Pathogenesis of infective endocarditis

(A) Pathogens gain (transient) access to the bloodstream as a result of healthcare procedures, via a dentogen pathway, or by intravenous drug use.
(B) Pathogens can rapidly (within minutes) adhere to an initially sterile platelet-fibrin nidus on a valve surface and become secondarily infected by micro-organisms.
(C) Some pathogen species, such as Staphylococcus aureus, obtain intracellular access to the valve endothelium, which adds to inflammation and aggressive tissue destruction by the pathogens.
(D) Proliferation of the pathogens on and in the endothelium leads to maturation of the vegetation on the valve.
(E) Consequently, embolization of vegetation particles and systemic haematogenous spreading of the pathogens often occurs, leading to complications such as ischaemic stroke, cerebral haemorrhage, meningitis or meningeal reaction, brain abscess, and mycotic aneurysm.