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Infective endocarditis !

Infective endocarditis is an infection of the heart's inner lining, usually a valve, where growths of germs can destroy it and break off into the blood.

Updated 2026-10-29

Structures involved

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Microorganisms that cause it

In histology

In the clinical exam

In physiology

Why it happens

What it is

Infection of the endocardial surface of the heart, usually a heart valve, forming vegetations of fibrin, platelets and microorganisms that can destroy the valve and break off as emboli.

Who gets it

Uncommon but serious. In high-income countries it is increasingly linked to prosthetic valves, devices and healthcare contact; in Colombia and Latin America rheumatic valve disease remains an important substrate, and injection drug use adds right-sided cases.

Causes

  • Staphylococcus aureus (most common in many series; acute course)
  • Viridans group streptococci (classically subacute, on damaged native valves)
  • Enterococci, often after urinary or bowel procedures
  • Coagulase-negative staphylococci on prosthetic valves and devices
  • HACEK organisms and fungi; culture-negative cases after prior antibiotics

Risk factors

  • Injection drug use (classically tricuspid valve)
  • Rheumatic heart disease and other damaged native valves
  • Prosthetic valve or intracardiac device
  • Previous infective endocarditis
  • Congenital heart disease
  • Haemodialysis, central lines and poor dental health

Pathophysiology

Turbulent flow damages the endothelium and a sterile platelet-fibrin deposit forms. Bacteria in the bloodstream adhere to it and multiply, protected from host defences, creating a vegetation. The vegetation erodes the valve, causing regurgitation, can spread to the annulus as an abscess, and sheds septic emboli and immune complexes.

Classification

  • Native vs prosthetic valve vs device-related
  • Left-sided vs right-sided (tricuspid, typical in injection drug use)
  • Acute (fulminant, often S. aureus) vs subacute (weeks, often streptococci)

Symptoms and signs

  • Fever, sometimes with night sweats, weight loss and fatigue
  • New or changing regurgitant murmur
  • Splinter haemorrhages and conjunctival petechiae
  • Janeway lesions (painless palm and sole macules) and Osler nodes (painful finger pads)
  • Roth spots on fundoscopy
  • Splenomegaly; septic pulmonary emboli with cough in tricuspid disease

Diagnosis

Clinical
Diagnosed with the modified Duke criteria: major criteria are typical organisms in repeated blood cultures and evidence of endocardial involvement on imaging; minor criteria include predisposition, fever, vascular and immunological phenomena.
Tests
At least three sets of blood cultures from separate venepunctures before antibiotics; full blood count, inflammatory markers, renal function and urinalysis (haematuria). ECG for conduction changes.
Imaging
Transthoracic echocardiography first; transoesophageal echo for prosthetic valves, suspected abscess or a negative but likely case. CT or PET-CT and brain imaging look for emboli and paravalvular spread.

Differential diagnosis

  • Acute rheumatic fever
  • Systemic lupus erythematosus
  • Atrial myxoma
  • Other sources of bacteraemia and sepsis
  • Lymphoma or other cause of prolonged fever

Goal of treatment

Sterilise the vegetation with prolonged bactericidal therapy, repair or replace destroyed valves when needed, and prevent embolic and heart-failure complications.

Treatment

Medical
Prolonged intravenous bactericidal antibiotics chosen by organism and sensitivity (penicillins, glycopeptides and others), usually for several weeks, guided by an endocarditis team.
Medical
Empirical antibiotic cover after cultures are taken when the patient is unwell, then narrowed to the cultured organism.
Surgical
Valve surgery for heart failure from valve destruction, uncontrolled infection or abscess, or high embolic risk.
Follow-up
Repeat blood cultures to confirm clearance, follow-up echocardiography and monitoring for drug toxicity.
Lifestyle
Harm-reduction support for people who inject drugs, and attention to dental health.

Drugs for this condition

Complications

  • Heart failure from acute valve regurgitation
  • Embolic stroke and brain abscess
  • Mycotic aneurysm
  • Perivalvular abscess and heart block
  • Septic emboli to spleen, kidneys or lungs
  • Immune-complex glomerulonephritis

Prognosis

Serious even with treatment, with substantial in-hospital mortality. Outcomes are worse with S. aureus, prosthetic valves, heart failure, stroke and older age; early diagnosis and timely surgery improve them. Relapse and recurrence are possible.

Prevention

  • Good oral hygiene and regular dental care in people with valve disease
  • Antibiotic prophylaxis before certain dental procedures in high-risk patients, per guidelines
  • Careful central line and device care
  • Prevention and treatment of streptococcal pharyngitis to limit rheumatic heart disease

Test yourself

Think of the answer, then tap the question to see it.

Which criteria are used to diagnose infective endocarditis?

The modified Duke criteria: major (positive blood cultures with typical organisms, imaging evidence of endocardial involvement) and minor criteria.

Which heart valve is classically affected in people who inject drugs?

The tricuspid valve, often with Staphylococcus aureus and septic pulmonary emboli.

How do Osler nodes differ from Janeway lesions?

Osler nodes are painful nodules on the finger pads (immunological); Janeway lesions are painless macules on palms and soles (embolic).

What should be done before starting antibiotics in suspected endocarditis?

Take at least three sets of blood cultures from separate venepunctures.

What does a new conduction block suggest in aortic valve endocarditis?

Extension of infection into the annulus as a perivalvular abscess, which usually needs surgery.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Infective Endocarditis (StatPearls (NCBI Bookshelf), 2026).

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