Infective endocarditis is microbial infection of the endovascular structures of the heart.
It often presents in an occult fashion and early diagnosis depends on a high index of clinical suspicion especially in patients with congenital heart disease, prosthetic valves or previous infective endocarditis.
The established diagnosis of infective endocarditis is demonstrated by a positive blood culture and involvement of the endocardium detected during sepsis or systemic infection. It may also be established if there is involvement of the endocardium detected during sepsis or systemic infection but blood culture is negative.


Infective Endocarditis (IE): An infection of the endocardial surface of the heart including infections of the large thoracic vessels & intracardiac foreign bodies characterized by the presence of vegetation which is a nidus for microorganism invasion

Native Valve Endocarditis (NVE): An endovascular microbial infection of native heart valves that may be local (cardiac) including valvular & perivalvular destruction or distal (non cardiac) due to detachment of septic vegetation w/ embolism, metastatic infection & septicemia. May also be broken down as acute & subacute; the only difference is that subacute endocarditis has a more indolent course than the acute form

Prosthetic Valve Endocarditis (PVE): An endovascular microbial infection of prosthetic heart valves (intracardiac foreign body) & may be classified as an infection likely to have been acquired perioperatively & thus being nosocomial (early PVE) or likely to have been community-acquired (late PVE). Early PVE occurs w/in 60 days of valve implantation & late PVE occurs 60 days after valve implantation



  • Staphylococcus sp: Causes approx 25% of NVE
  • S aureus (coagulase-positive staphylococci): Commonly cause PVE, IE in IV drug abusers (IVDA) & in patients w/ previously normal cardiac valves
  • IVDA often present w/ right-sided cardiac involvement
  • Non-IVDA usually present w/ left-sided cardiac involvement & have skin & soft tissue infections w/ underlying congenital abnormalities
  • S epidermidis, S lugdunensis (coagulase-negative staphylococci): Most common causes of PVE & have been known to cause NVE
  • Methicillin-susceptible S aureus (MSSA): May cause right-sided endocarditis in IV drug users
  • Methicillin-resistant S aureus (MRSA): Occurs particularly in PVE, right-sided endocarditis in IV drug users & nosocomial endocarditis
  • Streptococcus sp (viridans group of streptococci; S pneumoniae; S pyogenes; Lancefield group B, C, G streptococci; S bovis, S mitis, S mutans, S sanguis & Abiotrophia sp): Most common causes of NVE
    • Group B streptococci: Most common β-hemolytic streptococci & cause the most virulent IE among streptococci which is characterized by a fulminant disease w/ large crumbling vegetations w/ the frequency of embolization related to size
    • Group G streptococci: Both native & prosthetic valves can be affected w/ left-sided involvement being more common
      Viridans streptococci: Most common cause of NVE in patients w/ congenital heart disease or defects & in patients who are not IV drug users
    • S bovis: Also causes bacterial endocarditis
  • Enterococci
  • Culture-negative organisms: Common causative organisms of endocarditis producing culture-negative BCs
    • HACEK (Haemophilus parainfluenzae, aphrophilus, & paraphrophilus; Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans; Cardiobacterium hominis, Eikenella corrodens; & Kingella): Can cause NVE & PVE
    • Bartonella henselae: Exposure to infected cats may predispose patient to IE
    • Brucella
    • Chlamydia psittaci: Exposure to infected birds may predispose patient to IE
    • Coxiella burnetii: Exposure to infected sheep, cattle & wild rabbits may predispose patient to IE
    • Legionella
      • Characterized by a febrile course that extends up to mth w/ cardiac signs of newly developed murmurs & extremely high anti-Legionella titers
    • Mycobacterium
    • Pseudomonas aeruginosa: Most commonly occurs in IVDAs & is an important pathogen in early PVE
      • Commonly involves the tricuspid valve & may present as subacute infection w/ septic pulmonary emboli & right-sided HF


An increasing cause of PVE

  • Candida
  • Aspergillus
  • Nocardia

Signs and Symptoms

  • Embolic event(s) of unknown origin
  • Fever, plus:
    • Positive blood culture (organism identified is typical for NVE/PVE)
    • Previous history of IE, valvular or congenital heart disease
    • Evidence of CHF or pulmonary embolism
    • Focal or nonspecific neurological signs & symptoms
    • Cutaneous (Osler, Janeway) or ophthalmic (Roth) manifestations
    • Newly developed ventricular arrhythmias or conduction disturbances
    • Peripheral abscesses (renal, splenic, spine) of unknown origin
    • Predisposition & recent diagnostic/therapeutic interventions known to result in significant bacteremia
    • Prosthetic material inside the heart
    • Pulmonic infiltrations that are multifocal/rapid changing (right IE)
  • Hematuria, glomerulonephritis & suspected renal infarction
  • New valve lesion/regurgitant murmur
  • Sepsis of unknown origin

Risk Factors

Cardiac Risk Factors for IE

High Risk Factors

  • Aortic regurgitation
  • Aortic stenosis
  • Coarctation of aorta
  • Cyanotic congenital heart disease
  • Mitral regurgitation
  • Mitral stenosis w/ regurgitation
  • Patent ductus arteriosus
  • Previous IE
  • Prosthetic heart valves
  • Surgically repaired intracardiac lesion w/ residual hemodynamic abnormality
  • Ventricular septal defect

Intermediate Risk Factors

  • Asymmetrical septal hypertrophy
  • Bicuspid aortic valve disease
  • Calcific aortic sclerosis w/ minimal hemodynamic abnormality
  • Degenerative valve diseases in elderly patients
  • Mitral valve prolapse
  • Pulmonary stenosis
  • Pure mitral stenosis
  • Surgically repaired intracardiac lesion w/ minimal hemodynamic abnormality <6 mth after surgery
  • Tricuspid valve disease

Non-Cardiac Risk Factors Predisposing Patient to IE

  • Older age
  • Nonbacterial thrombotic vegetation (NBTV): Microorganisms may adhere more easily in the presence of fresh, platelet thrombi associated w/ leukemia,
  • cirrhosis of the liver, carcinomas which may cause hypercoagulability (marantic endocarditis), inflammatory bowel disease, SLE & steroid medication
  • Compromised host defense typical in steroid medication & possibly in chronic alcoholism
  • IVDA risk of IE is 12-fold higher than non-IVDAs
  • Compromised local non-immune defense mechanism
    • Found in increased transmucosal permeability in mucous membrane lesions eg chronic inflammatory bowel disease
    • Reduced capillary clearance in arteriovenous fistulas of patients on chronic hemodialysis
  • Increased risk or an increased frequency for bacteremia
    • Patients w/ broken skin (eg DM, burns), on intensive care (eg lines, respirators), w/ polytrauma, w/ poor dental status or on hemodialysis
    • Previous exposure to endocarditis-causing microorganisms

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