Development mechanisms and risk factors
The pathogenesis of infectious lesions is based on immune complex mechanisms and bacteremia (especially in septico-pyemia). Inflammation proceeds with a pronounced hyperergic reaction and can develop both in normal tissues and in the presence of pre-existing defects.
About 70% of cases occur on valves previously damaged by infections (syphilis, tuberculosis, tonsillitis, typhus) or rheumatic fever. The risk group also includes patients with mitral valve prolapse, hypertrophic obstructive cardiomyopathy, congenital heart defects, as well as individuals suffering from alcoholism, substance abuse, or receiving immunosuppressive therapy.
Acute and subacute infective endocarditis
Depending on the duration of the clinical course, several forms of the infectious process are distinguished:
- 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. The valve tissues swell, become infiltrated with fibrin and infiltrated by neutrophil 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. In contrast to the acute form, the necrosis foci are dominated by mononuclear infiltrates that involve not only the cusps but also the mural endocardium and trabeculae.
Protracted septic endocarditis (sepsis lenta)
This form has a chronic course, recurring over months and years. In half of the cases, it is caused by Streptococcus viridans.
Two clinico-morphological variants are distinguished:
- Secondary. Develops in individuals over 50 years of age against the background of sclerotic valves (following atherosclerosis or syphilis).
- Primary (Chernogubov's disease). Affects unchanged valves in younger patients.
The morphological picture is highly variegated: fresh foci of necrosis and thrombi coexist with old scars. A crucial histological hallmark of the protracted form is the complete absence of neutrophils in the lymphohistiocytic infiltrate.
Non-infective (non-bacterial) thrombotic endocarditis
A special form, also known as marantic endocarditis. It occurs in severely emaciated patients (cachexia) or in cases of severe intoxications.
The process proceeds as a verrucous or polypoid inflammation. Sterile thrombotic deposits appear on the margins of the left ventricular cusps (mitral and aortic valves). Microscopy reveals only small clusters of macrophages, monocytes, and fibroblasts beneath them. Signs of pronounced inflammation are absent, so the term "endocarditis" here is largely historical.
Morphology and severe complications
The classic manifestation of infectious forms is polypoid-ulcerative endocarditis. Microbial colonies settle on the margins of the destroyed cusps and thrombi are formed. As the process subsides, the thrombotic masses undergo organization, bacterial colonies become calcified, and the valve becomes irreversibly deformed.
If the process progresses, severe complications arise:
- Destruction: detachment of part of the cusps and rupture of chordae tendineae.
- Thromboembolic syndrome: detached infected thrombi cause infarctions (e.g., myocardial) and small abscesses in internal organs.
- Immune reactions: development of diffuse proliferative glomerulonephritis and the appearance of characteristic Osler's nodes on the skin.
Briefly: answers to topical questions
What macroscopic types of endocarditis are distinguished in pathological anatomy?
According to the provided sources, the following morphological variants of endocarditis are described in pathological anatomy:
- Diffuse endocarditis (valvulitis).
- Acute verrucous endocarditis — formation of small thrombi ("verrucae") along the closing margin of the cusps.
- Recurrent verrucous endocarditis.
- Fibroplastic endocarditis.
- Polypoid endocarditis — a variant that can occur in non-infective thrombotic endocarditis.
- Ulcerative endocarditis — a morphological variant of infectious septic endocarditis.
- Polypoid-ulcerative endocarditis — a combination of ulcerative valve defects with thrombotic deposits; massive, dry, crumbly thrombotic deposits are described in protracted septic endocarditis.
What are Lukin-Libman spots and where are they localized in infective endocarditis?
Lukin-Libman spots in infective endocarditis are described as petechial hemorrhages, as well as necrotic foci, often accompanied by hemorrhages.
Localization:
- Conjunctiva of the eyes — including the transitional fold of the lower eyelid conjunctiva.
- Mucous membranes — including the oral mucosa.
- Serous membranes.
In the sources, they are associated with hemorrhagic syndrome secondary to vasculitis; punctate hemorrhages on the conjunctiva are noted as a symptom of subacute infective endocarditis.
What extracardiac immune manifestations and symptoms are characteristic of infective endocarditis?
Extracardiac immune manifestations of infective endocarditis are driven by the circulation of immune complexes and the development of hypersensitivity reactions. Characteristic symptoms include:
- Kidney involvement — development of immune-complex diffuse proliferative glomerulonephritis (manifests as proteinuria).
- Spleen involvement — splenomegaly (formation of a "septic spleen").
- Skin and vascular changes — appearance of painful Osler's nodes, Janeway lesions, Roth spots on the retina, and petechial rash.
- Joint syndrome — development of arthritis due to the deposition of immune complexes on synovial membranes.
- Finger changes — clubbing of the terminal phalanges ("drumstick fingers") and watch-glass nails.
What changes occur in the spleen and kidneys in thromboembolic syndrome secondary to septic endocarditis?
In thromboembolic syndrome secondary to septic endocarditis, infarctions occur in the spleen and kidneys without suppuration.
- Kidneys — renal infarctions develop, subsequently leading to the formation of post-infarction scars.
- Spleen — due to the characteristics of its blood supply (main-stem type, poor anastomoses), true wedge-shaped infarctions form, which can also be replaced by scar tissue.
These changes result from the detachment of fragments of polypoid thrombotic masses from the affected heart valves and the occlusion of systemic arterial circulation.
Against the background of which diseases does secondary protracted septic endocarditis most frequently develop?
Secondary protracted septic endocarditis develops on altered valves — in the presence of sclerosis or deformity.
The sources explicitly indicate the following underlying conditions for secondary protracted septic endocarditis:
- Atherosclerosis.
- Syphilis.
- Congenital heart defects.
It is also noted that secondary endocarditis is more common in individuals over 50 years of age.
To quickly recall the cellular composition of the infiltrate: Acute endocarditis — Abundance of neutrophils. Protracted endocarditis — Predominance of lymphocytes and macrophages (no neutrophils).
Class and exam questions
How does primary protracted endocarditis differ from secondary endocarditis?
Primary endocarditis (Chernogubov's disease) develops on initially normal valves and is more common in young individuals. Secondary endocarditis develops on previously altered valves (sclerosis, valvular defects) in individuals over 50 years of age.
Which valves are most commonly affected in the protracted 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?
This is a form of infective endocarditis in which the causative agent cannot be detected in the blood using standard methods. It accounts for 10% to 30% of all cases of the disease.
Why does glomerulonephritis occur in endocarditis?
This is a manifestation of hypersensitivity. The pathogenesis is based on immune complex mechanisms that lead to systemic immune reactions, including renal involvement and the appearance of Osler's nodes.
What else to study on this topic
- Macro- and microscopic presentation of polypoid-ulcerative endocarditis depending on the pathogen (bacteria vs. fungi)
- Mechanisms of acquired heart defect formation during the organization of thrombotic masses
- Thromboembolic syndrome: pathways of emboli dissemination and development of metastatic abscesses
- Chernogubov's disease: historical perspective and current epidemiological trends
- Differential diagnosis of infective and non-bacterial thrombotic endocarditis
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