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Endocarditis infecciosa
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Pathogenesis of infective endocarditis (see figure next slid) A- Pathogens gain (transient) access to the bloodstream as a result of health-care procedures, via a dentogen pathway, or by intravenous drug use. B- Pathogens can rapidly (within minutes) adhere via platelet fibrin deposition ('nonbacterial thrombotic endocarditis') to a mechanically injured valve surface (pre-existing valvular disease) or to an inflamed valve surface (without pre-existing valve disease). 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.
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Werdan, K. et al. (2013) Mechanisms of infective endocarditis: pathogen–host interaction and risk states Nat. Rev. Cardiol. doi:10.1038/nrcardio.2013.174 Figure 1 Pathogenesis of infective endocarditis
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Sub-acute Endocarditis Persistent fever Constitutional symptoms New signs of valve dysfunction Heart failure Embolic Stroke Peripheral arterial embolism Other features
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