Pediatric Enterococcal Infection 

  • Author: Meera Varman, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Mar 12, 2012
 

Background

The French word enterocque first was used in 1899 by Thiercelin to describe gram-positive cocci of enteric origin that formed pairs and short chains. Enterococcus species, Streptococcus bovis, and Streptococcus equines originally were grouped together as group D streptococci (Lancefield classification). However, DNA hybridization studies showed that enterococci are biologically, serologically, and genetically different from streptococci, and enterococci now are placed in a separate genus. Enterococcus is currently recognized as one of the most common causes of nosocomial infections and is becoming increasingly resistant to numerous antibiotics, including vancomycin. See the image below.

This photomicrograph reveals cocci-shaped EnterocoThis photomicrograph reveals cocci-shaped Enterococcus species bacteria taken from a patient with pneumonia.
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Pathophysiology

Enterococci are gram-positive, catalase-negative, facultative anaerobes that grow as diplococci in short chains. They can be differentiated from other catalase-negative gram-positive cocci by their ability to hydrolyze esculin in the presence of 40% bile salts, grow in 6.5% sodium chloride at 45°C, and produce pyrrolidonylarylamidase (ie, PYR reaction).

The genus Enterococcus includes 17 species. Most human clinical isolates are due to either E faecalis (74-90%) or E faecium (5-16%). Occasionally, human infections can be due to Enterococcus raffinosus,Enterococcus casseliflavus,Enterococcus durans, or Enterococcus avium. Enterococci are normal flora of the gastrointestinal tract of humans and animals. They also may be found in oral secretions, the upper respiratory tract, skin, and the vagina.

Enterococci normally inhabit the bowel; thus, determining whether the microbe is a true pathogen or just happens to be associated with an illness is difficult. Enterococcus is frequently isolated from polymicrobial wounds and intra-abdominal and pelvic infections; however, whether enterococci contribute to the pathogenesis of these infections is often uncertain. Clinical trials have demonstrated that patients with such infections recover without any specific antienterococcal therapy. In animal models, injection of enterococci rarely causes peritonitis or subcutaneous infection, but synergy may be observed between enterococci and other organisms (especially anaerobes).

The pathogenesis of enterococcal infections is poorly understood, but several possible virulence factors exist. Hemolysin/bacteriocin is a plasmid-encoded protein that generally is accepted as a virulence factor. Hemolysin causes lysis of human erythrocytes, functions as a bacteriocin, and is active against other gram-positive cocci. This protein has been demonstrated to increase virulence in several animal models.

Aggregation substance is a plasmid-encoded surface protein that causes clumping or aggregation of enterococci. This substance may mediate adherence to urinary tract epithelial cells, resulting in urinary tract infection (UTI), and may promote adherence to endocardial tissue, resulting in endocarditis.

Gelatinase is an extracellular zinc endopeptidase similar to the elastase produced by Pseudomonas aeruginosa and has been found to be produced by a large percentage of Enterococcus faecalis isolates from hospitalized patients and patients with endocarditis. Enterococcus faecium may have a carbohydrate moiety that makes it resistant to phagocytosis. Enterococcus also contains lipoteichoic acid, which may cause an exaggerated host inflammatory response.

During chemotherapy, an imbalance was noted between colonization of anaerobic and aerobic bacteria in the gut. In pediatric patients with acute myeloid leukemia, chemotherapy is associated with a 10,000-fold reduction in fecal anaerobes and 100-fold increase in enterococci.[1]

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Epidemiology

Frequency

United States

Enterococcal infection is the second most common cause of hospital-acquired infection in the United States. Studies have demonstrated an increased incidence of enterococcal bacteremia in the general pediatric population, from 7 cases of bacteremia per 1000 in 1986 to 48 per l000 in 1991. A 12% increase in vancomycin-resistant Enterococcus (VRE) hospital-acquired infections in the ICU was reported in 2004, with a rate of about 28%.[2]

International

VRE and VRE infection have increasingly become a worldwide public health threat since the condition was first recognized in the mid 1980s. Among 210 bile samples obtained from 2001-2004 from 79 adult liver transplant recipients within 30 days of transplantation, approximately 75% yielded bacterial strains, of which 36% showed enterococci.[3] Among this same cohort, gram-positive organisms constituted about 78% of surgical site infections, and aminoglycoside-resistant enterococci was reported in 24%.

Mortality/Morbidity

Neonatal infections are associated with a 6% mortality rate in early onset septicemia, which rises to 15% in late-onset infections associated with necrotizing enterocolitis. In general, enterococcal sepsis is implicated in 7-50% of fatal cases.

Race

No racial predilection is noted.

Sex

No predilection is reported for either sex, although enterococcal endocarditis is more common in adult men.

Age

Adults are infected more commonly than children (excepting the neonatal period). Most of the literature regarding invasive enterococcal infections in children focuses on the neonatal period and indicates that approximately 50% of newborn infants are colonized with E faecalis by age 1 week. Older children who develop bacteremia have underlying risk factors.

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Contributor Information and Disclosures
Author

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 speaker; phamaceutical companies Grant/research funds clinical trials research

Coauthor(s)

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.

Walid Abuhammour, MD, FAAP  Professor of Pediatrics, Michigan State University College of Medicine; Director of Pediatric Infectious Disease, Department of Pediatrics, Hurley Medical Center

Walid Abuhammour, MD, FAAP is a member of the following medical societies: American Medical Association, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

José Rafael Romero, MD  Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center

José Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New York Academy of Sciences, and Pediatric Infectious Diseases Society

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.

Larry I Lutwick, MD  Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Warren C Johnson III, MD, to the development and writing of this article.

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This photomicrograph reveals cocci-shaped Enterococcus species bacteria taken from a patient with pneumonia.
 
 
 
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