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Changing Patient Characteristics and the Effect on Mortality in Endocarditis
Christopher H. Cabell, MD;
James G. Jollis, MD;
Gail E. Peterson, MD;
G. Ralph Corey, MD;
Deverick J. Anderson, MD;
Daniel J. Sexton, MD;
Christopher W. Woods, MD;
L. Barth Reller, MD;
Thomas Ryan, MD;
Vance G. Fowler, Jr, MD, MHS
Arch Intern Med. 2002;162:90-94.
ABSTRACT
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Background Limited data exist on recent demographic and microbiological changes
in infective endocarditis (IE) and the impact of these changes on patient
survival.
Methods Data were collected from all patients with definite or possible IE at
Duke University Medical Center, Durham, NC, from 1993 to 1999. Logistic regression
analysis was used to identify demographic and microbiological changes that
occurred in patients with IE over the study period. The impact of these changes
on survival was evaluated using Cox proportional hazards modeling.
Results Among the 329 study patients, rates of hemodialysis dependence, immunosuppression,
and Staphylococcus aureus infection increased during
the study period (P= .04, P=
.008, and P<.001, respectively), while rates of
infection due to viridans group streptococci decreased (P= .007). Hemodialysis was independently associated with S aureus infection (odds ratio, 3.1; 95% confidence interval, 1.6-5.9).
Patients with S aureus IE had a higher 1-year mortality
rate (43.9% vs 32.5%; P= .04) that persisted after
adjustment for other illness severity characteristics (hazard ratio, 1.5;
95% confidence interval, 1.03-2.3).
Conclusions The demographic and microbiological characteristics of IE at our institution
have changed over the past decade in ways that suggest a link between medical
practice and IE characteristics. Staphylococcus aureus
has emerged as a dominant cause of IE, and is an independent predictor of
mortality. These findings identify clinical settings that may warrant closer
surveillance and more aggressive measures in the identification and prevention
of endocarditis.
INTRODUCTION
HISTORICALLY, infective endocarditis (IE) was predominantly a disease
of patients with preexisting valvular abnormalities and community-associated
bacteremia. Streptococcal species accounted for 60% to 80% of all cases, and
most patients had rheumatic heart disease.1-2
Over the past 20 years, significant changes in the demographic characteristics
of IE have occurred. For example, the prevalence of rheumatic heart disease
has decreased,3-5
while the prevalence of chronically ill patients receiving intensive and invasive
care has increased.6-8
Approximately 20 years ago, leaders in IE research suggested that the
preceding demographic changes would have a dramatic impact on the manifestations
and outcomes of IE.4, 9 Specifically,
increased use of invasive procedures (eg, surgical procedures, central intravenous
catheters, hemodialysis) and steadily rising rates of nosocomial bacteremia
were cited as factors that could increase the frequency of endocarditis.9 In addition, advances in echocardiography and the
use of validated diagnostic criteria have enhanced the ability of clinicians
to diagnose endocarditis.10-15
Although descriptive studies on the epidemiology of IE in the 1980s and 1990s
have been published,16-24
there are limited data available to understand the relationships between changing
characteristics and outcomes in endocarditis.
We studied all patients with definite or possible IE seen at Duke University
Medical Center, Durham, NC, from 1993 to 1999 in an effort to identify changes
in demographic and microbiological characteristics in patients with endocarditis.
In addition, we sought to classify relationships between demographic characteristics
and microbiological etiologies and determine effects on survival.
PATIENTS AND METHODS
PATIENT SELECTION
The study received institutional review board approval. Patients were
identified in 3 ways: (1) a member of the endocarditis service screened patients
admitted to Duke University Medical Center between January 1, 1993, and December
31, 1999, and who underwent an echocardiogram for evaluation of suspected
IE; (2) referral to the infectious disease service for the evaluation of IE;
and (3) referral to the cardiology service for evaluation of IE. To preserve
the statistical assumption of independence of observations, only the initial
episode of endocarditis for each patient was included in the study. All patients
with definite or possible IE as determined by the Duke criteria10
were enrolled in this study. Data were collected from each patient's medical
record and clinical course. Immune suppression was defined as having received
more than 30 days of systemic corticosteroid therapy ( 10 mg/d of prednisone
or equivalent drug) or other immunosuppressive therapy (eg, organ transplantation
or cancer chemotherapy).
ECHOCARDIOGRAPHIC ASSESSMENT
Transthoracic echocardiography (TTE) and transesophageal echocardiography
(TEE) were performed as previously described.25-26
Images for TTE and TEE were recorded on -in super VHS (vertical helix
scan) videotape and in digital loop display format (EchoNet; Heartlab Inc,
Westerly, RI, or EnConcert; Agilent Technologies Inc, Andover, Mass). A cardiologist
member of the endocarditis team, specifically trained in echocardiography,
interpreted echocardiograms for research purposes. The cardiologist interpreting
echocardiograms was not part of the clinical care team and was blinded to
clinical information for each patient. Echocardiographic findings of IE such
as vegetations, oscillation, myocardial abscess, and prosthetic valve dehiscence
were defined as previously described.10, 25-26
MICROBIOLOGICAL ASSESSMENT
All blood cultures received from patients enrolled in this study were
routinely processed in the clinical microbiology laboratory and incubated
in an automated monitoring system for a minimum of 5 days. Duration of incubation
was extended (up to 14 days) when requested by the clinical team. Identification
of gram-positive organisms and yeasts was performed using standard microbiological
methods. Most gram-negative organisms were evaluated using an automated identification
system (MicroScan Walkaway; Dade MicroScan, Inc, West Sacramento, Calif).
FOLLOW-UP
Survival data were obtained on all patients by assessing the medical
record to determine dates of clinic visits, admissions, and deaths at Duke
Medical Center. To determine survival after hospitalization, a national death
index search was performed for those patients without documentation of death
in the hospital system.
STATISTICAL ANALYSES
Descriptive statistics are presented as percentages for discrete variables.
Continuous variables are presented as mean ± SD. Discrete variables
were compared with the 2 test. Logistic regression was used
to determine independent predictors of Staphylococcus aureus infection as well as the relationship between a later year of diagnosis
and a particular characteristic. Independent predictors of mortality were
determined with Cox proportional hazards models. A 2-sided P value of less than .05 was considered significant for all statistical
tests. All statistical analyses were done with the use of the Statistical
Analysis System, version 6.1 (SAS Institute Inc, Cary, NC).
RESULTS
DEMOGRAPHIC CHARACTERISTICS
During the study period, 1855 patients were screened; 375 patients met
criteria for definite or possible IE and were entered into the endocarditis
database. Forty patients had multiple episodes of IE (2 episodes in 36 patients,
3 episodes in 3 patients, and 5 episodes in 1 patient). Only the first episode
of IE was used for these 40 patients. Of the 329 patients enrolled in this
study, 185 (56.2%) had definite IE (Table
1). The mean age was 57 years and the male-female ratio was 1.2:1.
Diabetes and hemodialysis were more common than intravenous drug abuse and
human immunodeficiency virus infection. Sixty-three percent of patients were
transferred from outside facilities.
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Table 1. Demographic and Organism Characteristics of 329 Patients With
Endocarditis*
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ORGANISM FREQUENCIES
Forty percent (132/329) of the patients were infected with S aureus (Table 1). Of
these 132, 79 (60%) were infected with methicillin-susceptible strains, accounting
for 24% of the total cases. Patients with methicillin-resistant S aureus IE accounted for 40% (53/132) of patients with S aureus infection and 16% of the total cases. Coagulase-negative staphylococci,
viridans group streptococci, and enterococci were less common. Other organisms
classically associated with IE, such as Strepococcus bovis, were rare.
DEMOGRAPHIC AND ORGANISM CHANGES DURING THE 1990s
Demographic and microbiological characteristics were studied to determine
if significant changes in these characteristics occurred over the study period
(Table 2). The frequency of patients
with hemodialysis dependence, immunosuppression, and S aureus infection all increased significantly during the study period (P = .04, P = .008, and P<.001, respectively). In addition, the frequency of viridans group
streptococci infecting patients with IE decreased during the same interval
(P = .007) (Figure
1).
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Table 2. Time Trend Analysis for Changing Characteristics*
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Changing characteristics from 1993 to 1999 of 329 patients with infective
endocarditis.
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PREDICTORS OF S AUREUS
Multivariable logistic regression analysis was used to determine which
demographic characteristics were predictive of S aureus infection (Table 3). Characteristics
that increased during the 1990s (hemodialysis and immunosuppression) were
combined with clinically important characteristics that might be related to
infectious etiologies. These clinical characteristics included year of diagnosis,
prosthetic valve IE, age, sex, Duke diagnostic classification10
(possible or definite), diagnosis of diabetes mellitus, transfer from referring
hospital, and presence of myocardial abscess. Hemodialysis and year of diagnosis
were independently predictive of S aureus infection
(P<.001 for both), while patients with prosthetic
valve involvement were half as likely to be infected with S aureus (P = .03).
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Table 3. Predictors of Staphylococcus aureus Endocarditis in Patients With Endocarditis
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ECHOCARDIOGRAPHIC FINDINGS
Echocardiographic findings were also analyzed over the decade of the
1990s. There were no echocardiographic findings that showed a significant
change over the study period. Overall, 86% of patients underwent both TTE
and TEE. In most patients who had both studies, TEE was the most diagnostic.
MORTALITY AT 30 DAYS AND 1 YEAR
At 30 days, 16.4% of patients had died, and the mortality rate at 1
year was 37.1% (Table 4). When
stratified by S aureus infection, there was a trend
toward higher mortality at 30 days for those patients infected with S aureus (18.9% vs 14.7%; P =
.31). At 1 year, the mortality for patients with IE infected with S aureus was significantly higher than for those without S aureus infection (43.9% vs 32.5%; P = .04).
Those patients with methicillin-resistant S aureus
IE had a particularly high mortality at 1 year compared with patients with
IE due to other pathogens (49.1% vs 34.8%; P = .05).
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Table 4. Unadjusted 30-Day and 1-Year Mortality of Patients With Endocarditis
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A multivariable Cox proportional hazards model was used to determine
which patient characteristics were independently predictive of survival at
1 year. Variables included in the model were those found to change over the
study period (S aureus infection, hemodialysis, and
immunosuppression) and important characteristics that might affect survival
(age, year of diagnosis, hemodialysis, immunosuppression, surgical therapy,
and prosthetic valve infection). Staphylococcus aureus
infection, immunosuppression, and age were the only independent predictors
of mortality. Patients with endocarditis caused by S aureus had a 1.5-fold increase in the risk of death over 1 year (hazard ratio
[HR], 1.5; 95% confidence interval [CI], 1.03-2.3). Patients with IE and immunosuppression
had a similar increase in the risk of death over 1 year (HR, 1.7; 95% CI,
1.01-2.8). Finally, age at the time of diagnosis was also independently related
to an increase in the risk of death (HR, 1.02; 95% CI, 1.01-1.04).
COMMENT
This investigation of a large cohort of patients with well-characterized
endocarditis has identified important relationships between changing characteristics
and the effect of these changes on survival. The results of this investigation
yielded several key observations.
CHANGE IN DEMOGRAPHIC CHARACTERISTICS
The demographic characteristics of patients with endocarditis have changed
over the last decade. Patients diagnosed with IE later in the decade were
more likely to have recently undergone intensive and/or invasive medical care.
The primary manifestation of this change was an increase in the frequency
of patients undergoing hemodialysis or immunosuppressive therapy later in
the decade. These findings are consistent with previous studies documenting
an increase in the number of patients receiving hemodialysis8
and immunosuppressive therapy,27-28
and suggest that aggressively treated patients represent an emerging population
at risk for IE. Other recent cohort investigations also underscore the importance
of medical instrumentation as a risk factor for IE. For example, in one recent
report, 21 of 22 cases of nosocomial IE occurred as a consequence of a medical
or surgical procedure.29
CHANGES IN MICROBIOLOGICAL CHARACTERISTICS OF IE
During the 1990s, changes also occurred in the proportions of specific
pathogens causing IE. By the end of the decade, S aureus was the single most common cause of IE at our institution, accounting
for nearly 40% of all patients with IE. During the same period, IE caused
by viridans group streptococci became less common. The increasing importance
of S aureus as a cause of IE in our patients is consistent
with other studies showing increases in the overall rates of S aureus bacteremia30 and related infections
such as vertebral osteomyelitis31 and IE.32-36
RELATIONSHIP BETWEEN DEMOGRAPHIC AND MICROBIOLOGICAL CHARACTERISTICS
In this study we found a parallel increase in the frequency of patients
undergoing hemodialysis and/or immune suppression and those infected with S aureus. The association between these comorbid conditions
and S aureus IE may be due to several factors. First,
patients undergoing immunosuppressive therapy and those undergoing hemodialysis
are highly susceptible to bacterial infections, including S aureus.37 This susceptibility may
be due in part to both the underlying disease and its treatment. The susceptibility
is also related to the method by which the treatment is delivered: specifically,
intravenous catheters.
Studies have shown a strong relationship between immune suppression,
vascular catheters, and hospital-acquired infections.6-7
Intravascular devices are important risk factors for S aureus bacteremia and IE.34, 38
In this study, hemodialysis was independently predictive of S aureus infection, which was 3 times as likely to occur in hemodialysis
patients than in those not undergoing hemodialysis.
IMPACT OF CHANGING CHARACTERISTICS ON SURVIVAL
Patient outcome was also related to demographic and microbiological
changes. Consistent with previous reports,32-36
patients with S aureus IE experienced a significantly
higher unadjusted and adjusted 1-year mortality than patients with IE due
to other pathogens. If the proportion of cases caused by S aureus continues to increase, this finding may have important implications
on overall IE mortality rates.
STUDY LIMITATIONS
This study has several limitations. Although uniform data collection
methods were used, ascertainment bias may have been present. For instance,
our screening mechanism identified only those patients referred to the echocardiography
laboratory, the infectious disease service, or the cardiology service for
the evaluation of IE. It is possible that time trends in referral for echocardiography
or consultation may have affected our results. In addition, our patients were
hospitalized at a large tertiary care medical center, and most of these patients
transferred from another hospital. Thus, the frequency, type, and severity
of IE in our institution were likely to differ from IE encountered in a community
hospital setting.
CONCLUSIONS
The demographic and microbiological characteristics of IE at our institution
have changed over the past decade, which suggests a link between medical practice
and IE characteristics. Staphylococcus aureus infection
has emerged as a dominant cause of IE, and is an independent predictor of
mortality. These findings identify clinical settings that may warrant closer
surveillance and more aggressive measures to identify and prevent endocarditis.
Future investigations, ideally in the form of prospective, multicenter collaborations,
will be necessary to more precisely characterize the impact of changes in
medical practice on the clinical spectrum of endocarditis.
AUTHOR INFORMATION
Accepted for publication May 8, 2001.
This study was supported by the Four Schools Physician Scientist Program
sponsored by the Lucille P. Markee Charitable Trust, Philadelphia, Pa (Dr
Cabell); grants AI-01647 (Dr Fowler) and HL03995-01 (Dr Jollis) from the National
Institutes of Health, Bethesda, Md; and the Joseph C. Greenfield, Jr Scholars
Program, Durham, NC (Dr Cabell).
Presented in part at the 40th Interscience Conference on Antimicrobial
Agents and Chemotherapy, Toronto, Ontario, September 18, 2000.
Corresponding author and reprints: Christopher H. Cabell, MD, Duke
University Medical Center, Box 31020, Durham, NC 27710 (e-mail: chris.cabell{at}duke.edu).
From the Department of Medicine, Duke University School of Medicine
(Drs Cabell, Jollis, Peterson, Corey, Anderson, Sexton, Woods, Reller, Ryan,
and Fowler), Duke Clinical Research Institute (Drs Cabell and Jollis), and
Durham Veterans Administration Medical Center (Dr Peterson), Durham, NC.
REFERENCES
 |  |
1. Rabinovich S, Evans J, Smith IM, January LE. A long-term view of bacterial endocarditis: 337 cases 1924-1963. Ann Intern Med. 1965;63:185-198.
2. Weinstein L, Rubin RH. Infective endocarditis: 1973. Prog Cardiovasc Dis. 1973;16:239-274.
FULL TEXT
| PUBMED
3. Garvey G, Neu HC. Infective endocarditis: an evolving disease: a review of endocarditis at the Columbia-Presbyterian Medical Center, 1968-1973. Medicine (Baltimore). 1978;57:105-127.
PUBMED
4. Kaye D. Changing pattern of infective endocarditis. Am J Med. 1985;78(suppl 6B):157-162.
5. Bayer AS. Infective endocarditis. Clin Infect Dis. 1993;17:313-320.
ISI
| PUBMED
6. Ellis ME, Rhydderch D, Zwaan F, Guy ML, Baillie F. High incidence of line-related infection and mechanical failure of
an antiseptic-impregnated central venous catheter in highly immunocompromised
patients. Scand J Infect Dis. 1996;28:91-93.
ISI
| PUBMED
7. Burgner D, Dalton D, Hanlon M, Wong M, Kakakios A, Isaacs D. Repeated prevalence surveys of paediatric hospital-acquired infection. J Hosp Infect. 1996;34:163-170.
FULL TEXT
|
ISI
| PUBMED
8. United States Renal Data System. USRDS 1999 Annual Data Report. Bethesda, Md: National Institutes of Health, National Institute of
Diabetes and Digestive and Kidney Diseases; 1999:39-55.
9. Watanakunakorn C. Infective endocarditis as a result of medical progress. Am J Med. 1978;64:917-919.
FULL TEXT
|
ISI
| PUBMED
10. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of
specific echocardiographic findings. Am J Med. 1994;96:200-209.
FULL TEXT
|
ISI
| PUBMED
11. Bayer AS, Ward JI, Ginzton LE, Shapiro SM. Evaluation of new clinical criteria for the diagnosis of infective
endocarditis. Am J Med. 1994;96:211-219.
FULL TEXT
|
ISI
| PUBMED
12. Del Pont JM, De Cicco LT, Vartalitis C, et al. Infective endocarditis in children: clinical analyses and evaluation
of two diagnostic criteria. Pediatr Infect Dis J. 1995;14:1079-1086.
ISI
| PUBMED
13. Hoen B, Beguinot I, Rabaud C, et al. The Duke criteria for diagnosing infective endocarditis are specific:
analysis of 100 patients with acute fever or fever of unknown origin. Clin Infect Dis. 1996;23:298-302.
ISI
| PUBMED
14. Hoen B, Selton-Suty C, Danchin N, et al. Evaluation of the Duke criteria versus the Beth Israel criteria for
the diagnosis of infective endocarditis. Clin Infect Dis. 1995;21:905-909.
ISI
| PUBMED
15. Bayer AS. Diagnostic criteria for identifying cases of endocarditis: revisiting
the Duke criteria two years later. Clin Infect Dis. 1996;23:303-304.
ISI
| PUBMED
16. Hogevik H, Olaison L, Andersson R, Lindberg J, Alestig K. Epidemiologic aspects of infective endocarditis in an urban population: a 5-year prospective study. Medicine (Baltimore). 1995;74:324-339.
FULL TEXT
| PUBMED
17. Delahaye F, Goulet V, Lacassin F, et al. Characteristics of infective endocarditis in France, 1991: a one-year
survey. Eur Heart J. 1995;16:394-401.
FREE FULL TEXT
18. Tornos MP, Olona M, Permanyer-Miralda G, Almirante B, Evangelista A, Soler-Soler J. Is the clinical spectrum and prognosis of native valve infective endocarditis
in non-addicts changing? Eur Heart J. 1995;16:1686-1691.
FREE FULL TEXT
19. Siddiq S, Missri J, Silverman DI. Endocarditis in an urban hospital in the 1990s. Arch Intern Med. 1996;156:2454-2458.
ABSTRACT
20. Benn M, Hagelskjaer LH, Tvede M. Infective endocarditis, 1984 through 1993: a clinical and microbiologic
survey. J Intern Med. 1997;242:15-22.
FULL TEXT
|
ISI
| PUBMED
21. Strom BL, Abrutyn E, Berlin JA, et al. Dental and cardiac risk factors for infective endocarditis. Ann Intern Med. 1998;129:761-769.
FREE FULL TEXT
22. Dyson C, Barnes RA, Harrison GAJ. Infective endocarditis: an epidemiological review of 128 episodes. J Infect. 1999;38:87-93.
FULL TEXT
|
ISI
| PUBMED
23. Netzer RO, Zollinger E, Seiler C, Cerny A. Infective endocarditis: clinical spectrum, presentation and outcome. Heart. 2000;84:25-30.
FREE FULL TEXT
24. Strom BL, Abrutyn E, Berlin JA, et al. Risk factors for infective endocarditis: oral hygiene and nondental
exposures. Circulation. 2000;102:2842-2848.
FREE FULL TEXT
25. Heinle S, Wilderman N, Harrison JK, et al. Value of transthoracic echocardiography in predicting embolic events
in active infective endocarditis. Am J Cardiol. 1994;74:799-801.
FULL TEXT
|
ISI
| PUBMED
26. Fowler VG, Li J, Corey GR, et al. Role of echocardiography in evaluation of patients with Staphylococcus aureus bacteremia. J Am Coll Cardiol. 1997;30:1072-1078.
ABSTRACT
27. Budman DR, Korzun AH, Aisner J, et al. A feasibility study of intensive CAF as outpatient adjuvant therapy
for stage II breast cancer in a cooperative group. Cancer Invest. 1990;8:571-575.
ISI
| PUBMED
28. Tourani JM, Lucas V, Mayeur D, et al. Subcutaneous recombinant interleukin-2 (rIL-2) in outpatients with
metastatic renal cell carcinoma. Ann Oncol. 1996;7:525-528.
FREE FULL TEXT
29. Gouello JP, Asfar P, Brenet O, Kouatchet A, Berthelot G, Alquier P. Nosocomial endocarditis in the intensive care unit: an analysis of
22 cases. Crit Care Med. 2000;28:377-382.
FULL TEXT
|
ISI
| PUBMED
30. Steinberg JP, Clark CC, Hackman BO. Nosocomial and community-acquired Staphylococcus
aureus bacteremias from 1980 to 1993. Clin Infect Dis. 1996;23:255-259.
ISI
| PUBMED
31. Jensen AG, Espersen F, Skinhoj P, Rosdahl VT, Frimodt-Moller N. Increasing frequency of vertebral osteomyelitis following Staphylococcus aureus bacteremia in Denmark, 1980-1990. J Infect. 1997;34:113-118.
FULL TEXT
|
ISI
| PUBMED
32. Sanabria TJ, Alpert JS, Goldberg R, Pape LA, Cheeseman SH. Increasing frequency of staphylococcal infective endocarditis. Arch Intern Med. 1990;150:1305-1309.
ABSTRACT
33. Saiman L, Prince A, Gersony WM. Pediatric infective endocarditis in the modern era. J Pediatr. 1993;122:847-853.
ISI
| PUBMED
34. Watanakunakorn C. Staphylococcus aureus endocarditis at a community
teaching hospital, 1980-1991. Arch Intern Med. 1994;154:2330-2335.
ABSTRACT
35. Fernandez-Guerrero ML, Verdejo C, Azofra J, de Gorgolas M. Hospital-acquired infectious endocarditis not associated with cardiac
surgery. Clin Infect Dis. 1995;20:16-23.
ISI
| PUBMED
36. Roder BL, Wandall DA, Frimodt-Moller N, Espersen F, Skinhoj P, Rosdahl VT. Clinical features of Staphylococcus aureus
endocarditis. Arch Intern Med. 1999;159:462-469.
FREE FULL TEXT
37. Zimakoff J, Bangsgaard PF, Bergen L, et al. Staphylococcus aureus carriage and infections
among patients in four haemo- and peritoneal-dialysis centers in Denmark. J Hosp Infect. 1996;33:289-300.
FULL TEXT
|
ISI
| PUBMED
38. Fowler VG Jr, Sanders LL, Kong LK, et al. Infective endocarditis due to Staphylococcus aureus. Clin Infect Dis. 1999;28:106-114.
ISI
| PUBMED
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