states: Massachusetts, Michigan (two cases), Wisconsin, North Carolina, and Arizona (CDC, July 2011).  In four of the six cases, the infected individual developed HUS (CDC, July 2011).  One of the cases proved fatal (CDC, July 2011).

The E. coli strain responsible for the outbreak is “exceptionally virulent,” combining the virulence properties of entroaggregative E. coli (EAEC) and Shiga toxin-producing E. coli (STEC) (Frank et al., 2011).  The strain is also exceptional for its Shiga-toxin variant, which had previously been isolated in Germany from only the rare sorbitol-fermenting STEC E. coli O157:H-, which is a hypervirulent pathogen in children and is associated with high mortality rates (Frank et al., 2011).  The strain in the Germany outbreak also has a median incubation period of eight days, which is a much longer than the 3 to 4-day incubation period of E. coli O157:H7 (Frank et al., 2011).

There are a number of very important differences between previous outbreaks of Shiga-toxin producing E. coli and the recent outbreak in Germany.  First, HUS cases comprise about one-fourth of all reported cases, which is a figure much higher than those seen in previous outbreaks (Frank et al., 2011).  Second, approximately 89% of HUS cases occurred in adults, with the majority occurring in women; historically, children have been disproportionately affected by HUS (Frank et al., 2011).  Finally, the serotype of the E. coli responsible for the outbreak was O104:H4, a non-O157 strain (Frank et al., 2011).

2010 Freshway Foods Romaine Lettuce Outbreak

In April and May 2010, 33 people were infected with E. coli O145 (CDC, May 2010).  The infection was spread by shredded romaine lettuce produced at one processing facility (CDC, May 2010). This conclusion was reached by evaluating evidence that included identification of the outbreak strain in an unopened package of lettuce from the processing facility linked to the outbreak (CDC, May 2010).

On April 16, 2010, public health officials in Michigan reported 16 cases of bloody diarrhea (CDC, May 2010).  Within 10 days, Ohio and New York reported similar clusters of cases (CDC, May 2010).  On April 27, preliminary reports suggested lettuce as a possible vehicle of infection, and traceback investigations by the states indicated that a common supplier of shredded romaine lettuce, Freshway Products, might be the source (CDC, May 2010; Reuters, 2010).  The next day, the FDA determined that the lots of romaine lettuce implicated in the outbreak were produced on a single farm in late March, and that this lettuce accounted for all of the illnesses (CDC, May 2010).  These implicated lots were no longer in commerce (CDC, May 2010).  Thus, at that point, it was felt that no recall was necessary (CDC, May 2010).

However, subsequent laboratory investigation indicated that there had been at least intermittent contamination at the processor on later production days, triggering preemptive recalls (CDC, May 2010).  Initially, only a single contaminated lot was recalled; however, all production from the implicated farm was later included in the recall (CDC, May 2010).  As of the CDC’s final update on the outbreak, no illnesses had been associated with the later lots of recalled lettuce (CDC, May 2010).

Ultimately, 33 cases (26 confirmed and 7 probable) were linked to the outbreak (CDC, May 2010).  Michigan reported the most cases (11 confirmed and 2 probable), followed by Ohio (8 confirmed and 2 probable), New York (5 confirmed and 2 probable), Pennsylvania (1 confirmed), and Tennessee (1 confirmed) (CDC, May 2010).  Among the 30 patients the CDC was able to obtain information about, 40% (12 people) were hospitalized and 3 individuals developed HUS (CDC, May 2010).  No fatalities associated with the outbreak were reported (CDC, May 2010).

Due to the “limited public health surveillance data on the occurrence of non-O156 STECs,” including E. coli O145, cases may go unreported (CDC, May 2010).  This is exacerbated by the fact that many clinical laboratories do not test for non-O157 STEC infections because they are more difficult to identify (CDC, May 2010).  Thus, the number of cases implicated in this outbreak may be substantially greater than the number reported

2010 Bravo Farms Cheese Outbreak

The CDC reported that from October 16 through October 27, 2010, thirty-eight people from five different states became sick as a result of infection with an identical strain of E. coli O157:H7 (CDC, November 2010). Fifteen individuals were hospitalized, and one developed HUS (CDC, November 2010).

Tests, conducted by the New Mexico Department of Health on an unopened package of Bravo Farms Dutch Style Gouda Cheese that had been purchased from a Costco retail location, identified E. coli O157:H7 matching the outbreak strain (CDC, November 2010). These results were consistent with two previous tests that identified the outbreak strain in opened packages of Bravo Farms Cheese from two of the outbreak victims’ homes (CDC, November 2010).

After initially recalling its Dutch Style Gouda Cheese, which had been made with raw milk, Bravo Farms eventually expanded the recall to include all of its cheeses (FDA, 2010; CDC, November 2010).

2009 Nestle Cookie Dough Outbreak

Between March 1 and June 30, 2009, 69 people across 29 states were infected with a particular strain of E. coli O157:H7 (Layton and Gaudio, 2009). 34 were hospitalized, and 9 developed HUS (Layton and Gaudio, 2009).  Based on questions asked of infected individuals, preliminary results indicated a strong association between infection and consumption of raw cookie dough (CDC, June 2009).

The FDA confirmed presence of the bacteria in samples of Nestle Toll House refrigerated cookie dough produced at a plant in Danville, Virginia (Layton and Gaudio, 2009).  Investigators did not find E. coli in the factory or on the equipment, but instead in a tub of chocolate chip cookie dough made at the plant in February (Layton and Gaudio, 2009).

On June 19, 2009, after officials at the FDA and CDC indicated their suspicion that the outbreak was linked to Nestle Toll House Cookie Dough, Nestle voluntarily recalled 30,000 cases of its refrigerated cookie dough (Layton and Gaudio, 2009).

2007 Topps Ground Beef Outbreak

Between July 5 and September 24, 2007, public health officials identified 40 individuals infected with an identical strain of E. coli O157:H7.  Of those individuals, 21 were hospitalized, and 2 developed HUS.  Health officials in several states who were investigating reports of E. coli O157 illnesses found that many ill persons had consumed Topps brand frozen ground beef patties. Opened and unopened packages of Topps brand frozen ground beef patties collected from patients’ homes yielded E. coli O157 isolates with several different PFGE patterns. Investigators compared the PFGE patterns from ill persons and meat samples and found 40 patients PFGE patterns matching at least one of E. coli strains found in Topps brand frozen ground beef patties. 

2006 Taco Bell Outbreak

In November and December of 2006, public health officials identified 71 individuals in 5 states infected with an identical strain of E. coli O157:H7. Of those individuals, 53 were hospitalized, and 8 developed HUS.  An epidemiological investigation revealed that the consumption of lettuce, cheese, and ground beef at the Taco Bell restaurant chain was strongly associated with illness.

2006 Spinach Outbreak

Between August 1 and October 6, 2006, public health officials identified 199 individuals infected with an identical strain of E. coli O157:H7. Of those individuals, 102 were hospitalized, and 31 developed HUS, and 3 died.  An epidemiological investigation revealed that the consumption of fresh bagged spinach was strongly associated with illness.  E. coli O157:H7 was isolated from 13 packages of spinach supplied by patients living in 10 states.  Eleven of the packages had lot codes reflecting a common manufacturing date at a single manufacturing facility.  Two packages did not have lot codes available but had the same brand name as the other packages.  The “DNA fingerprints” of all of the samples matched that of the outbreak strain.

b) Waterborne transmission

Studies have shown that both drinking water (largely from municipal water systems and well water) and recreational water (contaminated swimming pools and lakes) can serve as transmission vehicles for E. colibacteria; this has been borne out by several outbreaks tied to contaminated water (Giannella, 2010).

It has been reported that small water systems (those that serve fewer than 3,300 people), collectively serve approximately 15% of the United States population.  These systems are less likely to be adequately chlorinated and monitored for contaminants than larger municipal water systems.  The outbreaks listed below confirm the potential of these small water systems to be an important source of infection with E. coli O157:H7. 

1999 New York Unclorinated Water Outbreak

In September 1999, a large waterborne outbreak of E. coli O157:H7 infections occurred at a fair in Washington County, New York. Epidemiological investigation revealed that the likely source was unchlorinated drinking water from a well serving a portion of the fairgrounds.  The water was likely contaminated when cow manure seeped into a well after a rainstorm. Of the 781 people infected, 71 were hospitalized, 14 contracted HUS, and 2 died.

1998 Wyoming Unchlorinated Water Outbreak

In the summer of 1998, a large outbreak of E. coli O157:H7 infections occurred in Alpine, Wyoming.  Over 150 people were sickened, including citizens of alpine and persons from14 other states. Four people contracted HUS, and no one died.  Illness was strongly associated with drinking unchlorinated drinking water from the Alpine municipal water system.

1991 Portland, OR Lake Outbreak

Another waterborne E. coli outbreak occurred in Portland, Oregon in 1991.  Of the 59 people infected, 21 contracted E. coli O157:H7.  An epidemiological investigation revealed that those infected had swum in a local lake in the 3 weeks preceding their illness.  Transmission was thought to have occurred when the swimmers accidentally swallowed lake water that had become fecally contaminated by other bathers.

1989 Missouri Water Main Outbreak

The first reported waterborne E. coli outbreak occurred in Missouri in 1989.  More than 240 people were infected, 32 were hospitalized, and 4 died.  Backflow from a broken water main was thought to be the source of contamination.

c) Animal to person transmission

The transmission of E. coli from animals to persons has been well documented (Craig and Zich, 2010).  Several outbreaks have originated in petting zoos, county fairs, and on farms, as shown below.

2005 Arizona Petting Zoo Outbreak

In July 2005, two children hospitalized with E. coli O157:H7 infection were reported to the Arizona Department of Health Services.  Isolates from the two children had indistinguishable PFGE patterns.  Both children had visited a petting zoo in Arizona. One child had direct contact with petting zoo animals; the second child only had possible contact with exterior railings at the petting zoo.  Both children had played in an area immediately adjacent to and downhill from the petting zoo facility.  Fecal specimens from petting zoo animals yielded 12 E. coli O157:H7 isolates with PFGE patterns indistinguishable from those taken from the children.  Upon notification of the results, zoo officials immediately closed the petting zoo and adjacent play area.

2005 Florida Petting Zoo Outbreak

In March 2005, Florida health officials identified a cluster of 22 E. coli O157:H7 infections, including seven HUS cases, related to attendance at Florida Fairs and Festivals during February 10–21, 2005, and March 3–13, 2005.  Early patient interviews identified no common food or water exposure but did implicate a common animal exposure (i.e., petting zoo attendance).  Three implicated fairs had one common animal vendor – an exhibitor of a farm animal petting zoo.  Stool samples from infected persons were sent to the Florida Department of Health for culture and PFGE typing of E. coli O157:H7 isolates.  Stool samples were also collected the environment and from 36 animals exhibited at the petting zoos.  The human, environmental, and animal samples yielded E. coli O157:H7 isolates with an identical PFGE pattern and the petting zoo was determined to be the source of the outbreak.  Of the 73 illnesses, 12 developed HUS.

2004 North Carolina Petting Zoo Outbreak

In October 2004, a large outbreak of E. coli O157:H7 occurred in North Carolina.  Of the 108 infected, 20 were hospitalized, and 15 contracted HUS.  Visits to a petting zoo at the state fair were associated with illness.  Environmental samples from the petting zoo yielded E coli O157:H7, with indistinguishable PFGE patterns from the stool samples of infected persons.  Persons were found to have become infected after contact with manure and engaging in hand-to-mouth behaviors with sheep and goats in the petting zoo. 

Person to person transmission

E. coli can also be transmitted by person to person contact, which frequently occurs in daycare centers, hospitals, and nursing homes (Giannella, 2010).  Hand washing and strict cleaning guidelines thus become an important issue in preventing such transmissions.

2009 Caregiver-to-Child Transmission

In February 2009, 21 children and a caregiver contracted E. coli in Chicago, Illinois.  Three were hospitalized and released.  The Cook County Health Department attributed the outbreak to inadequate hand-washing.

2000 Daycare Outbreak

In August 2000, a daycare facility in Folsom, California was linked to an E. coli O157:H7 outbreak that sickened 5 students.  In addition to the students, one parent and a sibling also contracted and tested positive for E. coli O157:H7.  The source of the outbreak was a sponge used to wipe down both the changing table and serving table.

Who gets STEC infections?

Though northern climates (e.g. Massachusetts, Minnesota, and other states in the Pacific Northwest) experience the highest frequency of STEC infections, the bacteria occurs and infects people throughout the US, and is also commonly found in Canada, Great Britain, and throughout Europe (Giannella, 2010).  Additionally, annual infection rates reach their peak between June and September (Giannella, 2010).

People of any age can become infected.  Very young children and the elderly are more likely to develop severe illness and hemolytic uremic syndrome (HUS) than others, but even healthy older children and young adults can become seriously ill.

What are the symptoms of STEC infections?

STEC symptoms manifest after an incubation period of 1 to 10 days; however, in the vast majority of cases, symptoms appear between 3 and 4 days after exposure (CDC, June 2011).  Individuals most commonly experience watery nonbloody diarrhea as the first symptom of infection. Severe abdominal cramping often accompanies the onset of diarrhea.  Subsequently, stools often turn visibly bloody (Giannella, 2010).

Though the symptoms of STEC infections vary for each person, victims may also experience fever (typically less than 101˚F/38.5˚C and experienced in fewer than one of every three cases), nausea, vomiting, and chills (Craig and Zich, 2010; CDC, June 2011). Diarrhea generally lasts somewhere between 3 and 8 days, though it may persist longer in children and the elderly (Craig and Zich, 2010; Giannella, 2010).  Some infections are very mild, but others are severe or even life-threatening, and a carrier state may persist for up to 1-2 weeks after symptoms resolve (Craig and Zich, 2010).

E.coli has emerged in recent years as the predominant cause of hemorrhagic colitis.  This illness, with the characteristic symptoms of abdominal cramps and bloody diarrhea, can progress into a severe, life-threatening complication known as hemolytic uremic syndrome. 

What are the complications of STEC infections?

Around 5–10% of those who are diagnosed with STEC infection develop a potentially life-threatening complication known as hemolytic uremic syndrome (HUS) (CDC, June 2011).  The CDC estimates that over 90% of HUS cases are associated with E. coli serotype O157:H7 (Craig and Zich, 2010).  The complication occurs more frequently in cases of children with STEC diarrhea; approximately 15% of these children develop HUS, which constitutes a significant cause of acute renal failure in children (Hunt, 2010).  Renal failure necessitates dialysis in approximately half of the cases, and the fatality rate is about 5% (Hunt, 2010).

Clues that a person is developing HUS include decreased frequency of urination, feeling very tired, and losing pink color in cheeks and inside the lower eyelids.  Persons with HUS should be hospitalized because their kidneys may stop working and they may develop other serious problems.  Most persons with HUS recover within a few weeks, but some suffer permanent damage or die.

75% of all HUS cases occur in children after experiencing diarrhea caused by STEC infection and illness (Hunt, 2010).  The greatest risk of developing HUS is associated with children under the age of 10.  Risk of developing HUS also depends on location and on what E. coli serotype caused the initial infection: about 90% of HUS infections in the United States are caused by STEC O157:H7.  In other countries, however, only 50% of HUS cases may be tied to serotype O157 (Hunt, 2010).

Approximately 22-40% of elderly individuals involved in nursing home outbreaks of STEC subsequently develop HUS.  Of these patients, 50-80% pass away due to complications from the disease (Craig and Zich, 2010).

Factors that increase the chance of developing HUS are presence of blood in the diarrhea, a high white blood cell count, age younger than five years, and attendance at a large daycare center (Giannella, 2010).  Complications of HUS include thrombocytopenia (abnormally low platelet count), hemolytic anemia (insufficient number of red blood cells), and acute renal failure.  Seizures, stroke, and other neurological sequelae may also later occur as a result of the disease (Taege, 2009).

How soon do symptoms appear after exposure?

The time between ingesting the STEC bacteria and feeling sick is called the “incubation period.”  The incubation period is usually 3-4 days after the exposure, but may be as short as 1 day or as long as 10 days (CDC, June 2011).  The symptoms often begin slowly with mild belly pain or non-bloody diarrhea that worsens over several days.  HUS, if it occurs, develops an average of 7 days after the first symptoms, when the diarrhea is improving (CDC, June 2011).

Timeline for Reporting of E Coli cases

To detect E. coli O157 outbreaks, public health laboratories perform a kind of “DNA fingerprinting” on E. coliO157 laboratory samples. Investigators determine whether the “DNA fingerprint” pattern of E. coli O157 bacteria from one patient is the same as that from other patients in the outbreak and from the contaminated food. Bacteria with the same “DNA fingerprint” are likely to come from the same source. Public health officials conduct intensive investigations, including interviews with ill people, to determine if people whose infecting bacteria match by “DNA fingerprinting” are part of a common source outbreak.

A series of events occurs between the time a patient is infected and the time public health officials can determine that the patient is part of an outbreak. This means that there will be a delay between the start of illness and confirmation that a patient is part of an outbreak. Public health officials work hard to speed up the process as much as possible. The timeline is as follows:

Three people in Winnebago County, Illinois, have become ill from e. coli contamination

Incubation time: The time from eating the contaminated food to the beginning of symptoms. For E. coli O157, this is typically 3-4 days.

Time to treatment: The time from the first symptom until the person seeks medical care, when a diarrhea sample is collected for laboratory testing.  This time lag may be 1-5 days.

Time to diagnosis: The time from when a person gives a sample to when E. coli O157 is obtained from it in a laboratory.  This may be 1-3 days from the time the sample is received in the laboratory.

Sample shipping time: The time required to ship the E. coli O157 bacteria from the laboratory to the state public health authorities that will perform “DNA fingerprinting”.  This may take 0-7 days depending on transportation arrangements within a state and the distance between the clinical laboratory and public health department.

Time to “DNA fingerprinting”: The time required for the state public health authorities to perform “DNA fingerprinting” on the E. coli O157 and compare it with the outbreak pattern.  Ideally this can be accomplished in 1 day.  However, many public health laboratories have limited staff and space, and experience multiple emergencies at the same time.  Thus, the process may take 1-4 days.

The time from the beginning of the patient’s illness to the confirmation that he or she was part of an outbreak is typically about 2-3 weeks.  Case counts in the midst of an outbreak investigation must be interpreted within this context.

How common are STEC infections?

The CDC estimates that every year, the United States experiences 110,000 cases and 2,100 hospitalizations due to STEC infection (Craig and Zich, 2010).  We can only estimate because we know that many infected people do not seek medical care, many do not submit a stool specimen for testing, and many labs do not test for STEC.  We think that a similar number of persons have diarrhea caused by non-O157 STEC.  Many labs do not identify non-O157 STEC infection because it takes even more work than identifying E. coli O157.

How are STEC infections diagnosed?

STEC infections are usually diagnosed through lab testing of stool specimens (feces).  Identifying the specific strain of STEC involved is very important for public health purposes, and is critical in detecting outbreaks.  Most labs can determine if an STEC is present and can identify E. coli O157.  To determine the O group of non-O157 STEC, strains must be sent to a State Public Health laboratory.

How long can an infected person carry STEC?

STEC typically disappear from the feces by the time the illness is resolved, but may be shed for several weeks, even after symptoms go away.  Young children tend to carry STEC longer than adults.  A few people keep shedding these bacteria for several months.  Good hand-washing is always a smart idea to protect yourself, your family, and other persons (CDC, June 2011).

What is the best treatment for STEC infection?

Non-specific supportive therapy, including hydration and monitoring of kidney function, is important (Hunt, 2010).  Antibiotics should not be used to treat this infection.  There is no evidence that treatment with antibiotics is helpful, and taking antibiotics may increase the risk of HUS.  Antidiarrheal agents like Imodium® may also increase that risk (CDC, June 2011).

Should an infected person be excluded from school or work?

School and work exclusion policies differ by local jurisdiction.  Check with your local or state health department to learn more about the laws where you live.  In any case, good hand-washing after changing diapers, after using the toilet, and before preparing food is essential to prevent the spread of these and many other infections (CDC, June 2010).

How can STEC infections be prevented?

  1. WASH YOUR HANDS thoroughly after using the bathroom or changing diapers and before preparing or eating food.
  2. WASH YOUR HANDS after contact with animals or their environments (at farms, petting zoos, fairs, even your own backyard)
  3. COOK meats thoroughly. Ground beef and meat that has been needle-tenderized should be cooked to a temperature of at least 160°F/70˚C. It’s best to use a thermometer, as color is not a very reliable indicator of “doneness.”
  4. AVOID raw milk, unpasteurized dairy products, and unpasteurized juices (like fresh apple cider).
  5. AVOID swallowing water when swimming or playing in lakes, ponds, streams, swimming pools, and backyard “kiddie” pools.
  6. PREVENT cross contamination in food preparation areas by thoroughly washing hands, counters, cutting boards, and utensils after they touch raw meat.

References (In Order of Appearance)

Donnenberg, Michael S. “Entrobacteriaceae.” Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. Ed. Gerald L. Mandell, John E. Bennett, and Raphael Dolin. 7th ed. Vol. 1. Philadelphia: Churchill Livingstone Elsevier, 2010. 2815-2833. 2 vols.

Centers for Disease Control and Prevention. “Diarrheagenic E. coli: Technical Information” Centers for Disease Control and Prevention: Your Online Source for Credible Health Information. Centers for Disease Control and Prevention, 27 Nov. 2009. Web. 16 June 2011. <http://www.cdc.gov/‌nczved/divisions/dfbmd/diseases/diarrheagenic_ecoli/technical.html>.

Giannella, Ralph A. “Infectious Enteritis and Proctocolitis and Bacterial Food Poisoning.” Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Ed. Mark Feldman, Lawrence S. Friedman, and Lawrence J. Brandt. 9th ed. Philadelphia: Saunders Elsevier, 2010. 1843-1887.

Ochoa, Theresa J. and Thomas G. Cleary. “Chapter 197: Escherichia Coli.” Nelson Textbook of Pediatrics. Ed. Robert Kliegman, et al. 18th ed. Philadelphia: Saunders Elsevier, 2007. 1193-1196.

Kumar, Vinay. “Infectious Entercolitis.” Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition. Ed. William Schmitt. 8th ed. Philadelphia: Saunders Elsevier, 2009.

Adachi, Javier A., et al. “Infectious Diarrhea from Wilderness and Foreign Travel.” Wilderness Medicine. Ed. Paul S. Auerbach. 5th ed. Philadelphia: Mosby Elsevier, 2007. 1418-1444.

Craig, Sandy A., and David K. Zich. “Gastoenteritis.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. Ed. John A. Marx, et al. 7th ed. Vol. 1. Philadelphia: Saunders Elsevier, 2010. 1200-1226. 2 vols.

Hunt, John M. “Shiga Toxin-Producing Escherichia Coli (STEC).” Clinics in Laboratory Medicine 30.1 (2010): 21-45.

Centers for Disease Control and Prevention. “Enterotoxigencic Escherichia coli: General Information” Centers for Disease Control and Prevention: Your Online Source for Credible Health Information. Centers for Disease Control and Prevention, 25 Nov. 2009. Web. 16 June 2011. <http://www.cdc.gov/‌nczved/divisions/dfbmd/diseases/enterotoxigenic_ecoli/>.

Centers for Disease Control and Prevention. “Escherichia coli O157:H7 and other Shiga-toxin Producing Escherichia coli (STEC): General Information” Centers for Disease Control and Prevention: Your Online Source for Credible Health Information. Centers for Disease Control and Prevention, 2 Jun. 2011. Web. 16 June 2011. <http://www.cdc.gov/‌nczved/divisions/dfbmd/diseases/ecoli_o157h7/>.

Bielaszewska, Martina, et al. “Shiga Toxin-Negative Attaching and Effacing Escherichia coli: Distinct Clinical Associations with Bacterial Phylogeny and Virulence Traits and Inferred In-Host Evolution.” Clinical Infectious Diseases 47.2 (2008): 208-217.

Centers for Disease Control and Prevention. “Investigation Update: Multistate Outbreak of E. coli O145 Infections Linked to Shredded Romaine Lettuce from a Single Processing Facility,” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 21 May 2010. Web. 14 Jul. 2011. <http://www.cdc.gov/ecoli/2010/ecoli_o145/index.html/>.

Frank, Christina, et al. “Epidemic Profile of Shiga-Toxin–Producing Escherichia coli O104:H4 Outbreak in Germany — Preliminary Report.” New England Journal of Medicine 10.1056 (June 2011): 1-11.

Centers for Disease Control and Prevention. “Investigation Update: Outbreak of Shiga Toxin-Producing E. coli O104 (STEC O104:H4) Infections Associated with Travel to Germany,” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 8 Jul. 2011. Web. 14 Jul. 2011. <http://www.cdc.gov/ecoli/2011/ecoliO104/>.

World Health Organization, “Outbreaks of E. coli O104:H4 Infection: Update 29.” World Health Organization Regional Office for Europe. World Health Organization, 7 Jul. 2011. Web, 14 July 2011. <http://www.euro.who.int/en/what-we-do/health-topics/emergencies/international-health-regulations/news/news/2011/07/outbreaks-of-e.-coli-o104h4-infection-update-29>.

Reuters, “Freshway Foods Recalls Romaine Lettuce,” Reuters. Thomson Reuters, 06 May 2010. Web. 15 Jul. 2011. < http://www.reuters.com/article/2010/05/07/lettuce-recall-idUSN0614523520100507>.

Sodha, Samir V., et al. “Foodborne Disease.” Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. Ed. Gerald M. Mandell, John E. Bennett, and Ralph Dolin. 7th ed. Vol. 1. Philadelphia: Churchill Livingstone Elsevier, 2010. 1413-1427. 2 vols.

Centers for Disease Control and Prevention. “Investigation Update: Multistate Outbreak of E. coli O157:H7 Infections Associated with Cheese,” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 24 Nov. 2010. Web. 14 Jul. 2011. <http://www.cdc.gov/ecoli/2010/cheeseO157/index.html>.

Food and Drug Administration, “FDA News Release: FDA, CDC, and Costco Warn Consumers to Avoid Bravo Farms Dutch Style Gouda Cheese,” U.S. Food and Drug Administration. FDA, 04 Nov. 2010. Web. 15 Jul. 2011. <http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm232748.htm>.

Layton, Lyndsey and Greg Gaudio. “FDA Confirms Presence of E. coli in Nestle Cookie Dough.” The Washington Post 20 June 2009. 16 Jul. 2011. <http://www.washingtonpost.com/wp-dyn/content/article/2009/06/29/AR2009062903813.html>.

Centers for Disease Control and Prevention. “Multistate Outbreak of E. coli O157:H7 Infections Linked to Eating Raw Refrigerated, Prepackaged Cookie Dough,” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 29 June 2009. Web. 14 Jul. 2011. <http://www.cdc.gov/ecoli/2009/0619.html>.

Taege, Alan. “Foodborne Disease.” Current Clinical Medicine. Ed. William D. Carey. 2nd ed. Philadelphia: Saunders Elsevier. 2010. 730-734.

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