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Infecctive Endocarditis
(IE)
Dr mirdamadi
Cardiologist, fellowship of echocardiography
Reference :
 Braunwalds heart disease
 Harrisons principles of internal medicine
 Acute IE is cused typically by staphylococcus
aureus, with marked toxicity and progresses over
days to weeks to valvular destruction and metastic
infection.
 Subacute IE usally caused by viridans
streptococci,enterococci,cougulase negative
staphlococci or gram-negative coccoba cilli,
evolves over weeks to months with only modest
toxicity and rarely causes metastatic.
#Prototypic lesion of IE ,the vegetation is mass of
platlets,fibrin ,microorganisms and inflammatory
cells.
# Site of infection :heart valves (native or prosthetic) ,
site of VSD, mural endocardium at site of aberrent
jets of blood or freign bodies ,on intracardiac
devices ,arteriovenousshunt, arterioarterial shunt
(PDA)or coarctation of aorta.
Predisposig conditin
Neonate : often TV involved as a consequencec of
infected intravascular catheters or cardiac surgery
Childern and adults : RHD,CHD,MVP,DHD
IV drug abuser:
Mostly involved TV ,then MV and AOV
 Multiple site involvement may occure
 Recurrent IE may occure
 Although S.aureus is characteristic but unusual
organisms and polymicrobial IE may occure.
 Infection with HIV is not a significant risk factor for IE
unless associated with IV drug abuse.
Prosthetic valve endocarditic (PVE):great frequency
during first 6 months
Early:within 60 days , as a complication of surgery
and s.epidermidis is prominent.
Late :after 60 days ,as a common microorganism.
Transvenous pacemaker lead and/or implanted
defibrillator :is usually nosocomial and is moe
within weeks of implantation or generator change
,mostly s.aureus or s.aureus or s.epidermidis
 Healthcare –associated :after hospitaliazation or as
a cnsequence of indwelling devices , or
hemodialysis catheter , s.aureus is the most
common cause.
Normal endothelium is resistant to infection and thrombus formation.
 Endothelial injury allows direct infection by virulent organisms or
development of an uninfected platelet-fibrin thrombus (nonbacterial
thrombotic endocarditis ,NBTE).
 Thrombus is a site of bacterial attachment during transient bacteremin
 NBTE: DIC,burn,SLE uremin ,valvular heart disease and intracardiac
catheters, marantic endocarditis (malignancy and ohronic disease).
Organisms enter the bloodstream from mucosal surfaces ,skin or site of
focal infection.
 Except for virulent bacteria (e.g.aureus) that can adhere to intact
endothelium , other microorganisms adhere to NBTE.
 Organism proliferate and induce a procoagulant state at the site.
 Fibrin deposition with platelet aggregation ,stimulated by tissue factor
and proliferating microorganisms,generate vegetation.
 Microorganisms can cause endocarditis have microbial surface
components recognizing adhesin matrix molecules (MSCRAMMs)
that mediate adherence to NBTE or injured endothelium
 Glucans or dextran is surface polysaccharides of streptococci

 Fibronectin is in lesion ofheart valves and produced by endothelial
cells platlets and fibroblasts in response to vascular injury
 Fibronectine-binding proteins present on many gram-positive bacterin.
9
10
Bacteria in vegetations reach to 10 - 10
organisms per pram and organisms deep in
vegetation are metabolically inactive (non growing)
and relatively resistant to killing by antimicrobial
agents
Clinical manifestations
Fever: is low –grade in subacute (<39.4c) but
temperatures of 39.4° - 40 °c are often in acute if
fever may be absent in elderly severely debilitated
patient or who have marked cardiac or renal failure
Cardiac manifestation
Valvula regurgitation due to valvular damage or ruptured
chordae
 CHF due to valvular regurgitation or myocarditis or
intracardiac fistula
 Perivalvular abscesses (mostly AOV)
 Pericarditis due to extension through epicardium (mostly
AOV)
 Heart block due to extension to conduction system (mostly
AOV)
Non cardiac manifestation
 Musculoskeletal symptom (arthralgin,myalgia,arthritis,back pain)
 Emboli to brain,coronary artery, extremities,mesenteric arteries
 Splenomegaly and clubbing
 Petechiae in conjunctiva ,buccal &palatal mucosa and extremities
 Splinter or subungual hemorrhages
 Osler nodes
 Janeway lesion
 Roth spot (oval retinal hemorrhage with pale center)
 Neurological symptum: stroke,ICH,cerebritis and microabscesses
headache(potentially due to mycotic
aneurysm),seizure,encephalopathy
 Renal insufficiency due to glomerulonephritis ,emboli, impaired
hemodynamic andvantimicrobial toxicities.
%50 of patients associated with IV drug use
,infection is limited to the tricupid valve.
 These patient present with fever ,faint or no
mumur,cough ,pleuritic chest pain ,pulmonary
infiltration ,pyopneumothorax.
Laboratory findings
Anemia (normochromic,normocytic),false positive
serologic test for syphilis and rheumatoid factor.
 ESR elevation (average 55mm/hr),positive CRP.
 Urinalysis (proteinuria, hematuria).
Blood culture :3 blood culture sets(two bottles per set
)with at least 1 h separation from different vien over
24 h should be obtained.
 If culture remain negative after 48-72 h ,two or three
additional blood culture sets should be obtained.
 5-10% of patiants with IE may have negative blood
cultures .due to previous antibiotic therapy or
fastidious organisms or fongal IE.
Echcardiography can confirmed IE, sizing of
vegetation,detection of intracardiac complications
assesment of cardiac function.
 TTE detects vegetation in 65% of patients and TEE
in 99%
Diagnosis
Definite diagnosis is when vegetation obtained at
cardiac surgery, an autopsy or from an artery
(embolus) and examined histologically &
microbiologically.
Duke criteria :
Developed on the basis of clinical , laboratory
&echocardiography.
‫جدول ص ‪ 792‬هارسون‬
Definite diagnosis according to documentation of 2
major ocriteria ,1 major &3 minor criteria or 5 minor
criteria
 Rejection if an alternative dianosis is established if
symptom resolve with <days of surgery or autopsy
after < 4 days of therapy yields no histologic
evidence IE
 Possible IE when 1 major &1 minor 0r 3 minor
criteria are identified.
Antimicrobial therapy
It is difficult to eradicate bacteria from the avascular
vegetation with largely nongrowing ,methabolically
inactive bacteria
 Therapy must be bactericidal and prolonged ,
prenterally with high serum concentrations that will
through passive diffusion lead to effective
concenterations in the depths of vegetation.
 Antibiotic toxicities ,including allergic reactions occur in 2540% of patients. blood test to detect renal ,hepatic &
hematologic toxicity should be performed periodically.
 In most patients ,effective therapy results in resolution of fever
in 5-7 days
 When fever persists for 7 days patients should be evaluated
for paravaluvlar abscess and for extracardiac abscesses
(spleen , kidney) or complications (embolic events) drug
reactions or complications of hospitalization.
 Vegetation become smaller with treatment ,but at 3 months
after cure half are unchanged and 25%are slightly larger.
Surgical treatment
Moderate to severe CHF due to value dysfunction
 Unstable prothesis, prosthesis orifice obstructed
 Uncontrolled infection
 Unavailable effective antimicrobial therapy

(fungi,brucellae,pseudomonas
aeruginosa)
 Relapse after optimal therapy
 Perivalvular extension
 Culture negative IE with persistent fever( >10d)
 Large (>10 mm) hypermobile vegetation
prevention
 Oral hygiene and dental health should be
addressed before prosthetic valves are placed
electively
 Oral irrigating devices are not recommended
 Use irrigating devices are not recommended
 Transient bacteremia occure after dental
manipnlation (daily or surgical)
Antibiotic prophylaxis recommended in
dental procedures that involve
gingival tissue or perforate oral
mucosa tonsilectomy a denoidectomy
or bronchoscopy, surgery of infected
skin or musculoskeletal tissue
Cardiac condition that need prophlaxis :
 Prosthetic valus
 Previous IE
 Unrepaired cyanotic CHD
 Repaired CHD with residual defect
 Completely repaired during the first 6 months after
procedure
 Cardiac transplantation with cardiac valvulopathy
Prophylaxy:30-60 min before procedure:
Amoxicillin 2g po
Cephalixin 2g po( azithromycin or clatrithromycin
500g or clindamycin 600g)