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Endocarditis

Q: Against the background of which diseases does secondary prolonged septic endocarditis most frequently develop?

Secondary prolonged septic endocarditis develops on altered valves—in the setting of sclerosis or deformity. Background conditions explicitly indicated for secondary prolonged septic endocarditis include: Atherosclerosis.Syphilis.Congenital heart defects. It is also noted that secondary endocarditis is more prevalent in individuals over 50 years of age.

For medical students2 min readUpdated 2026-10-10

Endocarditis is an inflammatory condition affecting the inner lining of the heart, most commonly involving the heart valves, but it can also extend to the chordae tendineae and mural endocarditis. The disease involves tissue destruction and thrombus formation, rapidly leading to acquired valvular heart disease and severe systemic complications.

Common LocationAortic and mitral valves

Main PathogenStreptococci and enterococci (60–80% of cases)

Risk GroupsPatients with congenital heart disease, IV drug users, hemodialysis patients

Acute CourseAbout 2 weeks (frequently caused by Staphylococcus aureus)

Pathophysiology and Risk Factors

The pathogenesis of infectious endocarditis is driven by immune complex mechanisms and bacteremia (especially in septicopyemia). Inflammation is accompanied by a pronounced hyperergic reaction and can develop on either previously healthy tissues or pre-existing cardiac defects.

Approximately 70% of cases occur on valves previously damaged by infections (syphilis, tuberculosis, tonsillitis, typhoid fever) or rheumatic heart disease. Risk groups also include patients with mitral valve prolapse, hypertrophic obstructive cardiomyopathy, congenital heart defects, as well as individuals suffering from substance abuse or receiving immunosuppressive therapy.

Acute and Subacute Infective Endocarditis

Based on the clinical course, infectious endocarditis is divided into several forms:

Acute bacterial endocarditis. Lasts about two weeks. It typically affects completely healthy (intact) valves in the setting of severe infections. In 80% of cases, the primary causative agent is Staphylococcus aureus. Valve tissues swell, become infiltrated with fibrin, and are invaded by neutrophilic leukocytes.
Subacute infective endocarditis. Lasts up to 6 weeks (occasionally up to 3 months) and accounts for half of all septic endocarditis cases. It frequently causes isolated destruction of the aortic valve. Unlike the acute form, necrotic foci are dominated by mononuclear infiltrates that involve not only the valve leaflets, but also the mural endocarditis and trabeculae.

Prolonged Septic Endocarditis (Sepsis Lenta)

This form has a chronic, relapsing course spanning months or even years. In half of the cases, it is caused by Streptococcus viridans.

Two clinical and morphological variants are distinguished:

Secondary. Develops in individuals over 50 years of age on sclerotic valves (following atherosclerosis or syphilis).
Primary (Chernogubov's disease). Affects unmodified valves in younger patients.

The morphological picture is highly heterogeneous: fresh foci of necrosis and thrombi coexist with older scars. A key histological feature of the prolonged form is the complete absence of neutrophils in the lymphohistiocytic infiltrate.

Non-Infective (Abacterial) Thrombotic Endocarditis

A distinct form, also known as marantic endocarditis, which occurs in severely wasted patients (cachexia) or during severe intoxications.

The process manifests as verrucous or polypoid inflammation. Sterile thrombotic deposits appear along the closure lines of the left ventricular valves (mitral and aortic valves). Microscopy reveals only small clusters of macrophages, monocytes, and fibroblasts beneath these deposits. Signs of marked inflammation are absent, making the term "endocarditis" largely historical in this context.

Morphology and Severe Complications

The classic manifestation of infectious forms is polypous-ulcerative endocarditis. Microbial colonies settle on the edges of destroyed leaflets, and thrombi form. As the process heals, the thrombotic masses undergo organization, bacterial colonies become calcified, and the valve sustains irreversible deformation.

If the disease progresses, severe complications arise:

Destruction: detachment of valve leaflet segments and rupture of chordae tendineae.
Thromboembolic syndrome: detached infected thrombi cause infarctions (e.g., myocardial infarction) and microabscesses in visceral organs.
Immune reactions: development of diffuse proliferative glomerulonephritis and the appearance of characteristic Osler nodes on the skin.

Mnemonic

To quickly recall the cellular infiltrate composition: Acute endocarditis = Abundance of neutrophils. Prolonged endocarditis = Presence of lymphocytes and macrophages (no neutrophils).

Frequently asked questions

What macroscopic types of endocarditis are distinguished in pathology?

Based on the referenced sources, morphological variants of endocarditis include:

Diffuse endocarditis (valvulitis).
Acute verrucous endocarditis — formation of small thrombi ("verrucae") along the closure margin of the valve leaflets.
Recurrent verrucous endocarditis.
Fibroplastic endocarditis.
Polypoid endocarditis — a variant through which non-infective thrombotic endocarditis may present.
Ulcerative endocarditis — a morphological variant of infective septic endocarditis.
Polypous-ulcerative endocarditis — a combination of ulcerative valve defects with thrombotic deposits; prolonged septic endocarditis features massive, dry, friable thrombotic vegetations.

What are Janeway lesions and Lukin-Libman spots, and where do they localize in infective endocarditis?

Lukin-Libman spots in infective endocarditis are described as petechial hemorrhages and foci of necrosis, often accompanied by bleeding.

Localization:

Conjunctiva — including the lower eyelid fornix.
Mucous membranes — including the oral cavity.
Serous membranes.

In the literature, they are associated with a hemorrhagic syndrome driven by vasculitis; petechial hemorrhages on the conjunctiva are noted as a sign of subacute infective endocarditis.

What systemic immune manifestations and symptoms are characteristic of infective endocarditis?

Extracardiac immune manifestations of infective endocarditis are caused by circulating immune complexes and hypersensitivity reactions. Characteristic symptoms include:

Renal involvement — development of immune-complex diffuse proliferative glomerulonephritis (manifesting as proteinuria).
Splenic involvement — splenomegaly (formation of a "septic spleen").
Skin and vascular changes — painful Osler nodes, Janeway lesions, Roth spots on the retina, and petechial rash.
Joint syndrome — arthritis resulting from immune complex deposition on synovial membranes.
Digital changes — clubbing of the fingers ("drumstick fingers") and watch-glass nails.

What changes occur in the spleen and kidneys during thromboembolic syndrome in septic endocarditis?

During thromboembolic syndrome secondary to septic endocarditis, bland (non-suppurative) infarctions occur in the spleen and kidneys.

Kidneys — renal infarcts develop, which subsequently heal to form post-infarction scars.
Spleen — due to its vascular supply pattern (terminal circulation, poor collateral anastomoses), true wedge-shaped infarcts form, which may also be replaced by scar tissue.

These changes result from the detachment of polypoid thrombotic fragments from damaged heart valves and the obstruction of systemic arterial circulation.

Against the background of which diseases does secondary prolonged septic endocarditis most frequently develop?

Secondary prolonged septic endocarditis develops on altered valves—in the setting of sclerosis or deformity.

Background conditions explicitly indicated for secondary prolonged septic endocarditis include:

Atherosclerosis.
Syphilis.
Congenital heart defects.

It is also noted that secondary endocarditis is more prevalent in individuals over 50 years of age.

How does primary prolonged endocarditis differ from secondary endocarditis?

Primary endocarditis (Chernogubov's disease) develops on initially normal valves and is more common in younger individuals. Secondary endocarditis develops on previously altered valves (sclerosis, defects) in individuals over 50 years of age.

Which valves are most commonly affected in the prolonged form?

In 73% of cases, the involvement is isolated, with the aortic valve being the absolute leader (53%). The mitral and tricuspid valves are affected significantly less often.

What is culture-negative endocarditis?

It is a form of infective endocarditis where the causative agent cannot be identified in the blood using standard laboratory methods. It accounts for 10% to 30% of all cases.

Why does glomerulonephritis occur in endocarditis?

It is a manifestation of hypersensitivity. The pathogenesis relies on immune complex mechanisms that drive systemic immune reactions, including renal involvement and the formation of Osler nodes.

Go deeper

Macro- and microscopic features of polypous-ulcerative endocarditis depending on the pathogen (bacteria vs. fungi)
Mechanisms of acquired valvular heart disease formation during the organization of thrombotic masses
Thromboembolic syndrome: pathways of emboli dissemination and development of metastatic abscesses
Chernogubov's disease: historical perspective and modern epidemiological trends
Differential diagnosis of infective versus non-infective thrombotic endocarditis