methicillin-resistant endocarditis: pathophysiology ... · introduction s taphylococcus aureus...
TRANSCRIPT
Methicillin-Resistant Staphylococcus aureus Prosthetic ValveEndocarditis: Pathophysiology, Epidemiology, ClinicalPresentation, Diagnosis, and Management
Alicia Galar,a,b Ana A. Weil,c,d David M. Dudzinski,d,e Patricia Muñoz,a,b,f,g Mark J. Siednerc,d
aClinical Microbiology and Infectious Diseases Department, Hospital General Universitario Gregorio Marañón, Madrid, SpainbInstituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Madrid, SpaincDivision of Infectious Diseases, Medicine Department, Massachusetts General Hospital, Boston, Massachusetts, USAdHarvard Medical School, Boston, Massachusetts, USAeCardiology Division, Medicine Department, Massachusetts General Hospital, Boston, Massachusetts, USAfDepartment of Medicine, School of Medicine, Universidad Complutense de Madrid, Madrid, SpaingCIBER de Enfermedades Respiratorias-CIBERES (CB06/06/0058), Madrid, Spain
SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2TIMING, PATHOPHYSIOLOGY, PATHOGENESIS, AND HISTOPATHOLOGY . . . . . . . . . . . . . . . . 2
Timing of Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Histopathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
EPIDEMIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5CLINICAL PRESENTATION, ASSESSMENT, AND DIAGNOSIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7TREATMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Vancomycin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14Rifampin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14Gentamicin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Alternative Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16The “Endocarditis Team” . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Choice and Timing of Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
PROGNOSIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18PREVENTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18CHALLENGES AND FUTURE PERSPECTIVES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19AUTHOR BIOS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
SUMMARY Staphylococcus aureus prosthetic valve endocarditis (PVE) remains amongthe most morbid bacterial infections, with mortality estimates ranging from 40% to 80%.The proportion of PVE cases due to methicillin-resistant Staphylococcus aureus (MRSA)has grown in recent decades, to account for more than 15% of cases of S. aureus PVEand 6% of all cases of PVE. Because no large studies or clinical trials for PVE have beenpublished, most guidelines on the diagnosis and management of MRSA PVE rely uponexpert opinion and data from animal models or related conditions (e.g., coagulase-negative Staphylococcus infection). We performed a review of the literature on MRSAPVE to summarize data on pathogenic mechanisms and updates in epidemiology andtherapeutic management and to inform diagnostic strategies and priority areas whereadditional clinical and laboratory data will be particularly useful to guide therapy. Majorupdates discussed in this review include novel diagnostics, indications for surgical man-agement, the utility of aminoglycosides in medical therapy, and a review of newer anti-staphylococcal agents used for the management of MRSA PVE.
KEYWORDS methicillin-resistant Staphylococcus aureus, prosthetic valve endocarditis
Citation Galar A, Weil AA, Dudzinski DM,Muñoz P, Siedner MJ. 2019. Methicillin-resistantStaphylococcus aureus prosthetic valveendocarditis: pathophysiology, epidemiology,clinical presentation, diagnosis, andmanagement. Clin Microbiol Rev 32:e00041-18.https://doi.org/10.1128/CMR.00041-18.
Copyright © 2019 American Society forMicrobiology. All Rights Reserved.
Address correspondence to Alicia Galar,[email protected].
Published 13 February 2019
REVIEW
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INTRODUCTION
Staphylococcus aureus prosthetic valve endocarditis (PVE) is a devastating infection.The mortality rate due to methicillin-resistant Staphylococcus aureus (MRSA) has
climbed in recent decades, reaching more than 15% of cases of S. aureus PVE (12) and6.6% of cases of PVE (4, 6).
Management for MRSA PVE is complex, and guidelines recommend both a multi-disciplinary team and an individualized approach to care. Given the lack of clinical trialstesting treatments for MRSA PVE, many aspects of management lack an empirical basis.For example, the timing and necessity of valve surgery remain unknown. In somestudies, hospital mortality rates for S. aureus PVE were significantly higher in patientswho had not undergone valve surgery (2, 3, 7, 8, 10, 13–15), prompting some investi-gators to conclude that early valve surgery (EVS) should be considered a standardtreatment for S. aureus PVE, especially in patients with early-onset infection (2, 11).However, recent literature and the experience of the International Collaboration onEndocarditis (ICE) have called into question the value of EVS (1, 11, 16–18). Specifically,work by Hill et al. (16) suggested that uncomplicated S. aureus PVE cases might besuccessfully managed without early valve surgery, and a multicenter study reported in2015 by the ICE found no association between EVS and a reduction of 1-year mortalityrates in patients with S. aureus PVE (11).
Furthermore, although multiple treatment guidelines advocate for incorporating anaminoglycoside into MRSA PVE therapy (19, 20) to promote sustained susceptibility torifampin, these recommendations are largely based on experimental models (21–23)and the use of aminoglycosides for treatment of coagulase-negative Staphylococcus(CoNS) PVE (24). Clinical data on the benefit of aminoglycoside combination therapy inhumans for MRSA PVE are lacking. Furthermore, the use of an aminoglycoside for othercauses of endocarditis, including methicillin-sensitive Staphylococcus aureus (MSSA)native valve endocarditis (NVE) and CoNS PVE, demonstrates either harm or a lack of asurvival benefit (24–27). Although current guidelines discuss this lack of evidence, mostcontinue to recommend the addition of an aminoglycoside based on expert opinion(28–31). Trimethoprim-sulfamethoxazole, clindamycin, ceftaroline, daptomycin, lin-ezolid, telavancin, oritavancin, tigecycline, and combinations that might result insynergy could have a role in treatment but have not yet been thoroughly studied.
TIMING, PATHOPHYSIOLOGY, PATHOGENESIS, AND HISTOPATHOLOGYTiming of Infection
MRSA PVE is often dichotomized based on duration of disease (32) into early,defined as the first year postsurgery, or late, defined as after 1 year postsurgery. Thesethresholds have been developed based on the risk of developing PVE and differencesin the microbiology of the disease between periods (33, 34). The risk of PVE is greatestduring the first 3 months after surgery. The risk peaks approximately 15 days aftersurgery, during which the PVE risk is estimated to be 45 cases/100,000 patient days (35).After this time period, it decreases steadily to approximately 1 case/100,000 patientdays from 150 days to 20 years postoperatively (35–39). The cumulative proportions ofpatients developing PVE range from 1 to 3% in the first 365 days after surgery accordingto several studies with close follow-up and from 3 to 6% in 5 years (35–39). S. aureus isa frequently encountered pathogen in both early and late PVE cases (6, 16, 40, 41),accounting for approximately 12 to 36% of early cases (53 to 69% at the first 2 monthsfrom surgery) and 18 to 30% of late cases (6, 41). A large, multicenter, internationalstudy (6) showed that MRSA was the causative microorganism in 18.9% of early casesof PVE, versus 3.3% of late cases.
Pathophysiology
Early PVE infection is believed to be caused by accidental seeding during surgery ordue to bloodstream dissemination in the first hours to months postoperatively. Earlyafter surgery, the prosthetic sewing ring and cardiac connection tissue and sutureshave not yet endothelized. Fibronectin and fibrinogen coat these areas and are
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believed to be a possible nidus for infection. In late PVE infection, these cardiacstructures become fully endothelized, and the pathogenesis of disease more resemblesthat of NVE (42).
The location and distribution of PVE also differ by the type of prosthetic valve andthe route of infection (Fig. 1). In cases where the infection is introduced via contami-nation around the surgical site, it typically affects the annulus and sewing ring union,causing pseudoaneurysms, dehiscence, fistulas, and abscesses around valves (43–45). Inone postmortem study, perivalvular invasion, which is commonly coupled with pros-thesis dehiscence and paravalvular regurgitation, appeared in approximately 40% ofautopsies performed for patients with PVE, and frank extension into tissue leading tomyocardial abscess was seen in 15% (46). Annular and/or myocardial abscesses werepresent in 68% of the 47 patients with PVE in another study (47). Dehiscence of theprosthesis was described in more than 80% of cases of aortic and mitral prosthesesexamined by Ben Ismail et al. (48), and vegetations were seen in 75% (48). More than1 year postoperatively, infection related to biological PVE is more commonly found atthe prosthesis leaflets. Complications of late PVE include leaflet rupture and perforationof an aortic valve prosthesis, which can extend through the intervalvar fibrosa andannulus to cause pericarditis or, more frequently, can spread into the membranousportion of the interventricular septum and cause arrhythmia (49–51). Large vegetationsmay also keep the prosthesis open, causing malfunction or encroachment on the valveorifice, resulting in functional stenosis or regurgitation via malcoaptation or perforation.
Pathogenesis
Several independent factors are involved in the development of MRSA PVE (Fig. 2).MRSA has microbial surface components recognizing adhesive matrix molecules(MSCRAMMs) that recognize and bind to adhesion molecules of the fibrin-plateletmatrices of “nonbacterial thrombotic endocarditis,” such as fibronectin, laminin, andcollagen, and these can also adhere to the normal endothelium or minimally injuredtissue (40, 52, 53). Once the thrombus is colonized by MRSA, this microorganism canproliferate, creating the characteristic vegetation of infective endocarditis (IE). Thepresence of cardiac prostheses introduces an additional variable that favors PVE, sinceMRSA can adhere by forming biofilms (Fig. 2 and 3) (40, 53). At initial placement, thering-prosthesis interface is not endothelized and favors fibrin-platelet thrombus for-mation. The suture points where the prostheses are placed constitute a mechanismwhereby MRSA can invade the heart tissue and form abscesses. In addition, thecontinuous stress caused by the repetitive movement in the bioprostheses may disruptthe surface of the leaflets and predispose to infection of the fibrin-platelet thrombus.MRSA can reach the prosthesis by contamination of the prosthetic valve during surgery(Fig. 4) or by a hematogenous route via a catheter-related infection, intravenous druguse, a surgical wound, or pulmonary or urinary tract infection (40, 53, 54). During thesurgical procedure (Fig. 4), the surgical site may be exposed to MRSA from the patient’sor health care practitioner’s skin. The ability of S. aureus strains to produce biofilms (Fig.3) in vitro has been linked to clinically persistent MRSA bacteremia (�7 days) and theevolution of prosthetic valve vegetation propagation (52, 55, 56).
Nonvalvular invasive infection may also cause bioprosthetic valve endocarditis. Forexample, annular and myocardial invasion was observed in 38 of 85 patients (45%) inone study and was more common among cases of bioprosthetic PVE occurring duringthe first year after valve placement than in cases presenting later (59 versus 25%) (57).Invasive disease was more frequent in patients with early than in those with latebioprosthetic PVE (79% versus 31%) in another series (58).
A large proportion of cases of PVE is nosocomial and correlates with a highproportion of MRSA infections (6). An international study including 556 patients withPVE demonstrated that 36.5% of infections were nosocomially acquired or related tofrequent health care visits (6). Similarly, the use of transcatheter aortic valve implanta-tion (TAVI) also increased the risk for MRSA PVE (59, 60), as did the use of orotracheal
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FIG 1 Prosthetic valves explanted from patients with MRSA prosthetic valve endocarditis, and received at the microbiology laboratory toperform valve culture and 16S PCR (courtesy of Mercedes Marín, Hospital General Universitario Gregorio Marañón, Madrid, Spain). Shownare a mechanical valve, a mitral ring, an aortic bioprosthesis, and a mitral bioprosthesis.
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intubation and percutaneous self-expandable valves (59). Further studies are needed tobetter establish a relationship between MRSA virulence factors observed experimen-tally in vitro and in animal models (61) and clinical disease in humans.
Histopathology
There is no typical pattern of PVE histological characterization in bioprostheticvalves. As bioprosthetic valves degenerate, they often create noninfective, calcific,vegetative-like lesions with inflammatory infiltrates, which can result in a noninfectiousprocess that can mimic and be misdiagnosed as PVE. A retrospective pathological studyof inflamed bioprosthetic valve tissues from 88 cases of resected bioprosthetic valves(21 for probable endocarditis and 67 for noninfective dysfunction) was performed tobetter define the histological criteria for PVE (62). PVE was histologically characterizedby neutrophil-rich inflammatory infiltrates and the presence of microorganisms. Inflam-matory infiltrates in valve tissue samples from the noninfective control group consistedmainly of lymphocytes and macrophages. In that study, having a neutrophil percentageexceeding 1.5% of the valve surface area was associated with a high specificity (94%)for infectious PVE (62).
EPIDEMIOLOGY
PVE occurs in 1% to 6% of patients after prosthetic valve placement (63), accom-panied by an incidence of 0.3% to 1.2% per patient year (6, 64–66) and accounting for16% to 31% of IE cases in several studies (1, 6, 67–70). The etiology of 146 early-PVEclinical cases and 140 late-PVE cases was summarized from 17 published reports (32).In that study, early S. aureus PVE accounted for 19.2% of the cases, and late compli-cations were less likely with increasing time after surgery, occurring in only 11.4% of thecases. The incidence of both early and late PVE was correlated with increasing under-lying comorbidity at the time of valve placement, surgeon experience, extracorporealcirculation duration, sterility of the heart-lung machine and the operating theater,extracardiac postoperative infection, and the length of time that the patient was
FIG 2 Pathogenesis of MRSA (methicillin-resistant Staphylococcus aureus) PVE. MSCRAMMs, microbial surface components recognizingadhesive matrix molecules.
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FIG 3 An original electron scanning microscope image of a methicillin-resistant Staphylococcus aureusbiofilm on a patient’s mechanical heart prosthesis. The image was prepared at both the ClinicalMicrobiology and Infectious Diseases Department and the Pathology Department of the Hospital GeneralUniversitario Gregorio Marañón and was taken at the National Center of Electron Microscopy (JSM 6400,CNME, Madrid, Spain).
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monitored after surgery (32). MRSA accounted for approximately 6.5% of PVE cases(n � 556) assessed by the ICE Prospective Cohort Study (6). Figure 5 shows a compar-ison of cases of S. aureus (P � 0.003) and MRSA (P � 0.001) involved in PVE acrossgeographic regions. The data provided by Wang et al. (6) are consistent with the globalepidemiology of S. aureus (P � 0.007) and MRSA (P � 0.001) PVE found and also kindlyshared by Murdoch et al. (4).
In one observational study, the prophylactic use of penicillinase-resistant penicillins(methicillin and oxacillin) during the perioperative periods reduced early postoperativeS. aureus PVE (71). Unsurprisingly, the incidence of PVE was higher when the valvereplacement occurred in the setting of active or recently treated endocarditis (36, 39,72, 73). In several observational studies, bioprosthetic valves appear to increase the riskfor infection over mechanical valves after 18 months (37, 72, 73). However, threerandomized trials including 1,418 patients monitored for 8 to 20 years could notdemonstrate a statistically significant difference in PVE occurrence between biologicaland mechanical valves (P � 0.45 [74], P � 0.71 [75], and P � 0.70 [76]). Anotherobservational study that included 38,000 patients �65 years of age demonstrated ahigher risk of endocarditis after a median of 12 years of follow-up among those withbioprosthetic valves (2.2% versus 1.4%; unadjusted hazard ratio, 1.69 [95% confidenceinterval {CI}, 1.43 to 2.00]) (77). Finally, Calderwood et al. (37) showed a higher risk ofoccurrence of PVE among patients (n � 116 out of 2,608 evaluated) who receivedmechanical valves than among those who received bioprosthetic valves at 3 monthspostsurgery (P � 0.02), but in contrast, Grover et al. (73) could not demonstrate anydifference between the valves in 66 patients who developed PVE out of 1,032 observedduring a mean length of follow-up of 7.7 years.
CLINICAL PRESENTATION, ASSESSMENT, AND DIAGNOSIS
PVE signs and symptoms are similar to those of native valve disease. Yet the clinicalpresentation of MRSA PVE is often nonspecific, especially soon after surgery, wheninflammation and fever might occur for other reasons. Due to the intracardiac compli-cations described above, clinical manifestations of PVE frequently include hemolysis,heart failure, valvular dysfunction, and/or new arrhythmia (13, 78, 79). Calderwood et al.(78) studied the outcomes of 116 patients with PVE and found that 64% of individualswith PVE suffered some combination of worsened or new cardiac failure, a changed ornew cardiac murmur, continuous fever, or irregularities upon electrocardiography(ECG). These complications were more common in the first year after valve replacementand in aortic valve prosthesis infections (Table 1). New or changing murmurs, heartfailure, and new electrocardiographic conduction disturbances are noted more often in
FIG 4 Surgery image (courtesy of Gregorio Cuerpo, Cardiac Surgery, Hospital General UniversitarioGregorio Marañón, Madrid). Shown is mitral prosthetic valve endocarditis caused by S. aureus.
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PVE than in NVE cases due to the likelihood of invasive infection. ECG (Fig. 6), chestradiograph, and blood cultures are considered part of the standard work-up if there isa clinical suspicion of PVE.
Pulmonary, neurological, kidney, and musculoskeletal complications or complica-
FIG 5 Global epidemiology of MRSA involved in prosthetic valve endocarditis (PVE). The causative agents of PVE differ geographically(4, 6). Data from Wang et al. (6) were collected between June 2000 and August 2005 from 556 patients with infective prosthetic valveendocarditis in 53 sites worldwide (P � 0.003 for Staphylococcus aureus; P � 0.001 for MRSA [methicillin-resistant Staphylococcusaureus]). MSSA, methicillin-sensitive Staphylococcus aureus.
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TAB
LE1
Key
artic
les
onep
idem
iolo
gy,d
iagn
osis
,man
agem
ent,
conc
lusi
ons,
and
pre
vent
ion
ofS.
aure
usPV
Ean
dIE
a
Aut
hor
(s)
(yr)
(ref
eren
ce)
Epid
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log
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nos
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anag
emen
tC
oncl
usio
n(s
)an
d/o
rp
reve
nti
onst
rate
gy
Béra
udet
al.(
2011
)(2
15)
137
phy
sici
ans
par
ticip
ated
inth
est
udy
Infe
ctiv
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astr
eate
dw
ithge
ntam
icin
dose
sof
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g/kg
/day
by
61%
ofp
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cian
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mg/
kg/d
ayb
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d5
mg/
kg/d
ayb
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.9%
Gui
delin
esw
ere
not
follo
wed
by
mos
tof
the
phy
sici
ans
for
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amic
indo
sing
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ese
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ient
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stea
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ens
from
pub
lishe
dst
udie
sBi
lle(1
995)
(216
)A
ntim
icro
bia
lth
erap
yre
view
Endo
card
itis
due
toSt
aphy
loco
ccus
Aco
mb
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ion
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antib
iotic
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anco
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inor
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illin
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ntam
icin
and
rifam
pin
)is
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este
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ring
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ast
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k
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her
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ies
are
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edto
inco
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ate
nove
ltr
eatm
ent
optio
ns,e
spec
ially
inp
atie
nts
affe
cted
by
MRS
AC
alde
rwoo
det
al.(
1985
)(3
7)2,
642
pat
ient
sw
houn
derw
ent
valv
ere
pla
cem
ent
for
the
first
time
wer
ein
clud
edin
the
stud
y11
6p
atie
nts
with
PVE
(4.4
%)
At
12m
o,th
eris
kof
PVE
was
3.1%
,and
at60
mo,
the
risk
was
5.7%
;por
cine
valv
esha
da
sign
ifica
ntly
low
erris
kof
PVE
durin
gth
efir
st90
days
from
surg
ery
than
mec
hani
cal
valv
esb
uta
sign
ifica
ntly
high
erris
kaf
ter
12m
op
osts
urge
ry
Ther
ew
ere
sign
ifica
ntdi
ffer
ence
sin
the
risk
ofPV
Ede
pen
ding
onth
ety
pe
ofva
lve,
but
nosi
gnifi
cant
diff
eren
ces
bet
wee
np
orci
nean
dm
echa
nica
lva
lves
wer
eob
serv
edin
the
risk
ofha
ving
PVE
afte
r5
yrC
erve
raet
al.(
2014
)(2
17)
Ana
lysi
sof
ast
udy
coho
rt93
case
sof
S.au
reus
infe
ctiv
een
doca
rditi
s(le
ftsi
ded)
57%
had
ava
ncom
ycin
MIC
of�
1.5
�g/
ml,
and
43%
had
anM
ICof
�1.
5�
g/m
lPe
rcen
tage
sof
in-h
osp
ital
deat
hva
ried
sign
ifica
ntly
bet
wee
nb
oth
grou
ps,
at30
and
53%
,res
pec
tivel
yC
hiro
uze
etal
.(20
04)
(1)
Eval
uatio
nof
mor
talit
yris
k61
case
sof
S.au
reus
PVE
Patie
nts
who
had
thei
rva
lve
rep
lace
dea
rly,d
esp
iteha
ving
hear
tco
mp
licat
ions
,sho
wed
low
erm
orta
lity
rate
s(P
�0.
09)
S.au
reus
PVE
isa
dise
ase
with
high
mor
bid
ityan
dm
orta
lity
rate
s(2
8.6–
85.7
%)
Chi
rouz
eet
al.(
2015
)(1
1)Im
pac
tof
early
valv
esu
rger
yon
clin
ical
outc
ome
ofS.
aure
usPV
Ew
ithin
the
Inte
rnat
iona
lC
olla
bor
atio
nof
Endo
card
itis
747
case
sof
defin
itele
ft-s
ided
PVE
Non
-S.a
ureu
sPV
Eca
used
sign
ifica
ntly
low
erra
tes
ofde
ath
afte
r1
yrth
anS.
aure
usPV
E;at
this
time,
pat
ient
sw
ithS.
aure
usPV
Ean
dEV
Sal
soha
dlo
wer
mor
talit
yra
tes
(P�
0.01
);EV
Sdi
dno
tdi
min
ish
mor
talit
yat
1yr
Diff
eren
tfa
ctor
ssh
ould
be
take
nin
toac
coun
tb
efor
ede
cidi
ngon
EVS
Cos
grov
eet
al.(
2009
)( 2
18)
236
pat
ient
sfr
om44
hosp
itals
and
4co
untr
ies
wer
ep
rosp
ectiv
ely
eval
uate
dS.
aure
usb
acte
rem
iaan
dna
tive
valv
ein
fect
ive
endo
card
itis
Vanc
omyc
inor
anan
tista
phy
loco
ccal
pen
icill
in�
low
-do
sege
ntam
icin
orda
pto
myc
inal
one
was
adm
inis
tere
dto
pat
ient
s;re
nal
adve
rse
even
tsw
ere
eval
uate
d
Low
-dos
ege
ntam
icin
shou
ldno
tb
eus
edro
utin
ely
for
S.au
reus
bac
tere
mia
and
nativ
eva
lve
infe
ctiv
een
doca
rditi
sdu
eto
the
nep
hrot
oxic
itysh
own
deFe
iter
etal
.(20
05)
(219
)Fu
sidi
cac
id,r
ifam
pic
in,v
anco
myc
in,o
xaci
llin,
and
gent
amic
intr
eatm
ent
failu
res
Patie
ntw
ithSt
aphy
loco
ccus
epid
erm
idis
PVE
Des
pite
the
nona
pp
rova
lfo
rth
isin
dica
tion,
linez
olid
was
adm
inis
tere
dto
this
pat
ient
Patie
ntha
da
favo
rab
leou
tcom
ew
ithlin
ezol
id
Del
Río
etal
.(20
14)
(220
)Re
scue
ther
apy
with
imip
enem
�fo
sfom
ycin
Com
plic
ated
bac
tere
mia
and
MRS
Aen
doca
rditi
sTr
eatm
ent
was
succ
essf
ulin
69%
ofca
ses;
the
mor
talit
yra
tedu
eto
MRS
Aw
as1/
5(2
0%)
Com
bin
atio
nth
erap
yw
assa
fean
def
fect
ive
asre
scue
ther
apy
Fern
ánde
zG
uerr
ero
etal
.(2
009)
(15)
Inci
denc
eof
infe
ctiv
een
doca
rditi
s,ep
idem
iolo
gy,
clin
ical
feat
ures
,pro
gnos
isD
efini
teS.
aure
usen
doca
rditi
s(r
ight
side
dan
dle
ftsi
ded)
NVE
was
ale
ssco
mm
onho
spita
l-acq
uire
din
fect
ion
than
PVE;
for
bot
hty
pes
ofen
doca
rditi
s,re
nal
and
card
iac
failu
rean
dce
ntra
lne
rvou
ssy
stem
com
plic
atio
nsw
ere
dete
cted
Valv
ere
pla
cem
ent
sign
ifica
ntly
imp
rove
dou
tcom
esfo
rp
atie
nts
with
PVE
Fow
ler
etal
.(20
06)
(157
)D
apto
myc
invs
stan
dard
ther
apy
S.au
reus
bac
tere
mia
and
endo
card
itis
Mic
rob
iolo
gica
lfa
ilure
was
mor
eco
mm
onin
the
grou
ptr
eate
dw
ithda
pto
myc
inth
anin
the
one
with
stan
dard
ther
apy
Ano
ninf
erio
rity
rate
was
obse
rved
inth
egr
oup
trea
ted
with
dap
tom
ycin
com
par
edto
the
one
trea
ted
with
stan
dard
ther
apy
for
bac
tere
mia
and
right
-sid
eden
doca
rditi
sca
used
by
S.au
reus
Has
bun
etal
.(20
03)
(221
)Pr
ogno
stic
fact
ors
Left
-sid
eden
doca
rditi
s(n
ativ
eva
lve)
with
com
plic
atio
nsFa
ctor
sre
late
dto
mor
talit
yaf
ter
6m
o,in
clud
ing
abno
rmal
men
tal
stat
us,b
acte
rial
caus
e,co
mor
bid
ities
,m
edic
altr
eatm
ent,
mod
erat
e/se
vere
cong
estiv
eca
rdia
cfa
ilure
4gr
oup
sof
pat
ient
sw
ere
iden
tified
dep
endi
ngon
the
mor
talit
yris
k6
mo
afte
rb
asel
ine
Hol
land
etal
.(20
14)
(222
)Re
view
onho
spita
lm
anag
emen
tBa
cter
emia
caus
edb
yS.
aure
usD
iagn
ostic
met
hods
and
antib
iotic
trea
tmen
tst
rate
gies
Ther
ear
egr
oup
sof
pat
ient
sw
hodo
not
need
TEE
John
etal
.(19
98)
(3)
Clin
ical
stra
tegi
esan
dp
rogn
ostic
fact
ors
Defi
nite
PVE
caus
edb
yS.
aure
usC
omp
licat
ions
affe
ctin
gth
ece
ntra
lne
rvou
ssy
stem
(33%
)an
dhe
art
(67%
)w
ere
foun
d;th
e3-
mo
mor
talit
yra
tew
as42
%
Mor
ep
atie
nts
died
due
tohe
art
pro
ble
ms
than
due
top
rob
lem
saf
fect
ing
the
cent
ral
nerv
ous
syst
em,b
utth
ism
orta
lity
was
dim
inis
hed
whe
nth
ere
was
surg
ery
for
valv
ere
pla
cem
ent
durin
gan
tibio
tictr
eatm
ent
Kang
etal
.(20
12)
(223
)6-
wk
occu
rren
ceof
emb
olic
even
tsan
dm
orta
lity
Patie
nts
with
larg
eve
geta
tions
,se
vere
dise
ase
inva
lves
,lef
t-si
ded
endo
card
itis
due
toin
fect
ion
Patie
nts
wer
era
ndom
ized
into
2gr
oup
s,co
nven
tiona
ltr
eatm
ent
orea
rlysu
rger
yRa
tes
ofem
bol
icev
ents
and
mor
talit
ysi
gnifi
cant
lyde
crea
sed
inth
egr
oup
with
early
surg
ery
com
par
edto
the
grou
pof
pat
ient
str
eate
dco
nven
tiona
llyKa
rchm
eret
al.(
1983
)(2
4)Re
tros
pec
tive
stud
yof
75PV
Eca
ses
Stap
hylo
cocc
usep
ider
mid
isPV
ETh
ege
ntam
icin
susc
eptib
ility
rate
was
78%
,and
thos
efo
rrif
amp
inan
dva
ncom
ycin
wer
e10
0%fo
ral
lis
olat
este
sted
;dys
func
tion
ofva
lves
and
tissu
ep
rogr
essi
onw
ere
the
mos
tco
mm
onp
rob
lem
s,ne
edin
gsu
rger
yin
30ca
ses
Ant
ibio
ticth
erap
yin
clud
ing
vanc
omyc
in�
rifam
pin
oran
amin
ogly
cosi
dein
crea
sed
favo
rab
leou
tcom
era
tes;
surg
ical
trea
tmen
tw
asal
soim
por
tant (C
ontin
ued
onne
xtp
age)
Staphylococcus aureus Prosthetic Valve Endocarditis Clinical Microbiology Reviews
April 2019 Volume 32 Issue 2 e00041-18 cmr.asm.org 9
on July 4, 2020 by guesthttp://cm
r.asm.org/
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nloaded from
TAB
LE1
(Con
tinue
d)
Aut
hor
(s)
(yr)
(ref
eren
ce)
Epid
emio
log
yD
iag
nos
isM
anag
emen
tC
oncl
usio
n(s
)an
d/o
rp
reve
nti
onst
rate
gy
Karc
hmer
(199
1)(2
24)
Infe
ctio
nco
ntro
lPV
ED
urin
ga
year
pos
tsur
gery
,the
noso
com
ial
risk
ofPV
Ew
as1.
4–3.
0%;t
hem
ost
com
mon
reas
onfo
rho
spita
l-ac
quire
dPV
Ew
asm
ethi
cilli
n-re
sist
ant
coag
ulas
e-ne
gativ
eSt
aphy
loco
ccus
Furt
her
stud
ies
are
need
edto
dete
ctp
osts
urgi
cal
caus
esof
hosp
ital-a
cqui
red
PVE
and
dim
inis
hth
em
Lean
dBa
yer
(200
3)(2
25)
Revi
ewon
antib
iotic
trea
tmen
tfo
ren
doca
rditi
sca
used
by
freq
uent
lyde
tect
edm
icro
orga
nism
sFe
wst
rate
gies
for
invi
tro,
exp
erim
enta
l,an
dcl
inic
alev
alua
tion
ofen
tero
cocc
alen
doca
rditi
sha
veb
een
show
n
Hum
ancl
inic
alda
taar
esc
arce
onco
mb
inat
ion
antib
iotic
trea
tmen
tfo
rin
fect
ive
endo
card
itis
due
toS.
aure
usM
ayer
and
Scho
enb
aum
(198
2)(2
26)
Revi
ewan
dap
pro
ach
PVE
Hig
her
rate
sof
mor
bid
ityan
dm
orta
lity
wer
ede
tect
edin
early
than
inla
tePV
Eca
ses;
the
etio
logy
ofte
nin
clud
edfu
ngi,
stap
hylo
cocc
i,an
dG
ram
-neg
ativ
ero
dsin
early
PVE
and
stre
pto
cocc
iin
late
PVE
Fact
ors
rela
ted
top
oor
outc
ome
wer
eea
rlyPV
E,p
arav
alvu
lar
leak
age,
emb
oli,
per
sist
ent
feve
r,no
nstr
epto
cocc
alm
icro
orga
nism
s,no
nhet
erog
raft
aort
icva
lve,
cong
estiv
eca
rdia
cfa
ilure
Muñ
ozet
al.(
2015
)(1
2)Ep
idem
iolo
gy,c
linic
alfe
atur
es,p
rogn
ostic
fact
ors
Infe
ctiv
een
doca
rditi
s(1
,804
case
s)Pr
evio
usca
rdia
csu
rger
y,at
rial
fibril
latio
n,ca
rdia
cco
mp
licat
ions
and
failu
re,s
eptic
shoc
k,ag
e,ce
reb
rova
scul
arco
mp
licat
ions
,or
Cand
ida
orSt
aphy
loco
ccus
caus
ew
asre
late
dto
in-h
osp
ital
deat
hs(2
8.9%
);af
ter
1yr
,ass
ocia
tion
was
foun
dfo
rca
ncer
,ca
rdia
cfa
ilure
,age
,and
rena
lin
suffi
cien
cy(1
1.2%
)
The
rate
sof
in-h
osp
ital
and
1-yr
deat
hsw
ere
elev
ated
,and
surg
ery
was
the
only
pro
tect
ive
fact
or
Mur
doch
etal
.(20
09)
( 4)
Glo
bal
infe
ctiv
eca
uses
and
clin
ical
feat
ures
Infe
ctiv
een
doca
rditi
sIn
fect
ions
ofm
itral
and
aort
icva
lves
due
toS.
aure
usw
ere
the
mos
tfr
eque
ntp
rese
ntat
ion,
also
com
plic
ated
with
hear
tfa
ilure
,str
oke,
and
othe
rem
bol
ian
dab
sces
sin
the
hear
t
Risk
fact
ors
for
in-h
osp
ital
mor
talit
yw
ere
lung
edem
a,ag
e,p
rost
hetic
infe
ctio
n,S.
aure
usor
coag
ulas
e-ne
gativ
est
aphy
loco
ccal
caus
e,m
itral
vege
tatio
n,an
dva
lve
pro
ble
ms
Raja
shek
arai
ahet
al.(
1980
)(2
6)Ev
alua
tion
ofto
lera
nce
(MBC
/MIC
�16
)S.
aure
usb
acte
rem
iaan
den
doca
rditi
sTo
lera
ntm
icro
orga
nism
sw
ere
acco
mp
anie
db
ym
ore
deat
hs,c
omp
licat
ions
,hos
pita
lizat
ion
inIC
U,
pro
long
atio
nof
feve
r
Poor
outc
omes
ofen
doca
rditi
sw
ere
mor
eco
mm
onin
case
sca
used
by
tole
rant
mic
roor
gani
sms
than
inca
ses
caus
edb
yse
nsiti
veon
esRi
ber
aet
al.(
1996
)(2
7)C
loxa
cilli
nvs
clox
acill
in�
gent
amic
indu
ring
2w
kS.
aure
usen
doca
rditi
s(r
ight
side
d)M
orta
lity
occu
rred
1an
d2
case
s,re
spec
tivel
yC
omb
inat
ion
trea
tmen
tw
asno
tm
ore
effe
ctiv
eth
anth
esi
ngle
one
Soha
ilet
al.(
2006
)(1
7)M
orta
lity
rate
sin
pat
ient
sw
hore
ceiv
edm
edic
alvs
surg
ical
trea
tmen
tS.
aure
usPV
EM
orta
lity
rate
sof
48%
and
28%
,res
pec
tivel
yTh
eno
.of
deat
hsw
aslo
wer
inth
esu
rgic
algr
oup
;bio
pro
sthe
ticva
lves
and
ASA
clas
sIV
wer
ep
rogn
ostic
fact
ors
Wan
get
al.(
2007
)(6
)G
lob
alin
fect
ive
caus
esan
dcl
inic
alfe
atur
esPV
ETh
em
ost
freq
uent
mic
roor
gani
smw
asS.
aure
us;3
6.5%
ofca
ses
wer
ere
late
dto
heal
thca
re;t
heof
in-h
osp
ital
deat
hra
tew
as22
.8%
and
was
rela
ted
tohe
alth
care
,ag
e,p
ersi
sten
tb
lood
stre
amin
fect
ion,
S.au
reus
caus
e,an
dca
rdia
can
dC
NS
pro
ble
ms
S.au
reus
isgl
obal
lyth
em
ain
caus
eof
PVE,
and
the
pre
senc
eof
com
plic
atio
nsis
anim
por
tant
pro
gnos
ticfa
ctor
War
eham
etal
.(20
05)
(227
)C
ases
trea
ted
with
linez
olid
MRS
Ean
dVR
Een
doca
rditi
sIn
vitr
ost
udy
ofSt
aphy
loco
ccus
epid
erm
idis
and
Ente
roco
ccus
faec
alis
infe
ctio
nstr
eate
dw
ithlin
ezol
id�
gent
amic
inor
vanc
omyc
in
Out
com
ew
asfa
vora
ble
inb
oth
case
s
Wat
anak
unak
orn
(197
9)(3
2)Tr
eatm
ent
with
pen
icill
invs
pen
icill
in�
gent
amic
inS.
aure
usen
doca
rditi
sTh
ede
ath
rate
was
40%
inb
oth
grou
ps
ofp
atie
nts
Ther
eis
nocl
inic
ally
dem
onst
rate
dad
vant
age
ofth
eus
eof
com
bin
atio
nth
erap
yw
ithge
ntam
icin
Wils
onet
al.(
1995
)(2
28)
Trea
tmen
tef
ficac
yex
per
ienc
eEn
doca
rditi
sca
used
by
ente
roco
cci,
stap
hylo
cocc
i,st
rep
toco
cci,
and
mem
ber
sof
the
HA
CEK
grou
p
Reco
mm
enda
tions
oftr
eatm
ent
bas
edon
pre
viou
sly
rep
orte
dst
udie
sLi
tera
ture
issc
arce
Yaw
etal
.(20
14)
(229
)C
linic
alou
tcom
eev
alua
tion
MRS
Aan
dM
SSA
bac
tere
mia
Reho
spita
lizat
ion
rate
sas
soci
ated
with
infe
ctio
nw
ere
sim
ilar
inb
oth
grou
ps
ofp
atie
nts
MSS
Ab
acte
rem
iaou
tcom
esw
ere
mor
efa
vora
ble
than
MRS
Ab
acte
rem
iaon
es;
pat
ient
sco
loni
zed
with
MRS
Ash
ould
be
trea
ted
care
fully
aA
SA,A
mer
ican
Soci
ety
ofA
nest
hesi
olog
ists
;EVS
,ear
lyva
lve
surg
ery;
MBC
,min
imal
bac
teric
idal
conc
entr
atio
n;M
RSA
,met
hici
llin-
resi
stan
tSt
aphy
loco
ccus
aure
us;M
RSE,
met
hici
llin-
resi
stan
tSt
aphy
loco
ccus
epid
erm
idis
;NVE
,na
tive
valv
een
doca
rditi
s;PV
E,p
rost
hetic
valv
een
doca
rditi
s;TE
E,tr
anse
sop
hage
alec
hoca
rdio
grap
hy;V
RE,v
anco
myc
in-r
esis
tant
Ente
roco
ccus
;IC
U,i
nten
sive
care
unit;
HA
CEK
grou
p,a
grou
pof
Gra
m-n
egat
ive
bac
illi
cons
istin
gof
Hae
mop
hilu
ssp
p.,
Act
inob
acill
usac
tinom
ycet
emco
mita
ns,C
ardi
obac
teriu
mho
min
is,E
iken
ella
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tions associated with systemic infections might also occur, at the same time, in somePVE cases (80–87). Of note, S. aureus is the pathogen most commonly related to IEcomplications compared to others (88). Lung complications are more frequently seenin patients with right-sided endocarditis, in several cases presenting manifestationssuch as pneumonia, abscesses, pleural effusion, and/or atelectasis.
Central nervous system (CNS) complications, primarily embolic infarcts or hemor-rhage, are also more common in PVE than in NVE cases, ranging from 20 to 40%, withovert arterial emboli being noted for 40% of patients with PVE (48, 89–91). Similar ratesof embolic stroke (18%) and ischemic stroke (20%) among patients with PVE werereported by Davenport and Hart (92) and Keyser et al. (89), respectively. FernándezGuerrero et al. (15) observed that, compared to NVE, S. aureus PVE clinical manifesta-tions were characterized by less-frequent cardiac murmurs and a shorter symptomaticprodrome.
In PVE patients with no prior antibiotic therapy, blood cultures are positive in at least90% of cases (63). Molecular techniques, such as DNA examination by pulsed-field gelelectrophoresis or 16S rRNA sequencing, can be used when standard blood or tissuecultures have not revealed a pathogen (93, 94).
Transesophageal echocardiography (TEE) has poorer diagnostic validity for PVE(including MRSA PVE) than for NVE (95). However, TEE with a high-resolution biplane ormultiplane transducer that allows continuous-wave and pulsed-wave Doppler andcolor flow imaging can increase the accuracy of diagnosis of PVE (96). TEE is consideredthe method of choice for diagnosis of PVE (97), because although transthoracicechocardiography (TTE) may lead to a diagnosis in some cases, TEE has a highersensitivity for PVE (98, 99) (Fig. 7A). This increase in sensitivity is not accompanied bya loss of specificity and is independent of the valve type or position (98–101). Forsuspected PVE, TEE sensitivity and specificity have been estimated at 77 to 90% and90%, respectively, compared to TTE, with a specificity and sensitivity estimated at 40 to70% and 90%, respectively (102). Nonetheless, TTE has value for the assessment ofventricular size and function and severe hemodynamic lesions in valves and can often
FIG 6 Electrocardiogram at 25 mm/s of a patient with aortic MRSA PVE with nonspecific findings, including tachycardia (heart rate of approximately 125 beatsper minute), a first-degree block with a PR interval exceeding a duration of 0.2 s (indicated by the arrow), and ST segment changes (indicated by the circle).
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FIG 7 Imaging modalities for MRSA prosthetic valve endocarditis diagnosis. (A) Transesophageal echocardiography demonstrating a 1.4- by1.2-cm highly mobile echodensity at the ventricular side of the bioprosthetic aortic valve (indicated by the arrow), without significant valvulardysfunction. (B) Transthoracic echocardiogram image showing a parasternal view with the prosthetic aortic valve, right ventricular outflow tract,and aorta on the top; the left atrium and mitral valve at the bottom; and the left ventricle on the left. The prosthetic aortic valve is not wellvisualized, but there is a vegetation on the ventricular side (indicated by the circle) and anterior aortic root thickening (indicated by the arrow),
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detect anterior aortic prosthetic valve abscesses (103) (Fig. 7B). Typically, the ventricularsurfaces of prostheses in the mitral, tricuspid, and aortic positions are better viewed byTTE, whereas TEE has additional value for viewing the aortic valve surfaces, tricuspidand mitral valves, and the exit of the prosthesis in the aorta; fistula and abscessdetection; detection of paraprosthetic leaks; and visualization of a mitral valve pros-thesis (104, 105). However, TEE will miss some cases of prosthetic valve dehiscence. Ina study of 26 patients with PVE, there were 14 (56%) cases of aortic valve dehiscenceintraoperatively, 4 (29%) of which were not detected upon TEE (106). One prospectivestudy that compared the paired use of TTE with TEE in 114 episodes of clinicallysuspected IE (34 PVE and 80 NVE) found that the results of the two tests wereconcordant in only 55% of cases (107). TEE prompted reclassification for 34% of patientswith prosthetic valves, compared with 11% of patients with native valves.
The Duke criteria have been described as being less useful for the diagnosis of PVEbecause of low sensitivity (108, 109) compared to the sensitivity of 70 to 80% (110, 111)in the diagnosis of NVE. Because of diagnostic challenges in PVE with standard testingand clinical scores, other techniques have been assessed. Magnetic resonance imaging(MRI) and multislice computed tomography (MS-CT) might improve the detection of anintra- or pericardiac anatomical complication (112). The value of ECG-gated multide-tector CT angiography (MDCTA) was addressed by three studies (113–115), whichdemonstrated a �90% sensitivity for the diagnosis of PVE (113), which was improvedto a sensitivity and a specificity of 100% and 83%, respectively, after completion ofroutine testing for endocarditis and resulted in modification of therapy in 25% of cases(115) (Fig. 7C).
Recently, nuclear imaging has shown promise for improving diagnostics. [18F]fluo-rodeoxyglucose positron emission tomography electrocardiogram-gated computer to-mography ([18F]FDG PET/CT) scans have shown utility as an additional diagnosticcriterion for PVE in cases where a diagnosis cannot be made with standard echocar-diography (116–119) (Fig. 7D). FDG PET/CT detects inflammation early in the infectionprocess (120). For suspected PVE, [18F]FDG PET/CT demonstrated a 67 to 100% positivepredictive value, a 50 to 100% negative predictive value, 73 to 100% sensitivity, and 71to 100% specificity (116–119, 121–123). As such, an algorithm reported by Saby et al.(116) shows that PET/CT is useful to assess probable PVE cases. This algorithm incor-porates the PET/CT 2013 modified Duke criteria for the diagnosis of possible PVE casesthat do not meet criteria for endocarditis by the modified Duke criteria but remainunder high clinical suspicion. The sensitivity of the modified Duke criteria significantlyincreased with the addition of PET imaging to the scoring system, from 70% (95% CI,52% to 83%) to 97% (95% CI, 83% to 99%) (P � 0.008). This result was the consequenceof a significant reduction (P � 0.0001) in the number of possible PVE cases from 56%to 32% (116).
Three retrospective studies have addressed the value of technetium-99m-hexamethylpropylene amine oxime (99mTc-HMPAO)-labeled leukocyte scintigraphywith single-photon emission tomography/computed tomography (SPECT/CT) for thedetection of PVE (119, 124, 125). Probable (125) or definite (119, 124) IE cases wereincluded. Globally leukocyte scintigraphy showed an 85 to 100% positive predictivevalue, a 47 to 81% negative predictive value, 64 to 90% sensitivity, and 36 to 100%specificity (126). Further evaluations with increased sample sizes will be helpful forbetter defining a role and optimal scenario of nuclear imaging in the diagnosis of PVE.
TREATMENT
The S. aureus PVE mortality rate remains high (25 to 42%) (3, 54) despite advancesin antibiotic treatment (1). Both the American Heart Association (AHA) and its European
FIG 7 Legend (Continued)suggestive of an aortic root abscess. There is also mild prosthetic aortic valve regurgitation, but it cannot be appreciated in the still image. (C)Electrocardiogram-gated multidetector CT angiography demonstrating a 4- by 8-mm vegetation on the bioprosthetic aortic valve. (D) PET/CTimage at the posterior prosthetic aortic valve, after 16.29 mCi [18F]fluorodeoxyglucose uptake. The arrow notes an area of hyperintensity,suggesting a focus of inflammation or infection consistent with prosthetic valve endocarditis.
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counterpart, the European Society for Cardiology (ESC), suggest a triple-drug regimen(class I; level of evidence C) with vancomycin and rifampin for �6 weeks and genta-micin during the first 2 weeks for the management of MRSA PVE (Table 2) (29, 30).
These recommendations are based on CoNS PVE therapeutic regimen activity, IEexperiments, and retrospective clinical series (57, 127–130). A single retrospective studyof valve cultures from 61 patients with staphylococcal PVE (29 due to S. aureus and 32due to CoNS) treated surgically showed that those receiving combination therapy were5.9 times more likely to have culture-negative valves than patients receiving mono-therapy (adjusted by the length of therapy prior to surgery) (128). In this study, the sixpatients treated with a triple-drug regimen including rifampin prior to surgery hadnegative valve cultures. Regarding surgical indication, all of the groups of therapyevaluated for S. aureus NVE and any staphylococcal NVE or PVE were similar (P � 0.53,P � 0.51, and P � 0.66, respectively). No data on clinical outcomes restricted to thosewith S. aureus PVE were reported.
Antibiotic recommendations for treatment of MRSA PVE are also partially based onex vivo and animal studies of Staphylococcus epidermidis PVE. A retrospective evaluationof 23 cases of methicillin-resistant S. epidermidis (MRSE) PVE (129) showed an increasein serum bactericidal activity when rifampin was added to vancomycin regimens (129).Studies regarding MRSE endocarditis in rabbit models also demonstrated that genta-micin, rifampin, and vancomycin in combination increased the efficacy of eradication ofS. epidermidis from vegetations compared to beta-lactam antibiotics alone (131, 132).Another study (130) found that when rifampin was added to the combination ofvancomycin and gentamicin in broth, there was an enhanced bactericidal effect inrabbits despite antagonism of the bactericidal rate. Notably, similar data for theserelationships on MRSA are lacking.
Vancomycin
Vancomycin remains the mainstay of therapy for MRSA PVE (29, 30). Vancomycindosing should be based on actual body weight and adjusted to achieve troughs of 15to 20 �g/ml (29). Vancomycin binds the terminal D-alanyl-D-alanine moieties ofN-acetylmuramic acid (NAM)/N-acetylglucosamine (NAG) peptides in the bacterial cellwall and thus prevents the addition of the NAM/NAG peptide subunits into thepeptidoglycan matrix of MRSA. It also acts by altering bacterial cell membrane perme-ability and RNA synthesis (133). Common vancomycin toxicities include hypersensitivity(“red man syndrome,” related to the infusion rate) after intravenous administration andnephrotoxicity when used concomitantly with aminoglycosides (134). Significantweight gain can also occur during prolonged treatment, particularly in older men (135).
Rifampin
The rifampin mechanism of action is based on the suppression of RNA synthesisthrough the inhibition of the bacterial DNA-dependent RNA polymerase. Rifampin isbelieved to bind to a pocket of the RNA polymerase �-subunit within the DNA/RNAchannel. This noncompetitive inhibitor prevents RNA synthesis by directly blocking RNAelongation and thus preventing the synthesis of host bacterial proteins (136). Hepaticand immunoallergic toxicities are the most common rifampin adverse effects. Hepato-
TABLE 2 International guidelines for therapy of MRSA PVEa
ESC guidelines for adults
AHA guidelines
Pediatric Adult
Vancomycin at 30–60 mg/kg Q24h i.v., BID or TIDduring �6 wk
Vancomycin at 40 mg/kg Q24h i.v. (maximum dose, 2 g Q24h),BID or TID during �6 wk
Vancomycin at 30 mg/kg Q24h i.v., BIDduring �6 wk
Rifampin at 900–1,200 mg Q24h i.v./orally, BID orTID during �6 wk
Rifampin at 20 mg/kg Q24h i.v. (maximum dose, 900 mgQ24h), TID during �6 wk
Rifampin at 900 mg Q24h i.v./orally, TIDduring �6 wk
Gentamicin at 3 mg/kg Q24h i.v./i.m., once a dayor BID during the first 2 wk
Gentamicin at 3 to 6 mg/kg Q24h i.v./i.m., TID during the first2 wk
Gentamicin at 3 mg/kg Q24h i.v./i.m., BIDor TID during the first 2 wk
aThe doses of these drugs must be adjusted in the setting of renal insufficiency. The intravenous (i.v.) route is preferred, particularly in infants and children. Q24h,every 24 h; BID, twice a day; TID, three times a day; i.m., intramuscular.
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toxicity usually affects patients with previous liver damage and is associated with thedose administered. Adverse immunoallergic events might be minor or major and arepredominantly observed after prolonged or intermittent treatment (137).
Animal model experiments, in vitro data, and clinical observations have each dem-onstrated an outsized beneficial effect of rifampin on foreign-material infections (24, 57,127, 130, 138–140). Nevertheless, S. aureus has a high intrinsic mutation rate at the rpoBgene, encoding the rifampin-binding site. When large numbers of S. aureus bacteria areexposed to rifampin alone or in combination with ineffective antimicrobials, singlemutations in this region allow the rapid selection of a rifampin-resistant subpopulation(57, 138). Consequently, recommended regimens support the selection of two addi-tional antimicrobials with rifampin, to protect against the development of resistance torifampin. Similarly, many have recommended waiting until vancomycin and gentamicinhave been administered for 3 to 5 days, bacteremia has resolved, and undrainedabscesses or collections have been debrided prior to initiation of rifampin (30). Thisapproach is supported by the in vitro antagonism demonstrated when rifampin isexposed to replicating bacteria in combination with other antimicrobials (141) and thesynergism detected when bacteria are instead in a latent state (142). This effect can beseen in biofilm-mediated foreign-body infections, such as those associated with ortho-pedic hardware, prostheses, or vascular grafts (143). Lowy et al. (131) prevented thedevelopment of rifampin-resistant S. epidermidis by adding either vancomycin orgentamicin in a rabbit endocarditis model, but these observations have unclear clinicalutility in treating PVE in humans.
Rifampin is recommended for a minimum of 6 weeks, at a dosing regimen of 300 mgevery 8 h, in combination with gentamicin for the first 2 weeks and vancomycin for thefull treatment course of 6 weeks (29, 31). Notably, some authors alternatively recom-mend rifampin at 600 mg once daily or 300 to 450 mg every 12 h with anotherantistaphylococcal antibiotic for S. aureus infections (31).
The data on synergy between rifampin and other antimicrobials are conflicting (144,145). Although several studies (146–148) have demonstrated that incorporating rifam-pin into failing therapies can increase bactericidal rates and the chances of eradicationof serious S. aureus and S. epidermidis infections, others have reported both in vitrosynergy and antagonism for rifampin in combination with beta-lactam agents, vanco-mycin, or gentamicin against S. aureus (149, 150). Another study concluded that therewas no synergy or antagonism against MRSE regarding the concomitant use of otherantibiotics (cephalothin, nafcillin, vancomycin, or gentamicin) with rifampin (127).
MRSE isolates harboring rifampin mutations appeared to be as virulent as theirrifampin-sensitive antecedents in rabbit endocarditis models, although a similar effectwas not seen in rifampin-resistant S. aureus isolates in a mouse model (151). Themechanism of decreased virulence may be due to decreased production of toxins byrifampin-resistant S. aureus (127). The emergence of rifampin resistance was notprevented in vivo by the combination of rifampin with a beta-lactam antibiotic,although it was prevented in vitro. There was no decrease in virulence of rifampin-resistant methicillin-resistant S. epidermidis in comparison to rifampin-sensitive ante-cedent strains (127). The MRSE study showed good bactericidal efficacy of rifampin invitro when there was a prevention of emergent rifampin-resistant mutants by abeta-lactam antibiotic.
Gentamicin
European and U.S. guidelines suggest intramuscular or intravenous gentamicin at adose of 3 mg/kg of body weight every 24 h, once daily or in 2 or 3 divided doses, forthe treatment of MRSA PVE. Gentamicin serum levels and renal function should beassessed at least once weekly, and more-frequent measurements are suggested incases of renal insufficiency. Gentamicin doses as high as 4 mg/kg/day have beendemonstrated to be successful in MRSA PVE treatment without additional toxicity inboth human and animal studies (152, 153). In nonobese adults, the gentamicin dose isbased on ideal body weight. Gentamicin is not distributed into adipose tissue, as it is
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highly hydrophilic. Therefore, corrected body weight should be used for dosing calcu-lations for obese patients, rather than ideal body weight. The gentamicin mechanismof action is based on irreversible binding to specific proteins on the 30S subunit of theMRSA ribosome and the decoding site of the 16S rRNA. This leads to a misreading ofthe mRNA, the addition of incorrect amino acids in the growing peptide chain, and theinterruption of MRSA protein synthesis (154).
Ototoxicity and nephrotoxicity are important adverse events limiting gentamicinclinical use. Both side effects are associated with the dose administered and might notappear until the end of treatment. Kidney damage, in contrast to inner ear damage, isusually reversible but can be fatal (155, 156). Gentamicin trough and peak values lowerthan 1 �g/ml and 3 to 4 �g/ml, respectively, are recommended when gentamicin isadministered every 8 h. When gentamicin is dosed daily, serum troughs should belower than 1 �g/ml. ESC guidelines recommend that peaks be assessed once afterinfusion, with a goal range of 10 to 12 �g/ml (per AHA/IDSA guidelines, there is no rolefor measuring peak gentamicin concentrations following single daily dosing).
The risk-to-benefit ratio of gentamicin therapy for MRSA PVE remains controversial.In a study of 35 ex vivo strains of S. aureus isolated from blood cultures of septic patients(23), vancomycin or nafcillin combined with tobramycin, gentamicin, or kanamycin hadimproved activity against most of the strains. In a rabbit model of S. aureus endocarditis,nafcillin and gentamicin altogether achieved a faster eradication of S. aureus at theheart vegetation than nafcillin in monotherapy (22).
Nonetheless, clinical data in support of gentamicin use in this setting are lacking. Ina recent study comparing daptomycin therapy with an antistaphylococcal penicillin orvancomycin in combination with gentamicin for MSSA or MRSA bacteremia and/orright-sided endocarditis (157), significantly more patients who received standard ther-apy with gentamicin suffered nephrotoxicity (18.1% versus 6.7% with renal tubularnecrosis and 46.8% versus 19.8% with worsening creatinine clearance), without animprovement in clinical outcomes for those who received gentamicin (157). Whetherthese results pertain to MRSA PVE is unknown, but this topic warrants urgent studygiven the ongoing guideline recommendations for the use of gentamicin in thetreatment of MRSA PVE.
Alternative Therapies
If an isolate is resistant to gentamicin and all available aminoglycosides, a fluoro-quinolone to which the strain is highly susceptible has been recommended (138–140).If the patient is treated with a fluoroquinolone instead of an aminoglycoside, athree-drug regimen for the entire course of treatment is preferred. In cases of resistanceto aminoglycosides and fluoroquinolones, ceftaroline, trimethoprim-sulfamethoxazole,or linezolid (158) has been proposed as the third agent during the first 2 weeks oftreatment, if the isolate is susceptible in vitro.
For cases of MRSA PVE with reduced vancomycin susceptibility (MIC � 1.0 �g/ml),substantial toxicity, or failure of vancomycin, the optimal treatment is not established.Options include high-dose daptomycin (8 to 10 mg/kg once per day, if the isolate isdaptomycin susceptible), linezolid, telavancin, ceftaroline, and daptomycin combinedwith ceftaroline, nafcillin, or fosfomycin, combinations that might result in synergy(159–165). Yet reported clinical experience with these treatments and combinationtherapies in MRSA PVE is limited. Daptomycin combination with rifampin and genta-micin has been recommended in these cases as a second-line therapy for MRSA PVE(30). Synergy between �-lactams and daptomycin is associated with several character-istics, including increased daptomycin binding and �-lactam-mediated potentiation ofinnate immunity, but the precise molecular mechanism is unknown (139). Dhand etal. (166) reported a series of seven cases with rapid clearance of persistent MRSAbacteremia when high-dose nafcillin was added to high-dose daptomycin. Otherexperts (167) suggested the use of high-dose daptomycin combined with fosfomy-cin for MRSA PVE.
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There are several case reports of ceftaroline being used to successfully treat refrac-tory or drug-resistant MRSA PVE, either alone (168) or in combination therapy (169). Inone case report, the efficacy and tolerability of ceftaroline were demonstrated in onepatient with osteomyelitis and endocarditis caused by an MRSA strain that was notsusceptible to daptomycin (170). A patient with MRSA aortic PVE was also cured withprolonged high-dose daptomycin plus ceftaroline after other therapeutic failures (169).
Ceftaroline fosamil was the most active bactericidal drug in a rabbit model of MRSAendocarditis (171). For each MRSA strain, rabbits were randomized to no therapy(controls), a ceftaroline fosamil dose equivalent to 10 mg/kg/12 h in humans (600 mgtwice daily), daptomycin at a dose comparable to 6 mg/kg/24 h in humans, or atigecycline dose equivalent to 100 mg/24 h in humans plus 50 mg/12 h. Both ceftaro-line and daptomycin exhibited high bactericidal efficacy based on MRSA vegetationreduction rates (�5 log10 CFU/g), whereas tigecycline did not show bactericidal effi-cacy, and MRSA vegetation reduction rates were �2 log10 CFU/g in comparison tocontrols. However, the MRSA vegetation sterilization rate by ceftaroline was 100%, incontrast to the rate of 57% reached by daptomycin, with resistant mutants being seenonly in the daptomycin therapy group. Recent clinical data also demonstrate ceftarolineas an alternative for MRSA bacteremia salvage treatment (170, 172–177). Two obser-vational studies also suggest that ceftaroline therapy alone (178) or in combinationwith trimethoprim-sulfamethoxazole (179) can be used to treat invasive MRSA infec-tion, although more experience and, if possible, adequately designed clinical studiesare needed before there is widespread recommendation for its use.
Linezolid is an alternate treatment in cases of MRSA PVE complicated by drug allergyor intolerance, although its use is limited by a relative scarcity of data and side effectsof prolonged use. Among 33 cases of endocarditis treated with linezolid, 21 (63.6%) hada favorable outcome. PVE accounted for 25% of the reviewed cases, and MRSAaccounted for 24.2% (1 case of MRSA PVE among 8 PVE cases [12.5%]). The one patientwith MRSA PVE treated with linezolid had a favorable outcome. Additional efficacy andtolerability data are required to better support the use of linezolid for PVE (180).
In an experimental rabbit model, Miró et al. (181) suggested that telavancin couldbe as effective as vancomycin in the treatment of endocarditis caused by glycopeptide-intermediate S. aureus (GISA). Other experimental IE models also showed telavancinbactericidal activity against different MRSA strains, including daptomycin-resistant S.aureus, vancomycin-intermediate S. aureus (VISA), and GISA (182–184). Telavancin (185)and also quinupristin-dalfopristin (186) have been reported as favorable rescue thera-pies in MRSA IE patients after vancomycin clinical failure.
The efficacy of oritavancin was also recently assessed in animal models of left-sidedMRSA endocarditis. The drug has gained attention for its single intravenous dosingschedule at 1,200 mg over 3 h, which allows treatment of complicated MRSA infectionswithout the need for indwelling central venous catheters, a particular concern forpatients with recent or active injection drug use, and has shown promise in otherrefractory and drug-resistant cases of PVE (187, 188). A left-sided MRSA endocarditisrabbit model suggested that oritavancin was superior to vancomycin in resolvingbacteremia and reducing bacterial counts in vegetations and tissues (189). Thoseinvestigators concluded that oritavancin was microbiologically effective and might bean alternative to vancomycin in treating similar infections in humans (189). Of note,Stewart et al. (190) reported a case series of 10 patients treated with oritavancin,including 1 patient with NVE due to group B Streptococcus, who unfortunately failedtreatment. Although oritavancin is currently indicated only for acute bacterial skin andskin structure infections, it has the potential to play an increasing role as an agentagainst MRSA PVE, particularly in light of the ongoing international opioid epidemic(191, 192).
Tigecycline has activity against MRSA; however, it has been demonstrated to havea lower efficacy than vancomycin against MRSA strains (193), and its peak serumconcentrations do not exceed 1 �g/ml (194, 195). As such, tigecycline is not typicallyrecommended as an agent for MRSA bacteremia or endocarditis. Similarly, although
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clindamycin and trimethoprim-sulfamethoxazole are theoretically alternative optionsfor MRSA PVE, experience with these agents for this condition is limited, and they aretypically considered only in the case of severe drug intolerance or as considerations insynergistic regimens (196).
The “Endocarditis Team”
A multidisciplinary team including specialists from different clinical fields (neurology,microbiology, infectious diseases, cardiology, imaging, surgery, and congenital heart dis-ease) (30) has been recommended for the management of PVE (197, 198). Early involve-ment of all team members is crucial to this strategy. Some studies have reported reductionsin 1-year mortality rates of PVE with the implementation of such teams (199, 200).
Choice and Timing of Surgery
Surgery is recommended for high-risk patients, particularly those with valvularfailures complicated by heart failure, abscess formation, or fistulas and those notresponding to maximally effective antimicrobial therapy (30). The timing of surgery forPVE is a topic of ongoing debate (2, 7, 16, 17, 201–203) and is a decision based onsurgeon- and patient-specific factors, including complications of disease, such as CNSemboli and hemorrhage, and overall surgical risk. A recent study of 4,166 cases ofinfective PVE and NVE in patients with heart failure found decreases in both hospitaland 1-year deaths with early surgery (during the index hospitalization) (65). Morerecently, two prospective cohort studies, reported by Chirouze et al. (11) and Lalaniet al. (204), found a crude reduction in 1-year mortality rates with early versus delayedsurgery but similar rates after consideration of confounding and survivor bias. Thus, thedecision on the timing of therapy continues to largely depend on surgical risk and inputfrom multidisciplinary teams.
PROGNOSIS
The PVE mortality rate remains high in the current era, ranging from 30 to 80% forearly PVE and 20 to 40% for late PVE (54, 63). The identification of high-risk subgroupsis critical to establishing more-effective treatment strategies (9). Health care-associateddisease, staphylococcal or fungal etiologies, older age, diabetes mellitus, early PVE,heart failure, CNS embolic disease, and intracardiac abscess are predictive of worseclinical outcomes (1, 3, 8, 13, 65, 205). Among these, staphylococcal infection (5) andcomplicated PVE (78) are the strongest indicators of poor outcomes. Patients withcomplications require aggressive management, including antibiotic therapy and, often,early surgery (30).
PREVENTION
The utility of antimicrobial prophylaxis for prevention of bacteremia and IE inhumans remains unclear (30, 206). Since the relaxation of antibiotic prophylaxis afterthe 2007 guideline revisions, no incremental increase in the IE incidence was observed(207, 208), with the exception of a recent ecological study showing increased rates ofStreptococcus but not staphylococcal IE cases since the guideline change (209). Accord-ing to current guidelines, antimicrobial prophylaxis is recommended for high-riskpatients (30, 33, 71, 210–213) undergoing high-risk procedures (30), including thosewith prosthetic heart valves. Probably as important as antibiotic prophylaxis is carefulattention to skin and dental hygiene. Moreover, procedures affecting gastrointestinal,respiratory, musculoskeletal, genitourinary, and dermatological systems do not typicallyrequire antimicrobial prophylaxis unless they are invasive (30).
CHALLENGES AND FUTURE PERSPECTIVES
MRSA is an increasingly common cause of PVE and continues to be among the mostmorbid infections in the modern era. Recent data have changed our approach to thisdisease. Multidisciplinary teams can improve outcomes (200, 214), and specializedcenters are an important aspect of optimizing care. Moreover, both nuclear imagingmodalities and molecular techniques that show promise in improving PVE diagnostic
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sensitivity are emerging. Finally, a number of newer agents that are active againstMRSA have recently been approved and have shown early efficacy in the managementof this condition. However, because prospective and randomized clinical data on themanagement of MRSA PVE remain scarce, recently updated international practiceguidelines for IE from the ESC and the American College of Cardiology (30) continue torely largely on nonhuman data and expert opinion. As such, important priorities for thefield include (i) validating newer diagnostic modalities, such as advanced cardiacimaging, that may increase the sensitivity and specificity of PVE diagnosis; (ii) clarifyingthe role and optimal timing of valve replacement; (iii) performing comparative effec-tiveness studies to assess newer alternatives to vancomycin with gentamicin andrifampin as the mainstays of therapy; and (iv) clarifying the role of aminoglycosides inMRSA PVE therapy.
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Alicia Galar, Pharm.D., Ph.D., studied Phar-macy at the University of Navarra and didboth her residency in Clinical Microbiologyand Parasitology and Ph.D. at the ClínicaUniversidad de Navarra. She was a Postdoc-toral Clinical Research Fellow/Specialist atBrigham and Women’s Hospital and HarvardMedical School. Dr. Galar worked at theWorld Health Organization (WHO) Collabo-rating Centre for Surveillance of Antimicro-bial Resistance and joined the Transplantand Oncology Team at the Infectious Diseases Division of Brigham andWomen’s Hospital/Dana-Farber Cancer Institute/Massachusetts GeneralHospital. She completed her education with several courses at theHarvard School of Public Health, Massachusetts General Hospital, andHarvard University. She is currently working at the Department ofClinical Microbiology and Infectious Diseases of the Hospital GeneralUniversitario Gregorio Marañón in Madrid. Dr. Galar’s main researchinterests include antimicrobial resistance, therapeutic drug monitoring,pharmacokinetic/pharmacodynamic (PK/PD) strategies, antimicrobialstewardship, vaccines, prosthetic-device-related infections, infective en-docarditis, and infections in patients with heart diseases.
Ana A. Weil holds an M.P.H. from the JohnsHopkins School of Public Health and an M.D.at Tufts University. She trained in internalmedicine and infectious diseases at Massa-chusetts General Hospital (MGH), where shealso served as a chief resident. Dr. Weil iscurrently a physician-scientist in the Infec-tious Diseases Division at MGH. The Weillaboratory is focused on understanding theinfluence of the gut microbiome in suscep-tibility to enteric infections and pathogen-gut microbe interactions at the mucosal surface, including identifyinggut species that may protect against infection and relationships be-tween gut microbial species and mucosal immune responses. Dr. Weilalso treats general medicine and infectious disease patients at MGH andhas held several leadership positions in medical education, including asa faculty advisor for an elective course at Harvard Medical School.
David M. Dudzinski studied Medicine atHarvard Medical School and trained at Mas-sachusetts General Hospital, where he was achief resident. He is board certified in inter-nal medicine, cardiovascular diseases, nu-clear cardiology, adult comprehensive echo-cardiography, and critical care medicine. Dr.Dudzinski is a cardiologist, cardiac intensiv-ist, and echocardiographer at Harvard Med-ical School and Massachusetts General Hos-pital and serves as a staff cardiac intensivistin the cardiac and cardiac surgical intensive care units, with a clinicalexpertise centered on the nascent field of critical care cardiology. Dr.Dudzinski’s academic interests are in pulmonary embolism, right ven-tricle function, procedural echocardiography, aortic disease, qualityimprovement, medical education, resuscitation science and emergencycardiovascular care, and critical care cardiology. Dr. Dudzinski is also anattorney with expertise in the scientific and legal aspects of the regu-lation of protein-based therapeutics, and he serves on the AmericanCollege of Cardiology’s national medical professional liability workinggroup.
Patricia Muñoz, M.D., Ph.D., studied Medi-cine at the Complutense University of Ma-drid (UCM) and trained at the HospitalClínico San Carlos. She was deputy editor ofClinical Microbiology and Infection and wasawarded the Young Investigator Award ofthe European Society of Clinical Microbiol-ogy and Infectious Diseases. She is currentlyProfessor in Medicine in Clinical Microbiol-ogy at UCM and Head of the Section ofClinical Microbiology and Infectious Diseasesat the Hospital General Universitario Gregorio Marañón (HGUGM). Dr.Muñoz’s research interests include fungal infections; infective endocar-ditis; infections in solid-organ transplant recipients, immunocompro-mised hosts, and heart surgery patients; and nosocomially acquiredinfectious diseases. She is an active member of the European StudyGroups for Nosocomial Infections and Infection in Compromised Hostand the Spanish Network of Infection in Transplantation. She is theSecretary of the Group for the Management of Infective Endocarditis atHGUGM and has been President of the Spanish Society for Cardiovas-cular Infections.
Mark J. Siedner is an Associate Professor ofMedicine at Harvard Medical School andholds an M.D. from the Johns Hopkins Uni-versity School of Medicine and an M.P.H.from the Johns Hopkins Bloomberg Schoolof Public Health. He trained in internal med-icine at Columbia University Medical Centerand in infectious diseases at MassachusettsGeneral Hospital (MGH). His clinical work fo-cuses on clinical infectious disease both atMGH and as an HIV care provider in south-western Uganda and Kwazulu-Natal, South Africa. He leads a researchprogram in Uganda and South Africa in partnership with MGH and theAfrica Health Research Institute, aimed at mitigating the causes ofmorbidity and mortality among people living with HIV in low-incomecountries.
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