Etiology of infective endocarditis
The disease can be caused by various microorganisms, but most commonly by bacteria.
- Streptococcus viridans (alpha-hemolytic streptococcus). This is the main causative agent, accounting for more than half of all cases. It is most characteristic of secondary endocarditis (when valves are already altered by a structural heart disease).
- Staphylococcus (S. aureus, S. epidermidis). Detected in 10–20% of cases. Staphylococcus aureus most commonly causes primary endocarditis, affecting initially healthy valves.
- Rare flora. The disease can be caused by enterococci, gram-negative bacteria (Pseudomonas aeruginosa, Salmonella, Klebsiella), as well as fungi (Candida, Histoplasma capsulatum). Mixed infection is sometimes observed.
Risk factors and classification
A key risk factor is altered hemodynamics. Turbulent blood flow arising from congenital or acquired valve defects, as well as the presence of prosthetic valves, constantly traumatizes the endothelium, creating conditions for the deposition of microorganisms. Dental and surgical procedures, as well as intravenous drug injections (especially in injection drug users), often serve as the portal of entry for the infection.
According to the predisposing (pre-existing) condition of the valves, the following are distinguished:
- Secondary endocarditis. The most frequent form (about 2/3 of cases). Infection superimposes on pre-existing pathology (rheumatic changes, valve defects).
- Primary endocarditis. Develops on previously unchanged, intact heart valves.
Pathogenesis: how the disease develops
The onset of endocarditis requires the simultaneous presence of predisposing factors and transient bacteremia. The process occurs in two stages:
- Abacterial phase. Healthy endothelium is resistant to infections. However, when damaged by turbulent blood flow, platelets and fibrin deposit on the exposed surface. A sterile vegetation is formed — non-bacterial thrombotic endocarditis.
- Bacterial phase. During transient bacteremia (e.g., after tooth extraction or even spontaneously), microbes settle on the prepared thrombotic "soil" and begin to multiply there. This leads to the formation of fully fledged infected vegetations, valve destruction, and massive systemic bacteremia.
The development of the disease is accompanied by immunological shifts (formation of circulating immune complexes affecting the kidneys and blood vessels) and hemostatic disorders (hypercoagulability with a risk of thromboembolism).
Clinical Forms
Depending on the acuteness of the process and the etiology, the disease can manifest in different ways:
- Acute endocarditis. Caused by highly virulent flora in the presence of a portal of entry (wounds, cardiac catheterization). It predominantly affects healthy valves. It presents with a picture of severe sepsis (fever, chills, purulent metastases). Without treatment, it leads to death within a timeframe ranging from a few days to 1.5 months.
- Subacute endocarditis. More commonly develops as a secondary process against the background of a heart defect. Onset is gradual, with a more subdued clinical picture. In the absence of therapy, the patient dies within six months.
Briefly: answers to topical questions
What specific hemostatic disorders and thromboembolic complications are characteristic of infective endocarditis?
Infective endocarditis is characterized by hypercoagulability, which creates a high risk of thrombosis and subsequent thromboembolism. Thromboembolic syndrome is associated with the detachment of vegetation fragments and embolism in the vessels of various organs; organ infarctions and strokes are possible.
Vascular and embolic complications mentioned in the sources include:
- Major systemic and pulmonary embolisms/infarctions.
- Cerebrovascular accidents of ischemic, hemorrhagic, or mixed type; intracranial ischemic or hemorrhagic lesions.
- Mycotic aneurysms, including those of peripheral vessels.
- Visceral abscesses.
- Hematogenous osteoarticular septic complications, such as spondylodiscitis.
- Conjunctival hemorrhages and Janeway lesions.
What diagnostic criteria (Duke criteria) are used to diagnose infective endocarditis?
The diagnosis is verified by a specific combination of major and minor Duke criteria.
- Major criteria — proven bacteremia (isolation of the pathogen from the blood) and echocardiographic signs of endocardial involvement (vegetations).
- Minor criteria — include several groups of signs:
- Predisposing conditions (heart disease or intravenous drug use).
- Fever (body temperature >38°C).
- Embolic complications (infarctions, mycotic aneurysms, conjunctival hemorrhages, Janeway lesions).
- Immunological criteria (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor).
- Microbiological or serological data indicative of active infection but not meeting major criteria.
What classical extracardiac manifestations (symptoms) occur in infective endocarditis?
Classic extracardiac manifestations are caused by systemic embolic and immunological phenomena.
The main peripheral and systemic signs include:
- Subungual hemorrhages — the most frequent vascular phenomena.
- Lukin-Liebman sign — petechial hemorrhages on the conjunctiva.
- Janeway lesions — vascular vasculitic-embolic manifestations.
- Osler nodes — belong to the immunological criteria of the disease.
- Roth spots — an immunological phenomenon.
- Glomerulonephritis — a manifestation of the immunoinflammatory syndrome.
These symptoms are rare and are characteristic primarily of severe or prolonged subacute courses of the infection.
Class and exam questions
What is the difference between primary and secondary infective endocarditis?
Primary endocarditis develops on initially healthy valves (more often caused by staphylococcus), while secondary endocarditis arises against the background of pre-existing valve pathology, such as rheumatic heart disease (more often caused by Streptococcus viridans).
What is non-bacterial thrombotic endocarditis?
This is the initial stage of pathogenesis, in which platelets and fibrin deposit on the damaged area of the endocardium, forming a sterile vegetation not yet colonized by bacteria.
Why are the kidneys affected in endocarditis?
In response to the infection, circulating immune complexes (CICs) are formed. They circulate in the blood and deposit on the basement membranes of the kidneys and in small vessels, causing an immunoinflammatory syndrome.
What else to study on this topic
- Pathophysiology of infectious-destructive syndrome
- Mechanisms of development of thromboembolic syndrome in IE
- Immunoinflammatory syndrome and its systemic manifestations
- Principles of antibiotic prophylaxis before invasive procedures
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