This document discusses infective endocarditis (IE), a serious infection of the heart valves or inner lining of the heart. It provides details on the epidemiology, symptoms, physical exam findings, causative organisms, risk factors, diagnostic criteria (Modified Duke Criteria), investigations including echocardiography and blood cultures, and treatment approach for IE. Staphylococcus aureus is a leading cause worldwide and viridans group streptococci are common causes after dental procedures. Diagnosis relies on modified Duke criteria incorporating positive blood cultures, echocardiogram findings, and clinical features.

1.  Dr. Nitin Das
 MD Pediatrics

2. Definition
 Infective endocarditis (IE) is a serious infection
characterized by colonization or invasion of the heart
valves or the mural endocardium by a microbe.

3. Epidemiology
 IE AFFECTS 3–7.5 PEOPLE PER 100,000 PERSON-YEARS WORLDWIDE
 INCIDENCE APPEARS TO VARY SIGNIFICANTLY AS REPORTED FROM
DIFFERENT GEOGRAPHIC AREAS EVEN WITHIN THE SAME COUNTRY
 STAPHYLOCOCCUS AUREUS IS THE LEADING CAUSE OF IE
WORLDWIDE AND HAS TAKEN PREDOMINANCE OVER VIRIDANS
GROUP STREPTOCOCCI IN MANY PARTS OF THE WORLD.
 GLOBALLY, IE IS ASSOCIATED WITH A SIGNIFICANT BURDEN AND
WAS RESPONSIBLE FOR 45,000 DEATHS IN 1990 AND 65,000
DEATHS IN 2013

4. Vegetation
 The prototypic lesion at the site of infection, the
‘vegetation’ is a mass of platelets , fibrin ,
microcolonies of micro-organisms and scanty
inflammatory cells.
 They may be single or multiple
 Range in size from a few millimeters to several
centimeters.

6. Sites
 Heart valves are most commonly involved.
 May occur at site of a septal defect,on
chordae tendineae or mural endocardium.
 Infection of arteriovenous shunt ,
arterioarterial shunt or coarctation of
aorta are also considered as IE.

7. Etiology
 Viridans-type streptococci(α-hemolytic
streptococci) & Staphylococcus aureus
remain the leading causative agent for
endocarditis in pediatric patient.
 Staphylococcal endocarditis is more
common in patient with no underlying heart
disease.
 Viridans group streptococcal infection is
more common after dental procedure.

8. Etiology(contd…)
 Group D enterococci—lower bowel or
genito-urinary manipulation
 Pseudomonas aeruginosa & Serratia
marcescens—I/V drug abusers
 Fungal organism after open heart surgey
 Coagulase negative staphylococci are
common in presence of indwelling central
venous catheter.

10. Classification
 Acc. to toxicity
Acute IE
Sub acute IE
 Acc . to culture
Culture positive
Culture negative
 Acc. to site of involvement
Left sided
Right sided

11. Culture-negative endocarditis
•CULTURE-NEGATIVE ENDOCARDITIS OCCURS WHEN A
PATIENT HAS TYPICAL CLINICAL OR ECHOCARDIOGRAPHIC
FINDINGS OF ENDOCARDITIS, WITH PERSISTENTLY
NEGATIVE BLOOD CULTURES
•COMMON CAUSES INCLUDE RECENT ANTIBIOTIC
THERAPY, OR INFECTION CAUSED BY A FASTIDIOUS
ORGANISM THAT GROWS POORLY IN VITRO.(COXIELLA
BURNETTI AND BARTONELLA SPP)

13. Pathogenesis
 Development of non bacterial thrombotic
endocarditis (NBTE)
1.Endothelial damage by jet of blood ,
turbulence or trauma
2.Platelet-fibrin deposition
3.Conversion of NBTE to IE by microorganism
colonization during bacteraemia.

14.  Biofilms form on the surface of implanted
mechanical devices such as valves, catheters, or
pacemaker wires that also serve as the adhesive
substrate for infection.
 Transient bacteremia then colonizes this Biofilm,
leading to proliferation of bacteria within the lesion.
 Bacterial surface proteins, such as the FimA antigen
in viridans streptococci, act as adhesion factor to the
NBTE or Biofilm.

15. BACTERIA CAN ENTER THE BODY IN MANY WAYS. ACCORDING
TO THE AMERICAN HEART ASSOCIATION (AHA), SOME OF THE
MOST COMMON WAYS INCLUDE THE FOLLOWING:
• Dental procedures
•Tonsillectomy or adenoidectomy
• Examination of the respiratory passage with a
rigid bronchoscope
• Certain types of surgery on the respiratory
passage, the gastrointestinal tract, or the urinary
tract
• Gallbladder or prostate surgery

16. Pathophysiology
Factors responsible for clinical
manifestations are
 Local destructive effect of intra cardiac
lesion
 Embolization of bland or septic fragments
of vegetations to distant sites , resulting in
infarction or infection
 Hematogenous seeding of remote sites
 Antibody response to infectious organism

17. Risk groups:
 prosthetic cardiac valves or other prosthetic
material used for cardiac valve repair
 unrepaired cyanotic CHD
 completely repaired defects with prosthetic
material or device during the 1st 6 mo after repair
 repaired CHD with residual defects at or adjacent to
the site of a prosthetic patch or device
 valve stenosis or insufficiency occurring after heart
transplantation,
 permanent valve disease from rheumatic fever
(mitral stenosis, aortic regurgitation),

18.  previous infective endocarditis.
 Dental procedures
 Patients with high-velocity blood flow lesions such as
VSD & AS are also at high risk.
 Surgical correction of CHD may reduce but does not
eliminate the risk of endocarditis, except for the repair
of a simple atrial septal defect or patent ductus
arteriosus without prosthetic material.

19. Clinical manifestations
History
1. history of an underlying heart defect..
2. recent dental procedure or
tonsillectomy is occasionally present,
but a history of toothache (from dental
or gingival disease) is more frequent
than a history of a procedure.
3. rare in infancy; at this age, it usually
follows open heart surgery.

20. Symptoms
The onset is usually insidious with
prolonged low-grade fever and somatic complaints including
 fatigue
 Weakness
 loss of appetite
 Pallor
 Arthralgia
 Myalgias
 weight loss
 diaphoresis.

21. Physical examination
 Heart murmur (100%).A new heart murmur and an
increase in the intensity of an existing murmur are
important.
 Fever (80%–90%) (101° and 103°F)
 Splenomegaly (70%).
 Skin manifestations (50%) (either secondary to
microembolization or as an immunologic phenomenon)
may be present in the following forms:
 a. Petechiae(most common),Osler’s nodes, Janeway’s
lesions ,Splinter hemorrhages

22.  Embolic or immunologic phenomena in other organs
are present in 50% of cases:
a. Pulmonary emboli (VSD, PDA, or a systemic-to-PA
shunt.)
b. Seizures and hemiparesis (embolization to CNS)
c. Hematuria and renal failure.
d. Roth’s spots
 Carious teeth or periodontal or gingival disease
 Clubbing
 Signs of heart failure

23. Osler’s node

24. Janeway lesions

25. Splinter hemorrhages

26. Roth spots

28. Modified Duke criteria
Definite infective endocarditis
Pathologic criteria
•Microorganisms demonstrated by culture or histologic
examination of a vegetation, a vegetation that has embolized,
or an intracardiac abscess specimen; or
•Pathologic lesions; vegetation or intracardiac abscess
confirmed by histologic examination showing active
endocarditis

29. Clinical criteria
•Two major criteria; or
•One major criterion and three minor criteria; or
•Five minor criteria
Possible infective endocarditis
•One major criterion and one minor
criterion; or
•Three minor criteria

30. Major criteria
Blood culture positive for IE
•Typical microorganisms consistent with IE from two separate
blood cultures: viridans Streptococci, Streptococcus bovis,
HACEK group, Staphylococcus aureus; or
•Community-acquired Enterococci, in the absence of a primary
focus; or
•Microorganisms consistent with IE from persistently positive
blood cultures, defined as follows:
•At least two positive cultures of blood samples drawn >12 h
apart; or
•All of three or a majority of ≥ four separate cultures of blood
(with first and last sample drawn at least 1 h apart)
•Single positive blood culture for Coxiella burnetii or antiphase
I IgG antibody titer >1:800

31. Evidence of endocardial involvement
•Echocardiogram positive for IE (TEE recommended in patients
with prosthetic valves, rated at least “possible IE” by clinical
criteria, or complicated IE (paravalvular abscess); TTE as first
test in other patients), defined as follows:
• 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 New valvular
regurgitation (worsening or changing of preexisting
murmur not sufficient)

32. Minor criteria
•Predisposition, predisposing heart condition or injection
drug use
•Fever, temperature >38·C (100.4·F)
•Vascular phenomena, major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, and Janeway
lesions
•Immunologic phenomena: glomerulonephritis, Osler’s
nodes, Roth’s spots, and rheumatoid factor
•Microbiologic evidence: positive blood culture but does not
meet a major criterion as noted above or serologic evidence
of active infection with organism consistent with IE
•Echocardiographic minor criteria eliminated

33. Investigations

34. Lab findings
 1.Positive blood cultures >90% of patients in the
absence of previous antimicrobial therapy.
Antimicrobial pretreatment reduces the yield of
positive blood culture to 50% to 60%.
 2. CBC shows anemia(80% of patients), and
leukocytosis
 3. ESR Increased (unless there is polycythemia)
 4. Urine Analysis-Microscopic hematuria (30% of
patients).

35. Blood culture
 3 to 5 separate blood collections should be obtained
after careful preparation of the phlebotomy site.
 The microbiology laboratory should be notified of
the clinical suspicion for endocarditis. Cultures
should be grown aerobically and anaerobically for at
least 1 week.
 If no growth is observed by the second day of
incubation, 2 more blood cultures should be
obtained.
 Blood cultures should be repeated during therapy to
demonstrate the clearance of bacteremia.
 An indwelling line should not be used to take
cultures.

36. • Echocardiography is the primary modality for detecting
endocarditis .
Typical findings include vegetations, abscesses, and new
valvular insufficiency.
Transthoracic echocardiography (TTE) has a greater
sensitivity in infants and children than in adults. Reported
sensitivity is as high as 81%.
ECHOCARDIOGRAPHY

37. Echo(contd..)
 Certain echocardiographic findings are included
as major criteria in the modified Duke criteria.
They include:
a. Oscillating intracardiac mass on valves or
supporting structures, in the path of regurgitation
jets, or on implanted material
b. Abscesses
c. New partial dehiscence of prosthetic valve
d. New valvular regurgitation

39. Investigations(contd…)
 ECG reveal conduction defect
 CXR shows evidence of cardiomegaly or
heart failure.
 S. Complement Reduced
 S. Gammaglobulin Raised
 B. Urea Elevated
 S. Creatinine Raised
 Rheumatoid factor maybe positive

40. Management

41. Objective of treatment
 Infecting micro organism must be
eradicated
 Invasive, intracardiac and focal
extracardiac complication of infection
must be resolved.

43. Contd..

47. Complications
 Heart failure
 Systemic emboli, often with CNS manifestations
 Pulmonary emboli may occur in children with
ventricular septal defect (VSD) or tetralogy of Fallot,.
 Other complications include mycotic aneurysms,
rupture of a sinus of Valsalva, obstruction of a valve
secondary to large vegetations, acquired VSD, and
heart block as a result of involvement (abscess) of the
conduction system.
 Additional complications include meningitis,
osteomyelitis, arthritis, renal abscess, purulent
pericarditis, and immune complex–mediated
glomerulonephritis.

48. Prevention

49.  Given that many invasive respiratory tract procedures do
cause bacteremia, prophylaxis for many of these
procedures is considered reasonable.
 In contrast to prior recommendations, prophylaxis for
gastrointestinal or genitourinary procedures is no longer
recommended in the majority of cases.
 Prophylaxis for patients undergoing cardiac surgery with
placement of prosthetic material is still recommended.

52. Prognosis
 Despite the use of antibiotic agents,
mortality remains at 20–25%.
 Serious morbidity occurs in 50–60% of
children with documented infective
endocarditis; the most common is heart
failure caused by vegetations involving the
aortic or mitral valve.