Infective endocarditis is an infection of the inner lining of the heart chambers and heart valves. It has varying presentations from subacute to acute. Diagnosis involves blood cultures, echocardiography, and clinical criteria. Common causes are bacteria like streptococci and staphylococci. Complications include heart failure, embolic events, and kidney or brain infections. Treatment involves prolonged antibiotics and sometimes surgery.

1. INFECTIVE ENDOCARDITIS
Prepared by KUTOSI Joseph (MBCh.B–V)
Kampala international university-WC.

2. EXPECTATIONS OF THIS PRESENTATION
• Introduction ( definition and important notes )
• Epidemiology
• Risk factors
• Etiology and pathophysiology
• Signs and symptoms
• Diagnosis [ Modified dukes criteria and ESC- criteria)
• Management and prognosis.
• Prevention.
• Q & A session and supplements.

3. INTRODUCTION
• Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci
or staphylococci) or fungi.
• It may cause fever, heart murmurs, petechiae, anemia, embolic phenomena, and endocardial
vegetations.
• Vegetations may result in valvular incompetence or obstruction, myocardial abscess, or mycotic
aneurysm.
• Diagnosis requires demonstration of microorganisms in blood and usually echocardiography.
• Treatment consists of prolonged antimicrobial treatment and sometimes surgery.

4. INTRODUCTION
• Endocarditis usually refers to infection of the endocardium (ie, infective
endocarditis).
• The term can also include noninfective endocarditis, in which sterile
platelet and fibrin thrombi form on cardiac valves and adjacent
endocardium.
• Noninfective endocarditis sometimes leads to infective endocarditis.
• Both can result in embolization and impaired cardiac function.
• The diagnosis of infective endocarditis is usually based on a
constellation of clinical findings rather than a single definitive test result.

5. EPIDEMIOLOGY OF INFECTIVE
ENDOCARDITIS
• In the United States, the incidence of IE is approximately 12.7 cases per
100,000 persons per year.
• The incidence of IE in other countries is similar to that in the United States.
• The proportion of patients with intracardiac devices has increased from
13.3% to 18.9%, whereas the proportion of cases with a background of HIV
infection or IV drug abuse has fallen.
• The mean age of patients has increased from 58.6 to 60.8 years and
continues to rise; more than 50% of patients are older than 50 years
• Infective endocarditis is 3 times more common in males than in females. It
exhibits no racial predilection.
Adapted from medscape mobile app [latest version Feb 2023].

6. EPIDEMIOLOGY OF INFECTIVE
ENDOCARDITIS IN AFRICA: A SYSTEMATIC
REVIEW AND META-ANALYSIS. 2022.
• Rheumatic heart disease was the most common risk factor for infective endocarditis in adults - 52%,
whereas congenital heart disease was the most common risk factor for infective endocarditis in
children (44·7%)
• Microbiological testing (mostly blood cultures) was positive in 48·6% of patients with infective
endocarditis, with Staphylococcus species 41.3% and Streptococcus species (34·0% ) the most
commonly identified microorganisms.
• The pooled rate of surgical treatment of infective endocarditis was 49·1%.
• The pooled in-hospital mortality rate was 22·6%.
• Other frequent complications included heart failure (47·0%), acute kidney injury (22·8), and embolic
events (31·1% ).
Adapted from https://www.thelancet.com/journals/langlo/article/PIIS2214-109X(21)00400-9/fulltext

7. RISK FACTORS OF INFECTIVE
ENDOCARDITIS
• Infective endocarditis can occur at any age.
• Men are affected about twice as often as women.
• Incidence of infection and mortality increase with increasing age.
• Patients who use illicit intravenous drugs, immunocompromised patients, patients with prosthetic
heart valves and other intracardiac devices are at highest risk.
• There is also an increased risk in patients with indwelling intravascular catheters.

8. ETIOLOGY AND PATHOPHYSIOLOGY
• The normal heart is relatively resistant to infection. Bacteria and fungi do
not easily adhere to the endocardial surface, and constant blood flow
helps prevent them from settling on endocardial structures. Thus, 2
factors are typically required for endocarditis:
1.A predisposing abnormality of the endocardium
2.Microorganisms in the bloodstream (bacteremia)
Important to note that Massive bacteremia or particularly virulent
microorganisms (eg, Staphylococcus aureus) cause endocarditis on normal
valves.

9. ETIOLOGY AND PATHOPHYSIOLOGY OF
INFECTIVE ENDOCARDITIS
The disease develops in 3 stages:
Bacteremia: Microorganisms are present in the blood
Adhesion: The microorganism adheres to abnormal or damaged
endothelium via surface adhesions
Colonization: Proliferation of the organism together with inflammation,
leading to a mature vegetation
Many of the causative microorganisms produce polysaccharide biofilms
that shield them from host immune defences and impede antibiotic
penetration.

10. ETIOLOGY AND PATHOPHYSIOLOGY OF
INFECTIVE ENDOCARDITIS
• The normal heart is relatively resistant to infection. Bacteria and fungi do
not easily adhere to the endocardial surface, and constant blood flow
helps prevent them from settling on endocardial structures.
Two factors are typically required for endocarditis:
1. A predisposing abnormality of the endocardium
2. Microorganisms in the bloodstream (bacteremia)
Massive bacteremia or particularly virulent microorganisms (eg, S. aureus)
cause endocarditis on normal valves.

11. ETIOLOGY AND PATHOPHYSIOLOGY
[ENDOCARDIAL FACTORS]
• Usually involves the heart valves
• Congenital heart defects, rheumatic valvular
disease, bicuspid aortic valves, calcific aortic
valves, mitral valve prolapse, hypertrophic
cardiomyopathy, and prior endocarditis.
• Prosthetic valves and other intracardiac
devices.
• Occasionally, mural thrombi, ventricular septal
defects, and patent ductus arteriosus sites
become infected.
• The nidus for infection is usually a sterile fibrin-
platelet vegetation formed when damaged
endothelial cells release tissue factor.
• Infective endocarditis occurs most often on the
left side (eg, mitral or aortic valve).
• About 10 to 20% of cases are right-sided
(tricuspid or pulmonic valve).
• Patients who use illicit intravenous drugs have
a much higher incidence of right-sided
endocarditis (about 30 to 70%

12. ETIOLOGY AND PATHOPHYSIOLOGY OF
INFECTIVE ENDOCARDITIS
The disease develops in 3 stages:
1.Bacteremia: Microorganisms are present in the
blood
2. Adhesion: The microorganism adheres to
abnormal or damaged endothelium via surface
adhesions
3. Colonization: Proliferation of the organism
together with inflammation, leading to a mature
vegetation
Many of the causative microorganisms produce
polysaccharide biofilms that shield them from host
immune defences and impede antibiotic
penetration.
• Causative organisms vary by site of
infection, source of bacteremia, and host
risk factors (eg, IV illicit drug use), but
overall, streptococci and Staphylococcus
aureus cause 80 to 90% of cases.
• Enterococci, gram-negative bacilli,
HACEK organisms (Haemophilus
species, Actinobacillus
actinomycetemcomitans,
Cardiobacterium hominis, Eikenella
corrodens, and Kingella kingae), and
fungi cause most of the rest.

13. ETIOLOGY AND PATHOPHYSIOLOGY OF INFECTIVE
ENDOCARDITIS
Local consequences.
• Myocardial abscesses with tissue destruction and
sometimes conduction system abnormalities (usually
with low septal abscesses)
• Sudden, severe valvular regurgitation, causing heart
failure and death (usually due to mitral or aortic valve
lesions)
• Aortitis due to contiguous spread of infection
• Prosthetic valve infections are particularly likely to
involve valve ring abscesses, obstructing vegetations,
myocardial abscesses, and mycotic aneurysms
manifested by valve obstruction, dehiscence, and
conduction disturbances.
Systemic consequences
• Systemic consequences of endocarditis are primarily due
to
• Embolization of infected material from the heart valve
• Immune-mediated phenomena (primarily in chronic
infection)
• Right-sided lesions produce septic pulmonary emboli,
resulting in pulmonary infarction, pneumonia, or
empyema.
• Left-sided lesions may embolize to any tissue,
particularly the kidneys, spleen, and central nervous
system.
• Mycotic aneurysms can form in any major artery.
• Cutaneous and retinal emboli are common.
• Diffuse glomerulonephritis may result from immune
complex deposition.

14. CLASSIFICATION OF INFECTIVE
ENDOCARDITIS
• Infective endocarditis may have an indolent, subacute course or a more
acute, fulminant course with greater potential for rapid decompensation.
• Classification is based on this and wether or not there is a prothethis, i.e
1. Sub acute Bacterial endocarditis
2. Acute bacterial endocarditis
3. Prosthetic valve endocarditis

15. SUBACUTE BACTERIAL ENDOCARDITIS
(SBE).
• Although aggressive, usually develops insidiously and progresses slowly
(ie, over weeks to months).
• Often, no source of infection or portal of entry is evident. SBE is caused
most commonly by streptococci (especially viridans, microaerophilic,
anaerobic, and nonenterococcal group D streptococci and enterococci).
• Less commonly by S. aureus, Staphylococcus epidermidis, Gemella
morbillorum, Abiotrophia defectiva (formerly, Streptococcus defectivus),
Granulicatella species, and fastidious Haemophilus species.
• SBE often develops on abnormal valves after asymptomatic bacteremia
due to periodontal, gastrointestinal, or genitourinary infections.

16. ACUTE BACTERIAL ENDOCARDITIS (ABE)
• Acute Bacterial endocarditis usually develops abruptly and progresses
rapidly (ie, over days).
• A source of infection or portal of entry is often evident.
• When bacteria are virulent or bacterial exposure is massive, ABE can
affect normal valves.
• It is usually caused by S. aureus, group A hemolytic streptococci,
pneumococci, or gonococci.

17. PROSTHETIC VALVULAR ENDOCARDITIS
(PVE)
• Develops in 2 to 3% of patients within 1 year after valve replacement and in 0.5%/year
thereafter.
• It is more common after aortic than after mitral valve replacement and affects
mechanical and bioprosthetic valves equally.
• Early-onset infections (< 2 months after surgery) are caused mainly by contamination
during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids,
coliform bacilli) or by fungi (eg, Candida species, Aspergillus species).
• Late-onset infections are caused mainly by contamination with low-virulence
organisms during surgery or by transient asymptomatic bacteremias, most often with
streptococci; S. epidermidis; diphtheroids; and the fastidious gram-negative bacilli,
Haemophilus species, Actinobacillus actinomycetemcomitans, and Cardiobacterium
hominis.

18. TYPES OF INFECTIVE ENDOCARDITIS
• Endocarditis has evolved into several variations, keeping it near the top
of the list of diseases that must not be misdiagnosed or overlooked.
• Endocarditis can be broken down into the following categories
1. Native valve endocarditis (NVE), acute and subacute
2. Prosthetic valve endocarditis (PVE), early and late
3. Intravenous drug abuse (IVDA) endocarditis.
4. Other terms commonly used to classify types of IE include pacemaker
IE and nosocomial IE (NIE)

19. SIGNS AND SYMPTOMS OF INFECTIVE
ENDOCARDITIS
• Symptoms and signs vary based on the classification but are usually
nonspecific.
In Sub acute bacterial endocarditis
Initially, symptoms of SBE are vague.
• low-grade fever (< 39° C), night sweats, fatigability, malaise, and weight loss.
• Chills and arthralgias may occur.
Symptoms and signs of valvular insufficiency may be a first clue.
• Initially, ≤ 15% of patients have fever or a murmur, but eventually almost all
develop both.
• Physical examination may be normal or include pallor, fever, change in a
preexisting murmur or development of a new regurgitant murmur, and
tachycardia.

20. SIGNS AND SYMPTOMS
• Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white
centers (Roth spots).
• Cutaneous manifestations include petechiae (on the upper trunk, conjunctivae,
mucous membranes, and distal extremities), painful erythematous subcutaneous
nodules on or near the tips of digits (Osler nodes), nontender hemorrhagic macules or
papules on the palms or soles (Janeway lesions), and splinter hemorrhages under the
nails.
• About 35% of patients have central nervous system (CNS) effects, including transient
ischemic attacks, stroke, toxic encephalopathy (due to infective microemboli), and, if a
mycotic CNS aneurysm ruptures, brain abscess and subarachnoid hemorrhage.
• Renal emboli may cause flank pain and, rarely, gross hematuria.
• Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause
splenomegaly or clubbing of fingers and toes.

21. SIGNS AND SYMPTOMS
Acute bacterial endocarditis and prosthetic valvular endocarditis.
• Symptoms and signs of acute bacterial endocarditis and prosthetic valvular
endocarditis are similar to those of subacute bacterial endocarditis, but the course is
more rapid.
• Fever is almost always present initially, and patients appear toxic; sometimes septic
shock develops.
• Heart murmur is present initially in about 50 to 80% and eventually in > 90%.
• Rarely, purulent meningitis occurs.
Right-sided endocarditis
• Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes
hemoptysis. A murmur of tricuspid regurgitation is typical.

22. OSLER NODES AND JANEWAY LESIONS

23. OSLER NODES , JANEWAY LESIONS AND
SPLINTER HEMORRHAGES

24. OCULAR MANIFESTATION OF
INFFECTIVE ENDOCARDITIS.

25. COMPLICATIONS OF INFECTIVE
ENDOCARDITIS
• Myocardial infarction, pericarditis, cardiac arrhythmia
• Cardiac valvular insufficiency
• Congestive heart failure
• Sinus of Valsalva aneurysm(an abnormal dilatation of the aortic root located between the aortic valve
annulus and the sinotubular junction)
• Aortic root or myocardial abscesses
• Arterial emboli, infarcts, mycotic aneurysms
• Arthritis, myositis
• Glomerulonephritis, acute renal failure
• Stroke syndromes
• Mesenteric or splenic abscess or infarct

26. DIAGNOSIS OF INFECTIVE
ENDOCARDITIS
• Because symptoms and signs are nonspecific, vary greatly, and may
develop insidiously, diagnosis requires a high index of suspicion.
• Endocarditis should be suspected in patients with fever and no obvious
source of infection, particularly if a heart murmur is present.
Diagnosis involves;
1. Blood culture
2. Echocardiography and sometimes other imaging modalities
3. Clinical criteria

27. BLOOD CULTURES
• Identification of the organism and its antimicrobial susceptibility is vital to guide
treatment.
• Three ( 3 ) blood samples for culture (20-mL each) should be obtained, ideally > 6
hours apart (if presentation suggests acute bacterial endocarditis, 2 cultures within the
first 1 to 2 hours).
• Each set of cultures should be obtained from a separate, fresh venipuncture site.
• When endocarditis is present and no prior antibiotic therapy was given, all 3 blood
cultures usually are positive because the bacteremia is continuous; at least one culture
is positive in 99%.
• Premature use of empiric antibiotic therapy should be avoided in patients with
acquired or congenital valvular or shunt lesions to avoid culture-negative endocarditis.
• If prior antimicrobial therapy was given, blood cultures should still be obtained, but
results may be negative.

28. OTHER LABORATORY INVESTIGATIONS
• Other than positive blood cultures, there are no specific laboratory
findings.
• Established infections often cause a normocytic-normochromic anemia,
elevated WBC , increased ESR, increased immun IG levels, the presence
of circulating immune complexes and RF's, but these findings are not
diagnostically helpful.
• Urinalysis often shows microscopic hematuria and, occasionally, red
blood cell casts, pyuria, or bacteriuria.

29. IMAGING STUDIES
• Transthoracic echocardiography (TTE) should be done initially and has
sensitivity of 50 to 90% and specificity > 90%. Transesophageal
echocardiography (TEE) can reveal vegetations too small to be seen on TTE
with a sensitivity of 90 to 100%.
• Transesophageal echocardiography should be done when
1. Patients have a prosthetic valve (where TTE sensitivity is limited)
2. Transthoracic echocardiogram is nondiagnostic
3. Diagnosis of infective endocarditis has been established clinically (done to
detect perforations, abscesses, and fistulas)
NOTE ; Serial TEE enables diagnosis of complications that evolve during
treatment, such as increasing vegetation size or abscess formation.

30. IMAGING STUDIES
• CT-Scan can fully define paravalvular abscesses and detect mycotic
aneurysms.
• Positron emission tomography (PET) scanning improves the sensitivity of the
modified Duke criteria without compromising specificity.
• PET scanning also detects extracardiac infection, such as septic emboli, and
is an emerging tool for the diagnosis of endocarditis originating in prosthetic
and intracardiac devices.
• CT and PET abnormalities are now included as major criteria in the European
guidelines.
• Routine brain imaging has been proposed because up to 60% of patients
have clinically silent lesions. It’s utility for prognosis and management is yet
to be defined.

31. DIAGNOSTIC CRITERIA
• Infective endocarditis is definitively diagnosed when microorganisms are
seen histologically in (or cultured from) endocardial vegetations
obtained during cardiac surgery, embolectomy, or autopsy.
• Because vegetations are not usually available for examination, there are
various clinical criteria for establishing a diagnosis.
• They include ;
1. Modified Duke Criteria —with a sensitivity and specificity > 90%, and
2. The European Society of Cardiology (ESC) 2015 modified criteria.

32. MODIFIED DUKES CRITERIA
Endocarditis is felt to be present in the following
conditions:
Direct evidence of endocarditis based upon
histological findings (a pathological criterion)
Positive Gram stain results or cultures of
specimens obtained from surgery or autopsy (a
pathological criterion)
-2 major clinical criteria
-1 major and any 3 minor clinical criteria
-5 minor clinical criteria
Possible endocarditis’ is defined by 1 major and 1
or 2 minor clinical criteria, OR 3 minor clinical
The diagnosis of endocarditis is ‘rejected’ in any
of the following cases:
- a firm alternate diagnosis is made
- clinical manifestations resolve after ≤4 days of
antibiotic therapy
- no pathological evidence of infective
endocarditis is found at surgery or autopsy after
antibiotic therapy for ≤4 days
- fail to meet criteria for for possible or definite
infective endocarditis

33. MODIFIED DUKES CRITERIA [MAJOR
AND MINORS]

34. THE EUROPEAN SOCIETY OF
CARDIOLOGY CRITERIA
• The ESC criteria are similar to the modified Duke criteria but include
expanded imaging results as major criteria as follows:
1. Vegetation, abscess, pseudoaneurysm, intracardiac fistula, valvular
perforation or aneurysm, or new partial dehiscence of prosthetic valve
identified by echocardiography
2. Abnormal activity around a prosthetic valve (implanted > 3 months
earlier) detected by PET/CT or single-photon emission computed
tomography (SPECT)/CT with radiolabeled leukocytes
3. Paravalvular lesions identified by cardiac
• The ESC also differs from the modified Duke minor criteria by specifying that
detecting silent vascular phenomena by imaging only is sufficient.

35. MANAGEMENT
• IV antibiotics.
• Sometimes valve debridement, repair, or replacement
• Dental evaluation and treatment.
• Removal of potential source of bacteremia.
• Withholding anticoagulation in patients with cerebral embolism

36. UGANDA CLINICAL GUIDELINES (UCG) ANTIBIOTICS FOR
INFECTIVE ENDOCARDITIS
Initial empirical antibiotic therapy
• Benzylpenicillin 5 MU IV every 6 hours for 4 weeks
• Plus gentamicin 1 mg/kg IV every 8 hours for 2 weeks.
If staphylococcus suspected, (acute onset) add:
• Cloxacillin IV 3 g every 6 hours.
If MRSA (Multi-Resistant Staphylococcus aureus).
• Vancomycin 500 mg IV every 6 hours for 6 weeks.

37. PROGNOSIS
Overall, the in-hospital mortality rate for endocarditis is 15 to 20%, with a 1-year mortality rate approaching 40%.
Untreated, infective endocarditis is always fatal. Even with treatment, death is more likely and the prognosis is generally poorer for
older people and people who have
• Infection with resistant organisms
• An underlying disorder
• A long delay in treatment
• Aortic valve or multiple valve involvement
• Large vegetations
• Polymicrobial bacteremia
• Prosthetic valve infections
• Mycotic aneurysms
• Valve ring abscess
• Major embolic events

38. PROGNOSIS
• Septic shock is more likely in patients with diabetes, acute kidney injury,
S. aureus infection, vegetation size > 15 mm, and signs of persistent
infection.
• The mortality rate for viridans streptococcal endocarditis without major
complications is < 10% but is virtually 100% for Aspergillus endocarditis
after prosthetic valve surgery.
• The prognosis is better with right-sided than left-sided endocarditis
because tricuspid valve dysfunction is tolerated better, systemic emboli
are absent, and right-sided S. aureus endocarditis responds better to
antimicrobial therapy.

39. PREVENTION OF INFECTIVE
ENDOCARDITIS
• Preventive dental examination and therapy before surgery to repair heart valves or congenital heart
lesions is recommended.
• Measures to reduce health care–acquired bacteremia aim to curb the rising incidence of iatrogenic
bacteremia and subsequent endocarditis are also recommended.
• During implantation of prosthetic devices, prophylaxis often involves use of amoxicillin/clavulanic acid.
• Dental and cutaneous hygiene is recommended for the general population but particularly for patients at
intermediate risk (those with native valve disease) and high-risk.

40. PREVENTION OF INFECTIVE
ENDOCARDITIS.
• Prosthetic heart valves, including transcatheter implanted prostheses
• Prosthetic material used for heart valve repair (eg, annuloplasty rings,
chords)
• Previous infective endocarditis
• Certain congenital heart diseases (CHD): Unrepaired cyanotic CHD
(including palliative shunts and conduits), completely repaired CHD
during the first 6 mo after surgery if prosthetic material or device was
used, repaired CHD that has residual defects at or adjacent to the site of
repair
• Heart transplant recipients with valvulopathy

41. LIBAN SACKS ENDOCARDITIS
• Non infection related endocarditis associated with Systemic lupus
erytheramatosus
• Antigen-antibody complexes.
• Affects mainly the mitral valve, but can affect both atrial and ventricular
endocardium.

42. THANK YOU NOTE AND REFERENCES
Thank you for paying attention, may you be able to prevent infective
endocarditis and efficiently manage patient presenting with the condition.
References
1.Davidsons
2. Uganda clinical guidelines (UCG)
3. Merck manuals (MSD) 2022.