2402
See ((Endocarditis))
Native-valve infective endocarditis incidence is approximately 2-10 cases per hundred thousand person-years.
It is initiated by injury to the valvular endothelium or endocardium that exposes subendothelial collagen and other matrix molecules to which platelets, and fibrin adhere and form a micro thrombotic lesion called a sterile vegetation.
Circulating bacteria in the bloodstream can subsequently bind to and colonize this lesion and the bacteria can replicate stimulating further platelet and fibrin deposition to form an infected vegetation that is the hallmark of infective endocarditis.
Vegetations are loaded with bacteria at high density and that promotes high-grade bacteremia and further growth of the vegetation when it becomes friable and readily fragments into the circulation.
Clinical features of infective endocarditis are due to bacterial densities, high-grade bacteremia, growth of the vegetation, increasing friability and fragmentation into the circulation.
Infective endocarditis complications: valvular disease, paravalvular extension of infection, heart failure, microvascular and large vessel embolization, metastatic infection to target organs, and immunologic manifestations of hypocomplementary glomerulonephritis, development of false positive rheumatoid factor, anti-neutrophil antibodies and syphilis.
Pre-disposing to infective endocarditis are congenital diseases and acquired valvular diseases.
Rheumatic heart disease is the most common predisposing condition for infective endocarditis in developing countries, and is uncommon in developed countries, were most frequent predisposing cardiac conditions or degenerative valvular disease is, congenita valvular abnormalities, and intracardiac devices.
Non-cardiac risk factors fot infective endocarditis include poor dentition, intravenous drug use, hemodialysis, chronic liver disease, diabetes, immunosuppression, neoplastic disease, and indwelling intravascular devices.
Fever and heart murmur are the two major features of infective endocarditis, and are present in approximately 90% and 75% of patients, respectively.
Infective endocarditis may present acutely with a progressive of course with CHF, stroke, systemic with pulmonary embolization, severe sepsis for septic shock,
Infective endocarditis may present subacute with non-specific symptoms such as low-grade fever, malaise, chills, sweats, dyspne, arthralgias, back pain, weight loss manifesting over weeks or sometimes months.
Micro embolic or immunologic phenomena such as splinter hemorrhage, conjunctival hemorrhage, Osler nodes(distal vascular lesions of the fingers and toes), Janeway lesions which are vasculitic lesions of the palms and soles, and rub spots with your hemorrhagic read the lesions, present in 5-10% of patients.
Worldwide, gram-positive bacteria count for approximately 80% of cases of native valve infective endocarditis.
The bacteria include: Staphylococcus aureus in 30-40%, streptococci in 30-40%, streptococci viridans approximately 20% and other streptococci approximately 15%, and enterococci about 10%.
Coagulase Negative staphylococci, which is a common pathogen in prosthetic valve infective endocarditis, or uncommon in need of valve infective endocarditis.
HACEK species, fungi, polymicrobial infection, and aerobic gram-negative bacilli are found in 5% of cases.