This document provides an overview of infective endocarditis including its classification, etiology, pathogenesis, clinical manifestations, diagnostic criteria, and management. It discusses the different types of infective endocarditis such as acute versus subacute and native versus prosthetic valve. Common causative organisms and their antibiotic treatment durations are outlined. The modified Duke criteria for diagnosis is explained. Indications for surgery and timing of surgical intervention are briefly covered.

1. DR. KALAIMANI
SENIOR RESIDENT
GENERAL MEDICINE
MGMCRI

2. Overview
• Introduction
• Classification
• Etiology/Epidemiology
• Pathogenesis
• Clinical features
• Complications
• Diagnostic criteria
• Management

3. INTRODUCTION
 What is infective endocarditis?
• infection of a native or prosthetic heart valve, the
endocardial surface, or an indwelling cardiac device
 What is infective endarteritis?
• arteriovenous shunts, arterio-arterial shunts (patent
ductus arteriosus), or a coarctation of the aorta
 What is a vegetation?
• is a mass of platelets, fibrin, microcolonies of
microorganisms, and scant inflammatory cells

4. CLASSIFICATION
Presentation
Acute
(ABE)
Subacute
(SABE)
Valve characteristics
Native
valve
(NVE)
Prosthetic
valve
(PVE)
Site involved
Rightsided
endocarditis
Left sided
endocarditis

5. Classification
• Acute endocarditis:
– Toxic
– Develops within few days
– Valvular destruction and embolic manifestation
– Most commonly by Staph aureus
• Subacute endocarditis:
– Develops in weeks to months
– More associated with immunologic phenomena
– Mostly caused by streptococci and others

6. Etiology
• Bacteria
• Fungi
Bacteria
Oral cavity
Skin
Upper resp tract
Strep viridans
Staph
HACEK
GIT
Streptococcus
gallolyticus
GUT Enterococci

7. Etiology/Epidemiology
• Health care associated NVE  S. aureus, CoNS,enterococci
( 55% nosocomial onset, 45% community onset)
• PVE within 2 months of surgery  nosocomial
• 68 – 85% of CoNS causing IE  resistant to methicillin
• IVDU related IE  most common S.aureus
• Polymicrobial endocarditis  IVDU
• Negative culture  5 – 15% (1/3 to ½ due to prior antibiotics)

8. High velocity jet striking endothelium
Flow from high to low pressure chamber
Flow across a narrow orifice at high velocity
Malignancy
SLE
Antiphospholipid antibody syndrome
DIC
Endothelial
injury
Hypercoagulable state
NBTE (sterile
platelet fibrin )
+
Bacteremia
Bacteria adhere to damaged endothelium and/or sterile platelet-fibrin nidus
Bacteria multiply
Further platelet and fibrin binding
Local tissue
destruction
Embolization
Hematogenous
spread
Antibody
response
Growth of vegetation
P
A
T
H
O
G
E
N
E
S
I
S

9. • Marantic endocarditis - uninfected vegetations seen in
patients with malignancy and chronic diseases
• Libman sacks endocarditis – bland vegetations in SLE

10. Organism enters bloodstream
Adherence
Infected vegetation

11. ADHESION MOLECULES
Clumping factor
Fss2
Ace
Ebp pili
Glucans
Fim A
Staph
aureus
Enterococcus
fecalis Streptococci

14. Clinical manifestations
Clinical
manifestations
Damage to
intracardiac
structures
Embolisation –
Infection or
infarction
Hematogenous
infection –
bacteremia
Circulating
immune
complexes

15. Clinical presentation
Acute
• β hemolytic
streptococci
• S.aureus
• Pneumococci
Subacute
• Viridans streptococci
• Enterococci
• CoNS
• HACEK
Indolent
• Bartonella
• T. Whipplei
• C.burnetti

16. ORGANISMS CAUSING ENDOCARDITIS

17. CLINICAL MANIFESTATIONS
Cardiac
• Heart murmurs
• Congestive cardiac failure
• Perivalvular abscess
• Pericarditis
• Heart block
• Intracardiac fistulae
• Myocardial infarction
Noncardiac
• Septic embolization
- CNS
- Skin
- Spleen
- Kidneys
- Skeletal system
• Immunological phenomenon
- Glomerulonephritis
- Roth’s spots
- Osler’s nodes

19. CLINICAL AND LAB FEATURES OF IE

20. EMBOLISATION
RIGHT LEFT

22. MODIFIED DUKE CRITERIA- MAJOR CRITERIA
1. Positive blood culture
 Typical microorganisms for IE from
2 separate blood cultures
Or
 Persistently positive blood culture,
defined as recovery of a
microorganism consistent with
infective endocarditis from:
 Blood cultures drawn >12 h
apart; or
 All of 3 or a majority of ≥4
separate blood cultures, with first
and last drawn at least 1 h apart
Or
 Single positive blood culture for
Coxiella burnetii or phase I IgG
antibody titer of >1:800
2. Evidence of Endocardial
involvement
 Positive echocardiogram
 Oscillating intracardiac mass on
valve or supporting structures or in
the path of regurgitant jets or in
implanted material, in the absence
of an alternative anatomic
explanation, or
 Abscess, or
 New partial dehiscence of
prosthetic valve,
Or
 New valvular regurgitation
(increase or change in preexisting
murmur not sufficient)

23. MODIFIED DUKE CRITERIA- MINOR CRITERIA
1. Predisposition:
predisposing heart conditions
or injection drug use
2. Fever ≥38.0°C (≥100.4°F)
3. Vascular phenomena:
– Major arterial emboli
– Septic pulmonary infarcts
– Mycotic aneurysm
– Intracranial hemorrhage
– Conjunctival hemorrhages
– Janeway lesions
4. Immunologic phenomena:
– Glomerulonephritis
– Osler’s nodes
– Roth’s spots
– Rheumatoid factor
5. Microbiologic evidence:
– positive blood culture but
not meeting major criterion
– or serologic evidence of
active infection with an
organism consistent with
infective endocarditiS

24. DEFINITE INFECTIVE ENDOCARDITIS
• Pathologic criteria
 Microorganisms demonstrated by
results of cultures or histologic
examination of a vegetation, a
vegetation that has embolized, or
an intracardiac abscess specimen;
or
 Pathologic lesions; vegetation, or
intracardiac abscess confirmed by
results of histologic examination
showing active endocarditis
• Clinical criteria
 2 major criteria, or
 1 major criterion and 3 minor
criteria, or
 5 minor criteria
• Possible Infective
Endocarditis
 1 major criterion and 1 minor
criterion, or
 3 minor criteria

25. • Rejected Diagnosis of Infective Endocarditis
 Firm alternate diagnosis explaining evidence of suspected IE,
or
 Resolution of IE syndrome with antibiotic therapy for ≤4 days,
or
 No evidence of IE at surgery or autopsy, on antibiotic therapy
for ≤4 days, or
 Does not meet criteria for possible IE

28. INVESTIGATIONS
• Blood cultures – 3 sets from different sites atleast 1
hour apart. Why?
• Complete blood count
– Leucocytosis
– Thrombocytosis
– Thrombocytopenia
– Anemia
• ESR, CRP
• Serology

29.  Electrocardiography
– to assess for conduction abnormalities (such as varying and
progressive degrees of atrioventricular [AV] block) suggestive
of abscess formation, which are particularly associated with
aortic valve endocarditis
– Ischemic/infarct changes suggestive of coronary emboli
 CXR
– Evidence of HF (pulmonary edema)
– Septic emboli, particularly in IV drug users with suspected
right-sided endocarditis

30. Transthoracic Echo (tte)
• TTE may detect valvular vegetations with or without positive blood
cultures
• It is used to characterize the hemodynamic severity of valvular
lesions in known IE
• It can also assess for complications of IE (e.g. abscesses, perforation,
and shunts)
• TTE can be used to reassess high-risk patients (e.g., those with a
virulent organism, clinical deterioration, persistent or recurrent
fever, new murmur, or persistent bacteremia)

31. ECHO
Vegetations attached to Aortic
valve
Aortic regurgitation ( Colour
doppler)

32. Transesophageal Echo
(TEE)
• Assess the severity of valvular lesions in symptomatic patients with
IE if TTE is nondiagnostic
• Diagnose IE in patients with valvular heart disease and positive
blood cultures if TTE is nondiagnostic
• Diagnose complications of IE with potential impact on prognosis and
management (e.g. abscesses, perforation, and shunts)
• First-line diagnostic study to diagnose PVE and to assess for
complications

33. TREATMENT
ORGANISM
• Streptococi
• Penicillin sensitive
• Relatively penicillin
resistant
• Moderately
penicillin resistant
DRUG ( DURATION)
• Penicillin G x 4 weeks
• Ceftriaxone x 4 weeks
• Vancomycin x 4 weeks
• Penicillin G + Gentamicin x 2 weeks
• Penicillin G or Ceftriaxone x 4 weeks
plus Gentamicin x 2 weeks
• Vancomycin x 4 weeks
• Penicillin or Ceftriaxone x 6 weeks
plus gentamicin x 6 weeks
• Vancomycin x 4 weeks

34. TREATMENT
ORGANISM
• Enterococci
DRUG ( DURATION)
• Penicillin G + Gentamicin x 4 - 6 weeks
• Ampicillin + gentamicin x 4 - 6 weeks
• Vancomycin + gentamicin x 4 - 6 weeks
• Ampicillin + ceftriaxone x 6 weeks

35. TREATMENT
ORGANISM DRUG ( DURATION)
• Staphylococi
• Native valve
 MSSA Nafcillin, Oxacillin or Flucloxacillin x 4 – 6 weeks
Or Cefazolin x 4 – 6 weeks
Or Vancomycin x 4 – 6 weeks
 MRSA Vancomycin x 4 – 6 weeks
• Prosthetic valve
 MSSA Nafcillin, Oxacillin or Flucloxacillin x 6 – 8 weeks
plus Gentamicin x 2 weeks
plus Rifampicin x 6 – 8 weeks
 MRSA Vancomycin x 6 – 8 weeks
plus Gentamicin x 2 weeks
plus Rifampicin x 6 – 8 weeks

36. Treatment
ORGANISM
• Coxiella burnetii
• Bartonella spp.
DRUG ( DURATION)
• Doxycycline + x 18 months (NVE)
Hydroxychloroquine x 24 months (PVE)
• Ceftriaxone or Ampicillin x 6 weeks
or doxycycline
plus Gentamicin x 3 weeks

37. DRUG DOSAGE
 Penicillin G 4 mU iv q4h
 Ceftriaxone 2 g iv qd
 Vancomycin 15mg/kg iv q12h
 Gentamycin 3 mg/kg iv or im single dose
Or 1 mg/kg iv q8h
 Ampicillin 2 g iv q4h
 Nafcillin/Oxacillin 2 g iv q4h
/Flucloxacillin
 Cefazolin 2 g iv q8h
 Rifampicin 300 mg PO q8h

38. INDICATIONS FOR SURGERY

39. TIMING OF SURGICAL INTERVENTION

42. REFERENCES
1. Harrison’s Principles of Internal Medicine 19th edition
2. Braunwald’s Heart disease 10th edition