INFECTIVE
ENDOCARDITIS
Vegetations (arrows) due to viridans streptococcal
endocarditis involving the mitral valve.
1
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Infective endocarditis (IE) is an infection
of the endocardial surface of the heart.
The intracardiac effects of this infection
include severe valvular insufficiency, which
may lead to congestive heart failure and
myocardial abscesses. IE also produces a
wide variety of systemic signs and symptoms
through several mechanisms, including both
sterile and infected emboli and various
immunological phenomena.
2
ETIOLOGY
Organisms Causing Major Clinical
Forms of Endocarditis:
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Staphylococcus aureus infection is the most
common cause of IE, including PVE, acute
IE, and IVDA IE.
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Approximately 35-60.5% of staphylococcal
bacteremias are complicated by IE.
More than half the cases are not associated with
underlying valvular disease.
The mortality rate of S aureus IE is 40-50%.
ETIOLOGY
Organisms Causing Major Clinical
Forms of Endocarditis:
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Streptococcus viridans
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This organism accounts for approximately 50-60% of
cases of subacute disease.
Most clinical signs and symptoms are mediated
immunologically.
Streptococcus intermedius group
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These infections may be acute or subacute.
S intermedius infection accounts for 15% of streptococcal
IE cases.
S intermedius is unique among the streptococci; it can
actively invade tissue and can cause abscesses.
ETIOLOGY
Organisms Causing Major Clinical
Forms of Endocarditis:
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Nonenterococcal group D organisms
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Group B streptococci
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The clinical course is subacute.
Infection often reflects underlying abnormalities of the large bowel (eg,
ulcerative colitis, polyps, cancer).
The organisms are sensitive to penicillin.
Acute disease develops in pregnant patients and older patients with
underlying diseases (eg, cancer, diabetes, alcoholism).
The mortality rate is 40%.
Complications include metastatic infection, arterial thrombi, and congestive
heart failure.
It often requires valve replacement for cure.
Group A, C, and G streptococci
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Acute disease resembles that of S aureus IE (30-70% mortality rate), with
suppurative complications.
Group A organisms respond to penicillin alone.
Group C and G organisms require a combination of synergistic antibiotics (as
with enterococci).
ETIOLOGY
Organisms Causing Major Clinical
Forms of Endocarditis:
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Coagulase-negative S aureus
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Pseudomonas aeruginosa
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This causes subacute disease.
It behaves similarly to S viridans infection.
It accounts for approximately 30% of PVE cases and less than 5% of NVE cases.10
This is usually acute, except when it involves the right side of the heart in IVDA IE.
Surgery is commonly required for cure.
HACEK organisms (ie, Haemophilus aphrophilus, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella
kingae)
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These organisms usually cause subacute disease.
They account for approximately 5% of IE cases.
They are the most common gram-negative organisms isolated from patients with IE.
Complications may include massive arterial emboli and congestive heart failure.
Cure requires ampicillin, gentamicin, and surgery.
ETIOLOGY
Organisms Causing Major Clinical Forms
of Endocarditis:
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Fungi
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These usually cause subacute disease.
The most common organism of both fungal NVE
and fungal PVE is Candida albicans.
Fungal IVDA IE is usually caused by Candida
parapsilosis or Candida tropicalis.
Aspergillus species are observed in fungal PVE and
NIE.

Acute endocarditis usually occurs
when heart valves are colonized by
virulent bacteria in the course of
microbemia. The most common
cause of acute endocarditis is
Staphylococcus aureus; other less
common causes are Streptococcus
pneumoniae, Neisseria gonorrhoeae,
Streptococcus pyogenes, and
Enterococcus faecalis.
8
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Patients with subacute endocarditis
usually have underlying valvular heart
disease and are infected by less
virulent organisms such as viridans
streptococci, enterococci,
nonenterococcal group D streptococci,
microaerophilic streptococci, and
Haemophilus species.
9
Bacteremia can result from various
invasive procedures
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Endoscopy
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Colonoscopy
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Rate of 0-20%
Enterococci, aerobic and anaerobic gram-negative rods
Rate of 40-100%
S viridans
Transurethral resection of the prostate
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Escherichia coli, Bacteroides species
Dental extractions
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Rate of 0-20%
Barium enema
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Rate of 0-20%
CoNS, streptococci, diphtheroids
Rate of 20-40%
Coliforms, enterococci, S aureus
Transesophageal echocardiography
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Rate of 0-20%
S viridans, anaerobic organisms, streptococci
primary
portals
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primary
portals
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PATHOPHYSIOLOGY
The clinical manifestations of IE result from:
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1. Local destructive effects of intracardiac infection
(distortion or perforation of valve leaflets, rupture of chordae
tendineae, perforations or fistulas between major vessels and
cardiac chambers, functional valvular stenosis) with
congestive heart failure;
2. Embolization of fragments of the vegetation, resulting
in infection or infarction including the spleen, kidney,
meninges, brain, bone, pericardium, synovium;
3. The hematogenous seeding of remote sites during
continuous bacteremia (hyper-gammaglobulinemia,
cryoglobulins, splenomegaly);
4. Immunologic response to the infection with tissue
injury due to deposition of preformed immune complexes or
antibody-complement interaction with antigens deposited in
tissues (glomerulonephritis, Osler’s nodes, rheumatological
manifestations).
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Clinical and Laboratory
Features of Infective
Endocarditis
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Fever 80-90 %
Chills and sweats 40-75 %
Anorexia, weight loss, malaise 25-50 %
Myalgias, arthralgias 15-30 %
Back pain 7-15 %
Heart murmur 80-85 %
New/worsened regurgitant murmur 10-40 %
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Clinical and Laboratory
Features of Infective
Endocarditis
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Arterial emboli 20-50 %
Splenomegaly 15-50 %
Clubbing 10-20 %
Neurologic manifestations 20-40 %
Peripheral manifestations (Osler's
nodes, subungual hemorrhages,
Janeway lesions, Roth's spots) 2-15 %
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Clinical and Laboratory
Features of Infective
Endocarditis
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Petechiae 10-40 %
Laboratory manifestations:
Anemia 70-90 %
Leukocytosis 20-30 %
Microscopic hematuria 30-50 %
Elevated erythrocyte sedimentation
rate>90 %
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Clinical and Laboratory
Features of Infective
Endocarditis
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Rheumatoid factor 50 %
Circulating immune complexes 65-100 %
Decreased serum complement 5-40 %
17
Common Peripheral Manifestations
of Infective Endocarditis.
Splinter hemorrhages (A) are
normally seen under the fingernails.
They are usually linear and red for
the first-two to three days and
brownish thereafter.
Panel B shows conjunctival
petechiae.
Osler's nodes (Panel C) are tender,
subcutaneous nodules, often in the
pulp of the digits or the thenar
eminence.
Janeway's lesions (Panel D) are
nontender, erythematous,
hemorrhagic, or pustular lesions,
often on the palms or soles.
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Noncardiac Manifestations
Janeway’s lesions.
Hemorrhagic, infarcted
macules and papules on
the volar fingers in a
patient with S. aureus
endocarditis.
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Noncardiac Manifestations
Septic vasculitis associated
with bacteremia. Dermal
nodule with hemorrhage and
necrosis on the dorsum of a
finger. This type of lesion
occurs with bacteremia (e.g.,
S. aureus) and fungemia (e.g.,
Candida tropicalis).
20
Noncardiac Manifestations
subconjunctival
hemorrhage. Submucosal
hemorrhage of the lower
eyelid in an elderly
diabetic with enterococcal
endocarditis; splinter
hemorrhages in the
midportion of the nail bed
and Janeway lesions were
also present.
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Noncardiac Manifestations
Splinter hemorrhages, embolic
Subungual hemorrhages in the
midportion of the nail bed (quite
different in comparison to traumatic
splinter hemorrhages) was noted in
several fingernails in a 60-year-old
female with enterococcal
endocarditis, who had associated
subconjunctival hemorrhage.
22
Splinter
haemorrhages are
linear
haemorrhages
lying parallel to
the long axis of
finger or toe nails.
23
Noncardiac Manifestations
Osler's nodes. Violaceous, tender
nodules on the volar fingers
associated with minute infective
emboli or immune complex
deposition.
24
Noncardiac Manifestations
Septic emboli with hemorrhage
and infarction due to acute
Staphylococcus aureus
endocarditis.
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Noncardiac Manifestations
Vasculitis
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Clubbing.
Seen in patients
with chronic lung
disease, cyanotic
heart disease,
cirrhosis and
infective
endocarditis.
27
Infective endocarditis: metastatic
infections due to emboli.
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Noncardiac Manifestations
Computed tomography
of the abdomen
showing large embolic
infarcts in the spleen
and left kidney of a
patient with Bartonella
endocarditis.
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The Duke Criteria for the Clinical
Diagnosis of Infective Endocarditis
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Positive blood culture for Infective Endocarditis
Typical microorganism consistent with IE from 2 separate blood
cultures, as noted below:
• viridans streptococci, Streptococcus bovis, or HACEK group, or
 • community-acquired Staphylococcus aureus or enterococci, in
the absence of a primary focus
 or
 Microorganisms consistent with IE from persistently positive
blood cultures defined as:
• 2 positive cultures of blood samples drawn >12 hours apart, or
 • all of 3 or a majority of 4 separate cultures of blood (with first
and last sample drawn 1 hour apart)
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The Duke Criteria for the Clinical
Diagnosis of Infective Endocarditis
MAJOR CRITERIA:
 Evidence of endocardial involvement
 Positive echocardiogram
- Oscillating intracardiac mass on valve or
supporting structures or in the path of regurgitant
jets or in implanted material, in the absence of an
alternative anatomic explanation, or
- Abscess, or
- New partial dehiscence of prosthetic valve, or
 New valvular regurgitation (increase or change in
preexisting murmur not sufficient)
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The Duke Criteria for the Clinical
Diagnosis of Infective Endocarditis
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MINOR CRITERIA :
Predisposition: predisposing heart condition or
injection drug use
Fever ≥38.0◦C
Vascular phenomena: major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, Janeway
lesions
Immunologic phenomena: glomerulonephritis, Osler's
nodes, Roth's spots, rheumatoid factor
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The Duke Criteria for the Clinical
Diagnosis of Infective Endocarditis
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MINOR CRITERIA :
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Microbiologic evidence: positive blood culture
but not meeting major criterion as noted
previously or serologic evidence of active
infection with organism consistent with infective
endocarditis
Echocardiogram: consistent with infective
endocarditis but not meeting major criterion
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The Duke Criteria for the Clinical
Diagnosis of Infective Endocarditis
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Documentation of two major criteria, of one
major and three minor criteria, or of five
minor criteria allows a clinical diagnosis of
definite endocarditis.
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INFECTIVE
ENDOCARDITIS
Vegetations (arrows) due to viridans streptococcal
endocarditis involving the mitral valve.
39
Characteristic sites of vegetations
within the heart. In the presence of
aortic insufficiency, vegetations
characteristically occur on the
ventricular surface of the aortic
valve (A) or on the chordae
tendinae or papillary muscles (B).
In mitral regurgitation, the
vegetations characteristically are
located on the atrial surface of the
mitral valve (C) or at sites of jet
lesions (D) on the atrial wall.
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Further Classification
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Acute
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Affects normal heart
valves
Rapidly destructive
Metastatic foci
Commonly Staph.
If not treated,
usually fatal within 6
weeks
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Subacute
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Often affects
damaged heart
valves
Indolent nature
If not treated,
usually fatal by one
year
Antibiotic Treatment for Infective
Endocarditis Caused by Common
Organisms
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Streptococci Penicillin-susceptible streptococci, S.
bovis
Penicillin G 2-3 million units IV q4h for 4 weeks
Penicillin G 2-3 million units IV q4h plus
gentamicin 1 mg/kg IM or IV q8h, both for 2 weeks
Ceftriaxone 2 g/d IV as single dose for 4 weeks
Vancomycind 15 mg/kg IV q12h for 4 weeks
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Antibiotic Treatment for Infective
Endocarditis Caused by Common
Organisms
Relatively penicillin-resistant streptococci
- Penicillin G 3 million units IV q4h for 4-6 weeks
plus gentamicin 1 mg/kg IV q8h for 2 weeks
 Penicillin-resistant streptococci, pyridoxalrequiring streptococci (Abiotrophia spp.)
- Penicillin G 3-4 million units IV q4h plus
gentamicinc 1 mg/kg IV q8h, both for 4-6 weeks
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Indications for Cardiac Surgical
Intervention in Patients with
Endocarditis
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Surgery required for optimal outcome
Moderate to severe congestive heart failure due to valve
dysfunction
Partially dehisced unstable prosthetic valve
Persistent bacteremia despite optimal antimicrobial therapy
Lack of effective microbicidal therapy (e.g., fungal or Brucella
endocarditis)
S. aureus prosthetic valve endocarditis with an intracardiac
complication
Relapse of prosthetic valve endocarditis after optimal
antimicrobial therapy
Persistent unexplained fever (≥10 days) in culture-negative
prosthetic valve endocarditis
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Indications for Cardiac Surgical
Intervention in Patients with
Endocarditis
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Surgery to be strongly considered for improved
outcomea
Perivalvular extension of infection
Poorly responsive S. aureus endocarditis involving the
aortic or mitral valve
Large (>10-mm diameter) hypermobile vegetations with
increased risk of embolism
Persistent unexplained fever (≥10 days) in culturenegative native valve endocarditis
Poorly responsive or relapsed endocarditis due to highly
antibiotic-resistant enterococci or gram-negative bacilli45
Prevention
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Approximately 15-25% of cases of IE are a consequence of
invasive procedures that produce a significant bacteremia.
Because only 50% of those who developed valvular infection
following a procedure were identified as being candidates for
antibiotic prophylaxis, only approximately 10% of cases of IE
can be prevented by the administration of preprocedure
antibiotics.
Maintaining good oral hygiene is probably more effective in the
overall prevention of valvular infection because gingivitis is the
most common source of spontaneous bacteremias.
The American Heart Association periodically compiles
recommendations for IE prophylaxis.