08: Infective Endocarditis

Question 1

Define infective endocarditis.

Answer 1

• Infection of cardiac valve or endocardium caused by bacteria, fungi or chlamydia.
• Presence of friable, valvular vegetations containing bacteria, fibrin, platelets and inflammatory cells.
• Valvular destruction with local intracardiac complications.
• Vegetation may break off and embolize or cause metastatic infections.

Question 2

Describe the epidemiology of endocarditis.

Answer 2

• Increased incidence of nosocomial endocarditis
• Increased risk:
  
  • IV drug users
  • Prosthetic/defective heart valves
  • Hemodialysis patients
  • Diabetics
  • HIV+
  • IV catheters
• Incidence of underlying valvular disease (atherosclerotic cardiovascular disease, mitral valve prolapse with insufficiency, rheumatic valvular disease).

Question 3

What are the most common organisms causing IE?

Answer 3

Predominantly a GP disease

1. Staph aureus (32%)
2. Viridans strep
3. Enterococcus bovis
4. Coag (-) staph (prosthetic valves)

Question 4

Identify the risk factors for specific pathogens that cause IE.

Answer 4

• Dental procedures, poor dental hygiene: viridans strep (major subacute), variant strep, HACEK (GNs)
• Prosthetic valves
  
  • Early: coag- staph (major in valves), s. aureus (80% acute; predominant IV drug related)
  • Late: coag- staph, viridans strep
• GI/GU procedures: enterococci, s. bovis (colon carcinoma)
• Nosocomial: s. aureus (MRSA), GNs, candida

Question 5

Describe the pathogenesis of IE.

Answer 5

1. Transient bacteremia (mucous membrane/peripheral tissue trauma)
2. Seeding on valvular surface
   
   1. Subacute IE: bacteria seed sites of previous micro/macro damage characterized by deposition of platelet-fibrin thrombus (nonbacterial thrombus [NBT]).
   2. Acute IE: more virulent organisms capable of colonizing normal cardiac valvular surfaces.
3. Elaboration of baterial factors (GP adhere to surfaces more avidly due to adhesins such as dextran; complement resistant; extracellular proteases)
4. Vegetaion formation (bacteria encased in meshwork of platelets and fibrin; barrier to host defenses)
5. Pathology (necrosis and friability, often with acute IE)

NB: Hemodynamic factors dictate that IE develops more often on left side of heart; right side (tricuspid valve) more common with acute bacterial endocarditis (ABE) and drug addicts. Due to presence of high-pressure source, high velocity flow through narrow orifice, and low-pressure sink beyond the orifice (vegetations exist on low-pressure side).

Question 6

Describe the clinical manifestations of IE.

Answer 6

• Systemic: fever, fatigue, anorexia, general malaise, weight loss.
• Cardiac: hear murmurs (99% SBE, 33% ABE); new regurgitant murmur leads to congestive heart failure (>90%).
• Bland/septic embolization: tissue infarction w/ most common sites being coronary vessels, kidneys, CNS, spleen.
  
  • Oftentimes bland in SBE, septic in ABE.
  • With tricuspid valvular ABE, lung frequently seeded (–>cavitary pneumonia)
• Sustained bacteremia
• Immunologic features
  
  • Rheumatoid factor (IgM antibody against IgG) in 50% pts w/ disease >6wks duration (titer declines w/ tx)
  • Vasculitis (circulating immune complexes, hypocomplementemia)
  • Sequela: glomerulonephritis, Osler’s nodes
• Other sites of involvement: petechiae, Janeway lesions, CNS emoli, ruptured cerebral aneurysms, Roth spots (eyes)

Question 7

Describe the laboratory findings/diagnosis of IE.

Answer 7

• Blood culture: In 2/3 of cases, 100% cultures positive; 3 sets of cultures results in >95% yield.
• Anemia, hematuria, RBC casts, hypocomplementemia common.
• Erythrocyte sedimentation rate almost uniformly elevated, circulating immune complexes detectable.
• Echocardiography: transesophageal echocardiography
• Cutaneous manifestations: splinter hemorrhages, Osler’s Node, Janeway Lesion
• Duke Criteria help to diagnose
  
  • 2 major; 1 major + 3 minor; 5 minor

Question 8

Describe the treatment of IE.

Answer 8

• Bactericidal antibiotics
• Prolonged therapy (weeks) necessary
• Treatment after blood cultures taken
• Urgency required for acute but not subacute IE
• Synergistic combinations when available
• Prophylaxis: prosthetic valve, complex congenital heart disease, previous endocarditis, cardiac transplantation with valvulopathy, dental procedures involving manipulation of gingival tissue, procedures involving respiratory tract, infected skin/skin structures