eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Escherichia Coli Infections

Author: Archana Chatterjee, MD, PhD, Professor of Pediatrics, Medical Microbiology and Immunology, and Pharmacy, Division of Pediatric Infectious Diseases, Chief of Division of Pediatric Infectious Diseases, Creighton University School of Medicine; Hospital Epidemiologist and Medical Director of Infection Control, Children's Hospital
Coauthor(s): Catherine O'Keefe, DNP, APRN, Assistant Professor of Nursing, Pediatric Nurse Practitioner, Pediatric Infectious Diseases, Creighton University School of Nursing; Sara L Cuthill, MD, Fellow, Developmental and Behavioral Pediatrics, Departmental and Behavioral Pediatrics, Interstate Medical Office East; Meera Varman, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Infectious Diseases, Creighton University School of Medicine
Contributor Information and Disclosures

Updated: Jan 8, 2009

Introduction

Background

Escherichia coli, a facultatively anaerobic gram-negative bacillus, is a major component of the normal intestinal flora and is ubiquitous in the human environment. First described in 1885, E coli has become recognized as both a harmless commensal and a versatile pathogen.

Pathophysiology

In contrast to the essential and beneficial role of most E coli isolates in the human intestine, pathogenic E coli are responsible for a broad spectrum of human disease. E coli has emerged as an important cause of diarrheal illness, with diverse phenotypes and pathogenic mechanisms. Hemolytic-uremic syndrome (HUS) is a potentially devastating consequence of enteric infection with specific E coli strains. E coli is also a commonly identified cause of urinary tract infections (UTIs), as well as neonatal sepsis and meningitis.

Uropathogenic E coli (UPEC) has the ability to colonize the uroepithelium by means of surface fimbriae. Although only partially understood, UPEC has been suggested to cause either direct cellular damage or direct invasion of the renal epithelial cells.1

Five pathotypes have of diarrheagenic E coli have been recognized; each pathotype has a distinct pathogenesis. The pathotypes are as follows:

  • Enterotoxigenic E coli (ETEC)
  • Enterohemorrhagic E coli (EHEC)
  • Enteropathogenic E coli (EPEC)
  • Enteroinvasive E coli (EIEC)
  • Enteroaggregative E coli (EAEC)
ETEC adheres to the small bowel mucosa by means of several different fimbrial colonization factor antigens (CFAs). Once colonization is achieved, one or both of the enterotoxins are released (ie, heat labile toxin [LT] and heat stable toxin [ST]). These toxins draw fluid and electrolytes from the small bowel mucosa. ST is reportedly the more virulent of the toxins.1 LTs are closely related in structure and function to the enterotoxin expressed by Vibrio cholerae. Immunity develops to ETEC surface antigens, confining most disease to immunologically naïve travelers and weaning infants.

EHEC, also known as Shiga-toxin producing E coli (STEC), induces an attaching and effacing (AE) lesion in the large bowel. Once established in the colon, EHEC releases one or more toxins known as Shiga-like toxin (Stx). Stx is related to the Shiga toxin of Shigella dysenteriae and is cytotoxic to the vascular endothelium. The systemic circulation of Stx accounts for the potential development of HUS but is not required for EHEC hemorrhagic colitis to occur. E coli O157:H7 is the most virulent of the EHEC.2,1

HUS consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. HUS typically develops in the second week of illness (range, 2-14 d), often after the diarrhea has resolved. Patients present with pallor, weakness, irritability, and oliguria or anuria.

EPEC also produce AE lesions; however, it does so in the absence of Shiga toxin production. The pathogenesis includes colonization of the small intestine, followed by the formation of AE lesions and a subsequent net secretory state.2,1

The pathogenesis of EIEC mimics that of the Shigella species. The EIEC invades the large bowel epithelial cells, producing secretogenic enterotoxins and subsequent colonic epithelial cell death. These enterotoxins are typically lactose nonfermenting and are responsible for the local colonic inflammatory response.2,1 Invasiveness derives from a virulence plasmid closely related to that possessed by Shigella species.

EAEC adheres to the small and large bowel by means of aggregative adherence fimbriae (AAFs), and colonization ensues. This colonization produces enterotoxins and cytotoxins, which, in turn, damages the intestinal mucosa.2,1

Systemic infections caused by E coli are frequently seen in neonates either by means of vertical or horizontal transmission. The characteristic serotype of this pathogenic E coli displays the K1 antigen, which is responsible for 40% of the cases of bacteremia and 80% of the cases of meningitis caused by E coli.2 The virulent activity of the K1 antigen reduces the ability of the host to develop an antibody specific response and to activate the alternative complement system. In addition, S fimbriae have been associated with many of the E coli of patients with CNS infections. S fimbriae enhance the ability of E coli to adhere to vascular epithelium as well as the spread of the bacterium within the CNS.1

Frequency

United States

Statistics on pathogenic E coli strains reflect increasing recognition and surveillance over the past 2 decades. According to the Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Disease Control and Prevention (CDC) Emerging Infections Program, in 2007, the incidence of Shiga-toxin–producing E coli (O157) was 1.20 cases per 100,000 population, and the incidence of Shiga-toxin–producing E coli (non-O157) was 0.57 cases per 100,000 population). Since the beginning of surveillance in 1996, the incidence of Shiga-toxin–producing E coli (O157) has decreased 25%.3

International

Many strains of diarrheagenic E coli primarily affect developing nations due to inadequate sanitary conditions. Statistics on the prevalence of the strains vary by location and surveillance activity. Worldwide, enterotoxigenic E coli are estimated to cause more than 600 million cases of diarrhea annually and 700,000 deaths in children younger than 5 years.

ETEC is the most common enteropathogen in developing countries, accounting for approximately 210 million diarrhea episodes and approximately 380,000 deaths.4,5 Traveler’s diarrhea is primarily caused by ETEC; thus, persons traveling to endemic areas regularly import the pathogen to the developed world.6,7,8  

Mortality/Morbidity

Several E coli pathotypes have been implicated in chronic diarrhea among severely immunocompromised patients (eg, patients with human immunodeficiency virus [HIV]).9,10,11  ETEC causes more dehydrating diarrhea cases among infants in developing countries than any other pathotype.12,13

Age

People of any age can become infected. Very young individuals and the elderly are the most likely groups to become seriously ill and to develop HUS.

Clinical

History

Symptoms of Escherichia coli infection may be subtle and nonspecific in infants and young children. Even in older children, symptoms may resemble those of common viral illnesses, leading to missed or delayed diagnosis. A thorough history, including any history of a prior urinary tract infection (UTI), and thoughtful analysis of the information provided is essential. Pertinent details can guide further diagnostic investigation.

  • Neonates and infants with UTIs, bacteremia, or sepsis may present with the following symptoms:
    • Fever
    • Hypothermia
    • Jaundice
    • Respiratory distress
    • Apnea
    • Poor feeding
    • Vomiting
    • Diarrhea
    • Fussiness
    • Irritability
    • Lethargy
  • Particularly in young infants, meningitis may be present without overt signs attributable to the CNS.
  • Infants with histories of prematurity, low birth weight, difficult or prolonged labor, intrapartum maternal fever, or antibiotic administration may have higher risk for serious bacterial infection.
  • Older children with bacterial enteritis or UTI may have fever, vomiting, abdominal pain, or diarrhea with or without blood or mucus. In young children with UTI, urinary symptoms (eg, frequency, urgency, dysuria) vary and are often not present; daytime urinary incontinence or new onset of bedwetting may be more suggestive of UTI. Always consider UTI in the differential diagnosis of fever without apparent source. Constipation is not a symptom of UTI but is instead associated with incomplete voiding and urinary stasis. Constipation may predispose a child to UTI and may complicate treatment. In children with recurrent UTI, aggressive treatment of constipation may reduce subsequent UTIs.
  • In cases of diarrheal illness, determine stool frequency (ie, number of stools or diaper changes in past 12-24 h), appearance (eg, loose, watery), and presence of blood or mucus. Inquire about a history of exposure to a child with bloody diarrhea or a known local outbreak of hemorrhagic colitis. Specific quantification of stool number and character is important because parents often describe a single loose stool as diarrhea. Also, remember various substances (eg, Kool-Aid, other foods containing red dyes) may tint stools red. Guaiac testing confirms the presence of blood.
    • Enterotoxigenic E coli (ETEC) diarrhea is watery without blood, mucous, or fecal leukocytes and ranges from mild to severe.
    • Enterohemorrhagic E coli (EHEC) disease ranges from mild watery diarrhea to severe hemorrhagic colitis, often accompanied by abdominal cramping and vomiting. Diarrhea becomes bloody in 1-2 days in most patients but is usually not associated with fecal leukocytes. Fever is present in about a third of cases.
    • Enteroinvasive E coli (EIEC) causes watery diarrhea, dysentery, fever, vomiting, painful abdominal cramps, and tenesmus. Stools often contain blood and leukocytes.
    • Enteropathogenic E coli (EPEC) and Enteroaggregative E coli (EAEC) cause watery diarrhea and dysentery. The resultant acute watery diarrhea may cause dehydration or become chronic and lead to failure to thrive.
  • Evaluate the ability of patients who are vomiting or at risk of dehydration to take and tolerate fluids orally. Assess frequency of urination (ie, last void or wet diaper, number of voids in past 8-24 h). Vomiting may occur with ETEC.
  • If the patient is experiencing abdominal pain, assess pain for the following features:
    • Severity and character (eg, sharp, dull, cramplike)
    • Location
    • Radiation
    • Duration
    • Nature (eg, constant, intermittent)
    • Aggravating and relieving factors

Physical

The child's overall appearance and behaviors (eg, alert, playful, fussy but consolable, lethargic, irritable, toxic) are valuable because these factors may direct diagnostic and therapeutic choices and influence decisions regarding outpatient management or admission.

  • Among the aspects of general appearance to consider are alertness, activity, tone, age-appropriate interaction, and whether the child can be consoled. Observe, for example, whether the child explores the room, clings to the parent, or lies still on the table.
  • Evidence of dehydration may be present in patients with bacterial enteritis. Ill appearance, tachycardia, and dry mucous membranes suggest significant volume depletion. Fontanelle and/or eyes may be sunken, but skin turgor change is a late finding and is often not present. If previous weight is known, documented weight loss can help approximate the degree of dehydration.
  • Assess peripheral perfusion by observing for extremity mottling, coolness, or delayed capillary refill. Evaluate the quality of central and peripheral pulses.
  • Patients may have abdominal pain from either bacterial enteritis or a UTI. Flank pain or costovertebral angle tenderness suggests pyelonephritis. Abdominal pain sometimes is sufficiently severe to mimic appendicitis. Examine the abdomen for distention, increased or decreased bowel sounds, diffuse or localized tenderness, and signs of acute abdomen (eg, rigidity, rebound, guarding).
  • Examine anogenital region in children who have urinary or abdominal symptoms or a history of bloody stools. Examination may reveal vulvovaginitis, perianal excoriation, or anal fissures.
  • Complete examination should include adequate visualization of all skin surfaces. Subtle findings, such as petechiae or bruising, may be overlooked if the examination is rushed or limited.

Causes

  • ETEC infection: ETEC is the primary cause of traveler's diarrhea and the major cause of infantile diarrhea in less affluent countries. ETEC is widespread in areas with poor sanitation and is a ubiquitous contaminant of food and water sources. ETEC's incubation period is 1-3 days. Infection usually is self-limited and persists less than 5 days.
  • EHEC infection
    • EHEC is an emerging cause of food-borne illness, particularly in the northern United States and Canada.
    • Recent highly publicized outbreaks of hemolytic-uremic syndrome (HUS) that caused fatalities have focused public attention on food safety.
    • Cattle are the primary reservoir of the EHEC strains that produce diarrhea in humans. Because EHEC is a common inhabitant of the bovine intestine, it may contaminate beef products or foods that contact bovine-exposed soil.
    • Sources identified in outbreaks include ground beef, apple juice, and alfalfa sprouts, as well as fecally contaminated drinking water and swimming pools.
    • Most outbreaks have been linked to 0157:H7 strains, although other serotypes have been implicated.14,9,15,16
    • Of particular concern in pediatric populations, E coli 0157:H7 requires a relatively small inoculum for infection and spreads easily from child to child by the fecal-oral route. The incubation period of EHEC is 1-5 days, with illness duration typically 4-10 days.
    • HUS develops in 10-15% of pediatric patients. Chronic renal failure develops in as many as 10% of patients with HUS, and HUS kills 3-5% of affected patients.17  
  • EPEC infection: EPEC is most often found in developing countries, primarily affecting infants and children. EPEC has been associated with outbreaks of diarrhea in newborn nurseries in the United States, primarily in the 1950s and 1960s.
  • EAEC infection: EAEC is similar in geographic distribution, mechanism, and effect to EPEC. The CDC's Traveler's Health Web site provides additional information to physicians and the public. 
  • UTIs
    • E coli is the most commonly isolated pathogen in pediatric UTIs. Virulence factors, such as pili, contribute to the pathogenicity of UTIs.
    • HUS has been reported following UTIs with enterohemorrhagic serotypes of E coli in patients who did not have a diarrheal illness.
  • Neonatal infections
    • E coli infection in neonates may manifest as bacteremia, sepsis, UTI, or meningitis; it rarely manifests as pneumonia, soft tissue, or bone infection.
    • E coli strains with the K1 capsular polysaccharide antigen cause approximately 40% of the septicemia cases and 80% of the meningitis cases attributed to E coli.
    • The usual source of E coli in neonatal infections is the maternal GI tract. The organism also may be acquired nosocomially, particularly in infants who are premature or who require mechanical ventilation.
    • Predisposing factors include maternal perinatal infection, low birth weight, prolonged rupture of membranes, and traumatic delivery. Fetal hypoxia and skin or mucosal defects also increase the risk of gram-negative infection. Infants with galactosemia appear to have an increased susceptibility to serious bacterial infection, particularly E coli sepsis.
    • In intensive care nurseries, mechanical ventilation, invasive procedures, indwelling catheters, and the frequent use of antimicrobial agents allow selection and proliferation of resistant strains of pathogenic gram-negative bacilli.

More on Escherichia Coli Infections

Overview: Escherichia Coli Infections
Differential Diagnoses & Workup: Escherichia Coli Infections
Treatment & Medication: Escherichia Coli Infections
Follow-up: Escherichia Coli Infections
References
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Further Reading

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Keywords

Escherichia coli infections, E coli infections, Escherichia coli, E coli, colibacillus, diarrhea, diarrheal illness, hemolytic-uremic syndrome, HUS, urinary tract infection, UTI, neonatal sepsis, meningitis, enterotoxigenic E coli, ETEC, enterohemorrhagic E coli, EHEC, enteropathogenic E coli, EPEC, enteroinvasive E coli, EIEC, enteroaggregative E coli, EAEC, hemolytic anemia, thrombocytopenia, renal insufficiency, diarrhea, oliguria, anuria, traveler's diarrhea, bacteremia, sepsis, respiratory distress, prematurity, low birth weight, hemorrhagic colitis, abdominal cramping, dysentery

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Contributor Information and Disclosures

Author

Archana Chatterjee, MD, PhD, Professor of Pediatrics, Medical Microbiology and Immunology, and Pharmacy, Division of Pediatric Infectious Diseases, Chief of Division of Pediatric Infectious Diseases, Creighton University School of Medicine; Hospital Epidemiologist and Medical Director of Infection Control, Children's Hospital
Archana Chatterjee, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, International Society for Infectious Diseases, Pediatric Infectious Diseases Society, and Society for Pediatric Research
Disclosure: GlaxosmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi-Pasteur Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; GlaxoSmithKline Grant/research funds Other; MedImmune  Other; Merck Grant/research funds Other; Novartis Grant/research funds Other; Sanofi-Pasteur Grant/research funds Other

Coauthor(s)

Catherine O'Keefe, DNP, APRN, Assistant Professor of Nursing, Pediatric Nurse Practitioner, Pediatric Infectious Diseases, Creighton University School of Nursing
Catherine O'Keefe, DNP, APRN is a member of the following medical societies: American Academy of Nurse Practitioners, National Association of Pediatric Nurse Practitioners, and Nebraska Nurse Practitioners
Disclosure: Nothing to disclose.

Sara L Cuthill, MD, Fellow, Developmental and Behavioral Pediatrics, Departmental and Behavioral Pediatrics, Interstate Medical Office East
Sara L Cuthill, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Meera Varman, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Infectious Diseases, Creighton University School of Medicine
Meera Varman, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: phamaceutical companies Honoraria Speaking and teaching; phamaceutical companies Grant/research funds clinical trials

Medical Editor

Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital
Ashir Kumar, MBBS, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association of Physicians of Indian Origin, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Mark R Schleiss, MD, American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota School of Medicine
Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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