Pediatric Escherichia Coli Infections 

  • Author: Archana Chatterjee, MD, PhD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Nov 9, 2011
 

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.

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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]

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Epidemiology

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 Ecoli (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]

The outbreak of gastroenteritis and hemolytic uremic syndrome caused by Shiga-toxin–producing E coli in Germany in May, June, and July, 2011 was linked to the consumption of sprouts.[9] Reported were 3816 cases, which included 54 deaths; 22% involved hemolytic uremic syndrome, which occurred predominantly in female adults.[10]

Mortality/Morbidity

Several E coli pathotypes have been implicated in chronic diarrhea among severely immunocompromised patients (eg, patients with human immunodeficiency virus [HIV]).[11, 12, 13] ETEC causes more dehydrating diarrhea cases among infants in developing countries than any other pathotype.[14, 15]

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.

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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: Nothing to disclose.

Coauthor(s)

Catherine O'Keefe, DNP, APRN  Assistant Professor of Nursing and Pediatric Nurse Practitioner, Pediatric Infectious Diseases, Creighton University Medical Center

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  Associate Professor, Department of Pediatrics, Section of Pediatric Infectious Diseases, Creighton University Medical Center

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

Specialty Editor Board

Ashir Kumar, MD, MBBS, FAAP  Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS, FAAP is a member of the following medical societies: American Association of Physicians of Indian Origin and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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 Medical School

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.

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: Novartis 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: Nothing to disclose.

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