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Infective Endocarditis (IE)

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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
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.
epidemiology
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
microbiology of native valve endocarditis
Microbiology of Native Valve Endocarditis

Karchmer, Scientific American Medicine, 1999

risk factors
Risk Factors
  • Intravenous drug abuse
  • Intravascular prostheses
  • Nosocomial exposure
  • Hemodialysis
  • Valvular Heart Disease
    • age-related valvular sclerosis
    • rheumatic heart disease
    • Congenital heart disease
risk factors1
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
factors contributing to the pathogenesis of endocarditis
Factors Contributing to the Pathogenesis of Endocarditis
  • Hemodynamics - blood flow patterns
  • Bacterial properties
  • Host factors
pathogenesis1
Pathogenesis

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

pathogenesis2
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
host factors involved in the pathogenesis of infective endocarditis
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
bacterial factors involved in the pathogenesis of infective endocarditis
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
classification
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
clinical findings
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
slide15

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
cutaneous manifestations of endocarditis
Cutaneous Manifestations of Endocarditis

Splinter Hemorrhages

A – C. Osler Nodes: D. Janeway lesion

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