Pediatric Enterococcal Infection Clinical Presentation

Updated: Jul 27, 2021
  • Author: Meera Varman, MD; Chief Editor: Russell W Steele, MD  more...
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  • Historical risk factors for acquisition of vancomycin-resistant Enterococcus (VRE) and enterococcal infections include history of the following [4] :

    • Prolonged hospitalization

    • Long stay in ICU

    • Surgical reexploration following liver transplantation

    • Prior use of antibiotics, mainly vancomycin and cephalosporins

    • Immunocompromised state

    • Breakdown of normal physical barriers (eg, GI tract, skin, urinary tract)

    • Neurosurgical procedures and use of neurosurgical devices

  • Recent surveillance by perirectal culture for VRE and nasal culture for methicillin-resistant Staphylococcus aureus (MRSA) conducted between 2002 and 2003 revealed a co-colonization rate of 2.7% in 65 of 2,440 patients in an ICU. Significant risk factors included older age, male sex, hospitalization in an ICU, and antibiotic use during previous hospitalization within a year.

  • The SENTRY Antimicrobial Surveillance Program, performed between 1997-2002 to assess blood stream infections (BSIs) in the United States, Europe, and Latin America, documented that the incidence of oxacillin-resistant S aureus (39.1%) and VRE (17.7%) were highest in the United States. [5]

  • In a review of 451 patients on chronic dialysis, 60 (13%) were found to be colonized with VRE associated with increased mortality of 50%, compared with 10% in noncolonized patients. [6] This also poses challenges to infection control measures and medical care for these patients.

  • In a 2-year study of 1330 ICU admissions, 638 patients were at risk for acquisition; any VRE-colonized room occupants within the previous 2 weeks and a positive room culture result were independent risk factors for the acquisition of VRE. [7] This reinforces the necessity of thoroughly cleaning rooms prior to admitting new patients.

  • Papadimitriou-Olivgeris conducted a prospective study to determine the prevalence of and risk factors for VRE colonization in 497 patients admitted to the intensive care unit (ICU) during a 24-month period. [8] Risk factors for VRE carriage upon admission to the ICU included the following: duration of previous hospitalization; glycopeptide administration; chronic heart failure; malignancy; insulin-dependent diabetes mellitus; and previous enterococcal infection (VRE and/or VSE). Risk factors for VRE colonization during ICU stay included the following: quinolone administration; chronic obstructive pulmonary disease; chronic renal failure; and number of VRE-positive patients in nearby beds. Risk factors for enterococcal infection during stays in the ICU included administration of third- or fourth-generation cephalosporins; use of cortisone before ICU admission; and VRE colonization. Enteral nutrition was found to be a protective factor. [8]



See the list below:

  • Urinary tract infections: VRE is an infrequent cause of urinary tract infection (UTI) in healthy children. When an enterococcal UTI occurs in children, it is usually acquired nosocomially. Risk factors for UTIs caused by enterococci include the following:

    • Indwelling urinary catheters

    • Instrumentation of the urinary tract

    • Structural abnormalities of the urinary tract: In a retrospective review of 257 episodes of UTI over 5 years, E faecalis was identified in 5.1% (13); 9 of these patients had significant underlying anatomic abnormality. [9, 10]

    • Bacteremia: This may be polymicrobial, probably reflecting the severity of the underlying disease. In adults, the genitourinary tract is the most common entry site for enterococcal bacteremia but is implicated much less frequently in the etiology of enterococcal bacteremia in children. However, in a study by Christie et al, urosepsis was the etiology of 12% of episodes of nosocomial enterococcal bacteremia in hospitalized children. [11]

    • BSI: BSI due to VRE is an independent predictor of mortality, and duration of hospital stay is prolonged in BSI secondary to VRE, compared with vancomycin-susceptible enterococci (VSE) (4.5 d vs < 1 d). In a study of more than 2000 hematology-oncology (including transplant) patients, rectal colonization of VRE was close to 5%, of which E faecium constituted 84%. [12] Among these patients with VRE, 29% eventually developed bacteremia. A negative predictive value as high as 99.9% for the risk of bacteremia was documented in this study.

  • Endocarditis: In contrast to adults, in whom enterococci cause as many as 15% of cases of endocarditis, these organisms rarely infect the heart valves of children.

  • Intra-abdominal infections: Enterococcus is often isolated from polymicrobial abdominal or pelvic abscesses. In a 1993 study by Bonadio, 5 cases of enterococcal bacteremia occurred in previously healthy infants with gastroenteritis, 6 cases were associated with bowel obstruction, and 1 case was associated with appendicitis without perforation. [13]

  • Meningitis: Although Enterococcus rarely causes meningitis in otherwise healthy children and adults, it is known to cause meningitis and ventriculitis in children with ventriculoperitoneal (VP) shunts.

  • Neonatal infections: Enterococci account for as many as 10% of cases of neonatal bacteremia and septicemia. Incidence of neonatal enterococcal septicemia increased from 0.12 per 1000 live births in 1982 to 0.8 per 1000 live births in 1986. Enterococcus may cause early onset (within 7 d of birth) or late-onset (>7 d) neonatal sepsis. Early onset sepsis caused by enterococci is milder than that caused by group B streptococcal sepsis. Most cases of enterococcal bacteremia in neonates are nosocomial. Central venous catheters, necrotizing enterocolitis, and intra-abdominal surgery are risk factors. Enterococcus may cause focal skin and soft tissue infections, meningitis, and conjunctivitis in the neonate. [14] Most neonatal infections are caused by E faecalis.

A study by Lubell et al that compared Gram-negative and enterococcal UITs reported that ≥ grade 3 vesicoureteral reflux and hydronephrosis were associated with enterococcal UTI and that urinalysis was more sensitive for the Gram-negative UTI group than the enterococcal UTI group. [15]



See Pathophysiology.