INFECTIVE

ENDOCARDITIS

EFRIDA WARGANEGARA

INTRODUCTION

Infective endocarditis is an
uncommon disease that often
present as a Pyrexia of Unknown
Origin (PUO), and is fatal if
untreated

Infection involves the endothelial

lining of the heart, including the
heart valves

INTRODUCTION

Term infective endocarditis,

first used by Thayer 1930,
and later popularized by
Lerner and Weinstein, is
preferable to the old term
bacterial endocarditis. Since
Chlamudia, Rickettsia,
Mycoplasma, fungi , and
perhaps even virus may be

INTRODUCTION
In

about 1/3 of patient, there is a

pre-existing : - heart defect
(congenital; acquired : result of
rheumatic fever) or a prosthetic
heart valve insitu

However,

the patient may be

unaware of any defect prior to
the infection

Etioloic Agent in Infective Endocarditis

Percentage of
Agent
Cases
Streptococci
60-80
Viridans streptococci
30-40
Enterococci
5-18
Other streptococci
15-25
Staphylococci
20-35
Coagulase-positive
10-27
Coagulase-negattive
1-3
Gram-negative aerobic bacilli
1.5-13
Fungi
2-4
Miscellaneous bacteria
<5
Mixed-infection
1-2
"culture negative"
<5-24

Aetiology
Almost

any organism can cause

endocarditis, but infection of native
valves is caused most commonly by
species of Oral Streptococci :
Viridans streptococcus (Strep.
sanguis, Strept. oralis, Strept. mitis)

Alfa-hemolytic

(but they may be

nonhemolytic), most prevalent
members of the normal flora of the
URT and important for the healthy

Aetiology
About

1/4 - 1/3 of cases are caused

by Staphylococcus and 80-90% of
these due to Coagulase positive S.
aureus attacks normal heart valves
in 1/3 patient
Staphylococcus epidernidis is an
important agent in prosthetic valve
endocarditis and in infant with
umbilical venous catheters in neonatal
intensive care unit.

Aetiology
Coagulase-negative

Staphylococcus are common

causes of early prostheticvalves endocarditis and are
probably acquired at the time of
surgery
The

species causing late infection

(>3 months) after cardiac
surgery resemble more closely

Aetiology
negative aerobic bacilli
Narcotic addicts, prosthetic valve
recipients, and patient with cirrhosis
appear to be at an increased risk for
the developed of gram negative
bacillary endocarditis.

Gram

Unusual

Gram negative bacteria, e.g.

Neisseria gonorrhoeae before the
introduction of penicillin, but is now
rarely.

Aetiology
Gram

Positive bacilli :
Infective endocarditis due to
various sprecies of Corynebcterium
(diphtheroid) is uncoomon and
usually occurs on damaged or
prosthetic velves, although native
valves infection are rarely reported
Other bacteria, include
Acinetobacter

Aetiology
Etiology Infective Endocarditis in
Addicts Staph. aureus, P.
aeruginosa, C. albicans,
Enterococcus .
Fungi Most of fungal
endocarditis can be grouped into
3 categories :
1) Narcotic addicts; 2) patient
after reconstructive
cardiovarcular surgery; and 3)

Pathogenesis
Endocarditis

is an endogenous infection
acquired when m.o. entering the
bloodstream establish themselves on
the heart valves. Thus any bacteriemia
may potentially result in endocarditis

Most

commonly streptococcus from the

oral flora enter the bloodstream (during
dental procedure or vigourus teeth
cleaning or flossing), and adhere to
damaged heart valves

Pathogenesis
In

the course of the bacteriemia,

viridans streptococci, penumococci, or
enterococci may settle on normal or
previously deformed heart valves
producing Accute Endocarditis
endocarditis often
involves abnormal valves
(congenital deformities and rheumatic,
or atherosclerotic lesion).
Subaccute endocarditis, most
frequently due to members of the

Subaccute

Pathogenesis
Subaccute Bacterial Endocarditis (SBE)
Viridans

streptococcus ordinarily the most

prevalen members of the upper resp trac
flora, are also the most frequent cause of
SBE

Group

D streptococcus (enterococcus and

S. bovis) also are common causes SBE,
that 5-10% cases are due to enterococcus
originating in the gut or urinary trac.

Pathogenesis
The

lesion is slowly progressive,

and a certain amount of healing
accompanies the active
inflammation : vegetation
consist of fibrin, platelet, blood
cells, and bacteria adherent to
the valve leaflets
multiplication attract further
deposition of fibrin and platelet
they are protected from the host
defences and vegetation can

Pathogenesis
The

clinical course is gradual,

quite slow process and
correspondingly the time period
between the initial bacteriemia
and the onset of symptom is
around 5 weeks

The

disease is variably fatal in

untreated cases

Clinical Feature
The

patient almost always has a fever,

anemia, weakness, a heart murmur,
embolic phenomena, and enlarged
spleen and renal lesion

Also

complain of nonspesific sympyom :

anorexia, weight loss, malaise, chills,
nausea, vomiting, and night sweats

Periheral

manifestation may also be

evident in the form of splinter
haemorrhages and Oslers nodes

Diagnosis
The

blood culture is he single

most important laboratory test.

Ideally

3 separate samples of
blood should be collected within a
24-hour periode and before
antimicrobial therapy

Isolation

of the causative is
essentially to enable antibiotic
susceptibility test to be

Treatment and Prevention

To

complete eradication takes

several weeks
Penicillin for susceptibility
streptococcus is a choice, if
allergy erythromycin
For enterococus : combination
penicillin/ampicillin with
aminoglycoside
For staphylococcus : b-lactamase
stable penicillin (oxacillin, may be

Treatment and Prevention

Prevention

: people with
known heart defect should be
given prophylactic antibiotic
to protec them during dental
surgery and any other
invasive procedure that is
likely to cause a transient
bacteriemia

Myocarditis and
Pericarditis

Efrida Warganegara

Aetiology and
Transmission
Group

B, and to a lesser extend

group A coxsackieviruses and
certain enteroviruses, are the
main viral causes of myocarditis
and pericarditis

Both

condition are seen

principally in adult male and are
important because they can be
mistaken for myocardial
infarction, yet the prognoses is

Aetiology and
Transmission
Spread

by fecal-oral and
occasionally from pharyngeal
sectretion

Mumps

and influenzae are

less common causes of
myocarditis or pericarditis

Rubella

can causes
myocardiris and associated

Clinical Features and

Pahogenesis

Ingested

coxsackievirus spread
from the pharynx or gut wall to the
lymphatics and then to the blood

Invasion

of heart or pericardium
takes place across blood vessels
and result in acute inflamation.

In

the heart and pericardium this

gives rise to dyspnoe, pain in the
chest, and sometimes mimics a
myocardial infarction

Diagnosis, treatment and

prevention
Coxsackievirus

may be isolated
from throat swab, fecal specimens
or pericardial fluid

Rising

titres of neutralizing
antibody may be demonstrable, or
the presence of IgM antibodies in
ELISA test

There

are no spesific treatments

Terima Kasih