Infective endocarditis is an infection of the endocardium, usually (usually streptococci or staphylococci) or fungi by bacteria. It causes fever, heart murmur, petechiae, anemia, embolic phenomena and endocardial vegetations. The vegetation can lead to heart valve insufficiency or -obstruktion to a Myokardabszess or mycotic aneurysm. The diagnosis requires detection of pathogens in the blood and usually an echocardiogram. The treatment consists of a long-term antibiotic therapy. Sometimes a surgical intervention is necessary.
Endocarditis can occur at any age. Men are affected twice as often as women. Particularly at risk are drug addicts with iv Drug abuse and immunocompromised patients.
Infective endocarditis is an infection of the endocardium, usually (usually streptococci or staphylococci) or fungi by bacteria. It causes fever, heart murmur, petechiae, anemia, embolic phenomena and endocardial vegetations. The vegetation can lead to heart valve insufficiency or -obstruktion to a Myokardabszess or mycotic aneurysm. The diagnosis requires detection of pathogens in the blood and usually an echocardiogram. The treatment consists of a long-term antibiotic therapy. Sometimes a surgical intervention is necessary. Endocarditis can occur at any age. Men are affected twice as often as women. Particularly at risk are drug addicts with iv Drug abuse and immunocompromised patients. Etiology The healthy heart is relatively resistant to infections. Bacteria and fungi do not adhere so easily to the surface of the endocardium, normal blood flow prevents colonization of the endocardial structures. Thus two factors for endocarditis typically needed: a predisposing abnormality of the endocardium microorganisms in the bloodstream (bacteremia) rarely causes massive bacteremia or particularly virulent pathogen endocarditis of healthy heart valve. Endocardial factors Endocarditis usually affects the heart valves. Common predisposing factors are congenital heart defects, rheumatic heart valve disease, bicuspid aortic valve or calcified, mitral valve prolapse, hypertrophic cardiomyopathy and a previous endocarditis. A particular risk is posed valve prostheses. Occasionally, infections of Gefäßwandthromben, ventricular septal defects or patent ductus arteriosus. The actual source of infection is usually a sterile vegetation of fibrin and platelets, which arises when damaged endothelial cells release tissue factor. Infective endocarditis occurs most often on the left side (mitral or aortic valve). In 10-20% of cases the right heart (tricuspid or pulmonary valve) is affected. For i.v. Drug addicts, the incidence of right-sided with about 30-70% especially hoch.Mikroorganismen may originate the microorganisms that cause an infection of the endocardium, from a distant focus of infection such as a skin abscess, or inflamed gums infectious or Harnsweginfekt. The obvious entry points for pathogens are central venous catheter or injection needle marks. In almost all implanted foreign materials (eg. B. ventriculoperitoneal shunt or prosthesis) the risk of bacterial colonization and thus a potential source of infection for a bacteremia with subsequent endocarditis there. Endocarditis can also develop from an asymptomatic bacteremia, which occurs typically during an invasive dental, medical or surgical procedure. Even the brushing and chewing can cause bacteremia (usually by Streptococcus viridans) in gingivitis. The causative agent are different depending on the infection, bacteremia and source of the risk factors of the host (eg. B. i.v. drug abuse), but the total endocarditis caused in 80-90% of cases by streptococci and Staphylococcus aureus. Enterococci, Gram-negative bacteria, HACEK-organisms (Haemophilus spp, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and King kingae) and fungi cause most of the remaining cases. Why streptococci and staphylococci often to vegetation stick and gram-negative aerobic bacteria rather rare, is still unclear. It is possible that the ability of S. aureus to adhere to fibronectin and produce the ability of Streptococcus viridans dextran, play a role. Have the microorganisms colonized vegetation, they are covered by a layer of fibrin and platelets, so that neutrophils, immunoglobulins and complement can not attack and thus the body’s immune system is blocked. Pathophysiology Endocarditis has local and systemic effects. Local effects to the local effects counts the formation of Myokardabszessen, which is associated with tissue damage and sometimes with conduction disorders (i. D. At low R. Septumabzessen). In addition (R. i. D. Caused by mitral or Aortenklappenläsionen) may develop severe valvular insufficiency and heart failure resulting in death lead abruptly. A spreading infection can lead to aortitis. Infection of prosthetic valves are particularly dangerous and can cause Klappenringabszesse, obstruction due to large vegetations, Myokardabszesse and mycotic aneurysms. The latter are formed by flaps obstruction, dehiscence and Reizleitungsstörungen.Systemische effects of becoming systemic implications of the endocarditis primarily due to emboli from infected valve material and, v. a. in chronic infections, immune-mediated diseases. Embolization right typically leads to septic pulmonary embolism with possible pulmonary infarction, pneumonia or empyema. Left-sided lesions can embolize in all tissues, but relate particularly common kidney, spleen and central nervous system. In all major arteries mycotic aneurysm can form. Even skin and retinal emboli are common. As a result, the immune complex deposits occur in some cases a diffuse glomerulonephritis. Classification Infective endocarditis may extend indolent-subacute or acute fulminant and with a relatively high potential for rapid decompensation. Although the subacute bacterial endocarditis (SBE) is an aggressive form, but usually develops slowly and progresses slowly over weeks or months. Often no source of infection or portal of entry is evident. The SBE will in most cases by streptococci (especially Streptococcus viridans, microaerophilic, anaerobic and nichtenterokokkale D streptococci and enterococci) gives less frequently are infections with S. aureus, Staphylococcus epidermidis, Gemella morbillorum, Abiotrophia defectiva (formerly Streptococcus defectivus) Granulicatella sp. and Haemophilus spp. THe SBE often develops at altered heart valves aysmptomatische bacteremia due to periodontal infections or infections of the gastrointestinal or genitourinary tract are already damaged. Acute bacterial endocarditis (ABE) suddenly develops normally and is progressing rapidly within days. The source of infection or portal of entry is usually clearly visible. In virulent bacteria or massive bacterial contamination, the ABE can also develop in healthy heart valves. Cause are usually infections with S. aureus, hemolytic group A streptococci, pneumococci or gonococci. Klappenprothesenendokarditis develops in 2-3% of patients within the first year after valve replacement and 0.5% / year in the following years. The PVE is common after aortic valve as mitral valve replacement. Mechanical and biological prosthetic valves are equally affected. Early onset infections (