Endocarditis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Altered blood flow around the valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).
Bacteremia
In a healthy individual, a bacteremia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with thrombus, these structures can provide a nidus for bacteria to attach themselves and an infection can be established.
Pathogens
The predominant pathogens in infective endocarditis include the following three gram-positive cocci:
- Viridans group streptococci, although the incidence is decreasing
- Staphylococcus species incidence is increasing
- Enterococcus species
Among the streptococcal viridans group the following are the most common:
- Species: sanguis, oralis (mitis), salivarius, mutans
- Anginosus (milleri) group: intermedius, anginosus, constellatus
- Gemella species: morbillorum, bergeriae,sanguinis, hemolysans, Abiotrophia defectiva
- Granulicatella species: elegans,
Causes of Bacteremia
The bacteremia is often caused by dental procedures, such as a cleaning or extraction of a tooth. It is important that a dentist or a dental hygienist therefore be told of any heart problems before beginning the procedure. Prophylactic antibiotics are administered to patients with certain heart conditions as a precaution.
Another cause of infective endocarditis is a scenario in which an excess number of bacteria enter the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of such bacteria. When a large burden of bacteria are introduced, a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus, but see below for others) is often responsible for infecting a normal valve.
Infections of the tricuspid valve and less frequently the pulmonic valve tend to occur in intravenous drug users given the high pathogen burden from their introduction in the vein. The diseased valve is most commonly affected when there is a pre-existing disease. In rheumatic heart disease this is the aortic valve and the mitral valves, on the left side of the heart.
Complications of Endocarditis
Complications of endocarditis can occur as a result of the locally destructive effects of the infection. These complications include perforation of valve leaflets, perforation of fistula between blood vessels or cardiac chambers, abscesses, embolization and disruption of conduction system.
Histopathological Findings in Non-Infective Endocarditis
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Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved
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Thrombotic Nonbacterial Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.
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Thrombotic Nonbacterial Endocarditis Infected: Gross close-up natural color vegetations or aortic cusps well shown secondarily infected with staphylococci micro is mitral valve also involved see and case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases
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Thrombotic Nonbacterial Endocarditis Infected: Micro low mag H&E large masses staphylococci in vegetation valvulitis is seen gross is mitral valve also involved and case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases