This document provides an overview of infective endocarditis (IE), including its introduction, classification, pathogenesis, clinical manifestations, diagnosis, and treatment. Some key points: - IE is defined as an infection of the inner lining of the heart (endocardium) that can involve heart valves, the inner lining of the heart chambers, or defects in the heart wall. - It is classified based on temporal evolution (acute vs. subacute) and location (native valve, prosthetic valve, device-related, right-sided). Common causes include streptococci, staphylococci, and enterococci. - Diagnosis is based on the Modified Duke Criteria, which considers

1. INFECTIVE ENDOCARDITIS
Dr. Ansuman Dash
GUIDE – Dr. Shakti Shankar Pattanayak

2. CONTENTS
 Introduction
 Etiology
 Pathogenesis
 Clinical manifestations and complications
 Diagnosis
 Treatment
 Prognosis

3. INTRODUCTION
 Infective endocarditis (IE) is defined as an infection of the
endocardial surface of the heart, which may include one or
more heart valves, the mural endocardium, or a septal defect.
 In 1674, Lazaire Riviere first described the gross autopsy
findings of IE in his monumental work Opera medica universa.
 In 1885, William Osler presented the first comprehensive
description of endocarditis in English.
 Lerner and Weinstein published about “Infective Endocarditis in
the Antibiotic Era,” in the New England Journal of Medicine.
 IE currently can be described as infective endocarditis in the era
of intravascular devices.

4. RISK FACTORS
 Valvular heart disease – MR with degenerative MVP m/c, 2nd
m/c is AR.
 Congenital heart disease – M/c is VSD.
 Prosthetic valves
 CIED
 IV drug use
 Chronic IV access
 H/O invasive dental procedures.
 Diabetes, malignancy, renal failure on hemodialysis.

5. CLASSIFICATION
 According to temporal
evolution of disease,
a) Acute
b) Subacute
 According to location of infection
a) Native valve endocarditis
b) Prosthetic valve endocarditis
c) Device related endocarditis
d) Right sided endocarditis

6. Acute Endocarditis –
 Develops over a period of days, rapidly damages cardiac
structures and seeds extracardiac sites.
 Presents as high grade fever, fatigue and tachycardia.
 Usually caused by S. aureus, Beta hemolytic streptococci and
Pneumococci .
Subacute Endocarditis –
 Develops over week to months.
 Indolent course
 Damages cardiac structures slowly. Rarely metastasizes.
 Presents with vague constitutional symptoms.
 Usually caused by Viridans streptococci, Enterococci, CoNS and
the HACEK group.

7. Native valve endocarditis (NVE) –
 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
 Health care associated NVE usually caused by S. aureus, CONS
and Enterococci.

8. Prosthetic Valve Endocarditis (PVE) –
 Between 16 to 30 % of all cases of endocarditis occur in
prosthetic valves.
 Risk of infection highest in first 6 to 12 months of valve
replacement.
 Early PVE if occurring within 1 year and late PVE if occurring
1 year.
 Early PVE caused by S. aureus and CoNS.
 Late PVE caused by same organisms as NVE.

9. Device – related Endocarditis
 IE related to Cardiovascular Implantable Electronic Devices
involves the device or the endothelium point of device contact.
 Mostly caused by S. aureus and CoNS.
 Risk factors are Renal failure, DM, hematoma at the site of
implantation.

10. 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.

11. ORGANISMS causing IE
 Streptococcus viridans – Cause native valve infection in RHD pts
 Beta Hemolytic Streptococci – Acute presentation. Frequent complications.
 Streptococcus gallolyticus - <10% cases of IE
 S. aureus – Both NVE and PVE. Acute presentation
 Coagulase negative staphylococci – Mostly in prosthetic valve. Subacute presentation
 Enterococcus – A/w CV catheter use. Multi drug resistance.
 HACEK group – Subacute presentation. Large vegetation.
 Aerobic gram –ve bacilli – E. coli, Klebsiella, Enterobacter, Pseudomonas
 Fungi – Candida m/c organism. a/w IV drug use and in prosthetic valve. Surgery needed.
 Atypical organisms – Coxiella, Bartonella, Brucella, T.whipelli, Legionella

12. PATHOGENESIS
 Organisms enter bloodstream from skin, mucosal surfaces or
focal sites of infection.
 Organisms express surface adhesins (MSCRAMMS) that
mediate adherence to NBTE or damaged endothelium.
 Adhesins are – Fibronectin binding proteins, clumping factor
in S. aureus, Fibrinogen binding surface proteins (Fss2),
Collagen binding protein in Enterococcus, Glucans or FimA
on streptococci.
 Prototypic lesion is the Vegetation which is a mass of
platelet, fibrin, microcolonies of organism and scant
inflammatory cells.

14. PATHOGENESIS OF INFECTIVE ENDOCARDITIS
Underlying valvular or non valvular structural abnormality
Blood flow turbulence and endothelial damage
Fibrin deposition and thrombus formation (NBTE)
Bacterial growth in thrombus and formation of dense microcolonies
Microorganisms induce further platelet deposition by eliciting tissue factor
Fibrin deposition, platelet aggregation and microorganism proliferation together
form infected vegetation

17. CLINICAL MANIFESTATIONS
SYMPTOMS
 Fever – m/c symptom but maybe absent in upto 20% cases.
 Constitutional symptoms like chills, night sweats, headache,
malaise, nausea, myalgia, arthralgia.
 Dyspnea if present is indicative of a severe hemodynamic lesion
probably a left sided valvular regurgitation.
 Orthopnea/ PND indicate onset of heart failure.
 Pleuritic chest pain may occur due to septic embolization and
infarction complicating tricuspid valve IE.

18. SIGNS
 Murmurs – Occur in less than half of the patients. New
or worsened regurgitant murmur occurs.
 Splenomegaly
 Clubbing may be seen
 Peripheral manifestations like Osler’s node, subungal
hemorrhages, Janeway lesions, Roth’s spot.

20. Roth Spot

21. JANEWAY LESIONS

22. DIAGNOSIS

23. MODIFIED DUKE CRITERIA
 A highly sensitive and specific diagnostic criteria known as the Modified Duke Criteria is
based on clinical, laboratory and echocardioagraphic findings commonly encountered
in patients of IE.
Definite Endocarditis –
 2 major criterion or
 1 major + 3 minor criterion or
 5 minor criterion
Possible IE –
 1 major + 1 minor
 3 minor criteria
Diagnosis of IE rejected if,
 Alternative diagnosis established
 If symptoms resolve with <4 days of antimicrobial therapy
 If surgery or autopsy reveals no histologic evidence of IE after <4days of antimicrobial
therapy

24. MAJOR CRITERIA
1. Blood culture positive
 a. Typical organism (Betα hemolytic streptococcus, Streptococcus bovis , HACEK
organisms, or community acquired Staphylococcus aureus or enterococcus
without a primary focus) from 2 separate blood cultures Or
 b. Persistent bacteremia with any organism (two positive cultures >12 hr apart or
three positive cultures or a majority of ≥4 cultures positive >1 hr apart) Or
 c. single positive blood culture for Coxiella burnetii or antiphase 1 IgG antibody
titer >1 : 800
2. Evidence of endocardial involvement
 a. Echocardiographic findings: mobile mass attached to valve or valve apparatus,
abscess, or new partial dehiscence of prosthetic valve
 b. New valvular regurgitation

25. MINOR CRITERIA
1. Predisposing condition: IV drug use or predisposing
cardiac condition
2. Fever ≥38° C
3. Vascular phenomena: arterial embolism, septic
pulmonary emboli, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, Janeway
lesions
4. Immunologic phenomena: glomerulonephritis, Osler
nodes, Roth spots, rheumatoid factor
5. Microbiologic evidence: positive blood cultures not
meeting major criteria or serologic evidence of active
infection consistent with endocarditis

26. ECHOCARDIOGRAPHY
ECHO confirms and measures vegetation, detects
intracardiac complication and assesses cardiac function.
TRANSTHORACIC ECHOCARDIOGRAPHY (TTE)
Non invasive and specific
can not detect vegetation <2mm in diameter
Inadequate in emphysema and obese.
Not optimal for evaluating prosthetic valve or detecting
intracardiac complications.

28. TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)
 Safe and detects vegetation in >90% with definite IE.
 Negative TEE does not exclude IE but requires repetition in 7 – 10
days.
 Optimal for diagnosis of PVE and intracardiac complications like
myocardial abscess, valve perforation or intracardiac fistulae, and
detection of vegetations in patients with CIED.

29. BLOOD CULTURE
Three 2-bottle blood culture sets , separated from one
another by at least 2 h should be obtained from
different venipuncture sites over 24 h.
If culture remain negative two or three additional
blood culture sets should be obtained.
Empirical antimicrobial therapy should be with held in
suspects of subacute endocarditis till cultures are
obtained.

30. NON BLOOD CULTURE TESTS
Serologic tests for Brucella, Bartonella, Legionella,
C.burnetti, C.psittaci.
PCR tests.
CBC – Anemia, Leukocytosis
Microscopic hematuria
Elevated ESR and CRP
Circulating Immune complexes
Decreased complement

31. TREATMENT

32. STAPHYLOCOCCI
MSSA infecting native valves –
 Cefazoline 2 g IV TID for 4 – 6 wks Or
 Vancomycin 15mg/kg IV BD for 4 – 6 wks Or
 Nafcillin, oxacillin or Flucloxacillin 2 g IV 4hrly for 4 – 6 wks
MRSA infecting native valves –
 Vancomycin 15mg/kg IV BD or TID for 4 – 6 wks
MSSA infecting prosthetic valves –
 Nafcillin, oxacillin or Flucloxacillin 2 g IV 4hrly for 6 – 8 wks plus
 Gentamycin 1mg/kg IM or IV TID for 2 wks plus
 Rifampicin 300mg PO TID for 6 – 8 wks
MRSA infecting prosthetic valves –
 Vancomycin 15mg/kg IV BD for 6 – 8 wks plus
 Gentamycin 1mg/kg IM or IV TID for 2 wks plus
 Rifampicin 300mg PO TID for 6 – 8 wks

33. STREPTOCOCCI
Penicillin susceptible Streptococci, S. gallolyticus
 Penicillin G 2 – 3 MU IV 4hrly for 4 wks or
 Ceftriaxone 2 g/day as a single dose for 4 wks or
 Vancomycin 15 mg/kg BD for 4 wks Plus
 Gentamycin 3mg/kg IV OD as a single dose for 2 wks
Relatively Penicilllin resistant
 Penicillin G 4 MU IV 4hrly for 4 wks or
 Ceftriaxone 2 g/day as a single dose for 4 wks plus
 Gentamycin 3mg/kg IV OD as a single dose for 2 wks
Moderately Penicillin resistant
 Vancomycin 15 mg/kg BD for 4 wks
 Gentamycin 3mg/kg IV OD as a single dose for 6 wks plus
 Penicillin G 2 – 3 MU IV 4hrly for 6 wks or
 Ceftriaxone 2 g/day as a single dose for 6 wks

34. ENTEROCOCCI
 Penicillin G 4 – 5 MU IV 4hrly + Gentamycin 1mg/kg IV TID both for 4 – 6 wks
 Ampicillin 2 g IV 4 hrly + Gentamycin 1mg/kg IV TID both for 4 – 6 wks
 Vancomycin 15 mg/kg BD + Gentamycin 1mg/kg IV TID both for 4 – 6 wks
 Ampicillin 2 g IV 4 hrly + Ceftriaxone 2 g IV BD both for 6 wks
HACEK organisms
 Ceftriaxone 2 g/day IV as a single dose for 4 wks
 Ampicillin/sulbactam 3 g IV 6hrly for 4 wks

35. SURGERY
Definite Indications for cardiac surgical interventions in
patients with Endocarditis
 Moderate to severe CHF due to valve dysfunction
 Partially dehisced unstable prosthetic valve
 Persistent bacteremia despite optimal antimicrobial therapy
 Lack of effective microbicidal therapy
 S. aureus prosthetic valve endocarditis with intracardiac complication
 Relapse of prosthetic valve endocarditis

36. Surgery considered for improved outcome
 Perivalvular extension
 Poor responsive S.aureus endocarditis involving aortic or mitral valve
 Large (>10mm) hypermobile vegetation with high risk of embolism
 Persistent fever in culture –ve NVE
 Poor responsive endocarditis due to high antibiotic resistant Enterococci or gram –ve