BACTERIAL/

INFECTIVE
ENDOCARDITIS
ALEX MUTUA
BSC CLINICAL MEDICINE
INTRODUCTION

Refers to a serious infection of the valvular and mural endocardium caused by different forms of
bacteria and is characterized by typical infected and friable vegetation.
There are two types;
1. Acute bacterial endocarditis; it is fulminant and destructive acute infection of the endocardium
by highly virulent bacteria in a previously normal heart and almost invariably runs a rapid fatal
course in a period of 2-6 weeks.
2. Subactute bacterial endocarditis (SABE); its caused by less virulent bacterial in a previously
diseased heart and has a gradual downhill course in a periods of 6 weeks to a few months and
sometimes years.
INCIDENCE
Introduction of antibiotics has greatly helped in lowering the incidence. Most cases occur to people
over 50 years of age and males are more affected than women.
ETIOLOGY

Is caused by streptococci and staphylococci. In acute bacterial endocarditis the most common
causative agent are virulent strains of staphylococci chiefly the staphylococci aureus.

Others include pneumococci, gonococci, B- streptococci and enterococci.

In sub acute bacterial endocarditis the commonest causative organism are the streptococci with low
virulence, predominantly streptococcus viridians which forms part of normal flora of the mouth and
pharynx.

Other less common agents include streptococcus boyis, streptococcus pneumonia and
staphylococcus epidermis . We also have gram –ve like pseudomonas, klebsiella
PREDISPOSING FACTORS
There are 3 main factors
1. Conditions initiating transient bacteraemia, septicaemia and pyaemia.
Include procedures or local infections which can enter blood hence resulting to BE eg. Periodontal
infection such as trauma from vigorous brushing of teeth, infections of the GUT and procedures eg
indwelling catheters, upper and lower respiratory tract infection, cardiac catheterization and cardiac
surgery for implantation of prosthetic, skin infections eg boils, abscesses, carbuncles
2. Underlying heart disease.
SABE occurs much more frequently in previously diseased heart valves whereas ABE is common in
normal heart. Some of the conditions include chronic rheumatic valvular disease in about 50% of the
case, congestive heart disease in about 20% of the cases, prosthetic heart valve
3. Impaired host defence.
All conditions where there is depression of specific immunity, deficiency of complement and
defective phagocytic function predispose to BE eg
Impaired specific immunity in lymphoma, leukaemia, cytotoxic therapy for various forms of cancer
and transplant patients, deficient functions of neutrophils and macrophages
PATHOPHYSIOLOGY

On the endocardia surface, the organism multiply and proliferate. Fibrin is deposited over the organism and
this gives coat against the defence of the host. Further growth of the organism and fibrin deposition results
in the formation of friable vegetation which show 3 layers as follows
Inner layer; made up of erythrocytes, leukocytes and platelets.
Middle layer; contains a heavy growth of the organisms
Outer layer; made of fibrin
As fibrin gets deposited further the vegetation grow and get emboli zed from time to time. Organisms which
reach the cardiac tissue adhere to the damaged valves and other parts within minutes. After adhesion to the
tissues, they multiply and envelope themselves in the fibrin and lead to the development of vegetation.
Monocytes which adhere to these sites do not engulf the organisms. On the other hand they produce
precoagulation which favour the development of further fibrin and vegetation. Normally adhesions of
platelets tends to inhibit organisms but in infective endocarditis this doesn’t happen but further growth of
vegetation cover. Tissue invasion and abscess formation follow.
Vegetation are located differently on the different valves. Chordae tendinae and papillary muscles maybe
affected and this may make them to rupture leading to acute vulvular incompetence.
CONT
Embolic episodes; form an integral clinical feature of infective endocarditis. The emboli maybe
septic or sterile. Embolisms leads to infarction of organs. Septic emboli reaching the vasa vasorium
lead to weakness of the arterial wall and formation of mycotic anursysms especially in the
intracranial vessels.
 DISTINGUISHING FEATURES OF ACUTE AND SUBACUTE BACTERIAL
ENDOCARDITIS

FEATURE ACUTE SUBACUTE

Duration < 6 weeks > 6 weeks
Most common organisms Staph aureus, B-strept Strept. viridans
Previous condition of Usually previously normal Usually previously
valves damaged
Lesions on the valves Invasive, destructive and Usually not invasive or
suppurative suppurative
Clinical features Features of acute systemic Splenomegaly, finger
infection clubbing, petechial
Virulence of organisms Highly virulent Less virulent
CLINICAL FEATURES

1. Features of sub acute infection

A. Low grade or high grade intermittent or continuous fever associated with chills and rigours
B. Painful digital clubbing may develop within weeks.
C. Unexplained fatigue, anaemia.
D. Palpable splenomegaly by 2nd week.
E. Brownish pigment over the face and limbs
2. Haemodynamic changes.
F. Destruction of valve may result to rupture resulting to development of fresh murmurs.
G. Papillary muscle and chordae tendinae may rupture giving rise to incompetence of the av valve.
3. Embolic phenomena.
H. Cutaneous embolism; this leads to painless erythematous or haemorrhagic lesions on the palms
and soles called janeway lesions.
I. Nails; splinter hemorrhage
CONT

C. speen; painful splenomegaly and splenic infarcts ma develop.

4. Immunological disturbances; these lead to vasculitis which manifests as oslers nodes, Roth's
spots and glomerulonephritis.

COMPLICATION AND SEQUALE

Are divided into cardiac and extra cardiac
Cardiac complication
1. Valvular stenosis and insufficiency
2. Perforation, rupture and aneurysms of valve leaflets.
3. Abscesses in the valve ring.
4. Myocardial abscesses
5. Suppurative pericarditis
6. Cardiac failure from one or more of the foregoing complications.
Extra cardiac complications

Since the vegetation is friable they tend to get dislodged due to rapid stream of blood and give rise to embolism
which is responsible for very common and serious extra cardiac complications

1. Emboli origination from the left side of the heart and entering the systemic circulation affects the organs like
the spleen, kidneys and brain causing infarcts, abscesses and mycotic aneurysm.

2. Emboli from the right side of heart enter pulmonary circulation and produce pulmonary abscesses

3. Petechial maybe seen in the skin and conjunctiva due to either emboli or toxic damage the capillaries

4. In SABE there are painful tender nodules on the fingertips of hands and feet called Osler's nodes while in
ABE there is appearance of painless non tender subcutaneous maculopapuar lesions on the pulp of fingers
called laneway lesions.

5. Focal necrotizing glomerulonephritis is seen more commonly in SABE than ABE

Treatment with antibiotics in adequate dosages kills the bacterial but complications and sequel of healed lesions
may occur even after successful therapy.
CAUSES OF DEATH IN BACTERIAL ENDOCARDITIS

1. Cardiac failure

2. Persistent infection leading to sepsis

3. Embolism of vital organs

4. Rupture of mycotic aneurysm of cerebral arteries

A high index of clinical suspicion is very essential for early diagnosis. In persons with congenital or acquired heart
disease fever, anaemia, clubbing, refractory cardiac failure, changing murmurs, development of emboli or even
vague health should suggest possibility of endocarditis

IE should be differentiated from activation of rheumatic fevers, disseminated lupus erythromatous ,drug toxicity and
other prolonged fevers.

Development of normocytic normochromic anaemia, mild leucocytosis, elevation of ESR, proteinuria and
microscopic or flank haematuria should strengthen the clinical diagnosis
DUKES CRITERIA FOR DIAGNOSIS OF INFECTIVE ENDOCARDITIS
A. Pathological criteria
1. Pathologic criteria; pathological lesions; vegetation or intracardiac abscess present, confirmed by
histology showing endocarditis
2. Micro-organisms; demonstrated by culture or histology in vegetation or in a vegetation that has
embolised or intracadiac abscess
B. Clinical criteria using specific definitions listed below
Two major criteria or one major and three minor criteria or 5 minor criteria ( definite diagnosis)
One major and one minor criteria or three minor criteria (possible diagnosis)
Echocardiogram; vegetation above 0.5 cm can be detected easily; smaller vegetation ay escape
detection and therefore a negative result should not be a reason for ruling out the diagnosis. In
practice demonstration of vegetation's by echocardiogram is the most rapid and definitive method to
establish the diagnosis. Since demonstrable vegetation's take days to weeks to develop repetition of
echocardiogram also helps to assess progress of treatment.
TREATMENT
Surgery ; when medical treatment fails to clear the infection, the underlying abnormality may have
to be corrected surgically and this has to be done as a life-saving procedure. Other indications for
surgery include acute vulvular incompetence leading to cardiac failure, large friable vegetation
which re likely to embolize unstable prosthesis and perivalvular extensions of infection.
Prognosis; with help of echocardiography and microbiological studies the diagnosis can be
confirmed in the most cases if clinical suspicion is high. Prognosis depends on the timely institution
and prolonged administration of appropriate antibiotic combination. Prognosis is best when the
specific organism and its antibiotic sensitivity are known.
Thank you

Questions ?