INFECTIVE

ENDOCARDITIS
Christine Joy F. Baquiran
MED-3C
 INFECTIVE
ENDOCARDITIS
It is a microbial infection
of the heart valves or the
mural endocardium.
 EPIDEMIOLOGY
• In developed countries, the incidence of endocarditis ranges from 4
to 7 cases per 100,000 population per year, with higher rates among
the elderly.
• Predisposing Conditions
oHealth care –associated
oCongenital heart disease
oIllicit IV drug use
oDegenerative valve disease
oIntracardiac devices
• Chronic rheumatic heart disease – risk factor in
low-income countries
• Of all endocarditis cases, 16-30% involve
prosthetic valves with the greatest risk during the
first 6-12 months after valve replacement.
 ETIOLOGY
TYPE OF IE FEATURES CAUSATIVE ORGANISMS
Acute Bacterial • Febrile illness • Staphylococcus aureus
Endocarditis • Rapid damage of cardiac • Beta hemolytic streptococci
structures • Pneumococci
• Seeding in extracardiac sites
• Progresses to death within
weeks
Subacute Bacterial • Indolent course • Viridans streptococci
Endocarditis • Slow structural cardiac damage • Coagulase-negative
• Rarely spread Staphylococci
• HACEK
• Causative microorganisms vary among clinical types of endocarditis due to
their different portals of entry.

Native-valve Healthcare- Prosthetic-valve CIED-related Endocarditis

Endocarditis associated endocarditis endocarditis among IV drug-
(NVE) NVE (PVE) users
Portal of Entry Oral, skin or Nosocomial Thru surgery - Involves the Through
URT Intraoperative or device itself or contaminated
postoperative the endothelium needles
at points of
device contact
Causative Viridans S. aureus, CoNS, S. aureus, MRSA S. aureus (MRSA),
microorganisms streptococci, CoNS and gram-negative bacilli, Pseudomonas,
staphylococci enterecocci diphtheroids or fungi Candida, Bacillus,
and HACEK Lactobacillus and
Corynebacterium
spp.
 PATHOGENESIS
• Vegetations
o Prototypic lesions of infective endocarditis
o Mass of platelets, fibrin, microorganisms and scant inflammatory cells
• It most commonly involve:
o Heart valves
o Mural endocardium damaged by jets of blood
o Foreign bodies
• Infective arteritis
o Analogous process involving AV shunts, arterio-arterial shunts or
coarctation of aorta
• Undamaged endothelium is resistant to infection by most
bacteria and to thrombus formation.
• Sites of endothelial injury
oHigh velocity blood jets
oLow pressure side of a cardiac structural lesion
• Endothelial damage
• Platelet-fibrin formation
• Nonbacterial Thrombotic Endocarditis (NBTE)
oThrombus which is the site of attachment of bacteria in transient
bacteremia
oRisk factors
§ Mitral regurgitation
§ Aortic stenosis
§ Aortic regurgitation
§ Congenital heart diseases such as VSD
oAlso arises as a result of hypercoagulable state
oMarantic endocarditis – uninfected vegetations in patients
with malignancy and chronic diseases
• Organisms enter the bloodstream from mucosal surfaces, skin or sites
of focal infection.
• S. aureus – a highly virulent bacteria. It can adhere directly to intact
endothelium or exposed subendothelial tissue
• Microbial Surface Component Recognizing Adhesin Matrix Molecules
(MSCRAMMS)
oSurface adhesin molecules
oMediate adherence to NBTE sites or injured epithelium
• Adherence molecules
oFibronectin-binding proteins – gram-positive bacteria. It is
required for S. aureus to invade intact endothelium
oClumping factor – S. aureus
oFibrinogen-binding surface proteins (Fss2), collagen-binding
surface protein (Ace), Ebp pili- E. faecalis
oGlucans or FimA – streptococci
• These organisms proliferation to form dense microcolonies
oPlatelet deposition
oLocalized procoagulant state
oInfected vegetation
• Organisms deep in vegetations are metabolically inactive and
resistant to antimicrobial agents
• Proliferating surface organisms are shed into the bloodstream
continuously.
Vegetations
 CLINICAL MANIFESTATIONS
ACUTE BACTERIAL IE
Fever High grade fever (39.4-40 C)
Course Rapid and seeds hematogenously to
extracardiac sites
Prognosis Poor if untreated
SUBACUTE BACTERIAL IE
Low grade fever (does not
exceed 39.4 C)
Indolent and rarely spreads
Better prognosis
 • Fever
• Chills
Constitutional
• Weight loss
Symptoms
• Myalgias
• Arthralgias
 • Heart murmurs – It is due valvular damage and
ruptured chordae. It is heard in 85% of patients
with acute NVE.
• Acute IE with normal valves – usually absent
initially
• CHF – develops in 30-40% of patients due to valve
Cardiac dysfunction and intracardiac fistulae.
Manifestations • Perivalvular abscess – infection beyond the valve
leaflets into adjacent annular or myocardial tissue
• Heart block – abscesses that burrow in the aortic
valve annulus
• Myocardial infarction – due to coronary artery
emboli
 • Classic nonsuppurative peripheral
manifestations of subacute IE
• These noncardiac manifestations are related
to prolonged infection
Noncardiac • Arterial emboli – present in 50% of patients
Manifestations with hematogenously seeded focal infection
evident in skin, spleen, kidneys, bones and
meninges.
 Noncardiac Description
Manifestations
Janeway lesions Nontender, slightly raised hemorrhages on the palms
and soles
Osler’s Nodes Tender, raised nodules on the pads of the fingers or
toes
Splinter hemorrhages Small blood clots that run vertically under the nails
Glomerulonephritis Immune complex deposition at GBM
Embolic events Minor emboli: splinter hemorrhages, Janeway
lesions, conjunctival hemorrhages
Major emboli: arterial emboli, intracranial
hemorrhage, pulmonary infarct, mycotic aneurysm
Mycotic Aneurysms Focal dilation in the artery wall that have been
weakened by infection or septic emboli
Janeway lesions Septic emboli
Osler nodes Splinter hemorrhage
 • Endocarditis related to injection drug use
o Limited to tricuspid valve
o Clinical features
§ Fever
§ Faint or no murmur
§ No peripheral manifestations
• Septic pulmonary emboli
Manifestations of o Common with tricuspid endocarditis
Specific Predisposing o Clinical features
Conditions § Cough
§ Pleuritic pain
§ Nodular pulmonary infiltrates
§ Empyema or pyopneumothorax
• CIED endocarditis
o Fever
o Minimal murmur
o Pulmonary symptoms
 DIAGNOSIS
• Diagnosis of IE is established with certainty only
when vegetations are examined histologically and
microbiologically.
• Modified Duke Criteria
oHighly sensitive and specific criteria based:
oClinical
§Laboratory
§Echocardiographic
Modified Duke Criteria
Criteria for Diagnosis
Blood Cultures
• Isolation of causative microorganism – critical for diagnosis and for treatment
planning
• For patients who have not received antibiotics during the prior 2 weeks:
• Three 2-bottle sets of blood culture samples— separated from one another
by at least 2 h—should be obtained from different sites within the first 24 h.
If blood cultures are negative after 48–72 h, two or three additional sets of
samples should be cultured.
Serology
• Helpful in implicating Brucella, Bartonella, Legionella, Chlamydia psittaci,
or C. burnetii in endocarditis.
• Examination of the vegetation by histology, culture, direct fluorescent
antibody techniques, and/or PCR may be helpful in identifying the
causative organism in the absence of a positive blood culture.
Cardiac Imaging
• Echocardiography – anatomically confirms, verifies the size of
vegetations, detects intracardiac complications, and assesses cardiac
function.
oTransthoracic Echocardiography (TTE)
§ Does not detect vegetations <2 mm in diameter
§ It is not adequate for evaluation of prosthetic valves or detection of
intracardiac complication
oTransesophageal echocardiography (TEE)
§ Detects vegetations in >90% of cases of definite endocarditis
§ Optimal for evaluation of prosthetic valves and detection of abscesses, valve
perforation, or intracardiac fistulas.
 Transthoracic Transesophageal
Echocardiography Echocardiography (TEE)
(TTE)
Transesophageal
Echocardiography
(TEE)
Other laboratory tests:
•CBC and Creatinine
•LFT
•Chest Xray and ECG
•ESR, CRP, RF, circulating immune complex
titer
 TREATMENT AND
MANAGEMENT
• Organism-specific therapies
• Empirical Therapy and treatment for culture-negative endocarditis
• Treatment for CIED endocarditis
• Outpatient antimicrobial therapy
• Monitoring antibiotic therapy
• Antithrombotic therapy
• Surgical Treatment
Antimicrobial Therapy

• To cure IE, all bacteria in the vegetation must be killed.

• Must be bactericidal and prolonged and given parenterally.
• Blood cultures should be repeated until sterile. Results should be
rechecked if there is:
• recrudescent fever
• 4–6 weeks after therapy to document cure.
• If patients are febrile for 7 days despite antibiotic therapy, an
evaluation for paravalvular or extracardiac abscesses should be
performed.
 ORGANISM-SPECIFIC ANTIMICROBIAL THERAPY
ORGANISM DRUG (DOSE AND DURATION)
Streptococci • Penicillin G (2-3 mU IV q4h for 4 weeks)
(Penicillin-sensitive) • Ceftriaxone (2 g/d IV as a single dose for 4 weeks)
• Vancomycin (15 mg/kg IV q12h for 4 weeks)
• Penicillin G (2–3 mU IV q4h) or ceftriaxone (2 g IV qd) for 2 weeks PLUS Gentamicin (3
mg/kg qd IV or IM, as a single dose or divided into equal doses q8h for 2 weeks)
Streptococci • Penicillin G (4 mU IV q4h) or ceftriaxone (2 g IV qd) for 4 weeks PLUS Gentamicin (3
(relatively Penicillin- mg/kg qd IV or IM, as a single dose or divided into equal doses q8h for 2 weeks)
resistant) • Vancomycin as noted earlier for 4 weeks
Streptococci • Penicillin G (4–5 mU IV q4h) or ceftriaxone (2 g IV qd) for 6 weeks PLUS Gentamicin (3
(moderately penicillin- mg/kg qd IV or IM as a single dose or divided into equal doses q8h for 6 weeks)
resistant)
Enterococci • Penicillin G (4–5 mU IV q4h) PLUS gentamicin (1 mg/kg IV q8h), both for 4–6 weeks
• Ampicillin (2 g IV q4h) PLUS gentamicin (1 mg/kg IV q8h), both for 4–6 weeks
• Vancomycin (15 mg/kg IV q12h) PLUS gentamicin (1 mg/kg IV q8h), both for 6 weeks
• Ampicillin (2 g IV q4h) PLUS ceftriaxone (2 g IV q12h), both for 6 weeks
MSSA infecting native • Nafcillin, oxacillin, or flucloxacillin (2 g IV q4h for 4–6 weeks)
valves (no foreign • Cefazolin (2 g IV q8h for 4–6 weeks)
devices) • Vancomycin (15 mg/kg IV q12h for 4–6 weeks)
 ORGANISM DRUG (DOSE AND DURATION)
MRSA infecting • Vancomycin (15 mg/kg IV q8–12h for 4–6 weeks)
native valve (no
foreign devices)
MSSA infecting • Nafcillin, oxacillin, or flucloxacillin (2 g IV q4h for 6–8 weeks) PLUS Gentamicin
prosthetic valves (1 mg/kg IM or IV q8h for 2 weeks) PLUS Rifampin (300 mg PO q8h for 6–8 weeks)
MRSA infecting • Vancomycin (15 mg/kg IV q12h for 6–8 weeks) PLUS Gentamicin (1 mg/kg IM or IV
prosthetic valves q8h for 2 weeks) PLUS Rifampin (300 mg PO q8h for 6–8 weeks)
HACEK • Ceftriaxone (2 g/d IV as a single dose for 4 weeks)
• Ampicillin/sulbactam (3 g IV q6h for 4 weeks)
Coxiella burnetti • Doxycycline (100 mg PO q12h) PLUS hydroxychloroquine (200 mg PO q8h),
both for at least 18 (native valve) or 24 (prosthetic valve) months
Bartonella spp. • Doxycycline (100 mg q12h PO) for 6 weeks PLUS Gentamicin (1 mg/kg IV q8h
for 2 weeks)
Empirical Therapy and Treatment for Culture-
negative Endocarditis
• Therapy administered before culture results are known.
• Consider etiology and epidemiologic clues
oVancomycin plus gentamicin OR cefepime: endocarditis related
to IV drug use, healthcare associated NVE
oVancomycin plus ceftriaxone: Subacute NVE
oVancomycin, gentamicin and cefepime: blood culture-pending
PVE (PV is placed for <1 year)
oTherapy is revised again once pathogen is identified.
Treatment for CIED endocarditis
• Antimicrobial therapy is adjunctive for complete removal of the
device
• Based on the causative organism and should be used as
recommended for NVE
• 4 to 6 weeks of therapy
• For generator pocket infection without bacteremia – 10-14 days
given orally
Outpatient Antimicrobial Therapy
• Fully compliant, clinically stable, no bacteremia, afebrile and no impending
complications may complete therapy as outpatients
Monitoring Antimicrobial Therapy
• Blood tests to detect toxicity
• Serum drug concentrations – aminoglycosides and vancomycin
Antithrombotic Therapy
• Indicated for
oMechanical prosthetic valve
oAtrial fibrillation
oDeep vein thrombophlebitis
• UFH or LMWH
Surgical
Treatment
Indications:
- CHF
- Perivalvular Infection
- Uncontrolled infection
- S. aureus endocarditis
- Prevention of systemic emboli
- CIED endocarditis
Timing of Cardiac
Surgical
Intervention
 OUTCOMES
• Death and other poor outcomes are related not to failure of antibiotic therapy but
rather to interactions of comorbidities and endocarditis- related end-organ
complications.
• Survival rates are 85–90% for NVE due to viridans streptococci, HACEK organisms,
or enterococci as opposed to 55–70% for NVE due to S. aureus in pts who are not
IV drug users.
• PVE beginning within 2 months of valve replacement results in mortality rates of
40–50%, whereas rates are only 10–20% in later-onset cases.
 PREVENTION
• Prophylaxis is recommended only for those dental procedures
involving manipulation of:
• gingival tissue
• periapical region of the teeth
• perforation of the oral mucosa (including respiratory tract surgery).
• Prophylaxis is not advised for pts undergoing GI or
genitourinary tract procedures unless the genitourinary tract is
infected.
THANK YOU!