Is endocarditis contagious?
Endocarditis is usually not contagious. It is only triggered by small amounts of bacteria, which are abundant in the oral cavity or body and can only enter the bloodstream through minor injuries. The infectious focus is then only on the heart, where small abscesses, encapsulations of the bacteria can form.
Disease development and cause
The prerequisite for an inflammation leading to structural damage to the heart valves is an increased outflow of pathogens into the blood (this is also called bacteremia). Common starting points (“foci” of endocarditis) are In a healthy person, the increased germ load leads to an activation of the immune system: white blood cells produce the body’s own proteins (so-called antibodies) to mark the pathogens as foreign invaders, so that they are then eliminated by scavenger cells (which represent a different subgroup of white blood cells and are also called macrophages). In the case of previous damage (see above), rapid valve destruction occurs, depending on the aggressiveness of the pathogen and the immune system of the affected person (acute is defined as a disease process within 40 days).
The so-called subacute endocarditis proceeds insidiously; the symptoms (see below) are much less pronounced here than in the acute form. The reason is that other, less aggressive pathogens are more prevalent.Another form of inflammation of the inner wall of the heart, which has become rare today due to prevention with antibiotics, is a hypersensitivity reaction of our immune system. In contrast to the form primarily caused by pathogens (and therefore also called “infectious endocarditis”), the inflammation takes place inside the valve.
Responsible for this is a preceding inflammation caused by so-called beta-hemolytic streptococci, in the course of which the body’s own defensive substances react not only as desired with wall components of the pathogens, but also with randomly similar-looking components of protein molecules of the heart or joints. While the term “rheumatic fever” describes the reaction of the entire body, the partial component specifically affecting the heart is called “endocarditis rheumatica” by analogy. Rarer special forms of endocarditis rheumatica occur: An allergic trigger is suspected in “Endocarditis parietalis fibroplastica Löffler”, which leads to cardiac insufficiency-heart failure due to excessive formation of connective tissue.
- Purulent skin inflammations (so-called boils = large pimples)
- Infections in the ear, nose and throat area (such as a: purulent tonsillitis, medical: tonsillitis inflammation of the paranasal sinuses = sinusitis, medical: sinusitis
- Purulent tonsillitis, medical: tonsillitis
- Inflammation of the paranasal sinuses = inflammation of the nasal sinuses, medical: sinusitis
- Pneumonia (pneumonia)
- Dental infections
- Bacteremia
- Purulent tonsillitis, medical: tonsillitis
- Inflammation of the paranasal sinuses = inflammation of the nasal sinuses, medical: sinusitis
- Cancer (“Endocarditis marantica”)
- Autoimmune disease lupus erythematosus (“endocarditis thrombotica Libman-Sacks”)
As a rule, various bacteria are the causative agents of infective endocarditis. The most common are staphylococci, especially the bacterium Staphylococcus aureus. This is responsible for about 45-65% of endocarditis.
The second most common endocarditis pathogen belongs to the streptococci and is called Streptococcus viridans. It causes about 30% of endocarditis. Other pathogens that come into question but occur significantly less frequently than those already mentioned are for example Staphylococcus epidermidis, Enterococci, other streptococci and fungi (Aspergillus fumigatus). The latter play a role above all in immunocompromised patients, for example in patients with HIV, after organ transplants or chemotherapy.
