Lecture conducted at the national heart hospital zambia

1. INFECTIVE ENDOCARDITIS
Dr Mulendele

2. OUT LINE
• Definition
• Classification/ Aetiology
• Epidemiology
• Pathogenesis
• Microbiology
• Clinical Presentation
• Diagnosis
• Investigations
• Management
• Complications
• Prevention
• Prognosis

3. DEFINITION
• Infective endocarditis (IE) is defined as an infection of the
endocardial surface of the heart (heart valves and mural
endocardium or septal defect) by microorganisms. This
includes:
1. Acute Bacterial Endocarditis
2. Subacute Bacterial Endocarditis
3. Non bacterial Endocarditis

4. CLASSIFICATION/AETIOLOGY
1. Acute Bacterial Endocarditis
- Caused by virulent organisms like S. aureus, enterococci and
streptococcus, which are harmful even on healthy
endocardium
- Onset of disease stormy with high grade fever, causes
destructive lesions on the endocardium- ulcerations,
perforation, regurgitation and ring abscesses especially
around prosthetic valves.

5. 2. Subacute Bacterial Endocarditis
- Caused by relatively low virulent organisms e.g S.viridans
and HACEK group (Haemophilus, Aggregatibacter,
Corynebacterium, Eikanella, Kingella).
- Runs a more insidious course
3. Non bacterial endocarditis - viral, fungi and others

6. EPIDEMIOLOGY
• Estimated annual incidence in USA 3.3 per 100, 000 in < 1 year, 0.3 to
0.8 per 100,000 per year in older children and adolescents
• 0.5-1 per 1000 pediatric hospital admissions
• Rates increased between 1960 and 2000 with improved survival of
children with CHD and use of central venous catheters
• Plateaued or slightly declined since 2000
• Streptococcus and staphylococcus account for more than 90% of
cases

7. RISK FACTORS
• Congenital heart disease (35-60% of IE), especially Cyanotic CHD
• Rheumatic heart disease
• Central venous catheters
• Prosthetic heart valves and other intracardiac devices
• History of endocarditis
• IV drug use or chronic IV access
• Immunocompromised (HIV, diabetes)

8. PATHOGENESIS
Infective endocarditis results from interaction of the following:
1. Blood borne pathogens,
2. Damaged endothelium
3. Fibrin
4. Platelets

9. • Endocardial surface is initially injured by shear forces
associated with turbulent blood flow
• At site of endothelial damage, fibrin, platelets and occasional
RBCs deposited forming an initially non infected thrombus/
non bacterial thrombotic embolus (NBTE)
• Transient bacteremia/fungemia ( which occurs in normal
children) results in adherence of microbes to injured
endocardium and thrombus, with subsequent fibrin and
platelet deposition permitting rapid proliferation of
infectious agent

10. • When infection is established, vegetations form composed
of organisms, fibrin & platelets
• May be large enough to cause obstruction
• An emboli may break away and occlude elsewhere
• Adjacent tissue may be destroyed & abscesses may form
• Valve regurgitation may develop or increase if the affected
valve is damaged by distorted tissue
• Extracardiac manifestations such as vasculitis and skin lesions
are due to emboli or immune complex deposition

12. MICROBIOLOGY – (Nationwide inpatient
sample data base 2000- 2010 study USA)
• Staphylococcci and Streptococci most common pathogens
• Among patients with underlying heart disease
- Strep. Viridans- 33%
- Staphylococcus aureus- 28%
- Other Strept- 17%
- Gram negative bacilli- 5%
- polymicrobial- 11%

13. • Among patients without underlying heart disease
- Staphylococcus aureus- 47%
- Strep. Viridans- 18%
- Other Strept- 6%
- Gram negative bacilli- 8%
- polymicrobial- 12%
• Staphylococcus epidermidis( central lines and post surgery)
• Candida albicans ( central lines, immunesuppressed)
• Apergilus, brucella, histoplasma, coxiella burnetti (rare)

14. CLINICAL FEATURES
03/18/2025 CCHS
• Can be divided into an acute or more insidious form
Subacute
• Subacute may abruptly develop acute life threatening
complications such as valve disruption or emboli
• The clinical presentation depends upon the extent of the
local cardiac disease, degree of involvement of other organs,
and causative organism

15. SUBACUTE
• Should be suspected in any patient with heart disease who
develops a persistent fever
• Unusual tiredness,
• Nights sweats
• Weight loss
• Osler’s nodes (painful tender swelling at the fingertips)
product of vasculitis
• Digital clubbing is a late sign
03/18/2025 CCHS

16. SUBACUTE
•Microscopic haematuria is common
•Janeway lesions
•Splinter haemorrhages
03/18/2025 CCHS

17. ACUTE
•Usually presents as a severe febrile illness
• Heart murmurs and petechiae
•Embolic events are common
03/18/2025 CCHS

18. DIAGNOSIS
Based on
• Careful history
• Physical examination
• Blood culture and laboratory results
• Echocardiogram

19. DIAGNOSTIC CRITERIA- Modified Duke criteria
Categorizes patients into
I. Definite Infective Endocarditis
II. Possible Infective Endocarditis
III. Rejected diagnosis of Infective Endocarditis

20. I. Definite Infective Endocarditis
# Pathologic Criteria
- Microorganisms demonstrated by culture/ exam of
vegetation/ intracardiac abscess
- Pathologic lesion- vegetation/ intracardiac abscess with
histological confirmed endocarditis
# Clinical Criteria
- 2 major
- 1 major 3minor
- 5 minor

21. 2 Possible Infective Endocarditis
# 1 major and 1 minor
#3 minor
3 Rejected diagnosis of Infective Endocarditis
#Firm alternate diagnosis
#Resolution with antibiotic < 4 days
# No evidence on autopsy/ surgery
#Does not meet criteria for possible IE

22. Major criteria
1. Positive blood culture
• Typical microorganism consistent with IE from ≥2 blood
cultures,
• Microorganisms consistent with IE from persistently
positive blood cultures, defined as:
- ≥2 Positive cultures of blood samples drawn >12 h
apart or
- All of 3 or a majority of ≥4 blood cultures, irrespective
of the timing
• 1 Positive blood culture for Coxiella burnetii or antiphase-I
immunoglobulin G antibody titre >1:800

23. 2. Evidence of endocardial involvement on ECHO as follows:
• Oscillating intracardiac mass on the valve or supporting
structures OR
• An abscess OR
• New partial dehiscence of prosthetic valve OR
• New valvular regurgitation

24. Minor criteria
• Predisposing heart condition or IV drug use
• Fever: temperature ≥38.0°C
• Vascular phenomena: major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival
haemorrhages, and Janeway lesions
• Immunologic phenomena: glomerulonephritis, Osler nodes, Roth’s
spots, and rheumatoid factor
• Microbiological evidence: positive blood culture but does not meet a
major criterion as noted above

25. INVESTIGATIONS
• Blood culture- 3 from separate venepunctures in first 24 hrs ,
2 in next 24hrs
• FBC ( leucocytosis, anaemia)
• Raised ESR, CRP
• Low C3 due to immune complex formation
• Serology ( Chlamydia, candida, coxiella and brucella)
• Urine- hematuria and proteinuria

26. • CXR – cardiomegaly, focal pulmonary infiltrates in pts with
pulmonary septic emboli
• ECG – new rhythm disorders ( ventricular ectopy, complete
heart block)
• Echo- Transthoracic/ transesophageal

27. MANAGEMENT
• Ideally Antimicrobial treatment should be guided by blood culture
results
• Antibiotic therapy ( as one await blood culture results). First line XPEN
and Gentamycin/ Ceftriaxone
Second line, Vancomycin plus gentamycin ( UTH protocol)
Treatment for at least 4 to 6 weeks
• Surgery
Indications : severe valve lesions with uncontrolled failure, failed
medical treatment, fungal endocarditis

28. Complications
• Myocarditis, Congestive cardiac failure
• Thromboembolic stroke
• Cerebral abscesses
• Peripheral embolism, gangrene
• Glomerulonephritis, kidney failure

29. PREVENTION
• Antimicrobial prophylaxis before dental and other surgical procedures
in high risk individuals
• Prompt identification and management of CHD and acquired heart
diseases
• Dental hygiene

30. PROGNOSIS
• Mortality is about 20-25%
• Severe morbidity 50-60%
• Highest mortality with staph infections and lowest with S. viridans

31. References
• Nelson textbook of paediatrics 21st
edition
• Coovadias textbook of paediatrics and child health
• Paediatric national protocol
• Medscape
• Up to date