Pathogenesis

The endothelial lining of the chambers of the heart and blood vessels is resistant to bacterial infection. Endothelial damage however, for example from a "jet lesion" caused by mitral regurgitation, may produce a localised, sterile vegetation of platelets and fibrin. This may then allow circulating micro-organisms to adhere to the valve. Once attached, the bacteria may become encased in fibrin and platelets and multiply rapidly. The causative organisms, sources of infection and pathological consequences of an infected vegetation are; (1)

Infected vegetations occurs along the edges of the heart valves, on the ventricular side for aortic lesions and on the atrial side in mitral or tricuspid lesions. Lesions on the left are most common, accounting for 95% of cases, with the mitral and aortic valves effected equally. Involved valves are often regurgitant prior to infection.

In the subacute form of endocarditis, vegetations may have arisen over a number of years following repeated bacteraemia with an organism of low virulence. The clinical course of this condition is therefore more insidious. This should be contrasted with the more dramatic presentation of acute infective endocarditis, where the infecting organism is more virulent, forming larger vegetations which tend to embolise.

Prosthetic valve endocarditis results from infection of a prosthetic valve. This may occur early, within 60 days of surgery, either during the operation or due to a perioperative bacteraemia e.g. urinary catheterisation.

Right sided endocarditis accounts for 5% of cases and is most often seen in IV drug abusers or the immunosuppressed; invariably the tricuspid valve is affected and the organism is usually a staphylococcus.

1. Kamde SP, Anjankar A. Pathogenesis, diagnosis, antimicrobial therapy, and management of infective endocarditis, and its complications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9572932/