1.
INFECTIVE ENDOCARDITIES:
RECENT TRENDS
Dr HIMANSHU SAMAIYA
MD GEN.MEDICINE
SSMC REWA M.P.

2.
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.
It may be caused usually by a bacterium, but may also involves a rickettsia,
chlamydia or fungus.
Its intracardiac effects include severe valvular insufficiency, which may lead
to intractable congestive heart failure, and myocardial abscesses.

3.
THE PROTOTYPE LESION
The vegetation
• Variable in size
• Amorphous mass of fibrin & platelets
• Abundant organisms
• Moderate inflammatory cells

4.
Predisposing Factors
Rheumatic Heart Disease
• 7 – 18% of cases in recent reported
series
• • Mitral site more common in women
• • Aortic site more common in men
Congenital Heart Disease
• • 10 – 20% of cases in young adults
• • 8% of cases in older adults
• • PDA, VSD,TOF, Bicuspid Aortic Valve
(esp. in men>60)
Intravenous Drug Abuse
• – Risk is 2 – 5% per pt./year
• – Tendency to involve right-sided
valves
Distribution in clinical series
• – 46 – 78% tricuspid
• – 24 – 32% mitral
• – 8 – 19% aortic
• – Underlying valve normal in 75 –
93%
• – S. aureus predominant organism

5.
Implantable pacemakers and
cardioverter defibrillators
• They are infected within a few months of
implantation
• – Generator pocket (most common)
• – Proximal leads
• – Portion of leads in direct contact with
endocardium, is the most challenging to treat.
• Of pacemaker infections, 75% are produced by
staphylococci.
Degenerative valve disease
• Myxomatous mitral valve
• Hypertrophic cardiomyopathy
• Degenerative calcific valvular stenosis
• Valvular damage from surgery, autoimmune
conditions or old age.

6.
CLASSIFICATION
Classified according to the temporal evolution of disease, the site of
infection, the cause of infection, or the predisposing risk factor.
• Acute (short incubation) vs. subacute (long incubation)
• Culture-positive vs. culture-negative
• Right sided vs. left sided
• Nosocomial vs. community-acquired
• Native-valve endocarditis vs. prosthetic-valve

7.
Acute and Subacute Bacterial Endocarditis
Acute
• Affects normal heart valves
• Rapidly destructive
• Metastatic foci
• Commonly Staph. aureus
• If not treated, usually fatal within
6 weeks
Subacute
Often affects damaged heart valves
• Indolent nature
• Most commonly Strepto. viridans
or Enterococcus
• If not treated, usually fatal by one
year

8.
Native Valve Endocarditis
1.Community acquired NVE:
• Among 25-35% of total cases of NVE ,45% belongs to community acquired endocarditis.
• Most common organisms includes: Streptococci>staph aureus>culture negative>CONS.
2.Health care associated NVE:
• 55% of total NVE cases belongs to this group.
• Most common organisms includes: Staph aures(MRSA)>Enterococci>streptocooci>CONS

9.
Prosthetic Valve Endocarditis
• PVE accounts for 16-30% of cases of IE.
• The valves in the mitral valve position are more susceptible than those in the aortic areas
Early PVE occurs within 60 days of valve implantation
• – usually due to intraoperative contamination or a postoperative bacterial contamination which is
usually nosocomial in nature.
• – staph aureus , coagulase-negative staphylococci, gram-negative bacilli, and Candida species
most common.
Late PVE occurs 60 days or more after valve implantation
• – Late prosthetic valve endocarditis is usually due to community acquired microorganisms
• – Staphylococci, alpha-hemolytic streptococci, CONS and enterococci are the common causative
organisms

10.
MICROBIOLOGY IN NUT SHELL
The oral cavity, skin, and upper respiratory tract are the respective primary portals
Streptococci
• – Alpha-haemolytic Streptococci (viridans – S. mitis, S. oralis) 30-40% (subacute)
• – Enterococci (E. faecalis) 5-18% (subacute)
• – Beta-haemolytic streptococci (e.g. Gp A Strep) – rare (acute)
Staphylococci
• – S. aureus 10-27% (acute)
• – Coagulase negative staphylococci (Staph epidermidis) :1-3 % (mainly prosthetic
valve risk, subacute)
Fungi
• – Candida – IVDU at risk (usually indolent)
• – Aspergillus – rare
Gram-negative bacteria – rare
Culture-negative endocarditis :HACEK, Q-fever – cases do occur, subacute

11.
Culture-negative endocarditis can be due to:
• Micro-organisms that require a longer period of time to be identified in the laboratory
• Prior antibiotic treatment. Fungal endocarditis
• HACEK Group (gram neg.coccobacilli.)
• • Haemophilus spp.
• • Aggregatibacter species
• • Cardiobacterium hominis
• • Eikenella corrodens
• • Kingella kingae
• Coxiella burnetii - Q fever endocarditis
• –farm animals
• –hepatic complications and purpura
• –Life-long antibiotic therapy may be required
• Brucella species, Chlamydia species:
• h/o contact with goats or cattle
• –often affects the aortic valve

12.
ETIOLOGY

13.
PATHOPHYSIOLOGY
Modes of endothelial injury
NonbacterialThrombotic
Endocarditis(NBTE) Bacteraemia…
• High velocity jet
• Flow from high pressure
to low pressure chamber
• Flow across narrow
orifice of high velocity
• Endothelial injury
• Hypercoagulable state
• Platelet-fibrin thrombi
• delivers organisms to the
damaged (sticky)endocardial
surface
• adherence & colonisation of NBT
infected vegetation

14.
PATHOPHYSIOLOGY

15.
Marantic Endocarditis
• NBTE due to hypercoagulable state- Malignancy, chronic diseases, SLE,
APLA
• Uninfected vegetation seen.

16.
Clinical
manifestation
• Cytokine production—arise from
damage to intracardiac structures;
• Embolization of vegetation
fragments, leading to infection or
infarction of remote tissues;
• Hematogenous infection of sites
during bacteremia;
• Tissue injury due to the deposition of
circulating immune complexes or
immune responses to deposited
bacterial antigens

17.
Cardiac Manifestations
 New regurgitant murmurs- Approx.85% of cases.
 CHF- 30 to 40%- due to valvular damage (aortic>mitral), myocarditis, intracardiac fistula
 Perivalvular abscess
Fistulae (Root of aorta to chambers/ between cardiac chambers)
Pericarditis
 Heart block/ MI due to embolic phenomena

18.
Noncardiac Manifestations
Nonspecific signs –
• Petechiae,
• Subungal or “splinter” hemorrhages,
• Clubbing, Splenomegaly
• Osler’s Nodes,
• Janeway lesions, and Roth Spots
Embolic phenomena include systemic, cerebral and pulmonary emboli are
common in >50 % cases.
Hematogenous seeded focal infection occurs most often in the skin, spleen,
kidneys, skeletal system, and meninges.

19.
Petechiae
• Common (40-50%) but nonspecific
finding
• Seen on palpebral conjunctivae, the
dorsa of the hands and feet, the anterior
chest and abdominal walls, the oral
mucosa, and the soft palate
• Result from local vasculitis or emboli

20.
Subungual (splinter) hemorrhages
• 1. Nonspecific,Nonblanching
(10%)
• 2. Usually 2-3mm long in long axis
of nail
• 3. Initially blue-purple in
colour,change to brown of black in
1-2 days
• 4. Move distal with nail growth

21.
Janeway Lesions
• 1. More specific
• 2. Erythematous, blanching macules
• 3. Nonpainful
• 4. Located on palms and soles
• 5. Micro abscesses of the dermis with
marked necrosis and inflammatory
infiltrate not involving the epidermis,
• Due to the deposition of circulating
immune complexes in small blood
vessels

22.
Osler’s Nodes
• More specific
• Painful and erythematous nodules
• Located on pulp of fingers and
toes
• More common in subacute IE
• Due to infective emboli or immune
complex deposits
• 4 P’s: Pink
Painful
Pea-sized
Pulp of the fingers/toes

23.
Roth Spots Eye
• Roth's spots are retinal
hemorrhages flame shaped with
white or pale centers composed of
coagulated fibrin.
• Observed via fundoscopy or slit
lamp examination

24.
 Signs of neurologic disease occur in as many as 40% of patients due to embolic
stroke with focal neurologic deficits, seizures, intracerebral hemorrhage and
multiple microabscesses.
 Signs of pulmonary and systemic septic emboli more common with tricuspid
endocarditis
 Signs of congestive heart failure, such as distended neck veins
 Splenomegaly (splenic rub d/t splenic infarction)
 Risk for emboli is increased when vegetation >1cm asso.with infection involving

25.
Blood cultures
• Blood cultures remain a cornerstone of the diagnosis of IE cases and should be taken prior to starting treatment
in all case. during the prior 2 weeks
• Sampling of intravascular lines should be avoided .
• As per AHA and ESC - At least three sets of blood cultures collected from different venipuncture sites, with at
least 1 h between the first and last draw.
• As per BSAC- Collection of two sets of blood cultures within 1 h of each other in patients with suspected
endocarditis and acute sepsis and three sets of blood cultures spaced from one another by at least 2 h, should
be obtained from different venipuncture sites over 24 h in cases of suspected subacute or chronic endocarditis.

26.
Three sets of blood cultures, with each set including one aerobic and one anaerobic
bottle, are collected.
 Alternatively, two sets may be collected, with two aerobic and one anaerobic bottle per
set (i.e., a total of six blood culture bottles)
10-20 ml of blood per Bactec or BacT/Alert bottle) being essential.
As per study done by M. Liesman Et al,2019 published in journal o f clinical microbiology -
routinely spacing blood culture draws in cases of suspected endocarditis not recommended.
There is no difference in yield if blood is collected simultaneously or several hours apart. (CMDT
2019)

27.
Culture Negative” IE (5-10%)
• Infective endocarditis may be culture negative either due to prior antibiotic treatment or
due to atypical microbial organisms or due to fungus etc non bacterial endocarditis.
• Less common with improved blood culture methods
• Special media required - Brucella, Mycoplasma, Chlamydia, Histoplasma, Legionella,
Bartonella
• Longer incubation may be required  HACEK
• Coxiella burnetii (Q Fever), Trophyrema whipplei will not grow in cell-free media

28.
Non-Blood-Culture Tests
1. Serologic tests---- Brucella, Bartonella, Legionella, Chlamydia psittaci,
and C. burnetii.
2. vegetations recovered at surgery or by embolectomy-
• culture;
• special stains;
• polymerase chain reaction (PCR) recovery of microbial DNA or DNA
encoding the 16S or 28S ribosomal unit (16S rRNA or 28S rRNA)

29.
Cardiac Imaging - Echocardiography
Transthoracic echocardiography (TTE)
– First line if suspected IE
– Native valves
Trans Esophageal echocardiography (TEE)
– Prosthetic valves
– Intracardiac complications
– Inadequate TTE
– Fungal or S. aureus or bacteremia

30.
Modified Duke Criteria
Definite IE
• Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or
intracardiac abscess
• Histologic evidence of vegetation or intracardiac abscess
Possible IE
• – 2 major
• – 1 major and 3 minor
• – 5 minor
Rejected IE
• Resolution of illness with four days or less of antibiotics
• presence of a firm alternative diagnosis
• No histological evidence of endocarditis are seen

31.
Differential Diagnosis(SBE Mimickers)
• Antiphospholipid syndrome
• • Primary cardiac neoplasms---atrial myxoma
• • Marantic Endocarditis(NBTE)
• • Systemic lupus erythematosus
• • Reactive arthritis

32.
Treatment
Case fatality is approximately 20% and even higher
• –those with prosthetic valve endocarditis
• –infected with antibiotic resistant
The major goals of therapy for infective endocarditis (IE) are to
• – eradicate the infectious agent from the thrombus
• – address the complications of valvular infection.
Parenteral (IV) antibiotics
• – High serum concentrations to penetrate avascular vegetation’s.
• – Prolonged treatment to kill dormant bacteria clustered in vegetation’s

33.
• Modify empiric therapy once cultures/sensitivities known
• Long duration 4-6 weeks Rx is required
Empirical treatment depends
• •on the mode of presentation,
• •suspected organism
• •whether the patient has a prosthetic valve
Acute: flucloxacillin and gentamicin
Subacute or indolent presentation: benzyl penicillin and gentamicin
Penicillin allergy, PVE or suspected methicillin-resistant Staph. aureus (MRSA) infection: triple therapy
with vancomycin, gentamicin and oral rifampicin

34.
Antibiotic Therapy
Effective antimicrobial treatment should
• lead to defervescence within 7 – 10 days
Persistent fever in:
• IE due to staph, pseudomonas, culture negative
• IE with paravalvular abscess, extracardiac abscesses (spleen, kidney), or
complications (embolic events)
• Drug reaction or complications of hospitalization

35.
ANTITHROMBOTIC THERAPY
• There is no indication for the initiation of antithrombotic drugs (thrombolytic
drugs, anticoagulant or antiplatelet therapy) during the active phase of IE.as it
dose not reduces the risk of emboli in patients with NVE
• In patients already taking oral anticoagulants, There is a risk of intracranial
haemorrhage which seems to be highest in patients with S. aureus

36.
Cardiovascular Implantable Electronic Device
(CIED) Endocarditis
• Most common microorganisms involve: staph
aureus > CONS
• Most Common Site : GENERATOR
POCKET>LEADS
• Complete device and lead removal in definite
CIED infection, as evidenced by valvular
and/or lead endocarditis or sepsis.
• Generator pocket infection without
bacteremia is treated with a 10- to 14-day
course, some of which can be given orally

37.
SURGICAL
TREATMENT

38.
Antibiotic Prophylaxis
Recommended only in manipulation
of gingival tissue or the periapical
region of the teeth or perforation of
the oral mucosa (including surgery on
the respiratory tract)
Not advised for gastrointestinal or
genitourinary tract procedures.

39.
What to give ?

40.
COMPLICATIONS OF ENDOCARDITIS
Systemic emboli
• –Risk depends on valve (mitral>aortic),
size of vegetation, (high risk if >10 mm)
• Splenic abscess—3-5%
• Mycotic aneurysms 2-15%---
headaches, focal neurologic symptoms,
or hemorrhage ,encephalitis
• Vertebral osteomyelitis, Septic arthritis
• Hypoxia from pulmonary emboli
Cardiac
• –congestive cardiac failure-valvular
damage,
• –more common with aortic valve
endocarditis,
• –higher mortality,
• –need for surgery,
• fascicular or bundle branch block,
• –pericarditis, tamponade or fistulae

41.
PREDICTORS OF POOR OUTCOME IN IE

42.
Take home message….
• IE is highly fatal condition with overall mortalities ranging from 20-40% mainly
due to cardiac and neurological complication.
• Patient present with Anemia Fever Splenomegaly and Clubbing : cardiac
examination is mandatory.
• Endocarditis is not just limited to valves.
• High risk of suspicion with early diagnosis and treatment may affect the outcome
favourably.