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Symptoms of infective endocarditis
Last reviewed: 06.07.2025
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Infective endocarditis has local and systemic symptoms.
Local changes of infective endocarditis include myocardial abscess formation with tissue destruction and (occasionally) conduction system disturbances (usually with inferior septal abscesses). Severe valvular regurgitation may develop suddenly, causing heart failure and death (usually with mitral or aortic valve involvement). Aortitis may result from contact spread of infection. Infection of prosthetic valves is likely to cause annular abscesses, vegetations leading to obstruction, myocardial abscesses, and mycotic aneurysms manifesting with valve obstruction, dissection, and conduction disturbances.
Systemic symptoms of infective endocarditis are primarily due to emboli of infected material from the cardiac valve and, mainly in chronic infection, immune-mediated reactions. Right-sided lesions usually produce infected pulmonary emboli, which may lead to pulmonary infarction, pneumonia, or empyema. Left-sided lesions may embolize to any organ, especially the kidneys, spleen, and central nervous system. Mycotic aneurysms may form in any major artery. Cutaneous and retinal emboli are common. Diffuse glomerulonephritis may result from immune complex deposition.
Classification of infective endocarditis
Infective endocarditis can have an asymptomatic, subacute, acute course, as well as a fulminant course with a high probability of rapid decompensation.
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Subacute infective endocarditis
Although this pathology is serious, it is usually asymptomatic, progressing slowly (over weeks or months). Often, the source of infection or portal of entry is not detected. PIE is usually caused by streptococci (especially S. viridans, microaerophile, anaerobic and non-enterococcal group D streptococci and enterococci), less commonly by Staphylococcus aureus, Staphylococcus epidermidis and Haemophilus influenzae. PIE often develops on altered valves after asymptomatic bacteremia due to periodontitis, gastrointestinal tract infections and genitourinary system.
Acute infective endocarditis (AIE)
Usually develops suddenly and progresses rapidly (within days). The source of infection or portal of entry is often obvious. If the bacteria are virulent or the bacteremia is massive, normal valves may be affected. AIE is usually caused by Staphylococcus aureus, group A hemolytic streptococcus, pneumococcus, or gonococcus.
Prosthetic valve endocarditis (PVE)
It develops in 2-3% of patients within 1 year after valve replacement, then in 0.5% per year. It is more common after aortic valve replacement than mitral valve replacement, and affects mechanical and bioprosthetic valves equally. Early infections (less than 2 months after surgery) are caused mainly by contamination during surgery with antibiotic-resistant bacteria (eg, Staphylococcus epidermidis, diphtheroids, enteric bacteria, Candida fungi, aspergilli). Late infections are caused mainly by infection with low-virulence microorganisms during surgery or by transient asymptomatic bacteremia. The most frequently detected bacteria are streptococci, Staphylococcus epidermidis, diphtheroids, gram-negative bacilli, Haemophilus influenzae, Actinobacillus actinomycetem comitans, and Cardiobactehum hominis.
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Subacute infective endocarditis
Initially, symptoms are vague: low-grade fever (< 39 °C), night sweats, fatigue, malaise, and weight loss. Cold-like symptoms and arthralgia may occur. Manifestations of valvular insufficiency may be the first finding. Up to 15% of patients initially have fever or a murmur, but eventually almost all develop both. Physical examination findings may be normal or include pallor, fever, changes in a preexisting murmur, or development of a new regurgitant murmur and tachycardia.
Retinal emboli may result in round or oval hemorrhagic retinal lesions with a small white center (Roth spots). Cutaneous manifestations include petechiae (on the upper trunk, conjunctiva, mucous membranes, and distal extremities), painful erythematous subcutaneous nodules on the fingers (Osler nodes), nontense hemorrhagic macules on the palms or soles (Janeway sign), and hemorrhages under the legs. About 35% of patients have CNS involvement, including transient ischemic attacks, stroke, toxic encephalopathy, and (if a mycotic CNS aneurysm ruptures) brain abscess and subarachnoid hemorrhage. Renal emboli may cause hemithoracic pain and occasionally macrohematuria. Splenic emboli may cause left upper quadrant abdominal pain. Long-standing infection may cause splenomegaly or clubbing of the fingers and toes.
Acute infective endocarditis and prosthetic valve endocarditis
Symptoms are similar to PIE, but the course is more rapid. Fever is almost always present initially, creating the impression of severe intoxication, sometimes septic shock develops. Heart murmur is present initially in approximately 50-80% of patients, and ultimately in more than 90%. Sometimes purulent meningitis develops.
Right-sided endocarditis
Septic pulmonary emboli may cause cough, pleuritic chest pain, and occasionally hemoptysis. A regurgitant murmur is typical with tricuspid insufficiency.