[1] Signs and symptoms may include fever, small areas of bleeding into the skin, heart murmur, feeling tired, and low red blood cell count.

[1] Improved diagnosis and treatment options have significantly enhanced the life expectancy of patients with infective endocarditis, particularly with congenital heart disease.

[7] Prosthetic valve endocarditis is commonly caused by Staphylococcus epidermidis as it is capable of growing as a biofilm on plastic surfaces.

[25] These bacteria are present in the normal oral flora and enter the bloodstream due to disruption of tissues in the mouth when dental surgical procedures are performed (tooth extractions) or genitourinary manipulation.

Similarly, HACEK organisms are a group of bacteria that live on the dental gums and can be seen with people who inject drugs who contaminate their needles with saliva.

[26] Viridans alpha-hemolytic streptococci, that are present in the mouth, are the most frequently isolated microorganisms when the infection is acquired in a community setting.

Cutibacterium spp., which are normal skin flora, have been responsible for infective endocarditis, preferably in patients with prosthetic heart valves, in rare cases leading to death.

It forms biofilms around thick-walled resting structures like prosthetic heart valves and additionally colonizes and penetrates endothelial walls.

[37] Risk factors for infective endocarditis are based on the premise that in a healthy individual, bacteremia (bacteria entering the bloodstream) is cleared quickly with no adverse consequences.

Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve.

[38] Specifically, the damaged part of a heart valve forms a local blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).

As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply.

This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis.

[11] For example, the sensitivity of the Duke criteria for detecting infective endocarditis decreases when prosthetic heart valves are present.

[11] As the Duke criteria rely heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among people who inject drugs[40][41][42] and among non drug-abusing patients.

The blood tests C reactive protein (CRP) and procalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis.

[11] Guidelines support the initial use of TTE over TEE in people with abnormal blood cultures, a new heart murmur, and suspected infective endocarditis.

[11] TEE is the preferred initial form of imaging in people with suspected infective endocarditis who have a moderate to high pretest probability of infective endocarditis, including people with prosthetic heart valves, blood cultures growing Staphylococcus, or have an intracardiac device (such as a pacemaker).

There is, however, insufficient evidence to support whether antibiotics are effective or ineffective at preventing IE when given prior to a dental procedures in people at high risk.

[55] In some countries e.g. the US, high risk patients may be given prophylactic antibiotics such as penicillin or clindamycin for penicillin-allergic people prior to dental procedures.

[11] In acute endocarditis, due to the fulminant inflammation, empirical antibiotic therapy is started immediately after the blood has been drawn for culture to clarify the bacterial organisms responsible for the infection.

This usually includes vancomycin and ceftriaxone IV infusions until the infecting organism is identified and the susceptibility report with the minimum inhibitory concentration becomes available.

[57] In cases of subacute endocarditis, where the person's hemodynamic status is usually stable, antibiotic treatment can be delayed until the causative microorganism can be identified.

[58] Relatively resistant strains of viridans group streptococci and Streptococcus bovis are treated with penicillin or ceftriaxone along with a shorter two-week course of an aminoglycoside during the initial phase of treatment.

[58] Some people may be treated with a relatively shorter course of treatment[58] (two weeks) with benzyl penicillin IV if infection is caused by viridans group streptococci or Streptococcus bovis as long as the following conditions are met: Additionally, oxacillin-susceptible Staphylococcus aureus native valve endocarditis of the right side can also be treated with a short 2-week course of a beta-lactam antibiotic such as nafcillin with or without aminoglycosides.

[24] However, adult patients with congenital heart disease can have relatively lower mortality down to 5% due to younger age, right-sided endocarditis and management by multidisciplinary teams.

It is no disparagement to the many skilled physicians who have put their cases upon record to say that, in fully one-half the diagnosis was made post mortem.Lazare Riviére first described infective endocarditis affecting the aortic valve in 1616.

[11] In 1806, Jean-Nicolas Corvisart coined the term vegetation to describe collections of debris found on a mitral valve affected by infective endocarditis.

[11] In 1909, William Osler noted that heart valves that experienced degeneration and were sclerotic or poorly functioning had a higher risk of being affected.

[11] Later, in 1924, Emanuel Libman and Benjamin Sacks described cases of vegetative endocarditis that lacked a clear microbial origin and were often associated with the autoimmune condition systemic lupus erythematosus.