Etiology, clinical features, complications, and treatment

Escherichia coli O157:H7: etiology, clinical features, complications, and treatment

Eileen Peacock

In recent years, Escherichia coli (E. coli) 0157:H7 has developed into an emerging cause of foodborne illness. It has been identified as the leading cause of postdiarrheal hemolytic-uremic syndrome (HUS) and acute renal failure in infancy and childhood. This article examines, the etiology, clinical features, complications, and treatment of this illness. Prevention strategies are also presented as well as a disaster management case study.


To discuss the etiology, transmission, clinical presentation, treatment and prevention of infection with Escherichia coli O157:H7 (E. coli O157:H7).


1. Discuss the association between enterohemmorhagic escherichia coli and hemolytic uremic syndrome.

2. Identify modes of transmission of E. coli O157:H7.

3. Describe the presenting symptoms, treatment and prevention of E. coli O157:H7 infection.

Escherichia coli (E. coli) O157:H7 is an emerging cause of food-borne illness, the leading cause of postdiarrheal hemolytic-uremic syndrome (HUS), and the leading cause of acute renal failure in infancy and childhood (Centers for Disease Control and Prevention [CDC], 1997 a,b; Klee, McAfee, & Greenleaf, 1993; Verweyen, Karch, Brandis, & Zimmerhackl, 2000). This emerging infectious agent was first identified in 1982 and continues to be isolated with increasing frequency (see Figure 1) (Mead & Griffin, 1998). According to the CDC, E. coli O157:H7 infects close to 20,000 people each year. Of those 20,000 infected, approximately 250 will die, mostly from HUS and other complications. A third of those who develop HUS will be left with varying degrees of permanent kidney damage, and another 8% will have other life-long complications such as hypertension. HUS following E. coli colitis has become the leading cause of pediatric renal failure requiring kidney transplantation in North America.


Both outbreaks and sporadic cases of E. coli O157:H7 infection have occurred in the United States, Canada, Western Europe, Australia, Japan, Central and South America, the Middle and Far East, as well as Africa (Pfeiffer & Nicotra, 2000).

In the United States, a total of 45 confirmed outbreaks were reported to the CDC in 1998. These outbreaks were reported from 25 states and affected 777 persons (see Table 1). Twenty percent of those infected were hospitalized, 4% developed HUS, and 0.4% died. A total of 38 confirmed outbreaks, which affected 1,897 people among 30 states, were reported in 1999 (see Table 1). Although this is fewer than the 45 reported outbreaks in 1998, 13% of the outbreaks in 1999 were multistate (involved two or more states), whereas in 1998 only 4% of the 45 reported outbreaks were multistate. Eleven percent of those infected were hospitalized, 2% developed HUS, and 0.2% died. Greater than 70% of the cases occurred in two large outbreaks in New York and Illinois (CDC 1999a; CDC, 2000a).

Etiology and Transmission

E. coli O157:H7 is one of hundreds of strains of the gram-negative bacterium Escherichia coll. There are more than 170 serogroups of E. coll. Within each serogroup there are one or more serotypes. E. coli O157:H7 is the most common serotype and the most well-known enterohemorrhagic strain. The numbers assigned to the strain refer to the molecules on the bacteria surface that indicate the specific strain of E. coli.

Enterohemorrahagic Escherichia coli (EHEC) is one of the five major categories of the diarrheogenic E. coli. The term enterohemmorhagic E. coli describes those strains of E. coli that are predominantly associated with the clinical presentation of acute bloody diarrhea and produce one or more of a family of Shiga toxins (ST). It is postulated that bacteria virus transferred the gene for the Shiga toxin from Shigella to E. coli during a pandemic in Central America in the 1970s. Hence, EHEC are a subgroup of Shiga toxin producing E. coli (STEC), also known as verocytotoxin or verotoxin producing E. coli (VTEC). There are at least 24 serogroups of STEC/VTEC associated with hemorrhagic colitis or diarrhea associated (D+) HUS (Robson Leung, & Kaplan, 1993). Not all STEC have been implicated as human pathogens, and nearly all understanding of the epidemiology of EHEC is derived from studies of E. coli O157:H7 (Pfeiffer, & Nicotra, 2000).

D+ HUS is associated with the Shiga toxin, which is produced in quantity only by STEC and by Shigella dysenterial type 1. Approximately 90% of HUS cases are diarrhea-associated. In the United States, S. dysenterial type 1 infections are rare making STEC infections the cause of virtually all D+ HUS (CDC, 1997a).

E. coli O157 is found regularly in the feces of healthy cattle (bovine reservoir) and is transmitted to humans through contaminated food, water, and direct contact with infected people or animals. Transmissions in outbreaks have mainly been through contaminated food, particularly undercooked ground beef.

Raw ground beef products present a significant public health risk because such products are often undercooked, and the E. coli O157:H7 organisms that have been introduced below the product’s surface by grinding are not sufficiently destroyed. In 1999 three multistate outbreaks were associated with eating commercially frozen ground beef patties and led to two nationwide recalls. E. coli O157:H7 transmission is not limited to raw ground beef products. An outbreak traced to venison jerky suggests a wild deer reservoir, making both cattle and feral deer manure areas of concern (Keene et al., 1997; Tauxe, 1997). The very low infectious dose, approximately [10.sup.2] organisms or less (the number of organisms required to cause disease) associated with foodborne disease outbreaks, and the very severe consequences of infection underscore the importance of proper food handling to adequately ensure that all food is not contaminated with the organism when consumed.

Other epidemiologically-associated food vehicles of transmission, beyond those directly related to the bovine reservoir, have included lettuce, cole slaw, hard shell tacos, fruit salad, and alfalfa sprouts (CDC, 1997b; Taormina, Beuchat, & Slutsker, 1999). Indirect contamination of such fruits and vegetable products by cattle feces has been implicated. In 1992, an outbreak caused by unpasteurized apple cider showed that this organism could be transmitted through a food with a pH level less than 4.0, possibly after contact of fresh produce with manure (Tauxe, 1997; Zhao, Doyle, & Besser, 1993). In 1996, unpasteurized commercial apple juice was again epidemiologically associated with an outbreak involving 45 individuals (CDC, 1996a). Raw milk and cheese curds have also been implicated with outbreaks illustrating the hazards of using raw milk to produce commercial products (CDC, 2000b).

Outbreaks continue to be associated with an expanding range of foods and activities. Contaminated water has served as a vehicle for transmission. Two outbreaks during the summer of 1998, one involving a drinking water supply and another involving recreational water exposure, resulted in a total of 140 infections and one death (Rice, Clark, & Johnson, 1999). In 1995, ingesting contaminated and untreated Illinois lake water resulted in 12 cases of infection. Bloody diarrhea occurred in nine of the cases; three of the cases in children ages 2, 4, and 5 years resulted in HUS with the children being hospitalized for at least 1 month each (CDC, 1996b). Two previous lake water-associated outbreaks that took place between 1991 and 1994 resulted from infected swimmers that had contaminated the water.

Contact with farm animals has been associated with both sporadic cases and outbreaks. In 1997, a 2-year-old boy from the United Kingdom died after a 7-day history of vomiting and blood-flecked, watery diarrhea. E. coli O157 was isolated from fecal specimens. The isolated E. coli bacteria had the same identical DNA banding as that isolated in five cows from the dairy and sheep farm where the boy had played (Barnham & Weightman, 1998). Most recently it was reported that 14 children between the ages of 1 and 10 became infected after visiting a farm petting zoo. Eight of the children were hospitalized, and two developed HUS.

Person-to-person transmission has also been reported. In fact, a study by the Canadian Pediatric Kidney Disease Registry found that person-to-person transmission is a significant source of VTEC in patients with D+ HUS (Robson, Leung, & Kaplan, 1993). Outbreaks of person-to-person transmitted infection have occurred in children’s day care facilities and institutions providing care for the elderly or for those with physical or mental disabilities (Parry & Salmon, 1998). In Wales, person-to-person spread was the most important factor in four out of five outbreaks, including those in children’s day nurseries, which were the settings for two of the largest outbreaks (Chalmers et al., 1999). Because person-to-person contact in families and child care centers is an important mode of transmission, measures to prevent cross contamination are critical. Bacteria in diarrheal stools of infected persons can be passed from one person to another when hygiene or handwashing practices are inadequate. Young children may shed the organism in their feces up to 2 weeks after the infection resolves. Infected toddlers who are not toilet trained may present a significant risk to family members and playmates. Household contacts in groups at high risk, such as children 5 years of age and younger, present a risk of spreading the infection to the wider community as well (Parry & Salmon, 1998). Because O157 can be transmitted from person to person, public health recommendations for measures to prevent transmission from infected persons have been developed and disseminated (CDC, 1997a).

Clinical Features and Complications

Infection with E. coli O157:H7 may cause nonbloody diarrhea or no symptoms, with the illness resolving in 5 to 10 days. However, clinical illness is commonly heralded by severe abdominal pain and watery diarrhea, followed within 24 hours by grossly bloody stools (see Table 2). This complex of symptoms constitutes the clinical picture, “hemorrhagic colitis.” Unlike those with other bacteria associated diarrhea, patients may be afebrile and inflammatory cells are seldom present in the stool (Wilson et al. 1998). Robson et al. (1993) reported that fever is present in only 5%-20% of cases. With the exception of the individuals who develop HUS, the illness is generally self-limiting.

After colitis caused by E. coli O157:H7, HUS develops in some patients. Approximately 2%-7% of infections lead to this complication, which is characterized by a triad of symptoms: acute renal failure, thrombotic thrombocytopenia purpura (TTP), and thrombotic microangiopathic hemolytic anemia (see Table 3) HUS is a worldwide problem that mirrors the distribution of E. coli O157:H7 and other Shiga and Shigalike toxin-producing microorganisms (Lindsay, 1997). Shiga toxins produced by E. coli O157:H7 are the key virulence factors in the pathogenesis of this STEC disease (Kimmitt, Harwood, & Barer, 2000). HUS develops when the bacteria enters the colon and releases the Shiga-like or verocytotoxins, which transfer across the epithelial cells and enter the systemic circulation affecting the endothelial cells primarily in the kidneys and may affect the endothelial cells of other organ systems as well. The toxin-mediated damage to the glomerular endothelial cells initiates the release of vasoconstrictive and platelet-aggregating substances that result in the formation of platelet thrombi in the renal microvessels causing acute renal injury (Robson et al., 1993). Multiple organ system involvement may also occur and can result in neurologic complications, hepatic damage, pancreatitis, and myocarditis from direct damage to related endothelial cells (Klee et al., 1993; Robson et al., 1993). Studies indicate that the toxins are specific for glycosphingolipid globotriasylceramide (Gb3) receptor sites, which are present on the renal tubular epithelial cells. Gb3 are present in the glomeruli of infants under 2 years of age but not in the glomeruli of adults, which may account for the differential sensitivity of renal cells to toxin-mediated damage (Lindsay, 1997). HUS tends to occur predominantly between the ages of 6 months and 4 years of age (Robson et al., 1993).

HUS commonly develops 7 days after the onset of diarrhea. Approximately 50% of patients who develop HUS will require dialysis (Pfeiffer & Nicotra, 2000). Severity of renal involvement measured by the duration of anuria is a marker of poor late prognosis with severe, long-term consequences (Zurowska, Gockowska, Czarniak, & Marczak, 2000).

Diagnostic Tests and Treatment

Early diagnosis is critical to preventing HUS and reducing associated mortality. Diagnosis is based on the typical clinical presentation and the isolation of the bacterium from the stool. Stool cultures specific to E. coli O157:H7 should be done within 4-7 days after onset of illness and before any antibiotic exposure, as antibiotics are contraindicated. Many laboratories that culture stool do not test for this specific organism (CDC, 1999b, CDC, 1997 a,b; CDC, 1995a). Stool specimens should be obtained on all patients with bloody diarrhea and the specimens tested on Sorbitol-MacConkey (SMAC) agar. It is vital that clinicians consider the diagnosis of E. coli O157:H7, that appropriate specimens are collected, and that laboratories use the necessary screening techniques to avoid the great potential for misdiagnosis and inappropriate clinical procedures or interventions (see Table 4) (Tapper, Tarr, Avner, Brandt, & Waldhausen, 1995).

Serologies to detect toxin-neutralizing antibody and anti-O157 antibody have been described but are not yet available for diagnostic use. In culture-confirmed postive cases, only 2/3 have a positive serology for the O157 antigen. (Pfeiffer & Nicotra, 2000).

Treatment for E. coli is dependent upon the patient’s reaction to the bacteria once ingested. Some patients recover without treatment with no adverse effects. For others, diarrhea occurs followed with complete recovery in 5-10 days.

Antibiotic therapy is contraindicated. Antibiotic therapy has been targeted as increasing the subsequent risk for HUS and has been associated with a higher case fatality rate in the more severe cases (Carter et al., 1987). A retrospective study showed that children treated with antibiotics had a higher risk of developing HUS compared with children who did not (Wong, Jelacic, Habeeb, Watkins, & Tarr, 2000). This may be because antibiotic treatment causes the release of the Shiga toxin from injured bacteria in the intestine. Antibiotic therapy also kills normal bowel flora allowing E. coli to flourish. Antimotility drags such as loperamide are also contraindicated because they slow metabolism in the bowel (Tapper et al., 1995). The contents stay in the bowel longer and increased amount of bacteria are absorbed. Their use has also been associated with a longer duration of bloody diarrhea and a greater propensity for central nervous system complications in HUS (Pfeiffer & Nicotra, 2000).

Infection with E. coli O157:H7 may result in the life-threatening complication of HUS requiring some form of renal replacement therapy. When this occurs, treatment is supportive with close attention to fluid, electrolyte and metabolic balance, nutrition, and blood pressure control (Robson et al., 1993). Supportive treatment must be given that includes replacing fluids and electrolytes. Intake, output, and weights should be monitored closely. The physician may order steroids to reduce inflammation. Early initiation of dialysis for acute renal failure may increase the chance of survival. If hemodialysis is required, the dialysate may need to be adjusted to accommodate the patient’s changing electrolytes. Ultrafiltration may be necessary to remove excess extracellular fluid and decrease hypertension especially in light of ongoing parenteral nutrition that is often required. Platelet and/or red blood cell transfusion may be necessary to support blood loss and corresponding drop in hemoglobin and hematocrit. Access usually involves a central venous line or femoral catheter, and anticoagulation is accomplished with minimal or no heparin due to the presence of coagulopathies. The usual complications may occur during dialysis. Care must be taken because of the acute nature of the illness. Careful monitoring of blood pressure is necessary along with observation of the dialyzer to avoid clotting and further blood loss. Continuous renal replacement therapy (CRRT), peritoneal dialysis (PD), plasmapheresis, or therapeutic plasma exchange (TPE) have also been used (Dan, Cardella, & Taft, 1983). TPE has been particularly effective in adult-type HUS and TTP. With TPE a specific volume of plasma is separated from the whole blood, collected, and discarded along with the dissolved contents of plasma (Price & McCarley, 1993), including the protein bound toxins.

The National Institutes of Health is now taking part in the phase III clinical trials of an immunoadsorbant drug, SYNSORB Pk[R], designed to prevent the serious complications of VTEC infections, including HUS. The drug is administered orally and works by binding and neutralizing the verotoxin while it is in the bowel preventing it from entering the blood stream. This 5-year study has been designed to determine the effect of SYNSORB Pk in children with HUS on mortality and extra-renal complications as well as the need for and the duration of dialysis (Ford, 1998).


Prevention strategies can be accomplished on several fronts. Avoid ingesting any food products that may contain E. coli O157:H7. Do not eat undercooked ground meat including meat products that may be served to you in a restaurant. Adequate cooking requires that the core meat temperature reach 155 [degrees] Fahrenheit or 68 [degrees] Celsius for at least a 15-second period. Examining the center portion of the meat to ensure that meat is gray or brown throughout and that the meat juices are clear can qualitatively assess adequate cooking temperatures (CDC, 1995b). Fresh fruit and vegetables should be washed well before eating. Unpasteurized beverages such as apple cider should be avoided. Federal regulations now require warning signs and labels whenever unprocessed fruit and vegetable juices and ciders are sold. Handwashing is another key strategy. Teach children to wash hands after using the bathroom, after petting farm animals, and before eating. To reduce the chance of person-to-person transmission, daycare workers should wash their hands thoroughly after diaper changes and before helping children with lunches. Children with E. coli may shed bacteria up to a week (7-17 days) after recovery. When caring for the hospitalized patient, strict enteric precautions must be followed. The public should be educated about the importance of handwashing, the dangers of swimming in untreated lakes, and in recognizing the symptoms of E. coli.

Development of an experimental vaccine is underway at the National Institute of Child Health and Human Development (NICHD). A polysaccharide from the capsule of the bacterium has been conjugated to a genetically-inactivated toxin protein obtained from the Pseudomonas aerugenosa bacteria and then used in vaccine development. Because humans do not develop the ability to make antibodies against polysaccharides until the age of about 2 years and because proteins are effective as antigens at all ages, conjugating the polysaccharides to proteins is an important advance in making an effective vaccine that can target young children at risk for developing HUS.

Consideration has also been given to mass vaccination of cattle, which would eliminate the pathogen at its source and, thus, significantly reduce the levels of E. coli O157:H7 excreted by cattle into the environment (Bioniche Life Sciences, Inc., 2000; Tauxe, 1997). More rigid regulation and inspection in slaughterhouses may also help reduce the bovine reservoir. Although debate continues, many organizations see food irradiation as a means of preventing many foodborne diseases.


E. coli O157:H7 exposure, as described, has serious potential risks for community outbreaks. It remains a health care concern. E. coli O157:H7 is the most common organism to cause HUS in young children. Early identification and treatment of symptoms and complications will make a difference in patient outcomes. Rapid investigation and reporting to state health departments and cluster management can identify the source of the outbreak (CDC, 1997 a,b; Tauxe, 1997). Prevention of exposure, which includes cooking ground beef well, cleaning fruits and vegetables, avoiding unpasteurized milk and juices (Tauxe, 1997), and handwashing will decrease the risk of infection. Education of the community and health care workers will increase the awareness of the potential risks of exposure to E. coli and prevent transmission.

Table 1

Outbreaks of E. coli 0157:H7 in vehicle 1998-1999

Suspected and Confirmed

1998 1999 Total

Drinking water (including well) 121 1,065 1,186

Fresh produce (fruits, vegetables, juice) 245 210 455

Other meat (roast beef, game sausage) 0 373 373

Ground beef 90 87 177

Unknown 110 54 164

Person-to-person 58 36 94

Dairy (milk, raw milk, cheese curds) 93 0 93

Swimming (pool, lake, beach) 26 49 75

Other food (cake, tacos) 20 21 41

Contact with cattle 14 2 16

Total 777 1,897 2,674

(Note: Adapted from Centers for Disease Control, 1998, 1999)

Table 2

Clinical Features of E. coli O157:H7

* Incubation period from 3-8 days

* Abdominal pain/cramping

* Nausea and vomiting

* Gastroenteritis

— usually preceded illness by 5-10 days

— diarrhea, bloody stool

— severe colitis

Table 3

Potential Complications

* Hemolytic uremic syndrome (HUS) develops in 2-7% or more of patients (highest risk for children, older adults, those with diminished immune systems).

* 75% of patients who develop HUS will require erythrocyte and/or platelet transfusions.

* 50% of patients with HUS will require dialysis.

* 5% of patients with HUS die.

* 10% of patients with HUS develop hypertension and chronic renal failure.

* Thrombotic thrombocytopenic purpura (TTP) is clinically similar to HUS but includes neurologic abnormalities (most common in adults).

Table 4

Laboratory Findings HUS (D+)

* Moderate to severe anemia

* Elevated serum bilirubin concentrations

* Low normal to markedly decreased platelet count

* Markedly elevates serum lactate dehydrogenase (LDH)

* Decreased urine output

* Elevated BUN and serum creatinine

* Elevated WBCs

* Proteinuria and hematuria may be seen


Barnham, M., & Weightman, N. (1998). Clostridium septicum infection and hemolytic uremic syndrome. Emerging Infectious Diseases, 4(2), 321-324.

Bioniche Life Sciences, Inc. (2000, September 20). Press release. New E. coli vaccine to be released in Canada. [Online]. Available: www.investorlook. com/BNC/BNCromote.shtml #newsitem9694 57280,94072.

Carter, A.O., Borczyk, A.A., Carlson, J.A., Harvey, B., Hockin, J.C., Karmali, M.A., Krishnan, C., Korn, D.A., & Lior, H. (1987). A severe outbreak of Escherichia coli O157:H7: Associated hemorrhagic colitis in a nursing home. New England Journal of Medicine, 317(24), 1496-1500.

Centers for Disease Control and Prevention (CDC). (1995a). Enhanced detection of sporadic escherichia coli O157:H7 infections — New Jersey, July 1994. MMWR, 44(22), 417-418.

Centers for Disease Control and Prevention (CDC). (1995b). Escherichia coli O157:H7 outbreaks at a summer camp — Virginia, 1994; MMWR, 4(22), 419-421.

Centers for Disease Control and Prevention (CDC). (1996a). Outbreak of Escherichia coli O157:H7 infections associated with drinking unpasteurized commercial apple juice. MMWR, 45(44), 975.

Centers for Disease Control and Prevention (CDC). (1996b). Lake-associated outbreak of Escherichia coli O157:H7. MMWR, 45(21), 437-439.

Centers for Disease Control and Prevention (CDC). (1997a). Hemolytic uremic syndrome surveillance to monitor trends with Escherichia coli O157:H7 and other Shiga toxin-producing E. coli. Emerging Infectious Diseases, 3(3).

Centers for Disease Control and Prevention (CDC). (1997b). Outbreaks of Escherichia coli O157:H7 Infection associated with eating alfalfa sprouts. MMWR, 46(32), 741-744.

Centers for Disease Control and Prevention (CDC). (1999a, March 8). Surveillance for outbreaks of Escherichia coli O157:H7 infection: Summary of 1998 data [Online]. Available: http :// dbmd/diseaseinfo/escherichia-coli_a.htm

Centers for Disease Control and Prevention (CDC). (1999b). Isolation of E. coli O157:H7 from sporadic cases of hemorrhagic colitis. MMWR, 48(LMRK), 83-87.

Centers for Disease Control and Prevention (CDC). (2000a, June 9). Surveillance for outbreaks of Escherichia coli O157:H7 infection: Summary of 1999 data [Online]. Available: dbmd/diseaseinfo/escherichia-coli_a.htm

Centers for Disease Control and Prevention (CDC). (2000b). Outbreak of Escherichia coli O157:H7 infection associated with eating fresh cheese curds. MMWR, 49(40), 911-913.

Chalmers, R.M., Parry, S.M., Salmon, R.L., Smith, R.M.M., Willshaw, G.A., & Cheasty, T. (1999). The surveillance of vero cytotoxin-producing Escherichia coli O157 in Wales, 1990 to 1998. Emerging Infectious Diseases, 5(4), 566-569.

Dau, P.C., Cardella, CJ., & Taft, E.G. (1983). Therapeutic plasma exchange disease compendium (1st edition). Lakewood, CO: COBE Laboratories, Inc.

Ford, D.M. (1998, October). Hemolytic uremic syndrome: Management and prevention treatments that are currently under investigation. Basic Nephrology Lecture Series.

Keene, W.E., Sazie, E., Kok, J., Rice, D.H., Hancock, D.D., Balan, V.K., Zhao, T., & Doyle, M.P. (1997). An outbreak of Escherichia coli O157:H7 infections traced to jerky made from deer meat. JAMA, 277(15), 1229-1231.

Kimmitt, P.T., Harwood, C.R., & Barer, M.R. (2000). Toxin gene expression by Shiga toxin-producing Escherichia coli: The role of antibiotics and the bacterial SOS response. Emerging Infectious Diseases, 6(5), 458-465.

Klee, K.M., McAfee, N., & Greenleaf, K. (1993). Pediatric case study: Hemolytic Syndrome. ANNA Journal, 20(4), 505-506.

Lindsay, J.A. (1997). Chronic sequelae of foodborne disease. Emerging Infectious Diseases, 3(4), 443-452.

Mead, P.M., & Griffin, P.S. (1998). Escherichia coli O157:H7. Lancet, 352(9135), 1207-1212.

Parry, S.M., & Salmon, R.L. (1998). Sporadic STEC 0157 infection: Secondary household transmission in Wales. Emerging Infectious Diseases, 4(4), 657-661.

Pfeiffer, J., & Nicotra, D. (2000). APIC text of infection control and epidemiology. Washington, DC: Association for Professionals in Infection Control and Epidemiology, Inc. (APIC).

Price, C., & McCarley, P.B. (1993). Technical considerations of therapeutic plasma exchange as a nephrology nursing procedure. ANNA Journal, 20(1), 41-46.

Rice, E.W., Clark, R.M., & Johnson, C.H. (1999). Chlorine inactivation of Esherichia coli O157:H7. Emerging Infectious Diseases, 5(3), 461-463.

Robson, W.L.M., Leung, A.K.C., & Kaplan, B.S. (1993, January). Hemolytic-Uremic Syndrome. Current Problems in Pediatrics.

Taormina, PJ., Beuchat, L.R., & Slutsker, L. (1999). Infections associated with eating seed sprouts: An international concern. Emerging Infectious Diseases, 5(5), 626-634.

Tapper, D., Tarr, P., Avner, E., Brandt, J., & Waldhausen, J. (1995). Lessons learned in the management of hemolytic uremic syndrome in children. Journal of Pediatric Surgery, 30(2), 158-163.

Tauxe, R.V. (1997). Emerging foodborne diseases: An evolving public health challenge. Emerging Infectious Diseases, 3(4), 425-434.

Verweyen, H.M., Karch, H., Brandis, M., & Zimmerhackl, L.B. (2000). Enterohemorrhagic Escherichia coli infections: Following transmission routes. Pediatric Nephrology, 14(1), 73-83.

Wilson, J.D., Braunwald, E., Isselbacher, KJ., Petersdorf, R.G., Martin, J.B., Fauci, A.S., & Root, R.K. (1991). Harrison’s principles of internal medicine (12th edition). New York: McGraw-Hill Professional Publishing.

Wong, C.S., Jelacic, S., Habeeb, R.L., Watkins, S.L., & Tarr, P.I. (2000). The risk of hemolytic uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. New England Journal of Medicine, 342(26), 1930-1936.

Zhao, T., Doyle, M.P., & Besser R.E. (1993). Fate of enterohemorrhagic Escherichia coli O157:H7 in apple cider with and without preservatives. Applied Environmental Microbiology, 59(8), 2526-2530.

Zurowska, A., Gockowska, Z., Czarniak, P., & Marczak, E. (2000). Changing clinical course of hemolytic uremic syndrome in children. Pol Merkuriuscz Lek, 8(46), 234-235.

E-coli Outbreak: Disaster Management Case Study

In August of 1999, a large outbreak of E-coli O157:H7 occurred in upstate New York. The cause of this exposure to E. col O157:H7 was a contaminated, unchlorinated well used during an annual county fair. There were 781 confirmed or suspected cases of E. coli infection.

* 71 people were hospitalized.

* All admissions took place within 7 days.

* 14 were diagnosed with hemolytic uremic syndrome (HUS).

* 12 of the 14 cases of HUS were children ranging in age from 15 months to 4 years.

* 2 people died; one child died within 48 hours after hospital admission.

* 10 developed acute renal failure (ARF) requiring dialysis.

Thirteen cases of HUS were transferred from area hospitals to Albany Medical Center (AMC) in Albany, NY, an academic health sciences center with a regional pediatric dialysis program. The program needed to provide treatment immediately.

AMC developed a disaster management plan outlining strategies that would enable us to provide care to the sudden large influx of patients. We used a multidisciplinary approach to formulate a strategic plan. It included the identification of internal and external resources, infection control issues, strategies to address patient and family concerns and to manage the large numbers of people including traffic control, and the provision of timely information for visitors and the media. Barriers to care included: (a) competency of registered nurses experienced in pediatric dialysis, peritoneal dialysis, and CRRT, (b) inadequate supplies of equipment and disposable supplies, and (c) possible burnout.

The identification of internal resources included: (a) nephrology nurses currently not working in the specialty, (b) education and development, (c) clinical engineering and plumbing. External resources included nephrology nurses and equipment recruited from local, regional, and national facilities. Corporate support was also requested for additional supplies and equipment.

A concise but cogent competency and orientation program was developed to orient nephrology nurses from other facilities. Clinical engineering provided support for machine maintenance on a 24-hour basis.

Outcomes to the strategic plan included: (a) the addition of nephrology nursing resources allowed the medical center staff to rest, (b) transmission of E. coli O157:H7 did not occur, (c) appropriate care was delivered to all patients, (d) nine patients recovered normal renal function, (e) the patients and their families received the proper support and reassurance from hospital staff.

The E. coli O157:H7 outbreak disaster was a learning opportunity for all involved. Essential components of a disaster plan learned from the experience included:

1. quick identification of the disaster and early communication to high-level management;

2. immediate activation of the plan;

3. establishment of a central communication location to address phone calls from family members and the media;

4. coordination of case updates;

5. daily debriefing with the staff, social workers, and crisis managers who support the families; and

6. security support.

Although this was a learning experience for all involved, it was rewarding in that the care delivered to our patients and their families provided positive patient outcomes.

Escherichia coli 0 157:H7: Etiology, Clinical Features,

Complications, and Treatment

Posttest — 2.2 Contact Hours

Posttest Questions

(See posttest instructions on the answer form, next page)

1. The term “enterohemorrhagic E.

coli” describes those strains of

E.coli that are predominantly

associated with

A. acute bloody diarrhea.

B. Mad cow disease.

C. hemolytic uremic syndrome.

D. thrombocytopenia.

2. Which of the following has been

most commonly identified with

transmission and E. coli outbreaks?

A. Lettuce.

B. Undercooked meat.

C. Poor hand-washing habits.

D. Recreational water exposure.

3. Young children may be particularly

susceptible to HUS after E.

coil infection because of the

presence of GB3 in the

A. renal microvessels.

B. liver endothelial cells.

C. gastrointestinal mucosa.

D. renal tubular epithelial cells.

4. The lowest infectious dose of E

coli O157:H7 associated with

food-borne disease outbreaks is

A. 10.

B. [10.sup.2].

C. [10.sup.3].

D. [10.sup.4]

5. E. coli O157:H7 is regularly

A. transmitted via indirect contact.

B. identified as a common strain

of the gram-positive bacteria

E. coli.

C. found in the feces of healthy


D. isolated as a common skin


6. HUS following E. coli infection

is the leading cause of

A. acute renal failure in children

and adults.

B. hypertension in children.

C. renal failure in children and


D. renal failure requiring transplantation

in children.

7. In establishing a diagnosis of

infection with E. coli O157:H7,

the nurse knows cultures specific

to E.coli O157:H7 should

be done on the patient’s

A. stool within 24 hours of onset

of diarrhea.

B. stool within 4-7 days of onset

of diarrhea.

C. blood within 5-10 days after

onset of diarrhea.

D. blood after one week of diarrhea.

8. J.W. is a 4-year-old male admitted

with a diagnosis of HUS

caused by infection with E. coli

O157:H7. The nurse would

expect J.W. to exhibit

A. a self-limiting illness.

B. high fever.

C. iron-deficiency anemia.

D. thrombocytopenia.

9. Verocytotoxin, produced in

large amounts by E. coli, transfers

across the epithelial cells

and mainly targets the

A. microvasculature of the kidney.

B. endothelial cells of the


C. endothelial cells in the kidney.

D. mucosal cells of the intestines.

10. HUS develops after colitis

caused by E coli O157:H7 in

A. 2%-7% of infections.

B. 10% of children.

C. 20% of adults.

D. 20,000 people annually.

11. The principal treatment for E.

coli includes the following:

A. Antibiotics for lysis of E. coli.

B. Antispasmotics to decrease


C. Plasmapheresis to reduce


D. Steroids to reduce inflammation.

12. Household contacts may be at

high risk for getting E. coli

O157:H7 because

A. children may shed the organism

in their feces for up to 17


B. handwashing does not reduce


C. contamination occurs frequently

via saliva.

D. of exposure to contaminated


13. Important steps to take to prevent

E. coli O157:H7 infection


A. utilize “dialysis precautions”

for infected individuals.

B. culture patients with diarrhea


C. avoid ingestion of contaminated


D. administer SYNSORB PK as

soon as possible.



Escherichia coli O157:H7: Etiology, Clinical Features, Complications, and Treatment

By Eileen Peacock, Virginia W. Jacob, and Susan M. Fallone

Posttest Instructions

* Select the best answer and circle the appropriate letter on the answer grid below.

* Complete the evaluation.

* Send only the answer form to the ANNA National Office; East Holly Avenue Box 56; Pitman, NJ 08071-0056.

* Enclose a check or money order payable to ANNA

* Posttests must be postmarked by October 20, 2003. If you receive a passing score of 70% or better, a certificate for 2.2 contact hours will be awarded by ANNA.

* Please allow 6-8 weeks for processing. You may submit multiple answer forms in one mailing, however, because of various processing procedures for each answer form, you may not receive all of your certificates returned in one mailing.

ANNA Member — $15

Non-Member — $25

Expiration Date (from membership card)

Complete the Following

Name: —

Address: —

Telephone: —

SS# —

ANNA Member — Yes — No — CNN Yes — No —

Source of Article: [] Journal [] ANNA Web site (ANNA link)

Note: If you wish to keep the journal intact, you may photocopy the answer sheet or access this posttest at


Eileen Peacock, MSN, RN, CNN, CIC, CPHQ, is Vice President, Clinical Resources and Special Projects, DaVita, Berwyn, PA.

Virginia W. Jacob, BS, RN, CNN, is Manager, Clinical Resources and Special Projects, Da Vita, Berwyn, PA.

Susan M. Fallone, MS, RN, CNN, is Clinical Nurse Specialist, Albany Medical Center, Albany, NY.

COPYRIGHT 2001 Jannetti Publications, Inc.

COPYRIGHT 2007 Gale Group