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Infective endocarditis is bacterial or rarely fungal infection of the heart valves. Infection of the extracardiac endothelium is called “endarteritis” and can cause disease that is clinically similar to endocarditis.
One of the most common predisposing aspects for infective endocarditis is the presence of structurally abnormal heart valves. Consequently, patients with a history of rheumatic or congenital heart disease, mitral valve prolapse with audible murmurs, prosthetic heart valves, or a history of previous endocarditis are at increased risk of developing infective endocarditis.
Infection involves the left side of the heart (mitral and aortic valves), except in patients using injection drugs or, less commonly, in patients with valve damage from a pulmonary artery (Swan-Ganz) catheter, which contains the virus. The right side of the heart (tricuspid or pulmonary valve) may occur.
Gram-positive bacteria, including Streptococcus viridans, S. aureus, and enterococci, are the most common infectious agents causing native valve infective endocarditis. The specific bacterial species causing endocarditis can be predicted based on host factors.
Injection drug users commonly introduce S. aureus into the bloodstream when unsterilized needles are used or the skin is not adequately cleansed before injection. Recent dental work is predisposed to transient bacteremia with normal oral flora, especially S. viridans, with subsequent endocarditis.
Genitourinary tract infections with enterococci can cause bacteremia and subsequent heart valve damage. Patients with prosthetic heart valves are at increased risk of infective endocarditis due to skin flora such as S. epidermidis or S. aureus.
Before the availability of antibiotics, infective endocarditis was a progressively fatal disease. Even with antibiotics, endocarditis has a mortality rate of up to 25%, and definitive treatment often requires prolonged antibiotic administration and immediate surgery to replace infected heart valves.
Several hemodynamic factors predispose patients to endocarditis: (1) high-velocity jet flow that creates turbulent blood flow, (2) flow from a high-pressure to a low-pressure chamber, and (3) relatively narrow orifice separation. Two chambers that create a pressure gradient.
Ulcers of infective endocarditis develop at low pressure on the valve surfaces in the cardiac chambers (eg, on the ventricular surface of an abnormal aortic valve and on the atrial surface of an abnormal mitral valve).
Damaged endothelium due to turbulent blood flow results in exposure to extracellular matrix proteins, which promote the accumulation of fibrin and platelets, leading to the formation of a sterile flora (nonbacterial thrombotic endocarditis or marentic endocarditis). Infective endocarditis occurs when microorganisms are deposited on sterile flora during bacteremia.
Not all bacteria adhere equally well to these websites. For example, E coli, a frequent trigger of bacteremia, is rarely implicated as a trigger of endocarditis. Conversely, virulent organisms such as S. aureus can invade intact endothelium, causing endocarditis in the absence of preexisting valvular abnormalities.
Once infected, these flora proliferate through further secretion of platelets and fibrin, providing sanctuary to the bacteria from host defense mechanisms, for example polymorphonuclear leukocytes and complement. As a result, once the virus takes hold, the infected plant continues to grow largely undisturbed.
Prolonged use (4-6 weeks) of bactericidal antibiotics is required to penetrate the plants and cure the disease. Bacteriostatic antimicrobial agents, which inhibit but do not kill bacteria, are inadequate.
Surgical excision of the infected valve is sometimes necessary for cure, especially in infections with gram-negative bacilli or fungi, resulting in mechanical dysfunction from the valve with congestive center failure, or in prosthetic valve infections. Infective endocarditis is characterized by persistent bacteremia, which stimulates both the humoral and cellular immune systems.
A variety of immunoglobulins are expressed, resulting in immune complex formation, elevated serum levels of rheumatoid arthritis, and nonspecific hypergammaglobulinemia. Immune complex deposition along the renal glomerular basement membrane can lead to acute glomerulonephritis and renal failure.
Infective endocarditis is a multisystem disease characterized by proteinuria. For these reasons, signs may be nonspecific and the diagnosis may not initially be included in the differential diagnosis. Skin findings suggestive of endocarditis include Osler’s nodes, painful papules about the pads of the fingers and toes that are thought to be secondary to immune complex deposition;
and Janeway lesions, painless hemorrhagic lesions on the palms and soles due to septic microemboli. Signs and symptoms of endocarditis can be acute, subacute, or chronic. Clinical manifestations mainly reflect hemodynamic changes from (1) valvular damage; (2) end-organ symptoms and indicators from septic emboli (right-sided emboli to the lungs, left-sided emboli to the brain, spleen, kidneys, and extremities); (3) end-organ symptoms and signs of immune complications; and (4) persistent bacteremia with metastatic seeding of the virus (abscesses or septic joints). Death is usually due to hemodynamic collapse or septic emboli to the CNS, resulting in brain abscess or mycotic aneurysm and intracerebral hemorrhage.
Risk factors for fatal outcome include left valvular disease, bacterial etiology other than S. viridans, medical comorbidities, complications from endocarditis (congestive heart failure, valve ring abscess, or embolic disease), and, in one study, valvular surgery without medical management.
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