Infective endocarditis is an infection of the heart valves or endocardial surfaces. It most commonly involves the mitral and aortic valves. Staphylococcus aureus is the most common cause of acute infective endocarditis while viridans streptococci most commonly cause subacute infective endocarditis. Diagnosis requires a high index of suspicion and is confirmed through blood cultures, echocardiography, and applying modified Duke criteria. Treatment involves prolonged intravenous antibiotics targeting the causative organism along with surgery to address valvular complications or poor prognostic factors. Prevention strategies focus on proper dental and skin care to reduce risk of infection from procedures.

1. INFECTIVE ENDOCARDITIS
By Dr Hafsat Mijinyawa Iya

2. OUTLINE
• INTRODUCTION/DEFINITION
• EPIDEMIOLOGY
• CLASSIFICATION
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• INVESTIGATION
• DIAGNOSIS CRITERIA
• MANAGEMENT
• PROPHYLAXIS
• CONCLUSION

3. INTRODUCTION/DEFINITION
• Infective endocarditis is an infection of the endocardial surfaces of the heart.
• Infection most commonly involves heart valves.
• The signs and symptoms vary widely including manifestations of infected and
sterile emboli as well as those of some immunological pathways.
• It is a life-threatening infection so if its diagnosis is unduly delayed or treatment is
inadequate, it is inevitably fatal.

4. EPIDEMIOLOGY
• In the United States and likely in other developed countries, the incidence of IE is
estimated to be 12 cases per 100,000 population per year, with progressive
increases during recent decades.
• The incidence of IE is notably increased among the elderly.
• In Africa, 42 studies with 2141 records were looked at.
• Rheumatic heart disease was the most common risk factor for infective
endocarditis in adults whereas congenital heart disease was the most common
risk factor for infective endocarditis in children and the most common pathogen
were Staphylococcus species and Streptococcus species.

5. EPIDEMIOLOGY IN NIGERIA
• Ninety cases of IE seen over a 10-year-period at University College
Hospital, Ibadan.
• The peak incidence was in the third decade.
• Rheumatic heart disease was the most common pre-existing lesion in 59
cases with subacute endocarditis.
• In most cases the source of infection was not known.
• In 41 of the 90 cases (44%) the diagnosis was made only at autopsy.
• The bacterial isolation rate was low, the commonest organisms being
staphylococci, streptococci, micrococci and gram-negative bacilli.
• The overall mortality was 70%.

6. TYPES OF IE
• Native valve endocarditis(NVE).
• Prosthetic valve endocarditis(PVE): Early or Late
• Intravenous drug use(IDU) related endocarditis

7. CLASSIFICATION OF IE
• AIE can be classified according to the temporal evolution of disease, the site of infection, the cause of
infection, or the predisposing risk factor.
• CUTE IE
ACUTE IE SUBACUTE IE
• HECTICALLY FEBRILE ILLNESS THAT’S
DEVELOPS OVER HOURS OR DAYS
• RAPID DESTRUCTION OF ENDOCARDIAL
TISSUE, SEEDS EXTRACARDIAC SITES
• RAPIDLY PROGRESSES TO DEATH.
• SLOWER ONSET, DEVELOPS OVER WEEKS
TO MONTHS.
• IT CAUSES STRUCTURAL DAMAGE MORE
SLOWLY
• IT IS MORE COMMON WITH
INDIVIDUALS WITH PRE-EXISTING
DAMAGE TO HEART VALVES,
STRUCTURAL HEART DEFECTS OR
PROSTHETIC VALVES.

8. AETIOLOGY
• Although many species of bacteria and fungi cause sporadic episodes
of IE, a few bacterial species cause the majority of cases and they
include:

9. ORGANISM
Staphylococcus aureus • Part of normal skin flora for follows procedures on the skin.
• Most common cause of ACUTE IE
• Affects healthy valves in addition to damaged valves. ONLY pathogen.
• Usually fatal within 6 weeks.
Viridan streptococci • Part of normal oral flora, mostly follows dental procedures.
• Most common cause of SUBACUTE IE
• Affects usually damaged valves.
• Produces DEXTRAN.
Staphylococcus
epidermidis
• Part of skin flora.
• Common cause of subacute IE in patients with prosthetic valves and
intracardiac devices.
Enterococci (esp
Enterococcus faecalis)
• Part of urogenital flora, follows GUT + GIT. Procedures.
• Causes multi-drug resistant IE.
Streptococcus gallolyticus • Associated with colorectal cancer and colonic polyps.
• Common among the elderly.
Grame –ve HACEK group • Formerly most common cause of subacute IE.

11. AETIOLOGY …..CONT’D
• About 5–15% of patients with IE have negative blood cultures.
• In one-third to one-half of these cases, cultures are negative because
of prior antibiotic exposure.
• The remainder are infected by fastidious organisms, such as some
streptococci, HACEK organisms, Coxiella burnetii, and Bartonella
species, Tropheryma whipplei, Corynebacterium species and
Propionibacterium acnes and Mycobacterium chimaera.
• Lastly, atrial myxoma, marantic endocarditis, and the
antiphospholipid antibody syndrome may mimic culture-negative IE.

12. RISK FACTORS
• Age: >60yrs
• Male sex
• Previous history of IE
• IV drug use or other skin procedures
• Poor dentition/Dental procedures (cleaning, root cannel)
• Catheter procedures (urethral, central venous)
• Long term hemodialysis
• HIV infection

13. …..cont’d
• Abnormal cardiac anatomy
– Abnormal native valve (most common predisposing factor)
– MVP(20%to30% of cases)
– RHD
– Bicuspid aortic valve
– Congenital heart disease including ASD,VSD and PDA
– Prosthetic heart valves

14. PATHOGENESIS
• The prototypic lesion of infective endocarditis (IE), the vegetation, is a
mass of platelets, fibrin, microorganisms, and scant inflammatory
cells
• Usually there is a predisposition; DAMAGED ENDOCARDIUM (E.G. an
abnormal valve). But S. aureus has the ability to cause infection on a
healthy endocardium or abnormal valve.
• Endothelial injury allows either direct infection by virulent organisms
or the development of a platelet–fibrin thrombus—a condition called
nonbacterial thrombotic endocarditis (NBTE).

15. • The cardiac conditions most commonly resulting in NBTE are mitral
regurgitation, aortic stenosis, aortic regurgitation, ventricular septal
defects, and complex congenital heart disease.
• This NBTE serves as a site of bacterial attachment during transient
bacteremia.
• NBTE + bacteria = Microbial vegetations.

16. • Microbial vegetations activate immune system with subsequent
release of cytokine, proteases and reactive oxygen species leading to
valve and perivalvular tissue destruction.
• Blood flow flicks off a piece of the vegetation = SEPTIC EMBOLI
• Plasma cells produce antibodies against the microbial antigen forming
and Ag-Ab IMMUNE COMPLEX. A part of this immune complex could
break off and get deposited in various tissues.
• The left side of the heart is more affected than the right side
(M>A>T>P valve). But in IV drug users; the tricuspid valve is more
affected.

18. CONSTITUTIONAL SYMPTOMS
• In patients with subacute presentations, fever is typically low grade
rarely exceeding 39.4°C (103°F); in contrast, temperatures of 39.4°–
40°C (103°–104°F) are often noted in acute IE.
• Fever may be blunted in patients who are elderly, are severely
debilitated, prior antibiotic use or have renal failure.
• Nonspecific symptoms of fatigue, weight loss, malaise, chills, night
sweat, and/or musculoskeletal aches.

19. CARDIAC MANIFESTATIONS
• Valve dysfunction
• New regurgitant murmurs
• Congestive heart failure
• Intracardiac fistulae
• Valvular and Perivalvular abscesses
• Periannular abscess
• Prosthetic valve dehiscence
• Varying degree of heart block (aortic paravalvular infection)
• Myocardial infarction from coronary artery emboli(2% of patients)

20. MANIFESTATIONS OF SEPTIC EMBOLI
LUNGS: pulmonary embolism, lung abscesses
BRAIN: cerebral abscess, ICH, SAH, acute iscahemic stroke,
encephalopathy.
LIMBS: Janeway lesions, splinter hemorrhges
BONES: discitis, osteomyelitis, spondylitis, septic arthritis
SPLEEN: splenic abcess, splenic infarct
KIDNEYS: renal infarct

21. IMMUNE COMPLEX MANIFESTATIONS
Immune complexes are distributed through systemic circulation
commonly
• Oslers nodes
• Roths spot
• Hypocomplementeric glomerulonephritis
• Positive rheumatoid factor

22. DIAGNOSIS
• The diagnosis of IE requires a high index of suspicion.
• Careful clinical, microbiologic, and echocardiographic evaluations
should be pursued when febrile patients have IE predispositions,
cardiac or noncardiac (e.g., stroke or splenic infarct) features of IE, or
blood cultures yielding an IE-associated organism.

23. INVESTIGATIONS
• Laboratory
– Non specific- anemia, leucocytosis, ↑c-reactive protein, ↑ESR, abnormal
urinalysis with hematuria, or red casts
– Blood culture
• Obtain blood culture before starting antibiotics.
• Exercise strict aseptic technique and optimal sin preparation
• In acute presentations obtain 2 or 3 sets rapidly within 5 to 10 mins of each
other prior to starting antibiotics
• In subacute presentations obtain 3 separate sets of blood cultures spaced
30 minutes apart Obtain 20 mL of blood for each sample drawn

24. INVESTIGATIONS
• ECHOCARDIOGRAPHY: TEE and TTE
TEE has more specificity and sensitivity than TTE
• TTE- to be used in patients with NVE who are good candidates for
imaging
• TTE may produce suboptimal images in 20% of patients- Obesity,
COPD
• TEE- has a negative predictive value of 92%
• TEE- is particular useful in PVE and for evaluation of myocardial
invasion
Color doppler

26. OTHER INVESTIGTIONS
• MRI (BRAIN, SPINE)
• ABD-PELVIC, RENAL USS
• CTPA/CHEST CT SCAN
• CXR
• FUNDOSCOPY
• URINALYSIS/URINE MICROSCOPY
• FBC
• RHEUMATOID FACTOR

27. …..CONT’D
• NON-BLOOD CULTURE TESTING:
• Serologic testing (Brucella, Bartonella, T. whipplei, and C. burnetii)
• Culture and histopathologic examination of vegetations recovered
from surgery or embolectomy
• Molecular testing: PCR

32. TREATMENT
• The major goals of therapy for IE are to eradicate the infectious agent
from the thrombus and to address the intra and extacardiac
complications of valvular infection.
• Some of the effects of IE require surgical intervention.
• Emergent care should focus on making the correct diagnosis and
stabilizing the patient.

33. TREATMENT
• Antibiotics are the mainstay of treatment for infective endocarditis.
• Goals to achieve maximize clinical outcomes are early diagnosis,
accurate microorganism identification, reliable susceptibility testing,
prolonged intravenous (IV) administration of bactericidal
antimicrobial agents, proper monitoring of potentially toxic
antimicrobial regimens

39. INDICATIONS FOR SURGERY

40. POOR PROGNOSTIC FACTORS

41. PREVENTION

46. CONCLUSION
Infective endocarditis is not a single disease, but rather may present
with very different aspects depending on the first organ involved, the
underlying cardiac disease (if any), the microorganism involved, the
presence or absence of complications and the patient’s characteristics
so its management should be based on multi-disciplinary approach.

47. QUESTIONS
• Rheumatoid factor in infective endocarditis
• Duration of ttt in IE
• When to repeat ECHO
• Mural endocardium
• Know criteria off head
• Read from manifestations in Harrison
• Pictures add to presentation.