Etiology

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Pathogens

Staphylococcus aureus	- Approximately 35–40% of native valve IE cases - Most common cause of acute IE, including persons who inject drugs and patients with prosthetic valves or pacemakers/ICDs - Typically affects healthy valves. - Usually fatal within 6 weeks if left untreated
Viridans streptococci	- Approximately 20% of native valve IE cases - Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve) - Common cause of IE following dental procedures, respiratory tract incision and biopsy - Produce dextrans from sucrose that facilitate binding of fibrin-platelet aggregates on heart valves. This ability also enable it to survive on teeth.
Staphylococcus epidermidis	- Bacteremia from infected peripheral venous catheters - Common cause of subacute IE in patients with prosthetic heart valves
Enterococci (especially Enterococcus faecalis)	- Multiple drug resistance - Common cause of IE following nosocomial UTIs - Following gastrointestinal or genitourinary procedures

Risk factors for infective endocarditis

• Cardiac conditions
  • Acquired valvular disease (e.g., Mitral valve prolapse (most common), rheumatic heart disease, aortic stenosis, degenerative valvular disease)
  • Prosthetic heart valves
  • Congenital heart defects (e.g., VSD, bicuspid aortic valve)
• Noncardiac risk factors
  • Poor dental status
  • Dental procedures
  • Nonsterile venous injections (e.g., in IV drug use)
  • Intravascular devices
  • Surgery

Pathophysiology

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• Pathogenesis
  1. Damaged valvular endothelium → exposure of the subendothelial layer → adherence of platelets and fibrin → sterile vegetation (microthrombus)
  2. Localized infection or contamination → bacteremia → bacterial colonization of vegetation → formation of fibrin clots encasing the vegetation → valve destruction with loss of function (valve regurgitation)
• Clinical consequences
  • Bacterial vegetation → bacterial thromboemboli → vessel occlusion → infarctions
  • Emboli can lead to metastatic infections of other organs.

Classifications

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Coagulase-negative staphylococci (CoNS): Staphylococcus epidermidis, Staphylococcus saprophyticus

Clinical features

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Cardiac manifestations

• Development of a new heart murmur or change in a preexisting murmur
  • Tricuspid valve regurgitation
    • Holosystolic murmur that is loudest at the left sternal border
    • Seen in persons who inject drugs, immunocompromised individuals, patients with congenital heart disease, and patients with instrumentation in the right heart (e.g., central venous catheters)
  • Aortic valve regurgitation: early diastolic murmur that is loudest at the left 3rd and 4thintercostal spaces and along the left sternal border
  • Mitral valve regurgitation: holosystolic murmur that is loudest at the heart’s apex and radiates to the left axilla

Extracardiac manifestations of IE

• Pulmonary manifestations: caused by septic emboli resulting from tricuspid valve involvement
  • Signs of pulmonary embolism (e.g., dyspnea)
  • Signs of pulmonary infection, e.g., multifocal pneumonia, lung abscess, and/or empyema.

Diagnostics

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vs rheumatic fever