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E COLI O157/O111

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Toxin-producing Shiga-toxigenic Escherichia coli (STEC) are rod-shaped, Gram negative bacteria that produce Shiga toxins (Stx). Enterohemorrhagic Escherichia coli (EHEC) are a subset of STEC capable of causing serious illness. Serotype O157:H7 is the prototypic EHEC strain, accounting for approximately 75% of EHEC infections worldwide
    B) All serotypes of E. coli can produce Shiga toxins and some may also cause diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS). Serotype O157 appears to be more prevalent in developed countries, however, the non-O157 serotypes may be of greater clinical and public health importance in other countries.
    1) Escherichia coli (E. coli) serotype O111:H2
    2) Escherichia coli (E. coli) serotype O157:H7
    3) Escherichia coli (E. coli) serotype O111:non-motile
    4) Escherichia coli (E. coli) serotype O26:H11
    5) Escherichia coli (E. coli) serotype O103:H2

Specific Substances

    1) E. coli O157:H7
    2) E. coli O111:H2
    3) E. coli O111:non-motile
    4) E. coli O26:H11
    5) E. coli O103:H2
    6) E. coli O104:H4
    7) Escherichia coli O111:H2
    8) Escherichia coli O157:H7
    9) Escherichia coli O111:non-motile
    10) Escherichia coli O26:H11
    11) Escherichia coli O103:H2
    12) Escherichia coli O104:H4
    13) Food Poisoning, E. coli O111:H2
    14) Food Poisoning, E. coli O157:H7
    15) Food Poisoning, E. coli O111:non-motile
    16) Food Poisoning, E. coli O26:H11
    17) Food Poisoning, E. coli O103:H2
    18) Food Poisoning, E. coli O104:H4
    19) Food Poisoning, Escherichia coli O157:H7
    20) Foodborne Poisoning, E. coli O111:H2
    21) Foodborne Poisoning, E. coli O157:H7
    22) Foodborne Poisoning, Escherichia coli O111:H2
    23) Foodborne Poisoning, Escherichia coli O157:H7
    24) O111:H2, E. coli, serotype
    25) O157:H7, E. coli, serotype
    26) O111:H2, Escherichia coli, serotype
    27) O157:H7, Escherichia coli, serotype
    28) Serotype, E. coli O111:H2
    29) Serotype, E. coli O157:H7
    30) Serotype, Escherichia coli O111:H2
    31) Serotype, Escherichia coli O157:H7
    32) E COLI 0157/O111
    33) E COLI 157/O111
    34) ESCHERICHIA COLI O157/O111
    35) FOOD POISONING-E COLI O157/O111

Available Forms Sources

    A) FORMS
    1) Toxin-producing Shiga-toxigenic Escherichia coli (STEC) are rod-shaped, Gram negative bacteria that produce Shiga toxins (Stx). Enterohemorrhagic Escherichia coli (EHEC) are a subset of STEC capable of causing serious illness. Serotype O157:H7 is the prototypic EHEC strain, accounting for approximately 75% of EHEC infections worldwide (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    B) SOURCES
    1) ROUTE OF EXPOSURE
    a) E. coli O157:H7 is a member of the enterohemorrhagic E. coli family (EHEC) which produces Shiga toxin and are capable of producing bloody diarrhea (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) While sporadic cases of E coli O157:H7 infection have been reported, most cases occur during outbreaks, usually due to food-borne bacterial contamination. However, spread of the infection may also be by: Person-to-person (fecal-oral), waterborne (drinking water), waterborne (swimming in feces-contaminated water), airborne (Belongia et al, 1993; Berkelman, 1994; Keene et al, 1994).
    c) TOXIN: Verotoxin and shiga-like toxin are closely related to the toxin produced by Shigella dysenteriae (Center for Food Safety and Applied Nutrition (CFSAN), 2009).
    1) Based on results from a national screening program in Japan, the rate of symptom-free shedding of shiga toxin-producing E. coli O157 was higher in adults than children. The authors speculated that this could result in secondary transmission from asymptomatic adults to healthy children (Terajima et al, 1999).
    2) E. COLI O104:H4: In Germany, contaminated raw sprouts resulted in an outbreak of E. coli O104:H4 infection. By July 2011, 852 cases of hemolytic uremic syndrome and 32 deaths were reported (Centers for Disease Control and Prevention (CDC), 2011).
    d) FOOD-BORNE OUTBREAKS
    1) Apple cider (fresh-pressed, untreated)
    2) Cantaloupe
    3) Cheese curds
    4) Cold cooked meats
    5) Cookie dough (frozen, raw)
    6) Deer meat (venison) jerky
    7) Dry-cured salami
    8) Incompletely cooked ground beef and beef products
    9) Juice (unpasteurized)
    10) Mayonnaise
    11) Milk (raw)
    12) Raw Sprouts
    13) Roast beef
    14) Salads/salad bars (eg, lettuce)
    15) Spinach (bagged)
    16) Sprouts (alfalfa/clover/radish)
    1) REFERENCES: (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Centers for Disease Control and Prevention (CDC), 2011; Schneideret al,null; Mohle-Boetani et al, 2001; Anon, 1998; Banatvala et al, 1996; Consensus Conference, 1995; Rodrique et al, 1995; Anon, 1995; Anon, 1995a; Anon, 1995b; Anon, 1994; Upton & Coia, 1994; Keene et al, 1994; Bell et al, 1994; Berkelman, 1994; Le Saux et al, 1993; Besser et al, 1993)
    2) MEAT: One of the largest food-borne outbreaks of E coli O157:H7 infection in the USA was due to incompletely cooked hamburger patties served by a fast food chain in the Western United States (Washington, Idaho, California, and Nevada) between November 1992 and February 1993. There were more than 500 laboratory-confirmed infections and four deaths. A hemolytic uremic syndrome cluster and an increase in children presenting to emergency departments with bloody diarrhea were sentinel events. Secondary transmission occurred in families and day care centers, and two secondary case patients developed fatal hemolytic uremic syndrome (Bell et al, 1994; Berkelman, 1994).
    a) An outbreak at a Virginia summer camp involving a total of 20 persons (18 campers; 2 counselors) who developed bloody diarrhea; one had hemolytic uremic syndrome. The only identified risk factor was consumption of rare (red or pink) ground beef cooked over campfires (Anon, 1995).
    b) Home-cooked ground beef has also resulted in food-borne outbreaks of E coli O157:H7 infection (Anon, 1994; Le Saux et al, 1993). One outbreak involving 21 cases (19 primary, 2 secondary) was thought to be due to insufficient cleaning and sanitizing of supermarket meat grinders, and also involved potential cross-contamination from other meats (Banatvala et al, 1996). An outbreak in Montana involved 17 persons who had consumed one brand of milk (Anon, 1995a).
    c) Roast beef served at a university graduation banquet was implicated in an unusually mild outbreak. Of 193 banquet attendees, 61 (32%) developed a mild gastrointestinal illness; only 2 were hospitalized and none developed hemolytic uremic syndrome or thrombocytopenic purpura, despite culture-proven E coli O157:H7 in the roast beef. CROSS-CONTAMINATION of SALAD was also a transmission vehicle (Rodrique et al, 1995).
    d) VENISON JERKY: Dried deer meet (venison jerky) was associated with an outbreak of a bloody diarrheal illness in Oregon. E coli O157:H7 was cultured from one victim's stool (Keene et al, 1997).
    e) DRY-CURED SALAMI: Dry-cured salami (which is NOT cooked) was responsible for 20 laboratory- confirmed cases of E coli O157:H7 infection (Anon, 1995b).
    3) APPLE JUICE: A large outbreak of 70 cases of E coli infection occurred due to contamination of unpasteurized apple juice in the fall of 1996 in California (26 cases), Colorado (5 cases), Washington (29 cases), and British Columbia (10 cases). Sixty-four of the 70 cases developed bloody diarrhea and 25 patients required hospitalization. Hemolytic uremic syndrome occurred in 14 patients, with 1 fatality. Thirteen of the 14 cases occurred in children 3 years or younger (Cody et al, 1999).
    e) WATERBORNE OUTBREAK
    1) A waterborne outbreak of E coli O157:H7 infection occurred in a small rural town with an unchlorinated drinking water supply. During the peak of the outbreak, bloody diarrhea was over 18 times more likely to occur in persons using municipal drinking water than in those using private well water. There were 243 cases, of whom 86 had bloody diarrhea, 32 were admitted to hospital, 2 developed hemolytic uremic syndrome, and 4 died. The outbreak occurred shortly after a number of water meters were replaced and two water mains had ruptured; the number of cases decreased after the water supply was chlorinated and residents were instructed to boil water before drinking (Swerdlow et al, 1992).
    2) An outbreak of E coli O157:H7 infection occurred at a county fair in upstate New York in August of 1999. E coli was isolated from 128 of 775 patients with suspected infections. Analysis of samples taken from 6 shallow wells on the fairgrounds (4 of which were unchlorinated) used as public water supply showed that one of the unchlorinated wells contained E coli. Two potential environmental sources of E coli contamination included a cow manure storage site approximately 80 feet from the contaminated well and a dormitory septic tank with a seepage pit approximately 36 feet from the contaminated well. This outbreak is considered the largest reported waterborne E coli O157:H7 outbreak in the United States (Bopp et al, 2003).
    f) AIRBORNE TRANSMISSION
    1) A case control study, involving patients who had attended a county fair in Ohio, identified an increased risk of E coli O157 infection in patients who had attended a dance in a building on the fairgrounds. Case-patients had laboratory-confirmed E coli O157 infection, hemolytic uremic syndrome, or bloody diarrhea within 7 days after attending the fair. Subjects in the control group attended the fair but did not have diarrhea. Six weeks after the fair ended, 24 of 54 specimens (44%) taken from the building, including isolates from the sawdust, rafters, railings, bleachers, walls, and doors, grew Shiga-toxin producing E coli O157:non-motile (NM). Forty-two weeks after the fair ended, the only specimens that continued to test positive for E coli O157:NM were all 6 of the sawdust specimens. Widespread contamination of the building indicated probable airborne dispersion of E coli O157, possibly from disturbance of the sawdust on the floor (Varma et al, 2003). The authors speculate that initial contamination of the building occurred following contact of the stools of an E coli O157-shedding animal with the building's sawdust.
    g) TIME TO ONSET
    1) Patients usually develop symptoms within hours or up to several days after ingestion (Schneideret al,null).
    h) DURATION
    1) Usually 5 to 10 days (Schneideret al,null).
    i) TARGET POPULATION
    1) Infants, young children, the elderly, and individuals who are immunosuppressed are at the greatest risk for severe infection (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    j) CHILD CARE CENTERS
    1) Person-to-person (secondary fecal-oral) transmission of E coli O157:H7 infection is common if infected children attend day care centers while still symptomatic (Belongia et al, 1993; Williams et al, 1997).
    a) In a Colorado child care center, 24 of 141 children developed symptoms of E coli O157:H7 infection. Thirteen of these children had positive stool cultures for the organism, 1 child developed hemolytic uremic syndrome (HUS), and 5 children were hospitalized (Williams et al, 1997).
    k) OCCUPATIONAL EXPOSURE
    1) A previously healthy 45-year-old laboratory technician who had been subculturing strains, performing agglutination reaction tests, and opening steamed broth cultures developed stool culture and serum antibody confirmed E. coli O157:H7 infection. There were no other risk factors and no documented laboratory mishaps. This patient subsequently developed severe renal failure requiring hemodialysis (Booth & Rowe, 1993).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) E. Coli O157:H7 is a member of the enterohemorrhagic E. coli family (EHEC) which produces Shiga toxin and are capable of producing bloody diarrhea. Sporadic cases of E. coli O157:H7 are usually a result of food-borne bacterial contamination, but can also be waterborne, airborne, person-to-person, animal-to-person and laboratory related.
    B) TOXIN
    1) Verotoxin and shiga-like toxin are closely related to the toxin produced by Shigella dysenteriae.
    C) EPIDEMIOLOGY
    1) Exposures are sporadic, but can result in severe toxicity. Undercooked or raw hamburger is the most common source of exposure. Enterohemorrhagic E. coli (EHEC) strain causes an estimated 70,000 cases of infection and 60 death annually in the USA.
    D) TARGET POPULATION
    1) Infants, young children, and the elderly are at the greatest risk for severe infections.
    E) MECHANISM
    1) Verotoxin breaks down vascular epithelium in small vessels in the gastrointestinal tract, causing hemorrhagic diarrhea. It may also affect the vascular endothelium in the glomerulus, causing hemolytic uremic syndrome.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) MILD TO MODERATE EFFECTS: Diarrhea, bloody diarrhea, abdominal pain, nausea and vomiting with occasional fever may occur, but all these effects may not always be present; absence of fever can often be diagnostic.
    b) SEVERE EFFECTS: Hemolytic-uremic syndrome (HUS) may develop about a week after diarrheal symptoms and is characterized by a triad of acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. Patients who also have neurologic dysfunction (ie, CNS depression, stroke, seizure), fever, and symptoms of HUS may also have thrombotic thrombocytopenic purpura (TTP). Hemorrhagic shock may also result in some cases.
    2) CHRONIC SYMPTOMS
    a) Patients who develop hemolytic uremic syndrome may have permanent renal failure. Patients may develop permanent neurologic dysfunction secondary to strokes.
    3) ROUTE OF EXPOSURE
    a) Undercooked or raw hamburger is the most common source of exposure. Other outbreaks have been associated with alfalfa sprouts, unpasteurized juice, dry-cured salami, lettuce, game meat, cheese curds, and raw milk.
    4) TIME TO ONSET
    a) Patients usually develop symptoms within hours or up to several days after ingestion.
    5) DURATION
    a) Usually 5 to 10 days.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Fever is usually low-grade or absent.
    0.2.5) CARDIOVASCULAR
    A) In children with hemolytic uremic syndrome (HUS), extrarenal complications have included myocardial dysfunction and pericardial effusions.
    0.2.6) RESPIRATORY
    A) In children with HUS, extrarenal complications have included adult respiratory distress syndrome (ARDS) and pleural effusions.
    0.2.7) NEUROLOGIC
    A) In children with HUS, extrarenal complications have included coma, stroke, hemiparesis, and seizures. Approximately 5% of patients who develop HUS have significant sequelae, including permanent neurological injury.
    0.2.8) GASTROINTESTINAL
    A) Up to 90% of children who develop hemolytic uremic syndrome (HUS) have a gastrointestinal prodromal syndrome.
    B) Common symptoms of E. coli O157:H7 infection are abdominal cramps, bloody or non-bloody diarrhea, nausea, vomiting, and fever.
    0.2.10) GENITOURINARY
    A) Hemolytic uremic syndrome (HUS) may occur in patients with E coli O157:H7 food poisoning, characterized by UREMIA and HEMOLYTIC ANEMIA. The risk of developing HUS has been reported to be 7% to 25% in children with E coli O157: H7 infection.
    1) Secondary case patients have developed fatal hemolytic uremic syndrome. One case of recurrent HUS following re-infection with E Coli O157:H7 has been reported.
    2) Based on case-control study of 12 fatal cases of HUS, WBC and hematocrit remained as independent predictors of death.
    0.2.13) HEMATOLOGIC
    A) Hemolytic uremic syndrome occurs in about 6% of patients, and is more common in children less than 5 years of age and the elderly. Thrombocytopenic purpura may also occur, but is more common in adults and the elderly.
    0.2.16) ENDOCRINE
    A) In children with HUS, extrarenal complications have included glucose intolerance.

Laboratory Monitoring

    A) Monitor serial complete blood counts, coagulation function, peripheral blood smears, serum electrolytes, renal function, urinalysis, and urine output very closely.
    B) Send stool for culture (inform the lab that you are concerned about E. Coli O157:H7) or test for verotoxin in stool.
    C) Food can be tested for the organism or the toxin, but this is only done as part of a public health investigation. Various assays can be utilized to detect the organism including enzyme-linked immunosorbent assay used on stool samples.
    D) Monitor for evidence of thrombotic, thrombocytopenic purpura (stroke, seizure or other neurologic deterioration, mucosal bleeding).
    E) Imaging including abdominal CT scans can also be utilized to help differentiate disease, along with direct bowel visualization with colonoscopy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) For a mild disease, treatment is symptomatic and supportive care, including intravenous fluids and antiemetics. Check stool for presence of E. coli O157:H7. Antibiotic therapy with antimotility agents may worsen the course of disease (especially in children under the age of 10). Monitor patients closely for the development of hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP).
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive care; however, these patients may require more aggressive critical care support, including aggressive airway management, central line placement for blood product replacement, and pressor support. Patients in renal failure may also require hemodialysis and treatment for hypertension. If patients develop signs of TTP, treat seizures or strokes with benzodiazepines and antiepileptics along with plasma exchange therapy if indicated. Antithrombotic agents or Shiga-binding toxin agents are not recommended.
    C) DECONTAMINATION
    1) Not indicated.
    D) AIRWAY MANAGEMENT
    1) Perform aggressive airway management as indicated by clinical presentation.
    E) ANTIDOTE
    1) None.
    F) HEMOLYTIC UREMIC SYNDROME
    1) Hemodialysis can be utilized in cases of renal failure from hemolytic uremic syndrome. Peritoneal dialysis may also be required. In one study, about 75% of patients who developed hemolytic uremic syndrome or thrombocytopenic purpura received red blood cell transfusions. About 50% of patients who developed hemolytic uremic syndrome or thrombocytopenic purpura required peritoneal or hemodialysis. Children have been treated with peritoneal dialysis, plasmapheresis, total parenteral nutrition (TPN), immune globulin, and platelet, fresh frozen plasma, and packed red blood cell transfusions. The efficacy of many of these treatments is unknown.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: All patients with hemorrhagic diarrhea or suspected E. coli O157:H7 should be referred to a healthcare facility for evaluation.
    2) OBSERVATION CRITERIA: Most patients should be admitted and closely monitored for the development of HUS or TTP.
    3) ADMISSION CRITERIA: Admit all patients with a high suspicion for infection.
    4) CONSULT CRITERIA: Infectious disease, nephrology, and critical care should all play a part in the management of these patients. Local public health departments should also be involved for monitoring of cases and incident management. HOTLINE: The United States Department of Agriculture (USDA) maintains a meat and poultry hotline for E coli O157:H7 and O111:H2 exposures -- (800) 535-4555 or (888) 674-6854.
    H) PITFALLS
    1) Administration of antibiotics and/or antimotility agents as these can worsen the course of disease, especially in children. Failure to consult your local infectious disease authority, so that they may investigate the report and identify the source of infection.
    I) DIFFERENTIAL DIAGNOSIS
    1) Inflammatory bowel disease, other EHEC bacteria, trauma, ulcers, and caustic or corrosive ingestion.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Although swimming in fecal-contaminated water has been associated with one outbreak of E. coli O157:H7 infection, this was more likely associated with SWALLOWING the water than with dermal contact.

Range Of Toxicity

    A) TOXICITY: The infectious dose of E. coli O157:H7 is very low; 10 to 100 organisms are capable of producing illness. Up to 15% of patients who develop hemorrhagic colitis may develop hemolytic uremic syndrome. In the elderly, the mortality rate of those who develop thrombotic thrombocytopenic purpura (hemolytic uremic syndrome, fever, and neurologic symptoms) may approach 50%. In general, patients who develop either hemolytic uremic syndrome or thrombotic thrombocytopenic purpura have a mortality rate of 3% to 5%

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) E. Coli O157:H7 is a member of the enterohemorrhagic E. coli family (EHEC) which produces Shiga toxin and are capable of producing bloody diarrhea. Sporadic cases of E. coli O157:H7 are usually a result of food-borne bacterial contamination, but can also be waterborne, airborne, person-to-person, animal-to-person and laboratory related.
    B) TOXIN
    1) Verotoxin and shiga-like toxin are closely related to the toxin produced by Shigella dysenteriae.
    C) EPIDEMIOLOGY
    1) Exposures are sporadic, but can result in severe toxicity. Undercooked or raw hamburger is the most common source of exposure. Enterohemorrhagic E. coli (EHEC) strain causes an estimated 70,000 cases of infection and 60 death annually in the USA.
    D) TARGET POPULATION
    1) Infants, young children, and the elderly are at the greatest risk for severe infections.
    E) MECHANISM
    1) Verotoxin breaks down vascular epithelium in small vessels in the gastrointestinal tract, causing hemorrhagic diarrhea. It may also affect the vascular endothelium in the glomerulus, causing hemolytic uremic syndrome.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) MILD TO MODERATE EFFECTS: Diarrhea, bloody diarrhea, abdominal pain, nausea and vomiting with occasional fever may occur, but all these effects may not always be present; absence of fever can often be diagnostic.
    b) SEVERE EFFECTS: Hemolytic-uremic syndrome (HUS) may develop about a week after diarrheal symptoms and is characterized by a triad of acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. Patients who also have neurologic dysfunction (ie, CNS depression, stroke, seizure), fever, and symptoms of HUS may also have thrombotic thrombocytopenic purpura (TTP). Hemorrhagic shock may also result in some cases.
    2) CHRONIC SYMPTOMS
    a) Patients who develop hemolytic uremic syndrome may have permanent renal failure. Patients may develop permanent neurologic dysfunction secondary to strokes.
    3) ROUTE OF EXPOSURE
    a) Undercooked or raw hamburger is the most common source of exposure. Other outbreaks have been associated with alfalfa sprouts, unpasteurized juice, dry-cured salami, lettuce, game meat, cheese curds, and raw milk.
    4) TIME TO ONSET
    a) Patients usually develop symptoms within hours or up to several days after ingestion.
    5) DURATION
    a) Usually 5 to 10 days.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Fever is usually low-grade or absent.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER is usually low-grade or absent (Boyce et al, 1995; Consensus Conference, 1995).

Cardiovascular

    3.5.1) SUMMARY
    A) In children with hemolytic uremic syndrome (HUS), extrarenal complications have included myocardial dysfunction and pericardial effusions.
    3.5.2) CLINICAL EFFECTS
    A) PERICARDIAL EFFUSION
    1) WITH POISONING/EXPOSURE
    a) In children with HUS, caused by E. coli O157:H7, extrarenal complications have included myocardial dysfunction and pericardial effusions (Brandt et al, 1994).

Respiratory

    3.6.1) SUMMARY
    A) In children with HUS, extrarenal complications have included adult respiratory distress syndrome (ARDS) and pleural effusions.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) In children with HUS, extrarenal complications have included adult respiratory distress syndrome (ARDS) and pleural effusions (Brandt et al, 1994).

Neurologic

    3.7.1) SUMMARY
    A) In children with HUS, extrarenal complications have included coma, stroke, hemiparesis, and seizures. Approximately 5% of patients who develop HUS have significant sequelae, including permanent neurological injury.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) About 25% of patients developing hemolytic uremic syndrome or thrombocytopenic purpura from E coli O157:H7 infection have neurological complications, including coma, hemiparesis, seizures, and stroke (Boyce et al, 1995; Brandt et al, 1994; Consensus Conference, 1995).
    b) SEQUELAE: Approximately 5% of patients who develop HUS have significant sequelae, including neurological injury (Boyce et al, 1995).

Gastrointestinal

    3.8.1) SUMMARY
    A) Up to 90% of children who develop hemolytic uremic syndrome (HUS) have a gastrointestinal prodromal syndrome.
    B) Common symptoms of E. coli O157:H7 infection are abdominal cramps, bloody or non-bloody diarrhea, nausea, vomiting, and fever.
    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH POISONING/EXPOSURE
    a) GI PRODROME: Up to 90% of children who develop hemolytic uremic syndrome (HUS) have a gastrointestinal (GI) prodromal syndrome (Siegler et al, 1994).
    1) This GI prodromal syndrome may vary in duration from 3 to 16 days (average: 5 to 7 days) (Taylor et al, 1986; Neill et al, 1987); clinical manifestations of HUS may follow a latent period during which the GI syndrome appears to be resolving (Tune et al, 1973).
    b) INCUBATION PERIOD: The typical incubation period is 3 to 4 days, but has been as short as 1 day and as long as 8 days (Boyce et al, 1995; Consensus Conference, 1995). Incubation periods of longer than 8 days may represent secondary person-to-person transmission (Boyce et al, 1995).
    c) MANIFESTATIONS: BLOODY DIARRHEA may occur in 35% to 90% of patients with E coli O157:H7 infection (Boyce et al, 1995). The illness typically presents with severe abdominal cramping and non-bloody diarrhea; stools often become bloody by the 2nd or 3rd day (Boyce et al, 1995; Consensus Conference, 1995; Anon, 1997; Keene et al, 1997).
    1) About 50% of patients also have nausea and vomiting (Boyce et al, 1995; Keene et al, 1997).
    2) Fever is usually low-grade or absent (Boyce et al, 1995).
    3) In the largest reported outbreak in the USA involving more than 500 persons who consumed ground beef from one fast-food restaurant chain, manifestations were: Abdominal cramps: 97%; bloody stools: 90%; fever: 63%; vomiting: 54% (Bell et al, 1994).
    4) In one outbreak involving 17 persons who consumed one brand of milk, manifestations were: Abdominal cramps: 100%; diarrhea: 94%; bloody stools: 89%; vomiting: 56%; fever: 40% (Anon, 1995a).
    5) In an outbreak involving 21 persons (19 primary, 2 secondary cases) involving ground beef, manifestations were: Abdominal pain: 95%; diarrhea: 95%; bloody stools: 81%; nausea: 76%; vomiting: 33%; fever: 24% (Banatvala et al, 1996).
    6) In one day care center fecal-oral person-to-person related outbreak, manifestations were: Hemolytic uremic syndrome: 17%; diarrhea: 17%; bloody stools: 50%; asymptomatic infection: 17% (Belongia et al, 1993).
    7) In an outbreak involving fresh-pressed untreated apple cider possibly contaminated with bovine fecal matter, manifestations were: Diarrhea: 96%; abdominal pain: 87%; bloody stools: 70%; vomiting: 35%; fever: 17% (Besser et al, 1993).
    8) In an outbreak of 70 cases (65 primary, 2 secondary, 3 undeterminable) due to contaminated unpasteurized apple juice, manifestations were: Bloody diarrhea: 91%; hemolytic uremic syndrome 20% (Cody et al, 1999).
    9) PERSON-TO-PERSON TRANSMISSION: In day care center person-to-person transmission, the mean interval between symptom onset in the primary case and the second case was 5 days (range: 1 to 15 days) (Belongia et al, 1993).
    a) FECAL BACTERIAL SHEDDING: In one day care center study, the duration of fecal bacterial shedding was a median of 17 days (range: 2 to 62 days), with 13% of children having fecal bacterial shedding for less than 7 days, 38% for more than 20 days, and the longest shedding period was 62 days (in a child administered amoxicillin 26 days after the onset of the acute diarrheal illness) (Belongia et al, 1993).
    10) HISTOPATHOLOGICAL CHANGES: generally include hemorrhage and edema in the lamina propria with areas of superficial focal necrosis (Mead & Griffin, 1998).
    11) LABORATORY STUDIES: Fecal leukocyte counts are less than 10 per high-powered field in most cases. "Thumb-printing", suggestive of edema and submucosal hemorrhage, particularly of the ascending and transverse colon, may be demonstrated with barium enema. Colonic mucosa often appears edematous and hyperemic when viewed with endoscopy and sometimes superficial ulceration or pseudomembranes are seen (Mead & Griffin, 1998).
    12) COMPLICATIONS: In children with HUS, extrarenal complications have included COLONIC NECROSIS and PANCREATITIS (Brandt et al, 1994). Diarrhea-associated HUS is the most common cause of acute renal failure in children, which is most often caused by Shiga toxin-producing strains of E coli (Trachtman et al, 2003).

Genitourinary

    3.10.1) SUMMARY
    A) Hemolytic uremic syndrome (HUS) may occur in patients with E coli O157:H7 food poisoning, characterized by UREMIA and HEMOLYTIC ANEMIA. The risk of developing HUS has been reported to be 7% to 25% in children with E coli O157: H7 infection.
    1) Secondary case patients have developed fatal hemolytic uremic syndrome. One case of recurrent HUS following re-infection with E Coli O157:H7 has been reported.
    2) Based on case-control study of 12 fatal cases of HUS, WBC and hematocrit remained as independent predictors of death.
    3.10.2) CLINICAL EFFECTS
    A) UREMIA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea-associated HUS may result in acute renal failure. Most cases are due to an intestinal infection with Shiga toxin producing strains of E Coli (O157:H7) (Trachtman et al, 2003; Siegler et al, 1994; Anon, 1997). It is characterized by uremia and hemolytic anemia. Up to 40% of patients may require temporary dialysis and 20% of patients can develop serious extrarenal events (Trachtman et al, 2003). It has a mortality rate greater than 3% to 5% (Trachtman et al, 2003; Boyce et al, 1995; Consensus Conference, 1995).
    b) HUS is usually diagnosed on days 2 to 14 following the onset of the diarrheal illness (Boyce et al, 1995). It occurs more often in children less than 5 years of age (especially in children less than 2 years of age) and in the elderly (Boyce et al, 1995; Consensus Conference, 1995).
    c) Secondary case patients have developed fatal HUS(Bell et al, 1994).
    d) RECURRENT HUS: One case of recurrent HUS following re-infection with E Coli O157:H7 has been reported (Siegler et al, 1993).
    e) RISK FACTORS
    1) RISK FACTORS: Diarrhea-associated HUS is the most common cause of acute renal failure in previously healthy children worldwide (Garg et al, 2003; Trachtman et al, 2003).
    a) Other potential risk factors include: treatment with antimotility drugs, elevated WBC, fever, severe gastrointestinal prodrome, anuria in the early stages of the infection, and bloody diarrhea (Boyce et al, 1995).
    f) INCIDENCE RATE
    1) The risk of developing HUS has been reported to be 7% to 25% in children with E coli O157:H7 infection (Belongia et al, 1993). Four of 23 patients with E coli O157:H7 infection associated with fresh-pressed untreated apple cider, possibly contaminated with bovine feces, developed HUS (Besser et al, 1993).
    g) PROGNOSIS
    1) SEQUELAE: Approximately 5% of patients who develop HUS have significant sequelae, including end stage kidney disease (ESRD) (Boyce et al, 1995). Although serum creatinine levels may return to normal in HUS survivors, persistently low glomerular filtration rates (GFRs) have been found in some (Brandt et al, 1994).
    2) CASE SERIES: A case-control study of 12 fatal cases of HUS demonstrated prodromal lethargy, oligoanuria, or seizures and white blood cell counts (WBC) greater than 20 X 10(9)/L or hematocrit greater than 23% to be predictive of poor prognosis and death. After multivariate analysis, only WBC and hematocrit remained as independent predictors of death (Oakes et al, 2006).
    3) META-ANALYSIS: In a systematic review of 49 studies (i.e., case series, cohort studies and randomized controlled trials) with 3476 patients and a mean follow-up of 4.4 years from 1950 to 2001, death or ESRD occurred in about 12% of patients with diarrhea-associated HUS, and 25% of survivors demonstrated long-term renal sequelae. Although the authors suggest some caution with interpreting results because of large between-study variability with wide ranging heterogeneity, death or permanent ESRD ranged from 0% to 30% with most cases occurring during the acute phase of HUS. The severity of acute illness, especially CNS symptoms (coma, seizures, or stroke), was associated with a worse long term prognosis in both univariate and multivariate analyses. In addition, the need for initial dialysis was also strongly associated with a worse outcome. It was noted that outcome was improved with prompt recognition and referral to specialized or higher level of medical care. During the acute phase of diarrhea-associated HUS, treatments such as corticosteroids, antiplatelet agents, anticoagulant therapy, and thrombolytics were not clearly shown to be effective (Garg et al, 2003).
    4) HUS developed in 1 to 40% of patients with E coli O157:H7 infection (22% in nursing home residents; 8% in a day care center; and 40% in a residence home for handicapped persons) (Robson & Leung, 1993).
    5) CASE SERIES: In the largest reported outbreak in the USA involving more than 500 persons who consumed ground beef from one fast-food restaurant chain, HUS developed in 9% of patients, and three of these patients died from complications (Bell et al, 1994).
    6) CASE SERIES: In a large outbreak of 70 cases in the western US and Canada due to contaminated unpasteurized apple juice, HUS developed in 14 patients (20%), with 1 fatality (Cody et al, 1999).
    B) CHRONIC RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) In a study of 387 children with HUS, patients who did not have prodromal diarrhea and did not have evidence of Shiga toxin-producing E coli (STEC) infection were more likely to go on to develop chronic renal failure or end stage renal disease. Only 34.5% (95% CI 18.6 to 54.3) of patients who did not have prodromal diarrhea and did not have STEC recovered normal renal function. In comparison, recovery rates were 65% to 75% in patients who had either prodromal diarrhea only (65.4% recovery, CI 51.3% to 77.4%), STEC infection (66.5% recovery, 95% CI 46% to 82.8%), or both prodromal diarrhea and STEC infection (75.8% recovery, CI 68.2% to 82.1%). A leukocyte count more than 2 standard deviations above normal, age less than 3 years, and the presence of CNS involvement were not associated with an increased risk of chronic renal failure in this study (Gianviti et al, 2003).
    C) URINARY TRACT INFECTIOUS DISEASE
    1) WITH POISONING/EXPOSURE
    a) Cases of HUS in patients with urinary tract infection with verotoxin-producing E coli (strains OX3:h2 and O145:H25) and without diarrheal illness have been reported rarely (Scheutz et al, 2000).

Hematologic

    3.13.1) SUMMARY
    A) Hemolytic uremic syndrome occurs in about 6% of patients, and is more common in children less than 5 years of age and the elderly. Thrombocytopenic purpura may also occur, but is more common in adults and the elderly.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Hemolytic uremic syndrome (HUS) may occur in patients with E coli O157:H7 food poisoning (Siegler et al, 1994; Morabito et al, 1998), and is characterized by UREMIA and HEMOLYTIC ANEMIA. HUS is usually diagnosed on days 2 to 14 following the onset of the diarrheal illness (Boyce et al, 1995). It occurs more often in children less than 5 years of age (especially in children less than 2 years of age) and in the elderly, and has a mortality rate greater than 3% to 5% (Boyce et al, 1995; Consensus Conference, 1995).
    b) Secondary case patients have developed fatal hemolytic uremic syndrome (Morabito et al, 1998; Bell et al, 1994).
    c) RISK FACTORS other than patient age associated with HUS include: treatment with antimotility drugs, elevated WBC, fever, severe gastrointestinal prodrome, anuria in the early stages of the infection, and bloody diarrhea (Boyce et al, 1995).
    d) HUS developed in 1% to 40% of patients with E coli O157:H7 infection (22% in nursing home residents; 8% in a day care center; and 40% in a residence home for handicapped persons) (Robson & Leung, 1993).
    e) CASE REPORT: An 8-month-old boy from Brazil, with a history of an acute diarrheal prodromal illness 3 weeks prior to admission, subsequently developed respiratory failure, hemolytic anemia, renal failure, and thrombocytopenia, indicative of hemolytic uremic syndrome. Laboratory analysis identified Shiga toxin-producing E Coli O26:H11 as the causative agent. The patient recovered following treatment with fresh frozen plasma and peritoneal dialysis (Guth et al, 2002).
    B) THROMBOCYTOPENIC PURPURA
    1) WITH POISONING/EXPOSURE
    a) This condition occurs more often in adults and the elderly (Boyce et al, 1995). It has all the features of HUS, but the kidney injury is usually less severe and the neurological manifestations more prominent (Boyce et al, 1995). Thrombocytopenia is thought to result from trapping of platelets in involved organs and removal by the liver and spleen (Mead & Griffin, 1998).
    C) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) In a chart review of 369 children with E coli O157:H7 enteritis, those who developed HUS presented with greater total leukocyte, polymorphonuclear leukocyte and monocyte counts that children who did not progress to HUS (Buteau et al, 2000).
    b) PROGNOSIS
    1) CASE SERIES: A case-control study of 12 fatal cases of HUS demonstrated white blood cell counts (WBC) greater than 20 X 10(9)/L or hematocrit >23% and prodromal lethargy, oligoanuria, or seizures to be predictive of poor prognosis and death. After multivariate analysis, only WBC and hematocrit remained as independent predictors of death (Oakes et al, 2006).
    D) COAG./BLEEDING TESTS ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) In a prospective study of 53 children with E coli O157:H7 infection, children who went on to develop HUS had higher plasma concentrations of various markers indicating activation of the clotting cascade (prothrombin fragments 1 and 2, tissue plasminogen activator (t-PA) antigen, t-PA-plasminogen activated inhibitor type 1 complex, and D-dimer) (Chandler et al, 2002).

Endocrine

    3.16.1) SUMMARY
    A) In children with HUS, extrarenal complications have included glucose intolerance.
    3.16.2) CLINICAL EFFECTS
    A) ABNORMAL GLUCOSE TOLERANCE TEST
    1) WITH POISONING/EXPOSURE
    a) In children with HUS, extrarenal complications have included glucose intolerance (Brandt et al, 1994).

Laboratory Monitoring

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) On barium enema examination, a thumbprinting pattern may be seen in the ascending and transverse colon due to edema and submucosal hemorrhage (Boyce et al, 1995).
    B) CT RADIOGRAPH
    1) Circumferential thickening of the colonic wall and adjacent small bowel loops, inflammatory changes in the mesentery, ascites, and involvement of the retroperitoneum have been seen on CT scan (Tanaka et al, 1992).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) An enzyme-linked immunosorbent assay (ELISA) can rapidly detect E. coli O157:H7 in stool specimens (Park et al, 1996). A direct immunofluorescent antibody stain technique can identify the organism directly from fecal smears (Park et al, 1994).
    2) Pulsed-field gel electrophoresis (PFGE) can be used to subtype E. coli O157:H isolates (Banatvala et al, 1996).
    3) E. coli O157 can be determined in stool specimens or by IgG or IgM O157 lipopolysaccharide (LPS) seropositivity (Banatvala et al, 1996).
    4) STOOL CULTURES - SORBITOL-MACCONKEY MEDIUM: Stool cultures for identification of E. coli O157:H7 must use Sorbitol-MacConkey medium; this particular test may NOT be a routine laboratory stool culture screening protocol, and SCREENING FOR E. COLI O157:H7 MAY NEED TO BE SPECIFICALLY ORDERED BY THE CLINICIAN (Berkelman, 1994; Boyce et al, 1995; Consensus Conference, 1995).
    a) This strain is more often isolated from stools with visible blood (Berkelman, 1994).
    b) This infectious agent is easily MISSED by stool culturing using standard media (Berkelman, 1994).
    c) Non-O157 serotypes of E. coli have none of the biochemical markers, such as lack of sorbitol fermentation, to currently facilitate screening in laboratories (Mead & Griffin, 1998). Newly available assays to test stool specimens for Shiga toxin-producing organisms may facilitate diagnosis of these non-O157 serotypes.
    5) Multiplex PCR assays of shiga toxigenic E. coli (STEC) in serogroups O111 and O157 have been developed for identification of the appropriate genotype in primary fecal cultures (Paton & Paton, 1998).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serial complete blood counts, coagulation function, peripheral blood smears, serum electrolytes, renal function, urinalysis, and urine output very closely.
    B) Send stool for culture (inform the lab that you are concerned about E. Coli O157:H7) or test for verotoxin in stool.
    C) Food can be tested for the organism or the toxin, but this is only done as part of a public health investigation. Various assays can be utilized to detect the organism including enzyme-linked immunosorbent assay used on stool samples.
    D) Monitor for evidence of thrombotic, thrombocytopenic purpura (stroke, seizure or other neurologic deterioration, mucosal bleeding).
    E) Imaging including abdominal CT scans can also be utilized to help differentiate disease, along with direct bowel visualization with colonoscopy.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) In high-risk patients (young children and the elderly), monitor for development of complications with peripheral blood smears and complete blood counts (Boyce et al, 1995).
    B) OTHER
    1) GLOMERULAR FILTRATION RATE (GFR): In hemolytic-uremic syndrome survivors, decreased GFRs have been documented in patients whose serum creatinine returned to normal. Accurate measurement of GFR by iothalamate clearance or other tests should be used in long-term follow-up of such patients (Brandt et al, 1994).
    4.1.3) URINE
    A) URINALYSIS
    1) In high-risk patients (young children and the elderly), monitor for complications with urinalysis (Boyce et al, 1995).
    4.1.4) OTHER
    A) OTHER
    1) FECAL
    a) Although only 1/3 of patients may have fecal leukocytes (Berkelman, 1994), methylene blue staining of stool or rectal mucous specimens may detect fecal leukocytes in approximately 65% of these patients (Tarr et al, 1992).
    b) Fecal organism stool shedding may last for a mean of 29 days (range: 11 to 57 days) (Williams et al, 1997).
    2) MONITORING
    a) COLONOSCOPY: The colonic mucosa has an edematous, hyperemic appearance, sometimes having superficial ulcerations, when visualized by colonoscopy (Boyce et al, 1995).
    b) On RENAL DOPPLER ULTRASOUND, urinary tract dilation, a hyperechoic urinary bladder (consistent with a blood clot), hyperechoic enlarged kidneys, and internal echoes consistent with blood or pus were seen in a 13-day-old neonate with hemolytic-uremic syndrome (Figueras et al, 1995).
    c) E. coli O157:H7 has been cultured from raw caribou meat in a remote Canadian village, from deer feces in Texas, and from water in a Pennsylvania reservoir in an area where there were no cattle and deer were abundant (Keene et al, 1997).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Admit all patients with a high suspicion for infection.
    B) PEDIATRIC PATIENTS: In one outbreak involving 3 children with HUS, one developed peritonitis and another developed catheter-related sepsis; the duration of hospitalization was from 11 to 41 days (Belongia et al, 1993).
    6.3.1.2) HOME CRITERIA/ORAL
    A) All patients with hemorrhagic diarrhea or suspected E. coli O157:H7 should be referred to a healthcare facility for evaluation.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Infectious disease, nephrology, and critical care should all play a part in the management of these patients. Local public health departments should also be involved for monitoring of cases and incident management.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Most patients should be admitted and closely monitored for the development of HUS or TTP.

Monitoring

    A) Monitor serial complete blood counts, coagulation function, peripheral blood smears, serum electrolytes, renal function, urinalysis, and urine output very closely.
    B) Send stool for culture (inform the lab that you are concerned about E. Coli O157:H7) or test for verotoxin in stool.
    C) Food can be tested for the organism or the toxin, but this is only done as part of a public health investigation. Various assays can be utilized to detect the organism including enzyme-linked immunosorbent assay used on stool samples.
    D) Monitor for evidence of thrombotic, thrombocytopenic purpura (stroke, seizure or other neurologic deterioration, mucosal bleeding).
    E) Imaging including abdominal CT scans can also be utilized to help differentiate disease, along with direct bowel visualization with colonoscopy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Decontamination is not indicated.
    6.5.2) PREVENTION OF ABSORPTION
    A) Decontamination is not indicated.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor serial complete blood counts, coagulation function, peripheral blood smears, serum electrolytes, renal function, urinalysis, and urine output very closely.
    2) Send stool for culture (inform the lab that you are concerned about E. coli O157:H7) or test for verotoxin in stool.
    3) Food can be tested for the organism or the toxin, but this is only done as part of a public health investigation. Various assays can be utilized to detect the organism including enzyme-linked immunosorbent assay used on stool samples.
    4) Monitor for evidence of thrombotic, thrombocytopenic purpura (stroke, seizure or other neurologic deterioration, mucosal bleeding).
    5) Imaging including abdominal CT scans can also be utilized to help differentiate disease, along with direct bowel visualization with colonoscopy.
    B) ANTIBIOTIC
    1) Antibiotic therapy may be associated with an increased risk of infection and a resultant poor prognosis in elderly persons (Carter et al, 1987).
    a) LACK OF EFFICACY: In 47 patients (with susceptible E. coli infections) entered into a prospective randomized controlled clinical trial, treatment with trimethoprim-sulfamethoxazole had NO SIGNIFICANT EFFECT on the progression of symptoms, fecal excretion of the organism, or incidence of hemolytic uremic syndrome (Proulx et al, 1992).
    b) CASE REPORT: In one child, administration of antibiotics prior to the onset of diarrheal illness did not prevent the development of HUS (Goldoft, 1999).
    2) INCREASED RISK OF HUS: In a prospective cohort study of children younger than 10 years of age with diarrhea caused by E. coli O157:H7, antibiotics increased the risk of HUS (Wong et al, 2000).
    3) Empirical antibiotic prescription (particularly with trimethoprim-sulfamethoxazole) in the treatment of bloody diarrhea subsequently proven to be due to E coli O157:H7 may predispose the patient to the development of hemolytic uremic syndrome (HUS) (Tarr et al, 1988; Olah & Gee, 1990; Cimolai & Carter, 1990; Cimolai et al, 1988; Pavia et al, 1990).
    a) However, in one study, administration of antibiotics during the prodromal phase was associated with milder acute disease and a good clinical outcome (Martin et al, 1990).
    b) Administration of antibiotics may eliminate competing bowel flora and predispose to overgrowth of E coli O157:H7, especially when this E coli serotype is resistant to the administered antibiotic(s).
    c) Sublethal damage to or lysis of the infecting E coli serotype may liberate bacterial cytotoxins into the gut lumen, which could precipitate hemolytic uremic syndrome (HUS) (Tarr et al, 1988).
    4) ANTIBIOTIC RESISTANCE: Of 176 strains of E. coli O157:H7 isolated between 1989 and 1991, 7.4% were resistant to streptomycin, sulfisoxazole, and tetracycline (Kim et al, 1994).
    C) HEMOLYTIC UREMIC SYNDROME
    1) Hemodialysis can be utilized in cases of renal failure from hemolytic uremic syndrome.
    2) About 50% of patients who develop hemolytic uremic syndrome or thrombocytopenic purpura require peritoneal or hemodialysis (Boyce et al, 1995).
    3) PEDIATRIC PATIENTS: Children have been treated with peritoneal dialysis, plasmapheresis, total parenteral nutrition (TPN), immune globulin, and platelet, fresh frozen plasma, and packed red blood cell transfusions. The EFFICACY of many of these treatments is UNKNOWN (Belongia et al, 1993; Boyce et al, 1995; Consensus Conference, 1995; Boyce et al, 1995).
    D) TRANSFUSION
    1) About 75% of patients who develop hemolytic uremic syndrome or thrombocytopenic purpura receive red blood cell transfusions (Boyce et al, 1995).
    2) PEDIATRIC PATIENTS: Children have been treated with peritoneal dialysis, plasmapheresis, total parenteral nutrition (TPN), immune globulin, and platelet, fresh frozen plasma, and packed red blood cell transfusions. The EFFICACY of many of these treatments is UNKNOWN (Belongia et al, 1993; Boyce et al, 1995; Consensus Conference, 1995; Boyce et al, 1995).
    E) CONTRAINDICATED TREATMENT
    1) ANTIMOTILITY DRUGS: These agents are likely CONTRAINDICATED, as their administration is a RISK FACTOR for development of the hemolytic uremic syndrome (Boyce et al, 1995; Olah & Gee, 1990; Pavia et al, 1990; Robson et al, 1990; Cimolai et al, 1988; Cimolai & Carter, 1990). ANTIBIOTICS are generally NOT INDICATED (Boyce et al, 1995).
    F) EXPERIMENTAL THERAPY
    1) EXPERIMENTAL VACCINE: A polyvalent E coli vaccine has been tested in human volunteers and found to be safe (Cross et al, 1994). It is efficacious in increasing antibody levels against E coli, but is NOT GENERALLY AVAILABLE (Cross et al, 1994; Stephenson, 1998).
    2) CASE REPORT: Plasma exchange was used to treat two patients with HUS (Downes et al, 2001). This therapy is of unproven benefit.
    3) ORAL SHIGA TOXIN-BINDING AGENT/LACK OF EFFECT: In a multicenter, randomized, double-blind, placebo-controlled trial of 145 children aged 6 months to 18 years with diarrhea-associated HUS, oral therapy with a Shiga toxin-binding agent was found to be ineffective at reducing the severity of symptoms or improving the overall clinical course. Prevalence rates of death or serious extrarenal events (described as central nervous system or cardiovascular complications) were similar in the treatment and control groups:18% vs 20% in the binding-agent and placebo-treated groups, respectively. The need for dialysis was also found to be similar, 42% in the binding agent group as compared to 39% in the placebo group. The authors suggested several possible reasons for the lack of effect which included a delay in treatment, impaired gastric motility limiting the delivery of the drug, and the interaction between Shiga toxins and gastrointestinal epithelium may limit the drug's ability to bind Shiga toxin in vivo (Trachtman et al, 2003).
    4) META-ANALYSIS: In a systematic review of 49 studies (ie, case series, cohort studies and randomized controlled trials) with 3476 patients and a mean follow-up of 4.4 years from 1950 to 2001, treatments such as corticosteroids, antiplatelet agents, anticoagulant therapy, and thrombolytics were not clearly shown to be effective during the acute phase of diarrhea-associated HUS (Garg et al, 2003).

Dermal Exposure

    6.9.2) TREATMENT
    A) SUPPORT
    1) POTENTIAL TRANSMISSION CONSIDERATIONS
    a) ETIOLOGY: Although swimming in fecal-contaminated water has been associated with one outbreak of E. coli O157:H7 infection, this was more likely associated with SWALLOWING the water than with dermal contact (Keene et al, 1994).
    b) CASE SERIES: E. coli O157:H7 infection resulting in 56 illnesses and 19 hospitalizations among school children occurred after farm visits in Pennsylvania and Washington. E coli O157 with a PFGE pattern the same as the infected children was isolated from 13% (28/216) of the cattle at the Pennsylvania farm. Stools from five animals were checked at the Washington location. All five samples were negative for E coli O157. This was the first report of direct transmission from farm animals to humans in the United States. Risk factors included contact with cattle and activities that promoted hand to mouth contact such as nailbiting. Handwashing prior to eating appeared to have a protective effect (Anon, 2001).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ADULT
    1) OCCUPATIONAL EXPOSURE: A previously healthy 45-year-old laboratory technician who had been subculturing strains, performing agglutination reaction tests, and opening steamed broth cultures developed stool culture and serum antibody confirmed E coli O157:H7 infection. There were no other risk factors and no documented laboratory mishaps or lapses in good laboratory techniques. This patient subsequently developed severe renal failure requiring treatment with hemodialysis (Booth & Rowe, 1993).
    B) PEDIATRIC
    1) FARM VISIT/FARM ANIMAL CONTACT
    a) A 3-year-old child developed hemorrhagic colitis after visiting a farm visitor's center in Wales. The mode of E coli O157:H7 infection transmission was possibly by animal feces carried on the coat of a dog which the child petted (Parry et al, 1995).
    b) Two children who developed hemolytic uremic syndrome following infection with E coli O157:H7 appeared to have contracted the illness following exposure to farm animals (Trevena et al, 1996).
    c) Direct transmission between infected calves and a 13-month-old child on a Canadian farm has been reported (Renwick et al, 1993).

Range Of Toxicity

Summary

    A) TOXICITY: The infectious dose of E. coli O157:H7 is very low; 10 to 100 organisms are capable of producing illness. Up to 15% of patients who develop hemorrhagic colitis may develop hemolytic uremic syndrome. In the elderly, the mortality rate of those who develop thrombotic thrombocytopenic purpura (hemolytic uremic syndrome, fever, and neurologic symptoms) may approach 50%. In general, patients who develop either hemolytic uremic syndrome or thrombotic thrombocytopenic purpura have a mortality rate of 3% to 5%

References

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