• Endocarditis is an inflammation of the inner layer of the

heart, the endocardium. It usually involves the heart

valves (native or prosthetic valves). Other structures

which may be involved include the interventricular

septum, the chordae tendinae, the mural endocardium,

or even on intracardiac devices.

• Endocarditis is characterized by a prototypic lesion, the

vegetation, which is a mass of platelets, fibrin,

microcolonies of microorganisms, and scant

inflammatory cells.

INFECTIVE ENDOCARDITIS

• Infectious endocarditis involves the heart valves and is most commonly found in people who have underlying heart disease. Sources of the infection may be transient bacteremia, which is common during dental, upper respiratory, urologic, and lower gastrointestinal diagnostic and surgical procedures.

• The infection can cause growths on the heart valves, the lining of the heart, or the lining of the blood vessels. These growths may be dislodged and send clots to the brain, lungs, kidneys, or spleen.

• Classified in to two types on the basis of etiology

1. Infective endocarditis

2. Non-infective endocarditis

INFECTIVE ENDOCARDITIS• Infective endocarditis (IE): is due to microbial infection

of heart valve(native or Prosthetic) . The lining of cardiac chamber or blood vessel, or congenital anomaly. The causative agent is usually bacterium, but may be arickettsia, chlamydia or fungus.

• Pathophysiology. Is occur typically at sites of prexisting endocardial damage. However ,infection in prviously normal heart occur by S aureus.

• Infection tend to occur at site of endothelial damage bcz these area attract deposit of platelets and fibrin, which are vulnerable to colonisation by blood born organisms. Adjecent tissue are destroyed and abscess may form, valve regurgitation may develop or increased.

If the affected valve is damage by tissue

distortion.

Extra cardiac manifestations e.g. vacuities

,infarcts of skin, spleen ,kidney and brain due

to emboli or immune complex deposits.

CLASSIFICATION

1.Sub-acute bacterial endocarditis

2.Acute bacterial endocarditis

3.Post operative endocarditis

CLASSIFICATION

• Infective endocarditis may have an indolent, subacute course or a more acute, fulminant course with greater potential for rapid decompensation.

• Subacute bacterial endocarditis (SBE), although aggressive, usually develops insidiously and progresses slowly (i.e, over weeks to months). Often, no source of infection or portal of entry is evident. SBE is caused most commonly by streptococci (especially viridans, microaerophilic, anaerobic, and nonenterococcal group D streptococci and enterococci) and less commonly by S. aureus, Staphylococcus epidermidis, Gemella morbillorum, Abiotrophia defectiva, Granulicatella sp, and fastidious Haemophilus sp. SBE often develops on abnormal valves after asymptomatic bacteremia due to periodontal, GI, or GU infections.

• Acute bacterial endocarditis (ABE) usually develops abruptly and progresses rapidly (ie, over days). A source of infection or portal of entry is often evident. When bacteria are virulent or bacterial exposure is massive, ABE can affect normal valves. It is usually caused by S. aureus, group A hemolytic streptococci, pneumococci, or gonococci.

• Post oprative or PVE endocarditis: develops in 2 to 3% of patients within 1 yr after valve replacement and in 0.5%/yr thereafter. It is more common after aortic than after mitral valve replacement and affects mechanical and bioprosthetic valves equally.

• Early-onset infections (< 2 mo after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids, coliform bacilli, Candida sp, Aspergillus sp).

• Late-onset infections are caused mainly by contamination with low-virulence organisms during surgery or by transient asymptomatic bacteremias, most often with streptococci; S. epidermidis; diphtheroids; and the fastidious gram-negative bacilli, Haemophilus sp, Actinobacillus actinomycetemcomitans, and Cardiobacterium hominis.

CAUSES OF INFECTIVE ENDOCARDITIS

Causes by gram- ve, gram+ve bact & fungi.

Most often caused by Staph and strep cocci an

recently recognise bact S lugdensis affect

previously normal valve

Patient wd native valve endocarditis:

70% a-hemolytic strep

25% S aures and S epidermidis

5% othe bact and fungi

Endocaditis in drug addicts: S aureus (55%),S

viridans (15%),gram neg-ve bact 1

Prosthetic valvular endocarditis (PVE):

MORPHOLOGY• The hallmark of IE is presence of friable, bulky, potentially destructive

vegetations containing fibrin, inflammatory cells and bacteria or other

organisms.

• Aortic and mitral valve most common sites, valves of right heart may be

involved particularly in intravenous drug abusers.

• Vegetations sometimes erode into the underlying myocardium and produce an

abscess (ring abscess).

• Emboli may shed from the vegetation leading to abscesses formation at the

site where emboli lodged, this may lead to sequelae such as septic infracts or

mycotic aneurysms.

• The vegetations of subacute endocarditis are associated with less valvular

destruction than acute endocarditis.

• Microscopically vegetations of typical subacute IE often have granulation

tissue indicating healing at the bases.

• With time fibrosis, calcification and a chronic inflammatory infiltrate can

develop.

The aortic valve with a large,

irregular, reddish tan vegetation

Here, infective endocarditis on the

mitral valve has spread into the septum

all the way to the tricuspid valve,

producing a fistula.

Microscopically, the valve in infective endocarditis demonstrates friable

vegetations of fibrin and platelets (pink) mixed with inflammatory cells and

bacterial colonies (blue). The friability explains how portions of the vegetation can

break off and embolize.

Here is a valve with infective endocarditis. The blue bacterial colonies on the lower

left are extending into the pink connective tissue of the valve. Valves are relatively

avascular, so high dose antibiotic therapy is needed to eradicate the infection.

Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of

the aortic valve and aortic valve vegetations.

Acute bacterial endocarditis caused by Staphylococcus aureus with

aortic valve ring abscess extending into myocardium.

The small pink

vegetation on the

rightmost cusp

margin represents

the typical finding

with non-bacterial

thrombotic

endocarditis (or so-

called "marantic

endocarditis"). This

is non-infective. It

tends to occur in

persons with a

hypercoagulable

state (Trousseau's

syndrome, a

paraneoplastic

syndrome

associated with

malignancies) and in

very ill persons

Bartonella henselae bacilli in cardiac valve of a patient with blood culture-

negative endocarditis The bacilli appear as black granulations.

SYMPTOM AND SIGNS:

SBE: Initially, symptoms are vague: low-grade fever (< 39°C), night sweats, fatigability, malaise, and weight loss. Chills and arthralgias may occur. Symptoms and signs of valvular insufficiency may be a first clue. Initially, ≤15% of patients have fever or a murmur, but eventually almost all develop both. Physical examination may be normal or include pallor, fever, change in a preexisting murmur or development of a new regurgitant murmur, and tachycardia.

� Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white centers (Roth's spots).

� Cutaneous manifestations include petechiae (on the upper trunk, conjunctivae, mucous membranes, and distal extremities), painful erythematous subcutaneous nodules on the tips of digits (Osler's nodes), nontender hemorrhagic macules on the palms or soles (Janeway lesions), and splinter hemorrhages under the nails.

Petechial rash. He was diagnosed with right-

sided staphylococcal endocarditis. Osler nodes

Osler's nodes on a finger and foot.

Janeway lesions are Flat, painless,

erythematous lesions seen on the palm

of this patient's hand. Frequently

associated with bacterial endocarditis.

Roth spots: red center with pale periphery; top

and left (The one on right is the optic disc, as it

has pale center and red periphery)

• About 35% of patients have CNS effects, including transient ischemic attacks, stroke, toxic encephalopathy, and, if a mycotic CNS aneurysm ruptures, brain abscess and subarachnoid hemorrhage.

• Renal emboli may cause flank pain and, rarely, gross hematuria.

• Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause splenomegaly or clubbing of fingers and toes.

Seen here in the finger at the right are small splinter hemorrhages in a patient

with infective endocarditis. These hemorrhages are subungual, linear, dark red

streaks. Similar hemorrhages can also appear with trauma.

• ABE and PVE: Symptoms and signs are similar to

those of SBE, but the course is more rapid.

Fever is almost always present initially, and

patients appear toxic; sometimes septic shock

develops. Heart murmur is present initially in

about 50 to 80% and eventually in > 90%.

Rarely, purulent meningitis occurs.

• Right-sided endocarditis: Septic pulmonary

emboli may cause cough, pleuritic chest pain,

and sometimes hemoptysis. A murmur of

tricuspid regurgitation is typical.

Duke Criteria for Infective Endocarditis• Major criteria:

• A. Positive blood culture for Infective Endocarditis

• 1- Typical microorganism consistent with IE from 2 separate blood cultures, as noted below:

• viridans streptococci, Streptococcus bovis, or HACEK* group, or

• community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus

• or

• 2- Microorganisms consistent with IE from persistently positive blood cultures defined as:

• 2 positive cultures of blood samples drawn >12 hours apart, or

• all of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart)

• B. Evidence of endocardial involvement

• 1- Positive echocardiogram for IE defined as :

• · oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or

• ab new partial dehiscence of prosthetic valveor

• 2- New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)

• Minor criteria:

• Predisposition: predisposing heart condition or intravenous drug use

• Fever: temperature > 38.0° C (100.4° F)

• Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions

• Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor

• Microbiological evidence: positive blood culture but does not meet a major criterion as noted above¹ or serological evidence of active infection with organism consistent with IE

• Echocardiographic findings: consistent with IE but do not meet a major criterion as noted above

• Clinical criteria for infective endocarditis

requires:

• • Two major criteria, or

• • One major and three minor criteria, or

• • Five minor criteria

• *HACEK group: Haemophilus sp, Actinobacilius

actinomycetemcomitans, Cardiobacterium

hominis, Eikenella rodens y Kingella sp

•

Non Infective Endocarditis

• Noninfected (sterile) vegetation are caused by

non bacterial thrombotic endocarditis

• The endocarditis of SLE called Libman-sacks

endocarditis.

• NBTE is characterized by deposition of small

sterilte thrombi on the leaflet of cardiac valve

• Grossly the lesions are 1mm-5mm in size occur

singly on the line of closure of leaflets.

• Histologically :they composed of bland thrombi

that are loosely attached.

• They are source of systemic emboli that

produce infarcts in brain,heart or elsewhere.

• NBTE or marantic endocarditis also occur in

debilitated patient.

• NBTE occur in DVT,

mucinousadenocarcinoma, is part of

Trousseau syndrome of migratory

thrombophelebitis.

�Endocarditis of SLE ( Libman-Sacks Disease).

Mitral and tricuspid valvulitis with small sterile

vegetations.

Here is

another

marantic

vegetation

on the

leftmost

cusp. These

vegetations

are rarely

over 0.5 cm

in size.

However,

they are

very prone

to embolize.

The valve is seen

on the left, and a

bland vegetation is

seen on the right. It

appears pink

because it is

composed of fibrin

and platelets. It

displays about as

much morphologic

variation as a

brown paper bag.

Such bland

vegetations are

typical of the non-

infective forms of

endocarditis.

• Grossly the lesion are small(1-4mm) single or

pink vegetation with warty appearance may

located on under surface of AV valve , valvular

endocardium, on the cords or on mural

endocardium.

• Histologically consist finally granular

eosinophilicmaterial that may contain

hematoxilin bodies.

Libman-sacks

endocarditis.

Here are flat, pale

tan, spreading

vegetations over

the mitral valve

surface and even

on the chordae

tendineae.

INVESTIGATIONS:

� Blood Examination.

�Blood culture

�ECG

�Echocardiography: esp transesophageal

echocardiography.

�Immunoglobulins and compliment.

�Urine exam: protein urea and microscopic

hemeturia is common