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What is endocarditis Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves (native or prosthetic valves). Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or even the surfaces of intracardiac devices

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Endocarditis is characterized by a prototypic lesion, the vegetation, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify. There are several ways to classify endocarditis. The simplest classification is based on etiology: either infective or non- infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms.

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Endocarditis begins as endothelial damage and sterile surface microthrombus, which, in the absence of bacteremia, regresses or grows into macrothrombi (noninfectious endocarditis). Malformed stenotic or regurgitant valves Malformed stenotic valves, or especially regurgitant valves, are predisposed to endocarditis. In the presence of bacteremia or fungemia, even transient or those with low microbe counts, microthrombi become infected, by adhesion and colonization of the thrombotic surfaces. Growth of organisms results in an inflammatory response, with neutrophil infiltration, enlargement of the thrombus, recruitment of matrix metalloproteinases (MMPs), and eventual destruction of collagen and cusp perforation. In approximately 25% of patients, however, neither structural valve abnormalities nor predisposing conditions are evident. Valve abnormalities, disease, prosthesis, and previous surgery Congenital valve abnormalities, acquired valve disease, prostheses, and previous cardiac surgery for structural congenital heart disease increase the risk for endocarditis and are indications for antibiotic prophylaxis for dental and other invasive procedures. In nosocomial endocarditis, bacteremic conditions are present in nearly 40% of cases and include intravenous drug abuse, hemodialysis, catheterizations, and intravascular devices

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Infective endocarditis Since the valves of the heart do not receive any dedicated blood supply, defensive immune mechanisms (such as white blood cells) cannot directly reach the valves via the bloodstream. If an organism (such as bacteria) attaches to a valve surface and forms a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications on treatment, since drugs also have difficulty reaching the infected valve. Normally, blood flows smoothly past these valves. If they have been damaged (from rheumatic fever, for example) the risk of bacteria attachment is increased

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Rheumatic fever is common worldwide and responsible for many cases of damaged heart valves. Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion, and shortening and thickening of the tendinous cords. The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Heart complications may be long-term and severe, particularly if valves are involved. While rheumatic fever since the advent of routine penicillin administration for Strep throat has become less common in developed countries, in the older generation and in much of the less- developed world, valvular disease (including mitral valve prolapse, reinfection in the form of valvular endocarditis, and valve rupture) from undertreated rheumatic fever continues to be a problem.

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Subacute bacterial endocarditis Also called ( endocarditis lenta ) is a type of endocarditis (more specifically, infective endocarditis). It is usually caused by a form of streptococci viridans bacteria that normally live in the mouth and throat (Streptococcus mutans, mitis, sanguis or milleri). Other strains of streptococci (bovis and equines) can also cause subacute endocarditis, usually in patients who have a form of gastrointestinal cancer. Additional causes are Enterococci (urinary tract infections) and coagulase negative staphylococci such as Staphylococcus epidermidis (skin).

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Diagnosis and Prognosis Osler's nodes as well as Roth's spots can indicate this condition. Nail clubbing is also often seen in subacute endocarditis. Underlying structural valve disease is usually present in patients before developing subacute endocarditis. It is less likely to lead to septic emboli than is acute endocarditis, but subacute endocarditis has a relatively slow process of infection and, if left untreated, can worsen for up to one year before it is fatal. In cases of subacute bacterial endocarditis, the causative organism (streptococcus viridans) needs a previous heart valve disease to colonize and cause such disease.

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On the other hand, in cases of acute bacterial endocarditis, the organism can colonize on the healthy heart valve, causing the disease. The standard treatment is with a minimum of four weeks of high-dose intravenous penicillin with an aminoglycoside such as gentamicin. The use of high-dose antibiotics is largely based upon animal models. Leo Loewe of Brooklyn Jewish Hospital was the first to successfully treat subacute bacterial endocarditis with penicillin. Loewe reported seven cases in 1944.

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Roths spot

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Non-infective endocarditis Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves. As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps. Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body. NBTE usually occurs during a hypercoagulable state such as system wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters. NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis

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Another form of sterile endocarditis, is termed Libman- Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations. These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.

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Causative organisms The organisms responsible for most cases of infectious endocarditis are gram-positive cocci: streptococci and, increasingly, staphylococci. The most common microbial infection is staphylococcus. Hospital-acquired infection is often associated with hemodialysis, prosthetic valvular infection, malignancies, and vascular interventions. Some cases of culture-negative endocarditis are caused by fastidious gram-negative organisms of the Haemophilus parainfluenzae, Actinobacillus, Actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae (HACEK) group, which constitutes approximately 1-3% of cases of community-acquired endocarditis on native and prosthetic valves, and may have a relatively good prognosis.

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Organisms causing community-acquired endocarditis include the following: Staphylococcus aureus (30-50%; minority, methicillin-resistant Staphylococcus aureus [MRSA]) Alpha-hemolytic (viridans) streptococci (10-35%) Enterococcus (5-10%) Culture negative (5-30%) Fungi (< 5%) Staphylococcus epidermidis (coagulase negative; < 5%) Others (eg, Escherichia coli, Klebsiella, Corynebacterium; < 5%)

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Organisms responsible for nosocomial endocarditis include the following: S aureus (60-80%; majority, MRSA) Alpha-hemolytic streptococci (< 5%) Enterococcus (5%) Culture negative (5%) Fungi (10%) S epidermidis (coagulase negative; < 5%) Others (eg, E coli, Klebsiella, Corynebacterium; 5-10%) The rate of culture-negative endocarditis varies from 7% to 33% and is increased in community-acquired infections because of antibiotic treatment before diagnosis. No association exists between culture negativity and underlying etiology or risk factors. If a full work-up is performed at a tertiary reference center, including serology and culture for esoteric organisms and polymerase chain reaction (PCR), an etiology is found in over 75% of cases of endocarditis with an initial negative culture. The most common organisms are C burnetii and Bartonella species.

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SIGNS AND SYMPTOMS Fever Chills Sweating Malaise Weakness Anorexia weight loss Splenomegaly flu like feeling cardiac murmur heart failure patechia of anterior trunk Janeway's lesions

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Diagnosis Examination of suspected infective endocarditis includes a detailed examination of the patient, complete history taking, and especially careful cardiac auscultation, various blood tests, ECG, cardiac ultrasound (echocardiography). In the overall analysis of blood revealed the typical signs of inflammation (increased erythrocyte sedimentation rate, leukocytosis). It is also necessary to sow twice venous blood in order to identify the specific pathogen (this requires two samples of blood). Negative blood cultures, however, does not exclude the diagnosis of infective endocarditis. The decisive role is played by echocardiography in the diagnosis (through the anterior chest wall or transesophageal), with which you can reliably establish the presence of microbial vegetation, the degree of valvular and violations of the pumping function of the heart

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TREATMENT Treatment of infectious endocarditis includes antibiotics, and, possibly, surgery if the valve is irreversibly insufficient. Surgical options include replacement, and repair if possible. In general, between 14% and 37% of cases require surgery.

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PROGNOSIS The overall mortality of infectious endocarditis is approximately 20-25%, and it is increased with advanced patient age, left- sided disease, methicillin-resistant S aureus (MRSA) infection, and chronic renal failure. For staphylococcal endocarditis, mortality is associated with age 60 years or older, female sex, community- acquired infection, absence of heart murmur, presence of congestive heart failure, and central nervous system involvement. The mortality rate of MRSA endocarditis in hemodialysis patients is as high as 90%. The long-term prognosis of patients with negative blood culture infective endocarditis has been found to be similar to that of patients with positive blood culture infective endocarditis across all age ranges.

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REFERENCES Fonager K, Lindberg J, Thulstrup AM, Pedersen L, Schnheyder HC, Srensen HT. Incidence and short-term prognosis of infective endocarditis in Denmark, 1980-1997. Scand J Infect Dis. 2003;35(1):27-30. Walpot J, Blok W, van Zwienen J, Klazen C, Amsel B. Incidence and complication rate of infective endocarditis in the Dutch region of Walcheren: a 3-year retrospective study. Acta Cardiol. Apr 2006;61(2):175-81. Burke AP, Kalra P, Li L, Smialek J, Virmani R. Infectious endocarditis and sudden unexpected death: incidence and morphology of lesions in intravenous addicts and non-drug abusers. J Heart Valve Dis. Mar 1997;6(2):198-203. Watanakunakorn C, Burkert T. Infective endocarditis at a large community teaching hospital, 1980-1990. A review of 210 episodes. Medicine (Baltimore). Mar 1993;72(2):90- 102. Chen SC, Dwyer DE, Sorrell TC. A comparison of hospital and community-acquired infective endocarditis. Am J Cardiol. Dec 1 1992;70(18):1449-52.

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