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Infective
Endocarditis
Management in the Era
of Intravascular Devices
edited by
John L. Brusch
Cambridge Health Alliance
Cambridge, Massachusetts, U.S.A.
New York London
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© 2007 by Informa Healthcare USA, Inc.
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International Standard Book Number-10: 0-8493-7097-3 (Hardcover)
International Standard Book Number-13: 978-0-8493-7097-7 (Hardcover)
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Library of Congress Cataloging-in-Publication Data
Brusch, John L.
Infective endocarditis : management in the era of intravascular devices / John L.
Brusch.
p. ; cm. -- (Infectious disease and therapy ; v. 41)
Includes bibliographical references and index.
ISBN-13: 978-0-8493-7097-7 (hardcover : alk. paper)
ISBN-10: 0-8493-7097-3 (hardcover : alk. paper)
1. Infective endocarditis--Treatment. 2. Cardiovascular instruments, Implanted. I.
Title. II. Series.
[DNLM: 1. Endocarditis, Bacterial. 2. Defibrillators, Implantable--adverse effects.
3. Heart Catheterization--adverse effects. 4. Heart Valve Prosthesis--adverse effects.
W1 IN406HMN v.41 2007 / WG 285 B912i 2007]
RC685.E5B78 2007
616.1’106--dc22 2006101797
Visit the Informa Web site at
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This book is dedicated to my beloved wife,
Patricia Brusch, whose support makes
all things possible. She is my heart and soul.
To my children Amy Claire, Meaghan, and
Patrick, who have accomplished so much
at an early age.
A special acknowledgment of my gratitude
for the prodigious efforts of my friend,
Fred Centanni, who ensured that the layout of the book and
the tables and figures are of the highest quality.
He has become a virtual author.
Preface
My experience with infective endocarditis extends back to my third year in medical
school when I was assigned to present a case on endocarditis on teaching rounds
to Dr. Louis Weinstein the next day. To prepare, I read Dr. Weinstein’s three-part
New England Journal of Medicine article, “Infective Endocarditis in the Antibiotic Era.”
Because of the lateness of the hour and the encyclopedic nature of Dr. Weinstein’s
review, the only thing I was able to comprehend was that I, a third-year medical
student, was presenting to a world’s expert on the subject. This unnerved me to the
point that when I opened my mouth really nothing came out. Dr. Weinstein calmed
me down and I managed to get through the presentation. Despite this less than
auspicious beginning, I persevered in learning as much as I could about endocarditis.
I became one of Dr. Weinstein’s fellows. In the early 1990s, he asked me to co-author
a text on infective endocarditis. It was a wonderful opportunity. I had access to his
case files, library, and his unique experience. His generation was the one that saw
the disease before and after the advent of antibiotics. Our book (Infective Endocarditis,
Oxford University Press, 1996) presented the disease from its first recognition
through the onset of AIDS.
This new volume covers the recent profile of this disease. Classic subacute
valvular infections still exist. However, Staphylococcus aureus and coagulase-negative
staphylococci have become the prominent pathogens. They have assumed this
prominence not simply because of their increasing resistance to antimicrobial
agents. The major reason for the increasing involvement of the staphylococci in
valvular infections is the proliferation of intravascular devices.
This realization inspired the title, Management of Infective Endocarditis in the Era
of Intravascular Devices. Subacute disease is thoroughly presented. However, the
dominant theme throughout this book is the ability of the staphylococci and other
bacteria to infect prosthetic material. I have attempted to cover this topic from the
perspective of the pathogenic properties of the organisms as well as of the defects in
the defenses of the hosts who require these intravascular devices.
Because of the specialized nature of many of the areas to be covered, I called
upon Drs. Cunha, Picard, Jassal, and Kradin to contribute their extensive knowl-
edge and experience to the book. I am deeply grateful for their efforts.
John L. Brusch
v
Acknowledgment
John L. Brusch, MD, and Louis Weinstein, MD
In grateful acknowledgment of the many contributions to the study of infective
endocarditis made by the late Louis Weinstein, M.D.
vii
Contents
Preface . . . . v
Acknowledgment . . . . vii
Contributors . . . . xi
1. Epidemiology 1
John L. Brusch
2. Microbiology of Infective Endocarditis and Clinical Correlates:
Gram-Positive Organisms 13
John L. Brusch
3. Microbiology of Infective Endocarditis and Clinical Correlates:
Gram-Negative and Other Organisms 51
John L. Brusch
4. Pathology of Infective Endocarditis 101
Richard L. Kradin
5. Pathoanatomical, Pathophysiological, and Clinical Correlations 119
John L. Brusch
6. Clinical Manifestations of Native Valve Endocarditis 143
John L. Brusch
7. Endocarditis in Intravenous Drug Abusers 167
John L. Brusch
8. Prosthetic Valve Endocarditis 183
John L. Brusch
9. Infective Endocarditis of Intracardiac Devices 203
John L. Brusch
10. Nosocomial and Health Care-Associated Infective Endocarditis
(Iatrogenic Infective Endocarditis) 211
John L. Brusch
11. Infective Endocarditis of Immunocompromised Patients 231
John L. Brusch
ix
x Contents
12. Diagnosis of Infective Endocarditis I 241
John L. Brusch
13. Echocardiography 255
Davinder S. Jassal and Michael H. Picard
14. Medical Management 273
John L. Brusch
15. Surgical Treatment of Native Valve and Prosthetic
Valve Infective Endocarditis 313
John L. Brusch
16. Prophylaxis of Infective Endocarditis 331
John L. Brusch
17. The Mimics of Endocarditis 345
Burke A. Cunha
Index . . . . 355
Contributors
John L. Brusch Harvard Medical School and Department of Medicine and Infectious
Disease Service, Cambridge Health Alliance, Cambridge, Massachusetts, U.S.A.
Burke A. Cunha Winthrop University Hospital, Mineola, New York, U.S.A.
Davinder S. Jassal Cardiac Ultrasound Laboratory, Division of Cardiology,
Massachusetts General Hospital and Harvard Medical School, Boston,
Massachusetts, U.S.A., and Bergen Cardiac Care Center, Division of Cardiology,
St. Boniface General Hospital, Winnipeg, Manitoba, Canada
Richard L. Kradin Departments of Pathology and Medicine, Massachusetts General
Hospital, Boston, Massachusetts, U.S.A.
Michael H. Picard Cardiac Ultrasound Laboratory, Division of Cardiology,
Massachusetts General Hospital and Harvard Medical School, Boston,
Massachusetts, U.S.A.
xi
1 Epidemiology
John L. Brusch
Harvard Medical School and Department of Medicine and Infectious Disease
Service, Cambridge Health Alliance, Cambridge, Massachusetts, U.S.A.
INCIDENCE
Infective endocarditis (IE) is an infection of the endocardium of one or more valves.
Rarely, it may involve the mural endocardium. It currently is classified into one of
the four major types: native valve endocarditis (NVE), prosthetic valve endocarditis
(PVE), intravenous drug abuser IE (IVDA IE), and healthcare-associated IE (HCIE).
Classically, this infection has been categorized as either acute or subacute. The
clinical courses were quite different with the pathogens that were highly associated
with one type or another. Acute IE was, and still is, a rapidly progressive disease
that can be fatal in a few days. Without treatment, subacute IE may smolder for
months or even longer than a year (Chapter 6). Until the 1980s, the vast majority of
cases were subacute, caused by viridans streptococci. In this era of IE of intravas-
cular devices (Table 1), there has been a dramatic reversal of this pattern. At times,
the differences between these two may be blurred by indiscriminately prescribed
antibiotic therapy. Infective endocarditis, caused by Staphylococcus aureus, may
assume an indolent course when exposed to inadequate dosage regimens of
antibiotics that are given on the basis of faulty diagnoses. This situation could be
labeled as “muted endocarditis.” Nonetheless, the clinical classification of acute
and subacute disease remains useful, as it still retains a good amount of clinical
predictive value.
An accurate rate of new cases of IE is difficult to determine. This is attributed
partly to the intermittent courses of antibiotics given because of failure to make the
correct diagnosis. The recognition of IE often may be very challenging, especially
when its signs and symptoms are noncardiac. Five to 10 percent of the cases of IE
have negative blood cultures. In the past, only postmortem examination reliably
differentiated uncomplicated bacteremia from that caused by cardiac infection. The
declining rate of autopsies has only worsened this situation. In 1981, von Reyn et al.
published strict case definitions for diagnosing IE (1). The Duke Endocarditis Service
combined echocardiographic findings with various clinical measures to improve
the accuracy of diagnosis (2). These criteria have positive and negative predictive
values of at least 92%. The International Collaboration on Endocarditis is an initiative
to establish a global database of IE patients who have been studied with standard
methodology (3).
Based on the studies conducted within the last 25 years, the incidence of IE
throughout the world varies from 1.5/100,000 to 6/100,000 per population per year
(4–7). There are marked variations in the incidence of IE among nations and even
within a given country. This probably is related to the proportion of urban versus
rural populations (8,9), and their differences in socioeconomic class and intravenous
drug abuse.
In 1940, Hedley estimated that there were approximately 5000 cases of IE in
the United States, at a rate of 4.2/100,000 per population per year (10). Overall, the
1
2 Brusch
TABLE 1 The Eras of Infective Endocarditis
The preantibiotic era (1725–1943):
1885––William Osler presented the first comprehensive account in English of infective
endocarditis
The antibiotic era (1943–1980s):
1966––Louis Weinstein presented an in-depth review of the pathophysiology, clinical
presentation, diagnosis, and treatment of infective endocarditis
1980s––Infective endocarditis in the era of intravascular devices
availability of antibiotics does not appear to have made a significant decrease in
the incidence of this disease (10,11). There might have been a transient decrease
during the early days of antimicrobial therapy (12). This could be attributed to
several factors, including (i) widespread use of antibiotics that decrease the rate of
sustained bacteremia, originating from many types of extracardiac infections;
(ii) antibiotic prophylaxis in patients with significant underlying heart disease; and
(iii) admission of patients with endocardial infection to referral hospitals. The increase
in the resistance of bacteria to various types of antibiotics and the increase in cardio-
vascular surgery and intravascular devices have blunted this advantage. These
same factors have changed the clinical profile of IE from a predominantly subacute
disease to an acute one. Newsom reported that the incidence of IE had changed
little since the 1930s (3.8/100,000 per population per year between 1950 and 1981)
(13). Currently, there are approximately 2000 to 15,000 new cases of IE yearly in the
United States (14).
The incidence and type of IE in any given hospital is dependent on the types
of patients it serves (15,16). Institutions that have a large population of IVDA,
congenital heart disease or patients with prosthetic valves, have a higher rate of IE
than a community hospital. The IE owing to S. aureus occurs more often than those
admitted to a community hospital, whereas enterococcal disease is cared for more
frequently in tertiary-care hospitals (1).
AGE AND SEX
The age distribution of IE has changed considerably since the 1940s. This was formerly
a disease of young adults. In 1920s, the patients were usually <34 years of age (17).
The mean age of those with subacute IE has increased from 36 (1923) to 32 (1930s
and 1940s) to 46 (1950s), and to 56 years (1960s) (18–20). The current median age is
58.0 (3). Gladstone and Rocco observed that the elderly are more susceptible to IE.
Older patients present with more subtle clinical manifestations than younger ones
to the degree that the correct diagnosis was missed in two-thirds of them
early in the course of disease. They postulated that their vulnerability is related
to a decrease in the activity of their immune system and to the dysfunction of the
heart and other organs that marks the aging process (21). Other proposed causes
of this “graying trend” include (22): (i) a heightened susceptibility of the
endocardium to infection during a transient bacteremia because of an increase in
calcific valvular disease; (ii) a marked increase in cardiac surgery and intravascular
devices among the elderly; (iii) 67% of those with nosocomially acquired staphylo-
coccal bacteremia are elderly compared with the 30% of those with community-
acquired staphylococcal infections (23); (iv) almost complete disappearance of
