INFECTIVE

ENDOCARDITIS
Dr/ Ashraf Alamir, MD
Ass. Prof. of Cardiology , Faculty of medicine
Al- Azhar University
1-Incidence/mortality didn’t decline over the past
30 years. Despite major advances in surgical and
medical therapy, mortality remains as high as
20%.

2-Variable presentation.

3-Lack of randomized trials and limited meta-

analysis.
Types of IE
According to site and the presence
of a foreign material:
1- Lt. side NVE.
2- Lt. side PVE:
-Early:<1 yr after surgery.
-Late:> 1 yr after surgery.
3- Rt. side IE.
4- CDRIE (PP or ICD).
 According to mode of acquisition:
1- Community-acquired (Ss/Ss develop < 48 hrs
of hospital admission).
2- Health-care associated:
-Non-nosocomial (Ss/Ss develop < 48 of
admission in a patient with history of health
care contact e.g. haemodialysis, IV chemo-
therapy or home-based IV therapy.
-Nosocomial (Ss/Ss develop > 48 of hospital
admission).
3- IVDA.
 According to microbiology:

1- Culture (+)ve ( = 85% ).

2- Culture (-)ve.
 Culture positive IE
(The most common oganisms are):
1-Streptococci:
a- Oral*( formerly viridans) streptococci; form a mixed group of
organisms that are almost always susceptible to penicillen G.
Viridans streptococci are part of the normal skin, oral,
respiratory and GI tract flora, and they cause at least 50% of
cases of community-acquired native valve IE not associated
with intravenous drug use.

b- Group D( formerly bovis) streptococci; include S.bovis and

S.equinus and are usually sensitive to penicillin G.

2- Enterococci: among them, there are 3 species that cause IE.

*Named so as they live as an oral microflora.

3-Staphylococci:*
a- S.aurius ( oxacillin sensitive esp. if community
acquired) usually cause NVE.
b- Coagulase negative staph. or CNS ( oxacillin
resistant) usually cause PVE**.

4-HACEK group: includes fastidiuos gram –ve

organisms that are normal flora in the URT.They
are commonly associated with large vegetations,
large-vessels embolism & CHF.***
 Culture negative IE
Culture negative IE due to prior antibiotic therapy (62%);
Culture may be negative for many days after antibiotic
discontinuation, the causative organisms are most often oral
strept. and CNS.
IE frequently associated with negative culture;
Fastidious( nutritionally variant) oral strept., fastidious G –ve
bacilli of the HACEK group( Haemophilus and Para-
haemophilus, Actinobacillus, Cardiobacterium, Eikenella and
Kingella), brucella and fungi.
IE associated with constantly negative culture ( 5%);
These are caused by intracellular organisms e.g. Coxiella
burnetii, Bartonella, Chlamydia and Trophyrema whipplei.
Diagnosis is made on the basis os serology, cell culture or
gene amplification.
Non-infective endocarditis:e.g.Libman-Sack’s endocarditis with
SLE.
AETIOLOGY
Predisposition
 1- 75% of cases have a preexisting
predisposing cardiac abnormality
I-NVE:
In developed countries; MVP with MR > RHD > CHD.
The most common CHD predisposing to IE are: bicuspid Ao valve, PDA, VSD,
AC and FT*.
II-PVE(10-20%):
Risk is max. in the 1st 6 mo.
Mechanical=Bioprothetic
Mitral=Aortic
Pacemaker/defibrillator endocarditis:
Incidence following device therapy is 0.2 - 7%.
Infection may involve G/D pocket, electrodes or endocardium.
Infection is usually d/t direct microbial seeding. Haematogenous spread is rare
and is usually d/t S.aurius bacteremia.
Infection of the pocket leads to thinning out of the overlying tissues ending in
device erosion.

*Secondum ASD isn’t associated with increasd risk of IE.

 2-Other risk factors include
immunosuppression, prolonged surgery,
previuos IE,…

*Despite the high virulence of this organism; the disease tends to be less severe with mortality
ranging from 2 – 6%
Pathophysiology
 THE NORMAL
ENDOTHELIUM IS
RESISTANT FOR
COLONIZATION AND
INFECTION BY
CIRCULATING
ORGANISMS.
 -1-
The 1ry event is either;
1- An endothelial damage by
- a turbulent flow
- a catheter/electrode
- degenerative changes
Leading to a healing process with PLT and fibrinogen deposition=

All organisms of IE can adhere to an injured endothelium.

2- Endothelial inflammation
 -2-
Transient bacteraemia related to invasive
procedures or chewing and brushing( leads to low grade short
timed spontaneous bacteraemia)

-3-
-The organism adheres to the endothelium and provokes pro-
coagulant response and nurture an infected
vegetations within which they can survive.Vegetations
form on the atrial surf. of regurgitant AV valves or ventr. surf. of
incompetent semilunar valves.
-Vegetations further impair leaflet coaptation, cause perforation or
chordal rupture leading to worsening regurge and HF.
-Veg. may dislodge causing septic/non-septic embolism.
-Infection may spread (esp. in PVE) to the adjacent valve ring,
myocardium/conductive system or M/A intravalvular
fibrosa….leading to PV dehiscence, abscess formation
,diverticul., fistul., aneurysm or conduct. abnormalities.
Clinical Picture
 C/P
Is highly variable;
Acute IE: arises with marked toxicity and
progresses, over days to weeks, to valve
destruction and metastatic manifestations.

Subacute IE: evolves over weeks to months

with mild toxicity and rarely cause
metastatic manifestations.
 C/P
Hallmarks of IE are:
FEVER AND A NEW MURMER
( > 85%)
Fever may be absent in elderly, uremic & immunosuppressed.
Murmer may be absent in mural or device infection.
 C/P
1- Fever and other non-specific
symptoms:

Such as malaise, anorexia, wt.loss, chills,

night sweats,…
 C/P
2-Cardiac:
-New / worsening valvular regurgitation.
-CHF…..55%
AV…75%
MV…50%
TV…20%
-HB, ACS, myocarditis& pericarditis.
 C/P
3-Neurologic:

-Overt cerebral embolism (15%)

-Enchephalopathy (10%)
-Mycotic aneurysm leak (<5%)
-Meningitis/ brain abscess (<5%)
 C/P
4-Vascular/immunologic:
-Splenomegaly (40%)
-Mucosal petechiae (30%)
-Splinter hge (20%)
-Clubbing (15%)
-Osler nodules (15%)
-Janeway lesions (<5%)
Splinter Hemorrhage
Conjunctival Petechiae
Osler Nodes
Janeway Lesions
 C/P
5-Embolic:
systemic embolism occurs in 25-50% of cases and may
mimic;
-CVS
-Acute limb ischemia
-ACS
-Acute abdomen; d/t renal, splenic or intestinal embolism.
-PE
 C/P
6-Ocular:

-Macular hge
-Roth’s spots
-Chorioretinitis / endophthalmitis
Roth’s spot
Diagnosis
 diagnosis of infective endocarditis is
often imprecise,

because bacteremia can occur without

endocardial infection,
and endocarditis can occur with negative blood
cultures,especially if a patient has received
antibiotics for minor undiagnosed febrile illness.
 Duke Criteria
Are, currently ,the most sensitive and specific set of
criteria ( 80% overall sensitivity and specificity) but
not yet validated for PVE.
Definite pathologic diagnosis:
-1 of the 2 pathologic criteria.
Definite clinical diagnosis:
-2 major,
-1 major + 3 minor or
-5 minor clinical criteria.
Possible clinical diagnosis:
-1 major +1 minor or
-3 minor clinical criteria.
Rejected diagnosis:
-Solid alternative diagnosis,
-Resolution of manifestations within 4 days of antibiotic
therapy or
-Absence of histopathologic characteristic features within 4
days of antibiotic therapy.
 (Duke criteria)
Pathologic criteria:
1-Microbiology: detection of typical organisms
by culture or microscopy in a vegetation, an
abscess or a vegetation that had embolized.

2-Histopathology: detection of active

endocarditis in a vegetation or an abscess.
 (Duke criteria)
Clinical criteria
Major criteria:
1-Positive blood culture =
# Typical organisms (S.viridans, S.bovis, S.aurius, HACEK
or com.acq. Enterococci in absence of 1ry focus)

Persistently i.e.
In 2 successive cultures 12 hrs apart
Or; In all of 3 or the majority of 4 or more cultures within at least 1 hr

or # Single +ve culture for C.burnetii or anti-phase 1

Ig G titre > 1/800
 (Duke criteria)
Major criteria:
2- Evidence of endocardial involvement:
#Echocardigraphic
-Vegetation= Oscilating intracardiac mass on a
valve, supporting structure, in the path of a
regurgitant jet or on implanted material.
In absence of alternative anatomical explanation.
-Abscess
-New partial dehiscence of a prosthetic valve.
#New valvular regurgitation.
 (Duke criteria)
Minor criteria:
1-Predisposition;
-Predisposing heart condition

2-Fever >38
3-Vascular phenomena;
-Major arterial embolism
-ICH
-Myc. Aneurysm
-Conj. Hge
-Janeway lesions
 (Duke criteria)
4-Immunologic phenomena;
-GN
-Roth’s spots
-Osler’s nodes
-RF
5-Microbiologic evidence;
- +ve culture but…..
- +ve serology
Investigations
 Lab workup
1-CBC:
-Modest leucocytosis
-Modest thrombocytopenia
-Normocytic normochromic anemia
2-Acute phase reactants:
-Elevated ESR, CRP and RF.
3-BUN & creatinine:
-Elevation indicates either ICGN or drug toxicity.
4-Urinalysis:
-May show microhematuria or proteinuria.
5-Blood culture:

-Treatment shouldn’t be delayed > 3 hours if acutely ill.

-Although critical in diagnosis, yet it is negative in a very
significant portion of cases…. 2.5 - 31% in recent
reports.
-Method;
*3 samples via 3 venepunctures under meticulous
aseptic conditions at intervals….sampling from a CV line
should be avoided.
*Each sample includes: 10 ml of blood added to an
aerobic flask & 10 ml of blood added to an
anaerobic flask.
*Culture for HACEK organisms should routinely be
done, while fungal culture should be made if
suspected.
6-Serology:
For Brucellosis, Legionella, Coxiella and
Psittacosis (culture negative).
ECG
Baseline and follow up ECGs for:
-Conduction abnormalities …reflect
intramyocardial extension with a (+)ve pred-
ictive value of 75% and sensitivity of 50%.
-MI is a rare complication.
 CXR
-Rt. side IE….nonspecific infiltrates.
-CHF / pleural effusion.
Echocardiography
The sensitivity of TTE is 40-70% & and of TEE is
90-100%.
Diagnosis is particulaely challenging in case of:
-PVE
-Small vegetations < 2mm
-Early before vegetating or already embolized
-Severe underlying lesion e.g. MVP, dege-
nerative calcified lesion.
 Investigations
TTE :
-A baseline TTE….sensitivity to detect valve vegetations is < 70%.
-A repeat TTE….if complications arise e.g. H.F. or conduction
abnormalities.
-A postoperative baseline TTE.
TEE:
Indications:
-PV/ICD + suspec. of IE.
-Poor quality TTE.
-A negative TTE + High suspec. of IE.
Vegetation on the mitral valve
 A transthoracic parasternal long axis view with harmonic imaging
illustrating a vegetation (arrow) involving the aortic valve during diastole
A transesophageal long axis view of the aorta in the same patient with
demonstration of the vegetation on the noncoronary cusp of the aortic
valve
 Investigations
CT/MRI brain
Indicated if:
-Neurological symptoms develop.
-Persistent headache.
-Routine CT brain/abdomen m/b useful in detection of
silent embolism.
CA
-Indicated if there is high suspecion of CAD (males > 35
yrs, females > 45 yrs*)
-Avoided as possible in Ao valve IE to avoid the risk of embo-
lization and if surgery is urgent ( do a high resolution CT
angio instead).
*ESC recommendations included: men>40yr,postmenopausal women,those with at least 1 CV
risk factor&those with PH of CAD.
Treatment
Antimicrobial therapy
Prevention of IE
(The new AHA guidelines)
‫و آخر دعوانا أن الحمد هلل رب العالمين‬
71