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Journal of Clinical Microbiology, February 2007, p. 631-635, Vol. 45, No. 2
0095-1137/07/$08.00+0     doi:10.1128/JCM.02188-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

CASE REPORT

Vancomycin-Resistant Enterococcus faecalis Endocarditis: Linezolid Failure and Strain Characterization of Virulence Factors{triangledown}

Constantine Tsigrelis,1,2* Kavindra V. Singh,3,4 Thais D. Coutinho,2 Barbara E. Murray,3,4,5 and Larry M. Baddour1,2

Division of Infectious Diseases,1 Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905,2 Division of Infectious Diseases, Department of Medicine,3 Center for the Study of Emerging and Re-emerging Pathogens,4 Department of Microbiology and Molecular Genetics, University of Texas Medical School, Houston, Texas 770305

Received 25 October 2006/ Returned for modification 27 November 2006/ Accepted 11 December 2006


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ABSTRACT
 
Infective endocarditis due to vancomycin-resistant (VR) Enterococcus faecalis has only rarely been reported. We report a case of VR E. faecalis endocarditis that failed to respond to linezolid therapy, outline the virulence traits of the isolate, and review previously published cases of VR E. faecalis endocarditis.


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CASE REPORT
 
A 37-year-old female was transferred to our institution for hemodialysis access and sustained vancomycin-resistant (VR) Enterococcus faecalis bacteremia. Her medical history was significant for medullary cystic kidney disease diagnosed at age 7, and she had required hemodialysis since age 10. She had four failed renal allografts, the first transplant having been performed at age 11. In addition, she had multiple failed arteriovenous grafts and fistulas, requiring placement of bilateral subclavian subcutaneous hemodialysis ports (LifeSite Hemodialysis Access System) 3 years prior to admission.

Seven months prior to admission, she developed methicillin-resistant Staphylococcus aureus bacteremia secondary to infection of her hemodialysis ports and was treated with 4 weeks of intravenous vancomycin. Two months prior to admission, she developed VR E. faecalis bacteremia secondary to hemodialysis port infection. The VR E. faecalis blood isolate was sensitive to penicillin, ampicillin, linezolid, high-level streptomycin (MIC, <1,000 µg/ml), and rifampin and resistant to high-level gentamicin (MIC, >500 µg/ml), erythromycin, and tetracycline. Due to a history of penicillin allergy, oral linezolid was given for 4 weeks. The hemodialysis ports were not removed at that time due to difficulty with obtaining additional vascular access. No valvular or catheter-associated vegetations were demonstrated on transesophageal echocardiography.

She was subsequently admitted to another institution for evaluation of fever and chills. Two sets of blood cultures grew VR E. faecalis with a susceptibility pattern similar to that of the previous VR E. faecalis blood isolate obtained 2 months prior. Linezolid, given 600 mg intravenously every 12 h, was initiated. Blood cultures remained positive for VR E. faecalis on hospitalization day 2. Both subclavian subcutaneous hemodialysis ports were removed on hospitalization day 3, and bacterial culture of the catheter tips grew VR E. faecalis.

The patient was transferred to our institution on hospitalization day 5. At hospital admission, her body temperature was 35.7°C, her blood pressure was 80/48 mmHg, and her heart rate was 101 beats/min. Physical examination did not reveal a cardiac murmur or peripheral stigmata of endocarditis. Laboratory testing showed a peripheral leukocyte count of 12,300/mm3. Two sets of blood cultures grew VR E. faecalis within 24 h; the blood isolate was sensitive to penicillin, ampicillin, linezolid, and daptomycin and resistant to quinupristin-dalfopristin and erythromycin. The isolate was resistant to high-level gentamicin (MIC, >500 µg/ml), although it lacked high-level resistance to streptomycin (MIC, <2,000 µg/ml). In addition, the isolate contained the vanA gene by PCR analysis.

Additional blood cultures taken on hospitalization days 7 and 9 were positive for VR E. faecalis, despite continued therapy with linezolid. A transesophageal echocardiogram on hospitalization day 7 showed mobile aortic valve vegetations (8-mm and 4-mm vegetations), a mobile mitral valve vegetation (10 by 8 mm), new mitral valve regurgitation, and new moderate-to-severe aortic valve regurgitation. She had more than 10 reported allergies, including penicillin, amoxicillin, cefazolin, tetracycline, and ciprofloxacin. Skin testing for penicillins and cephalosporins was performed and was negative. Antibiotic therapy was changed from intravenous linezolid to aqueous crystalline penicillin G sodium, 3 x 106 U given intravenously every 6 h, plus streptomycin, 300 mg given intravenously three times weekly, after each hemodialysis. Streptomycin levels were monitored. She improved clinically, and follow-up blood cultures performed on hospitalization day 15 were negative. She received 6 weeks of combined treatment with intravenous penicillin G and streptomycin. Relapsing VR E. faecalis bacteremia did not occur over the 9 months following the completion of antibiotic therapy.

Colony lysates of the VR E. faecalis blood isolate from hospitalization day 5 (TX2853) were prepared by previously described methods (29) and hybridized with probes representing 17 genes that encode proven or suspect virulence determinants. These included the gelatinase gene (22, 26, 28, 30); recently described pilus-encoding genes (16); genes encoding putative MSCRAMMs (microbial surface components recognizing adhesive matrix molecules) with predicted immunoglobulin (Ig)-like folds (17, 18, 27; J. Sillanpää, S. R. Nallapareddy, and B. E. Murray, unpublished data); genes, including esp (33), in a predicted pathogenicity island (PAI) (15); and an acquired gene that contributes to biofilm formation (32) (Table 1). The strain was examined for phenotypic production of gelatinase (22), hemolytic activity on Bacto Tryptic Soy Agar (Becton Dickinson and Company, Sparks, MD) plus 5% human blood agar plates, and biofilm formation (14). DNA was extracted with a DNeasy tissue kit (QIAGEN Sciences, Maryland) by following the manufacturer's instructions and tested by PCR as previously described to determine if the conserved junction of the PAI with chromosomal DNA was present (15). Pulsed-field gel electrophoresis and multilocus sequence typing of internal regions of five housekeeping genes were performed to determine if TX2853 belonged to the previously described beta-lactamase, vancomycin-resistant, endocarditis clone (15).


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  		TABLE 1. Potential virulence- and PAI-associated genes

TX2853 produced gelatinase; it also contained five of seven putative adhesin genes (including the ebpA and ebpB genes, which are related to pilus formation), one of two predicted hyaluronidase genes, esp, and two of six other PAI genes. The common PAI-chromosome junction point previously described (15) was also present. TX2853 tested negative by PCR for the bee (biofilm enhancer in enterococcus) locus (32). By pulsed-field gel electrophoresis and multilocus sequence typing, this strain did not belong to the beta-lactamase, vancomycin-resistant, endocarditis clone (or to one of the sequence types we have previously classified by this system). Biofilm assay showed that the strain was a medium biofilm producer (33). TX2853 tested negative for hemolytic activity on blood agar plates, which is consistent with cylM probe negative results.

Vancomycin-resistant enterococci have emerged as a well-defined cause of health care-associated and nosocomial infections (5, 8). Despite the increasing prevalence of vancomycin-resistant enterococci in most tertiary-care and other health care settings, infective endocarditis due to these organisms has been reported in only a limited number of cases (31). Moreover, endocarditis due to VR E. faecalis isolates is extremely rare. We performed a review of the PubMed database (English language) through the end of September 2006 with the search terms "vancomycin resistant enterococcus endocarditis" and "glycopeptide resistant enterococcus endocarditis." An article was included in our review if it described a case of VR E. faecalis infective endocarditis that fulfilled the modified Duke criteria for definite or possible infective endocarditis (13). There were only six previously reported cases of infective endocarditis caused by VR E. faecalis that met our criteria (Table 2). Two cases met criteria for definite infective endocarditis (patients 1 and 3), and four cases met criteria for possible infective endocarditis (patients 2, 4, 5, and 6). In the majority of previously reported cases of VR E. faecalis infective endocarditis in our review, the mitral or aortic valve was affected; our case report represents the first description of bivalvular endocarditis due to VR E. faecalis. Only one of seven isolates was resistant to ampicillin, which is consistent with the rates of ampicillin resistance (between 0.9 and 2.7%) observed in E. faecalis isolates in the United States (5, 8). The mechanism of resistance to ampicillin in the isolate from patient 5 (Table 2) was not mentioned in the case report (7). Most patients were treated with either ampicillin or penicillin, and synergistic bactericidal combination therapy with an aminoglycoside was given to four patients. There were two deaths, and two patients required valve replacement.


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  		TABLE 2. Characteristics of patients with infective endocarditis due to VR E. faecalis

Although there are some case reports of linezolid efficacy for infective endocarditis due to vancomycin-resistant Enterococcus faecium (31), there has been very limited experience with the use of linezolid to treat infective endocarditis due to VR E. faecalis. In the six previously reported cases of VR E. faecalis in our review, only two of the patients were treated with linezolid (Table 2, patients 5 and 6). Patient 5 was treated with linezolid for 6 weeks because he had an ampicillin-resistant strain of VR E. faecalis (7). He had multiple negative surveillance blood cultures during antibiotic therapy, although he died from an unknown cause 1 week after completion of linezolid therapy. Patient 6 was treated with linezolid for 12 weeks plus gentamicin for 6 weeks because of a previous anaphylactic reaction to penicillin (35). Six weeks after discontinuation of linezolid, blood cultures were positive for VR E. faecalis although subsequent blood cultures remained negative for 52 months of follow-up time. Our patient had persistent VR E. faecalis bacteremia for 9 days while on linezolid therapy but was subsequently cured after starting therapy with aqueous crystalline penicillin G sodium plus streptomycin. Based on the limited and conflicting data in these case reports, further studies are needed to elucidate the role of linezolid in the treatment of infective endocarditis due to VR E. faecalis.

Although there are multiple virulence factors that may contribute to the ability of enterococci to cause infective endocarditis, there have been limited studies of virulence traits in VR E. faecalis infective endocarditis isolates due to its rarity (Table 2). Our patient's VR E. faecalis infective endocarditis strain (TX2853) tested positive for five of seven genes thought to be involved in adhesion (ebpA, ebpB, ace, and two cell surface anchor family proteins with Ig-like fold-containing putative surface adhesin), enterococcal surface protein gene esp, gelatinase gene gelE, one of two putative hyaluronidase genes (hylA), and two of six PAI genes (xylA, which encodes a hypothetical protein) (Table 1). In addition, the strain was a medium biofilm producer by biofilm assay and tested negative for hemolytic activity on blood agar plates.

Microbial adherence to host cells is a pivotal stage in infection pathogenesis, regardless of the organism or infection syndrome. E. faecalis strains recovered from patients with endocarditis have a greater capacity to adhere to Girardi heart cells than to urinary tract epithelial cells in vitro (6), which suggests that adherence to vascular endothelium may be important. MSCRAMMs mediate binding of bacteria to extracellular matrix proteins and function as adhesins to damaged heart tissue (17, 18, 27). Ace is a specific collagen-binding adhesin of the MSCRAMM family, has been identified in E. faecalis endocarditis isolates (17), and mediates attachment of E. faecalis to collagen types I and IV and laminin (18). Subsequently, a family of seven genes encoding MSCRAMM-like proteins was found in 100% (nine out of nine) of the E. faecalis endocarditis strains tested, and elevated titers of IgG to these MSCRAMM-like proteins were found in the sera of nine patients with E. faecalis infections (27). Three of these genes, ebpA, ebpB, and ebpC (endocarditis- and biofilm-associated pili), control surface pilus formation and may be important in endocarditis pathogenesis (16).

Biofilm formation, which is modulated by many genes, including esp and the fsr locus, likely serves as an important factor in E. faecalis infections (16, 32). In one study, E. faecalis endocarditis isolates produced biofilm more often than did E. faecalis isolates from nonendocarditis sources and from hospital fecal specimens (14). The esp gene, which encodes an enterococcal surface protein (Esp), plays an important role in biofilm formation (33) and has been identified more often among E. faecalis isolates that cause endocarditis and other bloodstream infections than in E. faecalis fecal isolates (14).

A quorum-sensing fsr locus has recently been described that regulates the transcription of a gelatinase gene (gelE) and a serine protease gene (sprE) and could contribute to E. faecalis virulence (22, 26, 28). The fsr locus regulates biofilm formation (14, 20). One study showed that 100% (12 out of 12) of the E. faecalis endocarditis isolates tested had fsr compared to only 53% (10 out of 19) of the fecal isolates tested (21). In contrast, two subsequent studies did not show an increased prevalence of fsr in E. faecalis endocarditis and bloodstream isolates (11, 23). In a rat endocarditis model, an E. faecalis mutant that did not produce gelatinase or serine protease had an endocarditis induction rate that was significantly reduced compared to that of wild-type E. faecalis (28). Further investigation is needed to elucidate the role of the fsr locus in the pathogenesis of E. faecalis infective endocarditis.

There are several other potential virulence traits of enterococci that could be operative in endocarditis pathogenesis. These include aggregation substance (1, 12); multiple genes located in a PAI, including xylA, cbh, one that encodes a hypothetical protein, and others (15, 24); hyaluronidases (15); extracellular superoxide production (9); and cytolysins-hemolysins (1, 8, 10, 30).

There is only one previous description of pathogen virulence factors in a patient with VR E. faecalis infective endocarditis (2, 4) (Table 2, patient 3). That patient's isolate was similar to our strain (TX2853) in that it was positive for ace, was a biofilm producer, and did not display hemolytic activity. In contrast to our patient's isolate, that strain was esp negative. Although a molecular examination for the gelatinase gene (gelE) was not performed, phenotypically, the strain did not produce gelatinase. The strain was positive for the asa1 (aggregation substance) gene.

In conclusion, we report a case of VR E. faecalis endocarditis that failed to respond to linezolid therapy and review previously published cases of VR E. faecalis infective endocarditis. More information is needed in order to establish the role of linezolid in the treatment of VR E. faecalis endocarditis. In addition, we have also outlined the virulence traits of our patient's isolate. Further studies are needed to identify which virulence factors are operative in the pathogenesis of VR E. faecalis infective endocarditis and may lead to potential targets for novel therapeutic agents. Subsequent investigations should also include etiologic and prognostic cohort studies of patients with enterococcal bacteremia and infective endocarditis to identify which virulence traits play a role in the development of endocarditis and which affect outcome.


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ACKNOWLEDGMENTS
 
This work was supported in part by NIH grant R37 AI47923 from the Division of Microbiology and Infectious Diseases to B. E. Murray.


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FOOTNOTES
 
* Corresponding author. Mailing address: Division of Infectious Diseases, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905. Phone: (507) 255-1980. Fax: (507) 255-7767. E-mail: tsigrelis.constantine{at}mayo.edu. Back

{triangledown} Published ahead of print on 20 December 2006. Back


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Journal of Clinical Microbiology, February 2007, p. 631-635, Vol. 45, No. 2
0095-1137/07/$08.00+0     doi:10.1128/JCM.02188-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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