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Infective Endocarditis (IE)

Infective Endocarditis (IE). A microbial infection of a cardiac valve or the endocardium caused by bacteria, fungi, or chlamydia Often categorized as acute or subacute based on the rapidity of the clinical course

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Infective Endocarditis (IE)

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  1. Infective Endocarditis (IE) • A microbial infection of a cardiac valve or the endocardiumcaused by bacteria, fungi, or chlamydia • Often categorized as acute or subacute based on the rapidity of the clinical course • Alternatively described by type of risk factor e.g., nosocomial,prostheticvalve, intravenous drug use - associated • Pathological findings include the presence of friable valvularvegetations containing bacteria, fibrin and inflammatory cells. There is often valvulardestruction with extension to adjacent structures.

  2. Epidemiology • 3.6 to 7.0 cases per 100,000 patient-years • ~1 in 1280 pediatric admissions per year • age of subjects with endocarditis has increased over the past 60 years (30-40 to 47-69) • Among injecting drug users the incidence is as high as 150 - 2000/100,000 person years

  3. Microbiology of Native Valve Endocarditis Karchmer, Scientific American Medicine, 1999

  4. Risk Factors • Intravenous drug abuse • Intravascular prostheses • Nosocomial exposure • Hemodialysis • Valvular Heart Disease • age-related valvular sclerosis • rheumatic heart disease • Congenital heart disease

  5. Risk Factors • Dental procedures, poor dental hygiene • viridans streptococci, nutritionally variant streptococci, HACEK • Prosthetic valves • Early: coagulase negative staphylococci, S. aureus • Late: coagulase negative staphylococci, viridans streptococci • Gastrointestinal or genitourinary procedures • enterococcior S. bovis (colon carcinoma) • Nosocomial • S. aureus (including MRSA), Gram negatives, Candida species

  6. Pathogenesis

  7. Factors Contributing to the Pathogenesis of Endocarditis • Hemodynamics - blood flow patterns • Bacterial properties • Host factors

  8. Pathogenesis *Endothelial damage caused by turbulent blood flow seen in congenital or acquired heart disease

  9. Pathogenesis • Inoculation of bacteria colonizing a mucosal (e.g., oral mucosa) or peripheral tissue site into the bloodstream • Transient bacteremia of a serum-resistant pathogen capable of adhering to a cardiac valvular surface • Turbulent blood flow across the valve • Bacterial adherence to cardiac valvular surface • Pathogen - host tissue interaction resulting in vegetation formation and local tissue damage • Bacterial persistence • Dissemination of infection to other tissue sites and elicitation of systemic findings

  10. Host Factors Involved in thePathogenesis of Infective Endocarditis • Valvular surfaces • Nonbacterial thrombus forms on damaged valves • Direct adherence to the endovascular surface of normal valves • Suture line, valve surface of prosthetic valves • Platelets dual role • Platelet microbicidal proteins (α-granules) • Bacteria induce platelet aggregation • Part of nonbacterial thrombus surface • Leukocytes, complement, cytokines

  11. Bacterial Factors Involved in thePathogenesis of Infective Endocarditis • Serum resistance - i.e. complement • Bacterial adhesins mediate binding to the nonbacterial thrombus and to endothelial cells: dextran, fibrinogen-binding proteins • Invasive potential of bacteria • Ability to elaborate extracellular proteases • Capacity for metastatic seeding • Stimulation of tissue factor activity

  12. Classification • Subacute IE • develops insidiously and progresses slowly (over weeks to months) • caused most commonly by streptococci (especially viridans, microaerophilic, anaerobic, and nonenterococcal group D streptococci and enterococci) • Acute IE • develops abruptly and progresses rapidly (over days) • usually caused by S. aureus, group A hemolytic streptococci, pneumococci, or gonococci

  13. Clinical Findings • Secondary to 4 underlying phenomena • bacteremia (or fungemia) • Fever, fatigue,weakness, arthralgias, myalgias, weight loss, rigors, and diaphoresis (non-specific findings) • Valvulitis • changing cardiac auscultatory findings • development ofcongestive heart failure • Extracardiac manifestations • petechiae, hemorrhages, Roth’s spots, or splenomegaly • immunologic responses • Renal abnormalities (eg, glomerulonephritis,infarct) • Osler nodes • Emboli • Emboli to the abdominal viscera, the brain, or theheart may produce symptoms associated with ischemia and/or hemorrhage • Janeway lesions

  14. Roth spots • retinal hemorrhages with pale or yellow center • Osler's nodes • painful, palpable, erythematous lesions most often involving the pads of the fingers and toes • local inflammation associated with an immunologic reaction • Janeway lesions • nontender, macular lesions most commonly involving the palms and soles • caused by septic emboli

  15. Cutaneous Manifestations of Endocarditis Splinter Hemorrhages A – C. Osler Nodes: D. Janeway lesion

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