Infective endocarditis is an infection of the heart valves or endocardium. It is classified based on whether the infection involves native or prosthetic valves. Common causes are bacteria like staphylococcus aureus and streptococcus. Risk factors include rheumatic heart disease and intravenous drug use. Symptoms can include fever, heart murmur, and embolic complications. Diagnosis involves blood cultures, echocardiogram, and Duke criteria. Treatment is with long-term antibiotics with surgery for complications like heart failure or persistent infection. Prevention involves antibiotics for certain medical procedures to prevent bacteremia.

1. Infective Endocarditis

2. Outlines
• Definitions
• Pathogenesis
• Pathophysiology
• Clinical features
• Treatment
• Prevention

3. Definition
Infectious Endocarditis (IE):
• An infection of the heart’s endocardial surface
• Vegetation
– Variable in size
– Amorphous mass of fibrin & platelets
– Abundant organisms
– Few inflammatory cells
• Classified into four groups:
• Native Valve IE
• Prosthetic Valve IE
• Intravenous drug abuse (IVDA) IE
• Nosocomial IE

4. PREDISPOSING CONDITIONS ASSOCIATED WITH
INCREASED RISK OF ENDOCARDITIS
More Common
• Rheumatic heart disease
• Mitral valve prolapse with murmur
• Degenerative valvular disease
• Intravenous drug use
• Prosthetic valve
• Congenital abnormalities (valvular or septal
defect)

5. Less Common
• Hypertrophic obstructive cardiomyopathy
• Pulmonary-systemic shunts
• Coarctation of the aorta
• Previous endocarditis

6. Infecting Organisms
Common bacteria
– S. aureus
– Streptococci
– Enterococci
Uncommon bacteria
– Fungi
– Pseudomonas
– The HACEK grop
» Haemophilus sp.
» Actinobacillus
» Cardiobacterium
» Eikenella
» Kingella

7. Acute V Sub-acute
• Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection
developing in days to weeks
– Most commonly caused by S. aureus
• Subacute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus

8. Infective Endocarditis
• Intravenous Drug Abuse
- S. aureus
– Increased frequency of gram negative infection
such as P. aeruginosa & fungal infections
– High concordance of HIV positivity & IE
• HIV status does not in itself modify clinical
picture
• Survival is decreased if CD4 count < 200/mm3

9. Pathophysiology
• Turbulent blood flow disrupts the
endocardium making it “sticky”
• Bacteremia delivers the organisms to the
endocardial surface
• Adherence of the organisms to the
endocardial surface
• Eventual invasion of the valvular leaflets

10. Infective Endocarditis
• Pathology
– NVE infection is largely confined to leaflets
– PVE infection commonly extends beyond valve
ring into annulus/periannular tissue
• Ring abscesses
• Septal abscesses
• Fistulae
• Prosthetic dehiscence

11. Pathophysiology
• Local destructive effects
• Valvular distortion/destruction
• Chordal rupture
• Perforation/fistula formation
• Paravalvular abscess
• Conduction abnormalities
• Purulent pericarditis
• Functional valve obstruction

12. • Clinical Features Clinical manifestations
– Direct
• Constitutional symptoms of infection (cytokine)
– Indirect
• Local destructive effects of infection
• Embolization – septic or bland
• Hematogenous seeding of infection
» N.B. may present as local infection or persistent fever,
metastatic abscesses may be small, miliary
• Immune response
» Immune complex or complement-mediated
Clinical Features

13. Clinical Features
• Interval between index bacteremia &
onset of sx’s usually < 2 weeks
• Systemic manifestation like any other AFIs
• Fever most common sign
• Murmur present in 80 – 85%
• Generally indication of underlying lesion
• Frequently absent in tricuspid IE
• Changing murmur

14. Modified Duke criteria
Major criteria include---- Table-I
1. Positive blood culture with typical IE microorganism, defined as one of the
following:
– Typical microorganism consistent with IE from 2 separate blood cultures, as
noted below:
• Viridans-group streptococci, or
• Streptococcus bovis including nutritional variant strains, or
• HACEK group, or
• Staphylococcus aureus, or
• Community-acquired Enterococci, in the absence of a primary focus
– Microorganisms consistent with IE from persistently positive blood cultures
defined as:
• Two 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)
• Coxiella burnetii detected by at least one positive blood culture or
antiphase I IgG antibody titer >1:800

15. …Modified Duke criteria
2. Evidence of endocardial involvement with
positive echocardiogram defined as
– Oscillating intracardiac mass on valve or
supporting structures, in the path of regurgitant
jets, or on implanted material in the absence of an
alternative anatomic explanation, or
– Abscess, or
– New partial dehiscence of prosthetic valve or new
valvular regurgitation (worsening or changing of
preexisting murmur)

16. …Modified Duke criteria
Minor criteria include:
• Predisposing factor: known cardiac lesion, recreational drug
injection
• Fever >38°C
• Evidence of embolism: arterial emboli, pulmonary infarcts,
Janeway lesions, conjunctival hemorrhage
• Immunological problems: glomerulonephritis, Osler's nodes
• Positive blood culture (that doesn't meet a major criterion) or
serologic evidence of infection with organism consistent with
IE but not satisfying major criterion
• Positive echocardiogram (that doesn't meet a major criterion)
(this criterion has been removed from the modified Duke
criteria)

18. Classical Peripheral Manifestations
• Less common today
• Not seen in tricuspid endocarditis
• Petechiae most common

19. Janeway Lesions

20. Splinter Hemorrhage

21. Osler’s Nodes

22. Subconjunctival Hemorrhages

23. Roth’s Spots

25. Clinical Features
• Systemic emboli
• Incidence decreases with effective anti-microbial Rx
• Neurological sequelae
• Embolic stroke 15 – 20% of patients
• Mycotic aneurysm
• Cerebritis
• CHF
• Due to mechanical disruption
• High mortality without surgical intervention
• Renal insufficiency
• Immune complex mediated
• Impaired hemodynamics/drug toxicity

27. Additional Labs
• CBC
• ESR and CRP
• Complement levels (C3, C4, CH50)
• RF
• U/A
• Baseline chemistries and coags

28. Imaging
• Chest x-ray -Look for multiple focal infiltrates and calcification
of heart valves
• EKG-Rarely diagnostic Look for evidence of ischemia,
conduction
delay, and arrhythmias
• Echocardiography
TTE- - First line if suspected IE
– Native valves
• Transesophageal echocardiography (TEE)
» Prosthetic valves
» Intracardiac complications
» Inadequate TTE
» Fungal or S. aureus or bacteremi

29. Goals of Therapy
1. Eradicate infection
2. Definitively treat sequelae of destructive
intra-cardiac and extra-cardiac lesions

31. +

32. Antibiotic Therapy
• Effective antimicrobial treatment should lead
to defervescence within 7 – 10 days
– Persistent fever in:
• IE due to staph, pseudomonas, culture negative
• IE with microvascular complications/major emboli
• Intracardiac/extracardiac septic complications
• Drug reaction

34. Surgical Treatment of Intra-Cardiac
Complications
• Relative indications
– Perivalvular extension of infection
– Poorly responsive S. aureus NVE
– Relapse of NVE
– Culture negative NVE/PVE with persistent fever (>
10 days)
– Large (> 10mm) or hypermobile vegetation
– Endocarditis due to highly resistant enterococcus