Infective endocarditis from Harrison's

1. INFECTIVE ENDOCARDITIS – AN
UPDATE
PRESENTOR
- DR.HARSHITHA S

2. • Infective endocarditis (IE) is an evolving
disease with a persistently high mortality and
morbidity, even in the modern era of advanced
diagnostic imaging, improved antimicrobial
chemotherapy, and potentially curative surgery.
• Despite these improvements in health care, the
incidence of the disease has remained
unchanged over the past two decades and may
even be increasing.

3. EPIDEMIOLOGY
• Chronic rheumatic heart disease is now an
uncommon antecedent cause, whereas
degenerative valve disease of the elderly ,
congenital heart disease ,mitral valve
prolapse, intravenous drug misuse, valve
replacement, vascular instrumentation
hemodialysed cases and
immunocompromised have become
increasingly common.

4. ETIOLOGY
Common causes :
Viridans streptococci
Staphylococci aureus
HACEK group
Streptococci Gallolyticus ( Strep. Bovis )
Enterococci

5. • One of the changes in this spectrum stems from the
gradual rise in S.aureus ,particularly in prostheses
• Dangerous effects of S.aureus
a.Rapidly progressing
b.highly emboligenic with dissemination & spread
of infection
c.highly virulent causing valve infection in patients
with no h/o heart disease
d.increased antibiotic resistance
e.invasive procedures,prostheses and stents,iv drug
users

6. • NATIVE VALVE ENDOCARDITIS
Staphylococcus aureus, coagulase-
negative staphylococci (CoNS), and
enterococci
May have either a nosocomial onset
(55%) or a community onset (45%)

7. • PROSTHETIC VALVE ENDOCARDITIS
a.Early PVE : within 2 months
nosocomial
common causes : S. aureus, CoNS,
facultative gram-negative bacilli, diphtheroids,
and fungi
b.Delayed onset PVE : 2-12months
nosocomial
common cause : CoNS
c.Late onset PVE : >12months
causes : similar to community
onset NVE

9. • CARDIOVASCULAR IMPLANTABLE
ELECTRONIC DEVICE ENDOCARDITIS
-primarily permanent pacemakers and
implantable cardioverter defibrillator (mc )
- Causes : S. aureus and CoNS, both of
which are often resistant to methicillin, cause
the majority of cases

10. • INJECTION DRUG USE ENDOCARDITIS
-MC : right side endocarditis by S.aureus
-Left sided endocarditis : varied etiology
Pseudomonas aeruginosa,
Candida species, Bacillus, Lactobacillus, and
Corynebacterium species. Polymicrobial
endocarditis occurs among injection drug users

11. • ENDOCARDITIS WITH NEGATIVE
BLOOD CULTURE
Causes : Prior antibiotic exposure
Streptococci (Granulicatella and
Abiotrophia species)
HACEK organisms
Coxiella burnetii
Bartonella species

12. • C. burnetii has a predilection for prosthetic
valves.
• Corynebacterium species and Propionibacterium
acnes may involve intracardiac devices.
• Atrial myxoma, Marantic endocarditis, and the
antiphospholipid antibody syndrome may mimic
culture-negative infective endocarditis.

13. • MARANTIC ENDOCARDITIS
Non Bacterial Thrombotic
Endocarditis

14. PATHOGENESIS

17. • Why are vegetations in Infective
endocarditis common on the atrial side

18. • Infective endocarditis generally develops when
there is a pre-existing valvular lesion.
• The location where the vegetation in infective
endocarditis develops is based on the pressure of
the surroundings.
• Bacteria tend to colonise places where the
pressure is low.

19. • In mitral regurgitation, blood when pumped
from the left ventricle enters the atria due to the
patent bicuspid valve.
• Naturally, the pressure is more on the
ventricular side than the atrial side.
• Hence, the bacteria settle on the top of the leaf.
• Moreover, the do so at the edges of the leaves.
• This is because, since the blood has to squeeze
through, according to to bernoulli's theorem
(Venturi effect).
• Hence they form on the edges of the atrial side of
the valves

20. • In case of an aortic regurgitation, since there is a
backflow of blood from the aorta to the
ventricles, the vegetations are found on the
underside of the aortic valves.

21. • CLINICAL FEATURES

23. Major Criteria

24. Proposed modifications
Positive serology for Coxiella burnetti
Bacteraemia due to Staphylococcus aureus
Positive molecular assay for specific gene targets and universal loci for bacteria & fungi
Positive serology for Chlamydia psittaci
Positive serology for Bartonella species

27. To be added
Elevated CRP, elevated ESR, splenomegaly,
haematuria, clubbing,
splinter haemorrhages, petechiae and purpura
Identified IE organism from metastatic lesions

28. Definite Endocarditis
2 major or
1 major and 3 minor or
5 minor criteria
Rejected
If an alternative diagnosis is established,
If symptoms resolve and do not recur with ≤4 days of antibiotic therapy,
If surgery or autopsy after ≤4 days of antimicrobial therapy yields no histologic evidence of
endocarditis.

29. Possible Infective Endocarditis
Illnesses not classified as definite endocarditis
or rejected as such are considered cases of
possible infective endocarditis when either one
major and one minor criterion or three minor
criteria are fulfilled

32. High-Risk Cardiac Lesions
Prosthetic heart valves
Prior endocarditis
Unrepaired cyanotic congenital heart disease, including palliative
shunts or conduits
Completely repaired congenital heart defects during the 6 months after
repair
Incompletely repaired congenital heart disease with residual defects
adjacent to prosthetic material
Valvulopathy developing after cardiac transplantation

33. HIGH RISK ECHO FEATURES
Large vegetations
Valve insufficiency
Paravalvular infection
Ventricular dysfunction.

34. LIMITATIONS OF TTE IN DIAGNOSIS
• It cannot image vegetations <2 mm in diameter
• In 20% of patients the images are inadequate.
• TTE detects vegetations in 65–80% of patients
with definite clinical endocarditis but is not
optimal for evaluating prosthetic valves or
detecting intracardiac complications

35. • In addition, 18-fluorodeoxyglucose positron
emission tomography (FDG-PET)/CT, a
technique still under evaluation, may identify
perivalvular or perigraft infection not seen on
TEE in patients with PVE or prosthesis–aorta
graft infection (Bental procedure).

41. ANTITHROMBOTIC
TREATMENT
Patients who have a mechanical
prosthetic valve
Atrial fibrillation with either mitral
stenosis or a CHADS2 score ≥2,
Deep-vein thrombophlebitis.

50. Antibiotic Therapy after Cardiac Surgery
• When valve cultures are negative in
uncomplicated NVE caused by susceptible
organisms, the duration of preoperative plus
postoperative treatment should equal the total
duration of recommended therapy.
• For endocarditis complicated by perivalvular
abscess, partially treated PVE, or culture-
positive valves, a full course of therapy should be
given postoperatively.

51. Extracardiac Complications
• Splenic abscess develops in 3–5% of patients
with endocarditis. Effective therapy requires
either image-guided percutaneous drainage or
splenectomy.
• Mycotic aneurysms occur in 2–15% of
endocarditis patients; one-half of these cases
involve the cerebral arteries and present as
headaches, foca lneurologic symptoms, or
hemorrhage.

52. • Cerebral aneurysms should be monitored by
angiography. Some will resolve with effective
antimicrobial therapy, but those that persist,
enlarge, or leak should be treated surgically if
possible.
• Extracerebral aneurysms present as local pain, a
mass, local ischemia, or bleeding; these
aneurysms are treated surgically

53. Prevention

55. NEW DEVELOPMENTS
• Several exciting developments offer the prospect
of improved prevention and treatment of IE.
• Vaccines targeted at specific bacterial adhesins
may inhibit valve colonisation, and encouraging
results have been obtained with
antistaphylococcal vaccination in vitro and with
haemodialysis patients in vivo.

56. • Newer antibacterial agents with novel effects
may digest the essential Gram positive
peptidoglycan by triggering of bacteriophage
encoded bacteriolytic enzymes or they may
attenuate the invasive properties of S.aureus by
reducing secretion of haemolysins and toxins
• Lastly, modified biomaterials in development
may reduce the risk of IE in patients with
artificial heart valves or other intracardiac
prosthetic material.

57. Despite these advances, however, the
changing face of IE seems set to
challenge the endeavours of
cardiologists, microbiologists, and
cardiac surgeons for many decades
yet.