Infective endocarditis is a bacterial infection of the inner lining of the heart muscle (endocardium). This inner lining also covers the heart valves, and it is these valves which are primarily affected by infective endocarditis. If the infection remains untreated, multiplying bacteria may eventually destroy the valves and result in heart failure. Bacteria may also form small clots (emboli) which move through the blood and block small arteries. These clots may lodge in various parts of the body including the brain and cause serious damage.
There are several forms of infective endocarditis. Two types that have similar symptoms but are caused by different bacteria are acute bacterial endocarditis and subacute bacterial endocarditis. Acute bacterial endocarditis may affect normal heart valves, while subacute bacterial endocarditis more commonly affects heart valves which have been previously damaged by disease. A third type of infective endocarditis, prosthetic valvular endocarditis (PVE), may develop in patients who have previously had artificial (prosthetic) valve replacement or tissue valve replacement.
Infective endocarditis usually has a very sudden onset. Complaints of low back pain, pain in the joints (arthralgia) or in one or more muscles (myalgia) are common. These symptoms usually appear early in the disease, occasionally as the only initial symptoms. A fever which rarely exceeds 103 degrees fahrenheit is also common. Other symptoms may include night sweats, chills, headache and severe loss of appetite resulting in weight loss.
Heart murmurs are present in over 85% of individuals with infective endocarditis, and 60% have enlarged spleens. Blood or blood cells may be present in the urine (hematuria). Small red or purple spots composed of blood (petechiae) may cover the skin of the upper trunk. There may also be pale, oval spots on the retina of the eye (Roth’s spots) which may hemorrhage. Reddish-brown streaks (splinter hemorrhages) may occur under the nails of the fingers and toes, and small painful nodules may appear in the pads of the fingers or toes (Osler’s nodes). With prolonged infection, clubbing of the fingers may also occur.
In addition to the general symptoms of infective endocarditis, specific symptoms may occur more frequently in different types of the disorder.
Individuals with acute bacterial endocarditis may develop valve abscesses and experience rapid destruction of the heart valves. Painless, reddish-blue skin patches (Janeway lesions) may appear on the palms of the hands and the soles of the feet. The course of acute bacterial endocarditis is very rapid.
Subacute bacterial endocarditis progresses more slowly than acute bacterial endocarditis. Along with the general symptoms of infective endocarditis, there may be coughing or pain in the chest, abdomen, fingers and toes. A sensation of pricking, tingling or creeping of the skin (paresthesia) may be present. An individual with subacute bacterial endocarditis may experience changes in a preexisting heart murmur or develop a new murmur. There may also be a rapid heartbeat (tachycardia).
Individuals with prosthetic valvular endocarditis may develop abscesses on or near the valves. Bacteria may also grow in the heart and obstruct the flow of blood through it. Abscesses may form in the middle muscular layer of the heart (myocardium), or the surgical wound may separate leading to instability of the artificial valve. In addition to the general symptoms of infective endocarditis, there may be a heart murmur from blood flowing backward through a defective valve (regurgitative murmur) or a murmur suggestive of blood outflow obstruction (systolic murmur).
Clots (emboli) resulting from the infective endocarditis may produce serious damage. Symptoms depend upon the location of the clot. In 10% to 30% of individuals with infective endocarditis, clots lodge in the brain and may cause weakness on one side of the body, loss of vision or stroke. Clots may also cause abdominal pain, flank pain, or arterial insufficiency in an extremity. Damage from clots may be temporary or permanent.
Bacteria that cause infective endocarditis reach the heart through the bloodstream. Normally heart valves are highly resistant to the attachment of bacteria and resulting infection. Damage to a heart valve either by scarring (from such disorders as rheumatic heart disease) or trauma may leave the tissue susceptible to colonization by bacteria. As the microorganisms are rapidly swept past the damaged valve, those strains that can most strongly adhere to the surface are the bacteria that have the best chance of producing infective endocarditis.
Over 50% of infective endocarditis cases are associated with heart damage resulting from rheumatic fever. Other disorders which may damage the valves include congenital heart disease, syphilis infection and surgical heart valve replacement. Surgical procedures on the mouth, on the reproductive organs, or on the stomach and intestines (gastrointestinal tract) often risk the spread of bacteria. There is a even higher risk of introducing bacteria into the bloodstream through major heart surgery.
Acute bacterial endocarditis is most often caused by the bacteria Staphylococcus aureus. It may also be caused by group A Streptococcus and rarely by Brucella and Listeria. Approximately one-third of individuals with staphylococcal endocarditis will have a history of a preceding staphylococcal infection, with symptoms of endocarditis starting within two weeks of the initial infection.
Subacute bacterial endocarditis is usually caused by streptococcal bacteria and accounts for nearly two-thirds of reported cases of infective endocarditis. Subacute bacterial endocarditis usually develops on damaged valves after dental surgery involving infected gums, reproductive or urinary (genitourinary tract) surgery or operations on the gastrointestinal tract. A history of a preceding dental, genital or urologic procedure is common. Symptoms usually begin within two weeks following the procedure, but diagnosis is often delayed. A previous history of heart disease is present in approximately 80% of individuals with subacute bacterial endocarditis.
Prosthetic valvular endocarditis (PVE) develops in 2% to 3% of individuals in the year following artificial (prosthetic) valve placement, occasionally resulting from organisms accidentally implanted during surgery. The number of reported cases of prosthetic valvular endocarditis is highest with artificial aortic valve replacement. These infections frequently result from contamination during an operation. Approximately half of the reported cases are caused by staphylococcus.
Infective endocarditis appears to be approximately twice as common in men as women. In the past, disease onset occurred at an average age of 35. However, since antibiotics have become available, the average age at onset has increased to over 50 years.
Infective endocarditis most frequently affects individuals with heart valve damage due to rheumatic fever or birth defects of the heart (congenital heart defects) affecting heart chambers or valves. The condition is also common among those with artificial heart valves or changes of the valves due to aging. In individuals who have undergone surgical heart valve replacement, the risk of such infection appears to be highest within the first year after the procedure. Although the risk subsequently declines, it remains slightly higher than normal.
An increased risk of infective endocarditis is also associated with other invasive treatment and diagnostic procedures. In addition, because intravenous drug users may introduce bacteria directly into the bloodstream with unsterilized syringes or needles, they have an increased susceptibility to the condition.
Because particular procedures carry a risk of introducing bacteria into the bloodstream, preventive (prophylactic) antibiotic therapy is provided for certain individuals – e.g., those with known heart valve abnormalities, congenital heart defects, or artificial heart valves – before they undergo any surgical, dental, or invasive diagnostic procedures. Therefore, it is advised that individuals with such risk factors for infective endocarditis inform their physicians, dentists, or other health care professionals before undergoing such procedures.
Without prompt, appropriate treatment, infective endocarditis may result in life-threatening complications. Thus, early diagnosis and aggressive therapy are critical for successful treatment. Therapeutic measures typically include infusion of high doses of appropriate antibiotic drugs. Such therapy is often necessary for approximately two to four weeks or, in some cases, up to six or eight weeks. The specific drugs or drug combinations used may depend upon the bacterium responsible for the infection and other factors (e.g., bacterial strain resistance to certain antibiotics). Such drug or drug combination therapies may include the antibiotics penicillin, streptomycin, gentamicin, vancomycin, oxacillin, or ceftriaxone; the semisynthetic penicillin ampicillin; or the antibacterial medications nafcillin and rifampin. In some affected individuals, such therapy is not sufficient to control the infection, particularly for those with prosthetic valvular endocarditis. In such cases, heart surgery may be required, possibly on an emergency basis, to repair or replace damaged valves and eliminate the infection. Additional treatment is symptomatic and supportive.
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