Infective endocarditis is an infection of the heart valves or endocardial surface. It can be classified based on temporal evolution (acute vs subacute), site of infection, cause, or risk factors. Acute infective endocarditis typically affects normal valves and is caused by virulent organisms like S. aureus, while subacute infective endocarditis often affects damaged valves and has a more indolent course. Diagnosis involves blood cultures, echocardiography, and application of the Duke criteria. Effective treatment requires antibiotics, while complications include embolization, heart failure, and immune-mediated issues.

1. INFECTIVE ENDOCARDITIS
BY. Kifle Alamirew(MD)
1

2. DEFINITION
 Infective Endocarditis (IE): an infection of the
heart’s endocardial surface and or heart valves
that involves thrombi formation which may
damage endocardial tissues or valves
 Classified based on temporal evolution of
disease, the site of infection, the cause of
infection, or the predisposing risk factor.
2

3. CLASSIFICATION BASED ON TEMPORAL
EVOLUTION OF THE DISEASE
 Acute
 Affects normal heart valves
 Hectically febrile illness that rapidly damages cardiac
structures and hematogenously seed extracardiac sites
 If not treated, usually fatal within 6 weeks
 Commonly due to S.aureus
3

4. CONT’D….
 Subacute
 Often affects damaged heart valves
 Indolent nature,characterized by prolonged course of LGF,
and nonspecific compliants :fatigue, arthralgia, wt loss,
diaphoresis
 Rarely metastasize
 There is risk of immunologic sequelae:GN
 If not treated, usually fatal by one year
 Due to less virulent organisms: V.streptococci,CONS
4

5. CLASSIFICATION (BASED ON PREDISPOSING RISK FACTORS)
1. Native valve endocarditis
 Community acquired
 Health care-associated (nosocomial) endocarditis: defined as a
diagnosis of IE made more than 72 hours after admission in
patients with no evidence of IE on admission, or IE developing
within 60 days of a prior admission when there was a risk factor
for bacteremia or any risk factor for IE during the hospitalization
2. Prosthetic valve endocarditis
3. Endocarditis in IVD abusers
5

6. EPIDEMIOLOGY
 Incidence difficult to ascertain and varies according to
location but it is relatively uncommon disease
 Much more common in males than in females(M:F
ratiovaries from 2:1-9:1)
 May occur in persons of any age and increasingly
common in elderly
 Mortality ranges from 20-30% with Rx , up to100% fatal
with out Rx.
6

7. RISK FACTORS
 Intravenous drug abuse
 Artificial heart valves and pacemakers
 Acquired heart defects
 Rheumatic heart disease
 Calcific aortic stenosis
 Congenital heart defects(VSD,PDA,COA,TOF,BAV)
 Intravascular catheters
 Prior episode of infective endocarditis: recurrence is
9%
 NB. The higher gradient flow lesions( high pressure
to low pressure) are highly risk for IE. 7

8. ETIOLOGY( MICROBIOLOGY)
 Common bacteria
 Viridans group streptococci (S. mutans, S.
sanguis, S. mitis)
 Staphylococcus aureus
 Group D streptococcus (enterococcus) (S. bovis,
S. faecalis)
 Not so common bacteria
 Pseudomonas
 H.influenze
 HACEK (Haemophilus species, Aggregatibacter
aphrophilus, Actinomycetemcomitans,
Cardiobacterium species,Eikenella species, and
Kingella species)
 Fungi
8

9. PATHOPHYSIOLOGY1. Turbulent blood flow disrupts the endocardium making it
“sticky”
2. At the site of the damage, fibrin, platelet and occasionally
RBCs are deposited and form- nonbacterial thrombotic
endocarditis (NBTE)
3. Transient Bacteremia or fungemia delivers the organisms
to the endocardial surface
4. Adherence of the organisms to the injured endocardial
surface and thrombus
5. Eventual invasion of the valvular leaflets – further
deposition of platelets resulting in vegetation's
9

10. SYMPTOMS
 Acute
 High grade fever and
chills
 SOB
 Arthralgia/ myalgia
 Abdominal pain
 Pleuritic chest pain
 Back pain
 Subacute
 Low grade fever
 Anorexia
 Weight loss
 Fatigue
 Arthralgia/ myalgia
 Abdominal pain
 N/V
The onset of symptoms is usually ~2 weeks or less
from the initiating bacteremia
10

11. SIGNS
 Fever
 Heart murmur( new or changing murmur)
 Nonspecific signs – petechiae, subungal or “splinter”
hemorrhages, clubbing, splenomegaly, neurologic
changes
 More specific signs - Osler’s Nodes, Janeway lesions,
and Roth Spots
11

12. CLINICAL FEATURES OF IE
12

13. PERIPHERAL SIGN OF IE
 Janeway lesions: are macular, blanching, nonpainful, erythematous
lesions on the palms and soles
 Osler's nodes: are painful, papulopustular to violaceous nodular
lesions found in the pulp of fingers and toes and are seen more
often in sub acute than acute cases of IE
 Roth spots are exudative, edematous hemorrhagic lesions of the
retina
 Petechiae
 Splinter hemorrhage: are nonblanching, linear reddish-brown
lesions found under the nail bed
13

14. PETECHIAE
Photo credit, Josh Fierer, M.D.
medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Sciences
www.lib.uiowa.edu/ hardin/
md/cdc/3184.html
1.Nonspecific
2.Often located on extremities
or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
14

15. SPLINTER HEMORRHAGES
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
15

16. JANEWAY LESIONS
1.Erythematous, blanching macules
2.Nonpainful
3.More specific
4.Located on palms and soles
16

17. 17

18. OSLER’S NODES
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE 18

19. COMPLICATIONS
 Four etiologies
 Embolic eg stroke
 Local spread of infection
 Metastatic spread of infection
 Formation of immune complexes –
glomerulonephritis and arthritis
19

20. EMBOLIC COMPLICATIONS
 Occur in up to 40% of patients with IE
 Predictors of embolization
 Size of vegetation(>or= to 10mm)
 Left-sided vegetations
 Fungal pathogens, S. aureus, and Strep. Bovis
 Incidence decreases significantly after initiation of
effective antibiotics
20

21. EMBOLIC COMPLICATIONS
 Stroke
 Myocardial Infarction
 Fragments of valvular vegetation or vegetation-induced
stenosis of coronary ostia
 Ischemic limbs
 Hypoxia from pulmonary emboli
 Abdominal pain (splenic or renal infarction)
21

22. LOCAL SPREAD OF INFECTION
 Heart failure
 Due to extensive valvular damage or acute MI
 Commonest Couse of death
 Paravalvular abscess (30-40%)
 Most common in aortic valve, IVDA, and S. aureus
 May extend into adjacent conduction tissue causing
arrythmias
 Higher rates of embolization and mortality
 Pericarditis
 Fistulous intracardiac connections 22

23. METASTATIC SPREAD OF INFECTION
 Metastatic abscess
 Kidneys, spleen, brain, soft tissues
 Meningitis and/or encephalitis
 Vertebral osteomyelitis
 Septic arthritis
23

24. INVESTIGATION
 Blood Cultures
 3- 5 separate blood collection should be obtained after careful
preparation for phlebotomy site depending on severity of illness
 In most patients 3 BC are obtained with in the 1st 24 hrs
and additional 2 BC in the next 24 hrs if no growth
 In critically ill patients 3 venipuncture site for blood culture
should be obtained as fast as possible
 Obtain 10-20mL in adults and 0.5-5mL in children2
 Positive Result:
 Typical organisms present in at least 2 separate samples
 Persistently positive blood culture (atypical organisms)
 Two positive blood cultures obtained at least 12 hours apart
 Three or more positive blood cultures in which the first and
last samples were collected at least one hour apart 24

25. CONT’D……
 CBC
- Anemia: NCNC
- Leukocytosis
 U/A
- Microscopic hematuria
- Pyuria
- proteinuria
 Elevated erythrocyte sedimentation rate
 Elevated C-reactive protein level
 Rheumatoid factor
25

26. 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
26

27. INDICATIONS FOR
ECHOCARDIOGRAPHY
 Transthoracic echocardiography (TTE)
 First line if suspected IE
 Native valves
 Transesophageal echocardiography (TEE)
 Prosthetic valves
 Intracardiac complications
 Inadequate TTE
 Fungal or S. aureus or bacteremia
27

28. DIAGNOSIS
Modified Duke Criteria
 Definite IE
 Clinical criteria
 Two major criteria, or
 One major and three minor criteria, or
 Five minor criteria
 Pathologic criteria
 Microorganism: (via culture or histology) in a valvular
vegetation, embolized vegetation, or intracardiac
abscess
 Pathological lesions: vegetation or intracardiac
abscess present, confirmed by histology showing
active endocarditis 28

29. CON’D
 Possible IE
 One major criterion and one minor criterion
or three minor criteria
 Rejected IE
 Firm alternative diagnosis for manifestations
of endocarditis, or
 Sustained resolution of manifestations of
endocarditis, with antibiotic therapy for 4
days or less, or
 No pathological evidence of infective
endocarditis at surgery or autopsy, after
antibiotic therapy for 4 days or less 29

30. CON’D
 Major Criteria
 Positive blood culture
 Typical microorganism for infective endocarditis from two
separate blood cultures
 Persistently positive blood culture, defined as recovery of
a microorganism consistent with infective endocarditis
from:
 Blood cultures (≥2) drawn more than 12 hr apart, or
 All of three or a majority of four or more separate blood
cultures, with first and last drawn at least 1 hr apart
 Single positive blood culture for Coxiella burnetii or
antiphase I IgG antibody titer >1:800
30

31. CON’D
 Evidence of endocardial involvement
 Positive echocardiogram
 Oscillating intracardiac mass, on valve or supporting structures, or in
the path of regurgitant jets, or on implanted material, in the absence
of an alternative anatomical explanation, or
 Abscess, or
 New partial dehiscence of prosthetic valve, or
New valvular regurgitation (increase or change in
preexisting murmur not sufficient)
31

32. CON’D
 Minor Criteria
 Predisposition: predisposing heart condition or
intravenous drug use
 Fever ≥38.0°C (100.4°F)
 Vascular phenomena: major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, Janeway
lesions
 Immunological phenomena: glomerulonephritis,
Osler nodes, Roth spots, rheumatoid factor
 Microbiological evidence: positive blood culture but
not meeting major criterion as noted previously[*] or
serologic evidence of active infection with organism
consistent with infective endocarditis
32

33. CON’D
 The following minor criteria are added to those
already listed:
 splenomegaly
 splinter hemorrhages, and petechiae
 a high erythrocyte sedimentation rate
 a high C-reactive protein level
 the presence of central non feeding lines
 peripheral lines
 microscopic hematuria
33

34. TREATMENT
 Parenteral antibiotics
 High serum concentrations to penetrate vegetations
 Prolonged treatment to kill dormant bacteria clustered in
vegetations
 Surgery
 Intracardiac complications
 intractable heart failure
 failure to sterilize the blood despite adequate antibiotic
levels
 increasing size of vegetations while receiving therapy
 Surveillance blood cultures
34

35.  Acute endocarditis or prosthetic valvae endocarditis
vancomycin 30mg/kg/day(ceftriaxone 2gm/day) plus gentamycin
3mg/kg/day once daily or in 2-3 divided doses immedietly after blood
culture.
 Subacute endocarditis –if patient hemodynamically stable wait
for 2- 3 days till blood culture result.
 Culture positive treat based on the isolated organisms
 Culture is negative endocarditis
 SBE-ceftriaxone 2gm /day+gentamycin 3gm/kg for the 1st 2wks and
continue with ceftriaxone only for the remaining weeks of therapy
 Acute endocarditis –continue vancomycin +gentamycin for 2wks and
then vancomycin for the remaining wks of therapy
 patients with proven or suspected enterococcal endocarditis should
receive combination of vancomycin and gentamycin for the whole
duration of therapy.
 Duration of therapy- 4wks for most patients 35

36. PREVENTION
 Antimicrobial prophylaxis before various
procedures and other forms of dental
manipulation may reduce the incidence of
infective endocarditis in susceptible patients
36

37. HIGH-RISK CARDIAC LESIONS FOR WHICH ENDOCARDITIS
PROPHYLAXIS IS ADVISED BEFORE DENTAL PROCEDURES
37

38. ANTIBIOTIC REGIMENS FOR PROPHYLAXIS OF ENDOCARDITIS
IN ADULTS WITH HIGH-RISK CARDIAC LESIONS
38

39. POOR PROGNOSTIC FACTORS
 Female
 S. aureus
 Candida infection
 Vegetation size
 Aortic valve
 Prosthetic valve
 Diabetes mellitus
 Low serum albumen
 Heart failure
 Paravalvular abscess
 Embolic events
39