Bacterial Endocarditis

1. Submitted To :
Dr. KANCHAN VOHRA
Assistant Professor
Submitted By :
Mohd. Rafi Bhat
BACTERIAL ENDOCARDITIS

2. .

3. Definition
Endocarditis is an inflammation of the
endocardium, the membrane lining the
chambers of the heart and covering the cusps
of the heart valves. Bacterial endocarditis
refers to infection of the heart valves by
various microorganisms especially bacteria.

4. Classification
According to temporal evolution of the disease
1. Acute
2. Subacute
Acute endocarditis: develops over a period of
days, rapidly damages cardiac structures
• Presents as high grade fever and systemic
toxicity
• Usually caused by S. aureus
• If untreated death occurs within few days to
weeks

5. Subacute endocarditis: 1. develops over
weeks to months
2.Indolent infection
3.Caused by Viridans streptococci
4. Usually occuring in preexisting valvular
disease
According to location of infection
1. Native valve endocarditis
2. Prosthetic valve endocarditis
3. Device related endocarditis
4. Right sided endocarditis

6. Native valve endocarditis-
• Acute NVE frequently involves normal valves.
Virulent such as S.aureus and group B streptococci
are typically the causative agents of this type of
endocarditis.
• Subacute NVE typically affects only abnormal
valves .Alpha hemolytic streptococci or
enterococci are usual causative agent.
Prosthetic valve endocarditis (PVE)
• Between 16 to 30% of all cases of endocarditis
occur in prosthetic valve
•Risk of infection highest in first 6-12 months of
valve replacement

7. • Early PVE if occuring within 1 year and late
PVE if occuring after 1 year
• Early PVE caused by S.aureus
•Late PVE caused by Alpha hemolytic
streptococci or enterococci
Device related Endocarditis
• Endocarditis related to cardiovascular
implantable electronic devices invoves the
device or the endothelium point of device
contact
• Mostly caused by S.aureus

8. Right –sided Endocarditis
• Mostly associated with IV drug use
• S.aureus is the most common causative
organism
•Tricuspid valve is most commonly affected
•Pulmonary valve may also be involved

9. Etiology
• Mainly thre group of organism causes
endocarditis
• Streptococci
•Staphylococci
• Enterococci
• Preexisting cardiac valvular abnormalities

10. Risk factor
•Presence of a prosthetic valve
• Previous endocarditis
• Complex cyanotic congenital heart disease (e.g.,
single-ventricle states)
• Surgically constructed systemic pulmonary
shunts or conduits
• Acquired valvular dysfunction (e.g., rheumatic
heart disease)
• Hypertrophic cardiomyopathy
• Mitral valve prolapse with regurgitation
• Intravenous drug abuse

11. Pathophysiology
The development of endocarditis through
hematogenous spread ,the most common route
, requires the sequential occurrence of several
factors :
• The endothelial surface of the heart is
damaged:- This injury occurs with turbulent
blood flow associated with the valvular lesions.
• Platelet and fibrin deposition occurs on the
abnormal epithelial surface :- These platelet
fibrin deposits are reffered to as nonbacterial
thrombotic endocarditis (NBTE)

12. • Bacteremia gives organisms access to and result in
colonization of the endocardial surface
After colonization of the endothelial surface, a
vegetation of fibrin, platelets and bacteria forms:-
The protective cover of fibrin and platelets allows
unimpeded bacterial growth to
concentrations as high as 109 to 1010 organisms
per gram of tissue.
•Formation of vegetations may destroy valvular
tissue, and continued destruction can lead to acute
heart failure via perforation of the valve leaflet,
rupture of the chordae tendineae or papillary
muscle, or in the patient with PVE.

13. •Vegetations may be friable, and fragments may
be released downstream. These infected
particles, termed septic emboli, can result
in organ abscess or infarction.
•Septic emboli from right-sided endocarditis
commonly lodge in the lungs, causing pulmonary
abscesses.
•Emboli from left-sided vegetations commonly
affect organs with high blood flow, such as the
kidneys, spleen, and brain.
Circulating immune complexes consisting of
antigen, antibody,
and complement may deposit in organs,
producing local inflammation
and damage

14. Clinical presentation
Symptoms :-fever ,chills, weakness , dyspnea ,
night sweats , weight loss
Sign:- fever , heart murmur, may or may not have
embolic phenomenon , splenomegaly or skin
manifestations (osler nodes, janeway lesion)
• osler nodes :Purplish or erythematous
subcutaneous papules or nodules on the pads of
the fingers and toes. These lesions are
2 to 15 mm in size and are painful and tender

15. Osler node
Petechiae

16. Janeway lesions

17. Roth spot
.

18. Splinter hemmorhages
.

19. Janeway lesions:-Hemorrhagic, painless
plaques on the palms of the hands or soles of
the feet.
Splinter hemmorhages:- Thin, linear
hemorrhages found under the nailbeds of the
fingers or toes.
Petechiae:- erythematous, painless,
hemorrhagic lesions. These lesions
appear anywhere on the skin but more
frequently on the anterior trunk, buccal
mucosa and palate, and conjunctivae

20. •Clubbing of the fingers:-Proliferative change
in the soft tissues about the terminal
phalanges observed in long-standing
endocarditis.
•Roth spot:-Retinal infarct with central pallor
and surrounding hemorrhage.
Emboli:- Left-sided endocarditis can result in
renal artery emboli causing flank painwith
hematuria, splenic artery emboli causing
abdominal pain, and cerebral emboli, which
may result in alteration in mental status.
Right-sided endocarditis may result in
pulmonary emboli, causing pleuritic pain .

21. Diagnosis
1.The patient’s WBC count may be normal or only
slightly elevated.
2.Nonspecific findings include anemia
(normocytic, normochromic), thrombocytopenia,
an elevated erythrocyte sedimentation rate or C-
reactive protein, and altered urinary analysis
(proteinuria/
microscopic hematuria).
3.The hallmark of IE is a continuous bacteremia
caused by bacteria shedding from the vegetation
into the bloodstream; more than 95% of patients
with IE have positive blood cultures.

22. 4.Three sets of blood cultures cultures, each from
separate venipuncture sites, should be collected
over 24 hours, and antibiotics should be withheld
until adequate blood
cultures are obtained.
5.An electrocardiogram (ECG), chest radiograph,
and echocardiogram are performed commonly in
patients suspected of endocarditis.
6.Echocardiography using the transthoracic (TTE)
or transesophageal (TEE) technique plays an
important role in the diagnosis and management
of IE.

23. 7.TEE technique is more sensitive for detecting
vegetations (90% to 100%) as compared with
TTE (58% and TEE maintains good specificity
8.TEE is preferred in high-risk patients such as
those with a prosthetic heart valve, congenital
heart disease, previous endocarditis, a new
murmur, or stigmata of endocarditis

24. Normal person’s echocardiogram

25. Patient’s echocardiogram

26. Therapy for NVE due to
streptococcus
.ANTIBIOTIC DOSAGE AND ROUTE DURATION
Pencillin G OR
Ceftriaxone sodium
12-18 million units/24 hr
IV continuously or in 6
divided dose
2 gm once daily IV or IM
4 weeks
4 weeks
Pencillin G with
Gentamicin
As above
1 mg/kg IM OR IV /8hr
2 weeks
2 weeks
Vancomycin hydrochloride 30 mg/kg /24 hr in two
equally divided dose
4 weeks

27. Therapy for endocarditis due to
staphylococcus in the absence of prosthetic
material
.
ANTIBIOTIC DOSAGE AND ROUTE DURATION
Methicillin susceptible
staphylococci
Nafcillin sodium OR
Oxacillin sodium with
Gentamicin sulfate
2 g IV Every 4 hour
1mg/kg IM OR IV every 8 hr
4-6 weeks
3-5 days
Cefazolin with
Gentamicin
Vancomycin hydrochloride
2 g IV every 8 hr
1mg/kg IV or IM every 8 hr
30mg/kg/24 hr IV in 2
equal divided dose
4-6 weeks
3-5 days
4-6 weeks
Methicillin resistant
staphylococci
Vancomycin hydrochloride 30mg/kg / 24 h IV in two
equal divided dose
4-6 weeks

28. Staphylococcal Endocarditis in the Presence
of a Prosthetic Valve
.ANTIBIOTIC DOSAGE AND ROUTE DURATION (weeks)
For methicillin resistant
staphylococcal
Vancomycin hydrochloride
with Rifampicin
And with Gentamicin
sulfate
30mg/kg/24 hr IV in2 or 4
equal doses
300mg orally every 8 hr
1mg /kg IM OR IV 8 hr
>6
>6
2
For methicillin susceptible
staphylococcal
Nafcillin sodium or
Oxacillin sodium
With Rifampicin
And with Gentamicin
sulfate
2g IV every 4 hr
300mg orally every 8 hr
1mg/kg IM OR IV 8hr
>6
>6
2

29. Standard therapy for endocarditis
due to enterococci
.ANTIBIOTIC DOSAGE AND ROUTE DURATION (weeks)
Pencillin G
With Gentamicin sulfate
18-30 million units/24 hr IV
1mg/kg IM OR IV every 8 hr
4-6
4-6
Ampicillin sodium
With Gentamicin sulfate
12 g/24 hr IV
1mg/kg IM OR IV every 8 hr
4-6
4-6
Vancomycin hydrochloride
With Gentamicin sulfate
30 mg/kg per 24 h IV in two
equally divided dose
1mg/kg IM OR IV every 8 hr
4-6
4-6

30. Pencillin G
.

31. Side effects

32. Ceftriaxone

33. Side effects of ceftriaxone
.

34. Vancomycin MOA
.

35. .

36. Gentamicin MOA

37. Rifampicin
.