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PubMed2002

Formation of vegetations during infective endocarditis excludes binding of bacterial-specific host antibodies to Enterococcus faecalis.

Infectious endocarditis is a microbial infection of the endothelial lining of the heart that typically occurs on damaged or prosthetic heart valves. The characteristic lesion seen with infective endocarditis, termed "the vegetation," is composed of bacteria surrounded by a platelet/fibrin layer attached to the underlying endothelium. The vegetation has long been believed to exclude or hinder host defenses from clearing bacteria, although formal demonstration of mechanisms by which this occurs are lacking. This study investigated the ability of the vegetation to exclude host antibodies specific for the bacterial surface protein aggregation substance in vivo during experimental endocarditis caused by Enterococcus faecalis. The results demonstrate that, once the vegetation encloses bacteria, they are no longer accessible to high-titer bacterial-specific host antibodies, establishing a mechanism by which the vegetation functions to protect the bacteria from the humoral immune response.

Animals↗
PubMed2002

Genogrouping and incidence of virulence factors of Enterococcus faecalis in liver transplant patients differ from blood culture and fecal isolates.

Enterococcus faecalis is a leading cause of infections in liver transplant patients. This study reviewed the incidence of virulence factors such as hemolysin, gelatinase, aggregation substances (asa1 and asa373), or the enterococcal surface protein (Esp) in isolates from liver transplant patients. In total, 133 isolates from liver transplant patients were compared with 47 isolates from feces of healthy volunteers and 66 isolates from blood cultures. Amplified fragment length polymorphism (AFLP) analysis indicates that the isolates from different clinical subgroups can be divided into genogroups with an AFLP similarity of >80% and different virulence factors. Hemolysin and asa1 might be associated with infection, as they are more frequent in isolates from blood cultures and transplant patients. Esp might be associated with colonization and spread, because it is more frequent in isolates from feces of healthy volunteers and transplant patients. An epidemic esp gene-positive strain among liver transplant patients supports this hypothesis.

Bacteremia↗
PubMed2002

Association between the presence of enterococcal virulence factors gelatinase, hemolysin, and enterococcal surface protein and mortality among patients with bacteremia due to Enterococcus faecalis.

The potential virulence factors of enterococci include production of enterococcal surface protein (Esp), gelatinase, and hemolysin. Gelatinase- and hemolysin-producing strains of Enterococcus faecalis have been shown to be virulent in animal models of enterococcal infections. Esp production has been shown to enhance the persistence of E. faecalis in the urinary bladder. We determined the presence of the esp gene and production of gelatinase and hemolysin in 219 E. faecalis isolates from a larger prospective study of 398 patients with enterococcal bacteremia. Thirty-two percent of isolates carried the esp gene, 64% produced gelatinase, and 11% produced hemolysin. There was no significant association between 14-day mortality and any of the markers studied, singly or in combination.

Adolescent↗
PubMed2003

A potential virulence gene, hylEfm, predominates in Enterococcus faecium of clinical origin.

An open reading frame (hyl(Efm)) with homologies to previously described hyaluronidase genes has been identified in nonstool isolates of Enterococcus faecium. E. faecium isolates (n=577) from diverse sources were screened for the presence of hyl(Efm) and esp(Efm), a putative virulence gene associated with epidemic E. faecium strains. The presence of esp(Efm) was roughly twice that of hyl(Efm), but both were found primarily in vancomycin-resistant E. faecium isolates in nonstool cultures obtained from patients hospitalized in the United States. These data suggest that specific E. faecium strains may be enriched in determinants that make them more likely to cause clinical infections. Differences in the prevalence of these strains may help explain variations in the clinical importance of multiresistant E. faecium across different continents.

Anti-Bacterial Agents↗
PubMed2003

Linezolid-resistant, vancomycin-resistant Enterococcus faecium infection in patients without prior exposure to linezolid.

We describe 2 patients without prior exposure to linezolid who were infected with closely related strains of linezolid- and vancomycin-resistant Enterococcus faecium (LRVREF) that may have been hospital acquired. Polymerase chain reaction amplification of the domain V region of the 23S ribosomal RNA gene demonstrated the presence of the G2576U mutation previously reported to be associated with linezolid resistance. Nosocomial transmission of LRVREF is an ominous sign and underscores the importance of meticulous infection-control measures.

Acetamides↗
PubMed2003

Control of endemic vancomycin-resistant Enterococcus among inpatients at a university hospital.

We sought to determine the ability of surveillance cultures and isolation of vancomycin-resistant Enterococcus (VRE)-colonized patients to control nosocomial VRE infection and colonization during a 5-year period (November 1994 through October 1999). During this period, VRE colonization was limited to 0.82% of admissions. The incidence of VRE infection was 0.12 cases per 1000 patient-days (attack rate, 0.07%). Colonized patients were first identified by surveillance (95%) or routine clinical cultures (5%); 14% of colonized patients had a positive clinical culture a median of 15 days after a positive surveillance culture. Ten percent of colonized patients were identified by surveillance at the time of transfer from another health care facility. Identification of these colonized patients was associated with reduction from a peak incidence rate of 2.07% to a rate of 1.25% and stabilization at this lower level. The use of surveillance cultures to identify and isolate patients with asymptomatic colonization can provide sustained control of the spread of VRE within a health care facility.

Anti-Bacterial Agents↗
PubMed2003

Expression of glycopeptide-resistance gene in response to vancomycin and teicoplanin in the cardiac vegetations of rabbits infected with VanB-type Enterococcus faecalis.

VanB-type resistance in enterococci corresponds to resistance to vancomycin but not to resistance to the related glycopeptide teicoplanin, because the vanB gene cluster is activated by the VanR(B)-VanS(B) 2-component regulatory system in response to vancomycin but not to teicoplanin. Mutations in the vanS(B) gene allow for constitutive or teicoplanin-inducible expression of the resistance genes. To analyze in vivo expression of the van genes in rabbits with experimental endocarditis, a VanB-type Enterococcus faecalis with a transcriptional fusion between the P(YB) promoter of resistance genes and the gfpmut1 gene for the green-fluorescent protein in the chromosome was constructed. Rounded heaps containing fluorescent bacteria were detected in vegetation slides from rabbits treated with vancomycin but not in those from control rabbits, revealing induction of a tightly regulated vanB gene cluster. Teicoplanin-resistant mutants were detected as fluorescent bacteria in rabbits treated with teicoplanin. Thus, the reporter system monitored expression of a glycopeptide-resistance gene in vivo at a single-cell level.

Animals↗
PubMed2004

A putative sugar-binding transcriptional regulator in a novel gene locus in Enterococcus faecalis contributes to production of biofilm and prolonged bacteremia in mice.

A biofilm-negative transposon mutant was created from an Enterococcus faecalis strain that produces a lot of biofilm. The transposon had been inserted in the second gene of a locus consisting of 4 open-reading frames, designated bop (biofilm on plastic surfaces). A nonpolar deletion of this gene and of parts of the 2 flanking genes was created; production of biofilm by this deletion mutant was significantly enhanced, compared with that by the wild-type strain. Expression of a downstream gene was significantly lower in the transposon mutant than in the wild-type strain and the biofilm-enhanced deletion mutant. Transformation of this gene into the transposon mutant partially restored production of biofilm. Mice challenged by intravenous injection with the biofilm-negative mutant strain showed significantly reduced numbers of colony-forming units in the blood, compared with mice challenged with the biofilm-enhanced deletion mutant and the wild-type. These results indicate that bop is involved in production of biofilm and probably regulates expression of biofilm in the E. faecalis strain tested.

Animals↗
PubMed2004

Effects of glucose on fsr-mediated biofilm formation in Enterococcus faecalis.

Biofilm production is frequently dependent on such environmental factors as cell density and glucose concentration. The Enterococcus faecalis quorum-sensing locus (fsr) increases enterococcal virulence in multiple animal models. To date, fsr has been shown to regulate the transcription of 2 downstream protease genes. We demonstrate that the effect of fsr mutations on biofilm formation, as well as the fsr-mediated catabolite control of biofilm, is mediated via these proteases. The present study provides additional insight into the mechanisms used by E. faecalis to establish nosocomial infection.

Bacterial Proteins↗
PubMed2004

Importance of gls24 in virulence and stress response of Enterococcus faecalis and use of the Gls24 protein as a possible immunotherapy target.

Gls24 was previously identified as a general stress protein of Enterococcus faecalis. In the present study, we found that a gls24 disruption mutant (TX10100) of E. faecalis strain OG1RF showed a considerably increased 50% lethal dose in a mouse peritonitis model, and, at high inocula, TX10100 was either not lethal or was much less so than wild-type OG1RF (P<.001). TX10100 was also more sensitive to bile salts (mean+/-SD survival rate relative to wild-type OG1RF, 9.7%+/-2.0%) at late stationary phase, as previously found by Giard et al. with another strain. Inactivation of glsB, downstream of and cotranscribed with gls24, had no effect on E. faecalis virulence but resulted in reduced bile-salts resistance (to a mean+/-SD survival rate of 28.0%+/-5.1%) relative to wild-type OG1RF. Results of complementation of TX10100 with different combinations of gls24-glsB and 2 promoters--a remote promoter (P1) and an adjacent promoter (P2)--suggested that both genes and both promoters, especially P1, are important for bile-salts resistance. Anti-Gls24 immune rabbit serum, which showed some Gls24 on the cell surface, protected mice against a lethal challenge of OG1RF in the peritonitis model (e.g., survival of 12/18 mice vs. 1/18 mice with preimmune rabbit serum; P=.008). In conclusion, the E. faecalis gls24 gene is important for virulence as well as stress response, and anti-Gls24 immune rabbit serum shows protection against E. faecalis infection in a mouse peritonitis model.

Animals↗
PubMed2005

Glycosaminoglycans mediate invasion and survival of Enterococcus faecalis into macrophages.

Enterococcus faecalis is responsible for a large variety of nosocomial infections. The intestinal barrier is thought to be one of the preferential portals of entry of enterococci, and the ability of E. faecalis to survive within peritoneal macrophages may contribute to spreading to distant sites. We examined the ability of a polysaccharide-expressing (biofilm-positive) E. faecalis strain and an isogenic biofilm-negative mutant to enter and survive within professional and nonprofessional phagocytes. Biofilm-positive bacteria survived longer in all cell systems than did biofilm-negative bacteria, through a process of receptor-mediated endocytosis that is dependent on functional reorganization of microtubules and polymerization of microfilament and on activation of protein kinases but not ATPases or protein phosphatases. We suggest that glycosaminoglycans--specifically heparin, heparan sulfate, and chondroitin sulfate A--are the host receptors for enterococci on professional and, possibly, nonprofessional phagocytes, allowing entry of enterococci into cell compartments where killing mechanisms are inhibited.

Animals↗
PubMed2006

Genotyping and preemptive isolation to control an outbreak of vancomycin-resistant Enterococcus faecium.

BACKGROUND: Control of vancomycin-resistant Enterococcus faecium (VRE) in European hospitals is hampered because of widespread asymptomatic carriage of VRE by healthy Europeans. In 2000, our hospital (The University Medical Center Utrecht, Utrecht, The Netherlands) was confronted with a large outbreak of VRE. INTERVENTION: On the basis of genotyping (by pulsed-field gel electrophoresis), epidemic and nonepidemic VRE strains were distinguished, and infection-control measures were exclusively targeted toward epidemic VRE. The outbreak was retrospectively divided into 3 periods of different infection-control measures. Compliance with use of alcohol-based hand rubs was enforced during all periods. Period I involved active surveillance, isolation of carriers, and cohorting (duration, 4 months); preemptive isolation of high-risk patients for VRE colonization was added in period II (7 months); and cohorting and preemptive isolation were abandoned in period III (18 months). METHODS: When the outbreak was identified, 27 patients in 6 wards were colonized; 93% were colonized with an epidemic VRE strain. Detection rates of nonepidemic VRE were 3.5%, 3.0%, and 2.9% among 683, 810, and 977 screened patients in periods I, II, and III, respectively, comparable to a prevalence of 2% (95% confidence interval [CI], 1%-3.5%) among 600 nonhospitalized persons. The relative risks of detecting epidemic VRE in periods II and III, compared with period I, were 0.67 (95% CI, 0.41-1.10) for period II and 0.02 (95% CI, 0.002-0.6) for period III. Infection-control measures were withheld for patients colonized with nonepidemic VRE (76 [54%] of 140 patients with a test result positive for VRE). Use of alcohol-based hand rubs increased by 31%-275% in outbreak wards. CONCLUSION: Genotyping-targeted infection control, isolation of VRE carriers, enhancement of hand-hygiene compliance, and preemptive isolation successfully controlled nosocomial spread of epidemic VRE infection.

Disease Outbreaks↗
PubMed1999

Enteric carriage of vancomycin-resistant Enterococcus faecium in patients tested for Clostridium difficile.

OBJECTIVE: To identify independent risk factors for enteric carriage of vancomycin-resistant Enterococcus faecium (VREF) in hospitalized patients tested for Clostridium difficile toxin. DESIGN: Retrospective case-cohort study. SETTING: Tertiary-care teaching hospital. PATIENTS: Convenience sample of 215 adult inpatients who had stool tested for C difficile between January 29 and February 25, 1996. RESULTS: 41 (19%) of 215 patients had enteric carriage of VREE Five independent risk factors for enteric VREF were identified: history of prior C difficile (odds ratio [OR], 15.21; 95% confidence interval [CI95], 3.30-70.10; P < .001), parenteral treatment with vancomycin for > or = 5 days (OR, 4.06; CI95, 1.54-10.73; P = .005), treatment with antimicrobials effective against gram-negative organisms (OR, 3.44; CI95, 1.20-9.87; P = .021), admission from another institution (OR, 2.95; CI95, 1.21-7.18; P =.017), and age > 60 years (OR 2.57; CI95, 1.13-5.82; P = .024). These risk factors for enteric VREF were independent of the patient's current C difficile status. CONCLUSIONS: Antimicrobial exposures are the most important modifiable independent risk factors for enteric carriage of VREF in hospitalized patients tested for C difficile.

Adult↗
PubMed1999

Undetected vancomycin-resistant Enterococcus in surgical intensive care unit patients.

The rates of vancomycin-resistant Enterococcus (VRE) in a high-risk population were investigated prospectively using an active surveillance method. The costs of conducting active surveillance were calculated. Among the 10 patients found to have VRE, routine cultures identified 3 (30%); thus, 70% of the VRE-colonized patients would have gone undetected in the absence of active surveillance. The total cost for 5 weeks of active surveillance was $2,234. Although active surveillance identified a high rate of VRE-colonized patients who otherwise may not have been identified, it remains to be determined if the additional costs are justified and result in reduced transmission.

Bacterial Typing Techniques↗
PubMed1999

The prevalence of colonization with vancomycin-resistant Enterococcus at a Veterans' Affairs institution.

OBJECTIVE: To study vancomycin-resistant Enterococcus (VRE) prevalence, risk factors, and clustering among hospital inpatients. DESIGN: Rectal-swab prevalence culture survey conducted from February 5 to March 22, 1996. SETTING: The Veterans' Affairs Medical Center, Atlanta, Georgia. PATIENTS: Hospital (medical and surgical) inpatients. RESULTS: The overall VRE prevalence was 29% (42/147 patients). The VRE prevalence was 52% (38/73 patients) among patients who had received at least one of six specific antimicrobials during the preceding 120 days, compared with only 5% (4/74) among those who had not received the antimicrobials (relative risk, 9.6; P<.001). The longer the period (up to 120 days) during which antimicrobial use was studied, the more closely VRE status was predicted. Among 67 hospital patients in 28 multibed rooms, clustering of VRE among current roommates was not found. CONCLUSIONS: At this hospital with relatively high VRE prevalence, VRE colonization was related to antibiotic use but not to roommate VRE status. In hospitals with a similar VRE epidemiology, obtaining cultures from roommates of VRE-positive patients may not be as efficient a strategy for identifying VRE-colonized patients as obtaining screening cultures from patients who have received antimicrobials.

Aged↗