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)

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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.



  • 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



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



  • 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



  • 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

Infective endocarditis ie

  • 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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