Infective endocarditis: susceptibility, vegetations and tissue injury
THE CONTEXT
Endothelial damage favours infection during bacteraemia, followed by vegetation formation, local destruction and systemic complications.
Susceptible hearts and lesions
•
Infective endocarditis usually occurs at sites of pre-existing endocardial damage, but aggressive organisms such as Staphylococcus aureus can infect a previously normal heart.
•
Staphylococcal endocarditis of the tricuspid valve is a common complication of intravenous drug use.
•
High-pressure jets can damage endocardium and predispose to infection in ventricular septal defect, mitral regurgitation and aortic regurgitation, even when these lesions are haemodynamically insignificant.
•
A large atrial septal defect is a low-pressure lesion with minimal endocarditis risk at its site, despite potentially being haemodynamically important.
Vegetation formation
•
Damaged endothelium attracts platelet and fibrin deposits that can be colonised by blood-borne organisms during bacteraemia.
•
Avascular valve tissue and fibrin–platelet aggregates protect proliferating organisms from host defences.
•
Vegetations contain organisms, fibrin and platelets. They can enlarge enough to obstruct flow, detach and embolise.
Local and systemic complications
•
Infection destroys adjacent tissue and may form abscesses. Tissue distortion, cusp perforation or chordal disruption can cause or worsen valve regurgitation.
•
Emboli can cause stroke, myocardial infarction or abdominal organ infarction.
•
Vasculitis, skin lesions and glomerulonephritis may result from emboli or immune complex deposition.
•
Mycotic aneurysms may develop in arteries at sites of infected emboli.
Microbiology
•
Over half of cases are caused by Staphylococcus aureus or oral streptococci.
•
Viridans streptococci, including Streptococcus mitis and Streptococcus sanguis, are oral commensals that can enter the bloodstream during chewing or tooth-brushing.