Infections Due to Beta-Lactamase-producing, High-Level Gentamicin-resistant <i>Enterococcus faecalis</i>

Wells, Virginia D.; Wong, Edward S.; Murray, Barbara E.; Coudron, P E; Williams, Denise; Markowitz, Sheldon M.

doi:10.7326/0003-4819-116-4-285

Cited by 103 publications

(65 citation statements)

References 15 publications

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“…Ten of 12 patients experienced VRE BSI during the neutropenic period (median 15 days post transplant, range [8][9][10][11][12][13][14][15][16][17][18][19][20][21], and mainly this occurred in patients with refractory or relapsed disease at the time of transplantation (70%). All VRE BSI patients were co-infected with other organisms including gram-negative bacilli, fungi or CMV, and five patients had intra-abdomial complications (GVHD, cholecystitis or typhlitis).…”

Section: Discussionmentioning

confidence: 99%

“…[6][7][8] Up to 73% of enterococcal BSIs are due to vancomycin-resistant strains. 9 Risk factors for vancomycin-resistant enterococcal (VRE) colonization and infection include prolonged hospitalization, intensive care unit (ICU) stay, advanced age, immunocompromised state, neutropenia, high severity of underlying illness, antibiotic exposure, and indwelling urinary and vascular catheters, 8,[10][11][12][13] characteristics commonly found in patients on HSCT units. Several studies have investigated the significance of VRE infections in different patient populations and controversy exists as to whether VRE infections are associated with worse outcomes compared to vancomycin-sensitive enterococci.…”

Section: Introductionmentioning

confidence: 99%

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Vancomycin-resistant enterococcal bloodstream infections on a hematopoietic stem cell transplant unit: are the sick getting sicker?

Dubberke

Hollands

Georgantopoulos

et al. 2006

Bone Marrow Transplant

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Patients with hematologic malignancies and hematopoietic stem cell transplant (HSCT) recipients are at high risk for bacterial bloodstream infections (BSI) owing to resistant organisms. Data describing the outcomes of vancomycin-resistant enterococcal (VRE) BSI in this patient population are limited. We performed a retrospective cohort study of all cases of VRE BSI that occured between February 1996 and December 2002 on the Leukemia/HSCT unit at Barnes-Jewish Hospital. There were 68 episodes of VRE BSI in 60 patients with acute (53%) or chronic (8%) leukemia, non-Hodgkin's lymphoma (22%) or other malignant hematologic disorders (17%). A total of 13, 32 and 32% were recipients of autologous, related and matched-unrelated transplants, respectively. Forty-two of allograft recipients had active acute graft-versus-host disease (GVHD) and 32% chronic GVHD. Only 57% were neutropenic, 52% had refractory/relapsed malignancy and 60% had end organ dysfunction with a median APACHE II score of 17. Median survival after VRE BSI was 19 days. Pneumonia, receipt of anti-fungal drugs and low APACHE II score at the time of the VRE BSI remained significant risk factors for death on multivariable analysis. Our analysis suggests that in patients with hematological malignancies or HSCT, VRE may not have the behavior of a virulent pathogen. VRE BSI may simply be a marker of these patients' already existing critical medical condition.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vancomycin-resistant enterococcal bloodstream infections on a hematopoietic stem cell transplant unit: are the sick getting sicker?

Dubberke

Hollands

Georgantopoulos

et al. 2006

Bone Marrow Transplant

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“…Scenarios to explain these results include the possible existence of an ancestral lineage that spread and evolved slowly over many years, until its disease-causing and resistance acquisition potentials were recognized, or that the group recently evolved into a more favorable form and then spread rapidly, achieving distribution of a subpopulation in various locations. This clonal cluster is notable because it has not only demonstrated pathogenic potential (causing serious infections in outbreaks [8,13,33,40] as well as endocarditis) but also has acquired two uncommon to rare (for E. faecalis) resistances. Vancomycin resistance, seen predominantly in the species E. faecium, is an uncommon property of E. faecalis, found in Յ2% of isolates, while Bla producers are even more rare; of note, however, a vancomycin-resistant E. faecalis was the donor of the vanA genes in at least one of the recent descriptions of vancomycin-resistant methicillin-resistant S. aureus (39).…”

Section: Vol 187 2005 Evolution Of An E Faecalis Clonal Complex Anmentioning

confidence: 99%

“…The earliest isolate of this clone, HH-22, the first known Bla ϩ isolate of E. faecalis, is a multidrug-resistant urine isolate recovered in Texas in 1981 (18); the blaZ gene of this strain is located on a plasmid that also harbors a gene for high-level gentamicin resistance (HL-Gm r ) (16). Other members of this clone (which represents the majority of known Bla ϩ isolates) were subsequently found in five states of North America (20), including a large, prolonged outbreak in a Virginia hospital (33,40) and a hospital outbreak that included five bloodstream infections in North Carolina (13). Surprisingly, the first known U.S. vancomycin-resistant enterococcus, E. faecalis strain V583 (32) (from Missouri), which has recently been sequenced (28), was also found to be a member of this clonal cluster (ST-14), differing from ST-6 by a single nucleotide in efaA.…”

Section: Vol 187 2005 Evolution Of An E Faecalis Clonal Complex Anmentioning

confidence: 99%

Molecular Characterization of a Widespread, Pathogenic, and Antibiotic Resistance-Receptive Enterococcus faecalis Lineage and Dissemination of Its Putative Pathogenicity Island

Nallapareddy¹,

Huang²,

Weinstock

et al. 2005

J Bacteriol

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Enterococcus faecalis, a common cause of endocarditis and known for its capacity to transfer antibiotic resistance to other pathogens, has recently emerged as an important, multidrug-resistant nosocomial pathogen. However, knowledge of its lineages and the potential of particular clones of this species to disseminate and cause disease is limited. Using a nine-gene multilocus sequence typing (MLST) scheme, we identified an evolving and widespread clonal complex of E. faecalis that has caused outbreaks and life-threatening infections. Moreover, this unusual clonal complex was found to contain isolates of unexpected relatedness, including the first known U.S. vancomycin-resistant enterococcus (E. faecalis strain V583), the first known penicillinaseproducing (Bla ؉ ) E. faecalis isolate, and the previously described widespread clone of penicillinase producers, a trait found in <0.1% of E. faecalis isolates. All members of this clonal cluster (designated as BVE for Bla ؉ Van r endocarditis) were found to contain a previously described putative pathogenicity island (PAI). Further analysis of this PAI demonstrated its dissemination worldwide, albeit with considerable variability, confirmed its association with clinical isolates, and found a common insertion site in different clonal lineages. PAI deletions, MLST, and the uncommon resistances were used to predict the evolution of the BVE clonal cluster. The finding of a virulent and highly successful clonal complex of E. faecalis with different members resistant to the primary therapies of choice, ampicillin and vancomycin, has important implications for the evolution of virulence and successful lineages and for public health monitoring and control.

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“…Bacteremia with E. faecalis is a life-threatening condition that causes death in 28 to 75% of patients (1,14,17,29,31,37,44,53) and has a mortality rate of 1.7 to 20% in patients who develop endocarditis (3,14,32,37,52,53). Bloodstream infections with E. faecalis can occur due to contamination of intravenous catheters, ascending urinary tract infections following catheterization, intravenous drug abuse, or abdominal surgery (2,4,12,17,25,26,31,33).…”

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confidence: 99%

Intravenous Mouse Infection Model for Studying the Pathology ofEnterococcus faecalisInfections

et al. 2003

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An intravenous mouse infection model was used to compare the virulence of Enterococcus faecalis strains, to study bacterial localization and organ histopathology, and to examine the effects of Nramp1 and gamma interferon (IFN-␥) on the course of infection. Infection of BALB/c mice with 5 ؋ 10 8 CFU of E. faecalis JH2-2, MGH-2, 418, DS16C2, or OG1X revealed the following virulence ranking (from highest to lowest): MGH-2, 418, DS16C2, JH2-2, and OG1X. Discernible differences in the number of MGH-2 and JH2-2 bacteria were observed at 7 days (168 h) in the blood (P ‫؍‬ 0.037), at 72 h in the liver (P ‫؍‬ 0.002), and at 8 h in the spleen (P ‫؍‬ 0.036). At these time points, the number of MGH-2 bacteria was higher in the blood and liver while the number of JH2-2 bacteria was higher in the spleen. At 72 h, livers from MGH-2-infected mice had higher numbers of coalescing aggregates of leukocytes and a greater degree of caseous necrosis than those from JH2-2-infected mice. These results indicate a correlation between the virulence of the E. faecalis strain, the number of bacteria in the liver, and the degree of histopathology of the liver at 72 h postinfection. IFN-␥ was important in E. faecalis infection, since IFN-␥ gene knockout mice had reduced mortality and massive coagulative necrosis was observed in wild-type mice. The contribution of Nramp1 was unclear, since Nramp1 ؊/؊ mice and the respective control mice were innately resistant to E. faecalis. The mortality of mice in this model is probably due to induction of cytokine release and massive coagulative necrosis.Enterococcus faecalis is the third leading nosocomial isolate from patients with bacteremia (11). Bacteremia with E. faecalis is a life-threatening condition that causes death in 28 to 75% of patients (1,14,17,29,31,37,44,53) and has a mortality rate of 1.7 to 20% in patients who develop endocarditis (3,14,32,37,52,53). Bloodstream infections with E. faecalis can occur due to contamination of intravenous catheters, ascending urinary tract infections following catheterization, intravenous drug abuse, or abdominal surgery (2,4,12,17,25,26,31,33). Many studies have focused on demonstrating that the presence of specific virulence factors such as aggregation substance, cytolysin, surface protein EspA, and extracellular superoxide production are closely associated with E. faecalis isolates from bacteremic patients (20,21,30,42). Results from these studies suggest that the presence of these virulence factors (or a subset of these factors) may augment the ability of E. faecalis to exist in the bloodstream, since fecal isolates less frequently contain these factors.Animal studies to determine the role of virulence factors in disease (41,45,46) or to study antimicrobial efficacy (5, 6, 34-36) have often relied on intraperitoneal injection of mice with E. faecalis, either alone (23) or in conjunction with a virulence adjuvant such as mucin or sterile rat fecal extracts (5,35,46). Preliminary studies in our laboratory have shown that the use of the intraperitoneal inf...

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Infections Due to Beta-Lactamase-producing, High-Level Gentamicin-resistant Enterococcus faecalis

Cited by 103 publications

References 15 publications

Vancomycin-resistant enterococcal bloodstream infections on a hematopoietic stem cell transplant unit: are the sick getting sicker?

Vancomycin-resistant enterococcal bloodstream infections on a hematopoietic stem cell transplant unit: are the sick getting sicker?

Molecular Characterization of a Widespread, Pathogenic, and Antibiotic Resistance-Receptive Enterococcus faecalis Lineage and Dissemination of Its Putative Pathogenicity Island

Intravenous Mouse Infection Model for Studying the Pathology ofEnterococcus faecalisInfections

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