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Case Presentation


Case I 97/03/12 0468013
• 70 y/o male P’t
• Complain of intermittent spiking fever
(39C) for the past 1 month.
• Presented to ER with fever 38C and mild
SOB and chest tightness was also noted
• Denied any other systemic disease
PE and Lab Data
• Chronic ill looking p’t
• Grade 4/6 systolic murmur over LSB
• WBC: 10100/cumm N/L: 87/5
• AST:27 Cr: 1.1
• U/A : Negative
Further Studies
• Blood Culture : Streptococcus Gr.Viridians X IV
• Cardiac Echo :
• Normal LV contractility with severe LVOT
obstruction with LVOT PG~ 80-120 mmHg.
• Dilated LA and Aortic sclerosis
• MV vegetation with severe eccentric MR, mild
• Diagnosis :Infective endocarditis ( IE ):definite,
Case II 97/04/13 0248419
• 46 y/o male P’t
• Sent to ER the chief complaint of fever,
headache and R’t side weakness
• Denied any other systemic disease
PE and Lab Data
• Acute ill looking p’t
• GCS : E3V2M5
• WBC: 17500/cumm N/L: 85/9
• AST:24 Cr: 0.9
• CXR and Brain CT
Further Studies
• Blood Culture : Streptococcus Gr.Viridians X III
• Cardiac Echo:
• 1.A vegetation at the anterior leaflet of mitral
valve(about 1.3*0.8cm) with severe MR
• **Diagnosis:infective endocarditis : definite
• Abd Sono:
• Spleen:one irregular shaped hypoechoic mass with
small hyperechoic nodules in the margin 5.8X3.7cm at
lower pole of spleen
• R/O intrasplenic hematoma, abscess, or post-infaction
• related intrasplenic hemorrhage
What is Infective Endocarditis (IE)?
• IE is a microbial infection of the inner lining of the heart, the

• A vegetation commonly found on the valvular leaflets is the

characteristic lesion of IE.

• The incidence of IE in the United States is between 10,000 and 20,000

cases per year.

• While incidence has remained steady over the past five decades, the
disease has evolved drastically.

• The mortality rate of IE is 25%.

Anatomy of the Heart

• The heart has four valves. In counterclockwise order, they are: the aortic valve, the
tricuspid valve, the pulmonary valve, and the mitral valve.
• The arrows indicate blood flow. Red arrows indicate the flow of oxygen-rich blood
and blue oxygen-poor.
• Unable to facilitate the one-way flow of blood, damaged heart valves hinder the
pumping of blood efficiently throughout the body, leading to congestive heart
failure. This is one reason the mortality rate of IE remains high even today.
• At a previously-damaged cardiac valve, a jet stream of blood with an abnormally
high velocity damages the endothelium

• This damaged surface becomes a starting point for the deposition of platelets and
the formation of a platelet-fibrin clot, causing nonbacterial thrombotic endocarditis

• IE develops after bacteria enter the bloodstream and colonize the clot.

• Platelets and fibrin accumulate over the bacteria, increasing the size of the

Leukocytes are unable to penetrate the vegetation as additional layers of fibrin are
added. Treatment with antibiotics can also be problematic because the bacteria
within the vegetation often become less metabolically active, and many antibiotics
require active bacterial growth to be effective.

Not every incidence of bacteremia leads to IE. Not only must the blood-borne pathogen be
present in significant enough numbers to establish infection, it must possess the capacity
(determinants of virulence) necessary to adhere to and colonize the damaged endothelium.
Infective Endocarditis requires bacteremia and quite often requires
an underlying heart defect to be exploited by the blood-borne

With this in mind, the following groups of people are more

susceptible to IE:
• People with congenital heart defects
• People who have had rheumatic fever
• The elderly
• Intravenous drug users
• People with compromised immune systems
– AIDS patients
– Cancer patients

Prevalence of disease per group changes over time, but overall

incidence of IE remains constant.
Principle causative agents include:
• Streptococci
– Represent approximately 50% of cases of IE – down from 80% in
the preantibiotic era
– Viridans streptococci (30-40% of Streptococcal IE)
• S. sanguis and S. mitis each account for 30%-50% of the cases
caused by the oral viridans streptococci
• Enterococci
– Cause 5-15% of cases of IE
• Staphylococci
– Responsible for about 20% of cases of IE
• Coagualse-negative staphylococci (e.g. S. emidermidis) cause 60% of
prosthetic-valve IE
• Mortality rates associated with CONS in PVE have been decreasing,
although the mortality rates of IE due to S. aureus remain ominously
Less prevalent causative agents include:

• Other bacteria
– The HACEK Group
• Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium
hominis, Eikenella corrodens, and Kingella species
– Usual bacterial causes
• Bacillus cereus, Clostridium perfringens, Mycobacterium tuberculosis, Nocardia
asteroides, Coxiella burnetii, etc.
• Fungi
– Candida and Aspergillis species

(A number of organisms on this list are responsible for culture-negative IE)

Microbiology of Infective Endocarditis

© 2007 About, Inc

Splinter hemorrhage
Roth Spots
Janeway Lesion
Osler Nodes

© 2005 The Regents of the University of California

Definition of Major and Minor criteria used in the Duke criteria
Definition of Infective Endocarditis according to the Duke criteria
Figure 1 Algorithm for using echocardiography in suspected infective

Haldar SM and O'Gara PT (2006) Infective endocarditis: diagnosis and management

Nat Clin Pract Cardiovasc Med 3: 310–317 doi:10.1038/ncpcardio0535
The figure on the left is of a mitral valve vegetation shown by echocardiogram.

The figure to the right shows one portion (called a leaflet) of the mitral valve.

Cabell, C. H. et al. Circulation 2003;107:e185-e187

Copyright ©2003 American Heart Association

How is Infective
Endocarditis treated?
Antimicrobial Therapy
• Antibiotics are usually administered intravenously for 2-6 weeks.
Duration depends on the virulence of the pathogen.

• The drug of choice for most cases of viridians streptococcal

endocarditis is penicillin.
– The cure rate for viridans streptococcal endocarditis is above 90%.
– Without treatment, VSE is typically fatal within six months.

• Antifungals alone are not enough to cure fungal IE, although

Amphotericin B is often administered in conjunction with surgery.
Surgical Treatment
• 15-25% of patients with IE are treated surgically

• When removal of an infected valve is necessary:

– Antibiotic therapy fails (first reported case: 1965)
– Persistent vegetation after systemic embolization
– Increase in vegetation size after antimicrobial therapy
– Valvular dysfunction
– Fungal endocarditis

• “The surgeon wields a double-edged scalpel”

– Surgery can introduce organisms and initiate an infection

• 50% of some valvular infections do not respond to antimicrobial therapy

or surgery
– Today’s highly virulent causative agents have led to an increase in dangerous
Congestive heart failure
• Greatest impact on mortality
• Native valve IE, acute CHF occurs more
frequently in aortic v (29%), mitral v (20%),
tricuspid v (8%)
• Poor surgical outcome is predicted by
preoperative NYHA class III or IV, renal
insufficiency and old age
Risk of Embolization
• Occurs in 22%-50%
• Up to 65% embolic events involve the CNS,
and > 90% lodge in MCA distribution
• Most emboli occur within the first 2-4 wks of
• Presence of vegetation and involved site
and vegetation size
• Embolic event was 1 of 4 early independent
predictors of in-hospital death caused by IE
Splenic Abscess
• Splenic infarction : Lt sided IE (40%)
• Estimated about 5% will develop abscess
• Viridians streptococci and S aureus each
account for about 40%
• Abd CT and MRI
• Splenectomy and antibiotics
Mycotic Aneurysms
• ICMA : mortality rate about 60%
• Clinical presentation highly variable –
severe headache, altered sensorium,
focal neurological deficits
• CTA, MRA or cerebral angiography
• Antimicrobial therapy and endovascular
• ECMA : surgical intervention
• Cure rate for NVE is > 90% for streptococci,
75-90% for enterococci, and 60-75% for S
• Usual cause of death: heart failure, emboli,
rupture of MA, postoperative complications,
renal failure and overwhelming infection
• Prognosis is worse in PVE
• Late PVE has a better prognosis than early
PVE; mortality rate 19-50% vs 41-80%
A retrospective study of IE at Changhua Christian
Hospital during 1989-1999

• 58 p’ts: 46 males vs 12 females

• Pathogens: Viridians streptococcus (32/58)
and Staphylococcus auerus (12/58)
• A total of 17 (29.3%) p’ts died
• Complications occurred in 40(69%) p’ts,
16(27.6%) with neurological and 24(41.4%)
with cardiovascular complications
• Neurological and cardiovascular
complications were the most likely causes of
• Emergency medicine; A comprehensive
study guide 6th edition (Oct 2003): Judith
E Tintinalli
• Color atlas of infective endocarditis
(2006): David R. Ramsdale
• Infective Endocarditis : Circulation
2005;111:e394-e433 Larry M. Baddour,
Walter R. Wilson