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Rheumatic fever – symptoms, prevention and treatment

Rheumatic fever – symptoms, prevention and treatment

Rheumatic fever is an infectious-allergic disease, caused by beta-hemolytic streptococcus group A. Streptococcal infection usually runs in the form of prolonged and/or recurrent purulent tonsillitis. The long presence of this microorganism in the pus in the tonsils leads to rheumatism as a second disease. Of all the microorganisms only the beta-hemolytic streptococcus group A can lead to development of rheumatic fever.

Rheumatic fever

Rheumatic fever

Why exactly this microorganism? When the usual inflammatory reaction can not cope with a cause of disease, on the stage comes the immune system. Antibacterial immunity is humoral . This means that in the fight against streptococcus the organism relies on the production of antibodies by plasma cells (activated B- lymphocytes). These cells for about ten days produce large amounts of antibodies (immunoglobulins) against the surface proteins of the streptococcus. Immunoglobulins are spread through the bloodstream to all tissues in order to seek and destroy the cause of inflammation (streptococci). However, this microbe has surface antigens (membrane proteins), that are completely similar to some antigens of the human tissues. For example, M-protein of streptococci is almost identical to the protein myosin in human muscle cells; the hyaluronic capsule of the bacteria is identical in structure and composition with human hyaluronic acid, which is represented in the body as the main ingredient of connective tissue. This similarity “confuses” the antibodies and they are not in the condition to differentiate the streptococci from the cells of normal tissues. Consequently, the antibodies circulate throughout the body and they attach not only to the throat, but also they begin to attach to the membranes of normal cells. These are called cross-reactive antibodies and can be found in the serum – elevated titers of antistreptolysin O, antistreptokinase and antistreptohyaluronidase. These immunoglobulins deplete the body’s own cells, “thinking” that they are bacteria. The inflammatory processes in organs, running from these “autoantibodies”, define the clinical picture, the severity of the course of  rheumatic fever and the prognosis for the patient’s life.

Early symptoms of rheumatic fever:
• Fever
• Headache, sweating
• Tachycardia (palpitations)
• Swolling and pain in large joints that migrate from joint to joint

All these symptoms develop 2-4 weeks after purulent tonsillitis!

Rheumatic fever can develop unnoticed, hidden. Its only appearance may be unwellness and sub feverish temperature (37.2 to 37.4 C). Other hidden symptoms could be rheumatic subcutaneous nodules and red spots on the skin (erythema, purpura).The involvement of the nervous system (chorea minor) may also give symptoms, valuable for the diagnosis The change in the student’s handwriting can be a sign of rheumatic fever.
Normal ESR excludes the presence of rheumatic fever!
The tissues are sterile. The microbiological tests find no streptococci, excluding purulent exudate of the tonsils.

Organ damage and complications of rheumatic fever

Heart – Rheumatoid carditis
The damages of the heart engage the three layers – the pericardium (heart sac and the outer surface of the heart), myocardium (heart muscle) and endocardium (inner lining).

Pericarditis – The outer covering (pericardium) suffers in the form of acute fibrinous inflammation. The surface of the heart is covered with a whitish fluid, which can be drained in the form of fiber and the heart gets a filamentous form. This type is called fibrinous pericarditis- Cor villosum. Inflammatory exudate is mostly absorbed, but some rare focal adhesions remain, which does not difficult the heart function.

Myocarditis – involvement of the myocardium (heart muscle) of the inflammatory process leads to the development of rheumatic myocarditis. The typical morphological picture includes granulomatous inflammatory reaction in heart muscle. These focal chronic inflammatory infiltrates are called granulomas of Ashoff and contain macrophages, histiocytes, cells of Anichkov and giant multinuclear cells of Ashoff.

Endocarditis – involvement of the inner lining of the heart in rheumatic fever goes through several phases:

Initial endocarditis
Valve lanes are juicy, swollen. Microscopic changes are dominated by their softened stroma and change of the basic substance of the connective tissue, which is proved by the reaction of metachromasia stained with Toluidine Blau. The altered tissues change the basic color of blue paint and are painted in purple.

Verrucous endocarditis
The blood flow, passing through the cardiac ventricles, is strongest in the center of the stream. There are the edges of the valves, that are already damaged by previous stages of rheumatic inflammation. Endothelial cells at the edges of the boards are shed by the force of blood flow, because they are no longer firmly attached to the stroma (the base) of valve sails. The coagulation system is activated and in the place of the damaged endothelial cells forms a thrombotic layer that looks like the beads of rosary. These thrombs, composed primarily of platelets and fibrin are located on the surface of the canvas flap that is coming from the side of the blood. Thus, the knots in mitral valve are located on the side of the left ventricle and those in the aortic valve – on the side of the left ventricle.

Fibrous endocarditis
The growth of scar tissue in the valves as a result of the inflammatory process leads to deformities of the valves and heart defects. Valve defects in rheumatic fever commit most often mitral valve and the valve of the aorta. Depending on the type of deformation of the valve lanes, there are two main types of defects – stenosis and/or insufficiency. Stenosis is a narrowing of the valve orifice due to scarring of the valve sheets. This narrowing prevents the receipt of a sufficient amount of blood in the heart cavity. In mitral valve stenosis appears to be injured left ventricle .Due to the small amount of blood coming in, the valve works less for a long time (less redundancy) and over time undergoes atrophy (reduced size). At the same time, retained blood in the left atrium leads to its enlargement (hypertrophy and dilatation).The movements of blood created by impaired hemodynamics favor the development of thrombosis. Formed thrombus in the left ventricle can grow “in place”, spinning with blood flow in the heart cavity. This clot is round and can reach up to the size of egg yolk. If at one point it starts going through a funnel like narrowed mitral orifice, most likely it will stuck in the narrowed valve and would cause sudden death by stopping the blood flow.

Reccurent endocarditis
If a new bout of rheumatic fever follows and the process is repeated again on the already deformed valve canvas, it deepens and aggravates valve defects.
Myocarditis defines the severity of the course of acute rheumatism, and valve defects remaining after endocarditis are responsible for disability and prognosis in these patients.

Joints – migratory polyarthritis
Affected are large joints – knee, ankle, elbow, wrist. The damaged joint is swollen, red and very painful. After two to three weeks symptoms decrease and inflammation is transferred to other joints. So called migratory arthritis.

Cutaneous manifestations of rheumatic fever
Annular erythema marginatum – rose-red, partly scattered spots on the body, especially around the navel (paraumblical) spots.
Subcutaneous nodules – Red-blue spots, painful for pressure and usually located on the legs.

Nervous system – chorea minor (Sydenham)
Develops as a late symptom (up to months!) of rheumatism and is expressed in uncontrolled movements of arms and acts of clumsiness in children. They spill the soup, broke cups, start to write ugly …

Treatment and prevention of rheumatic fever
Purulent angina should be treated with antibiotics prescribed by a doctor. Self-treatment is just as dangerous as the lack of treatment! After completion of the course of antibiotic therapy there should be an examination to establish their effect! Treatment of patients with streptococcal angina shoud be with penicillin antibiotic. In all streptococcal infections penicillin is the drug of choice, because without exception all streptococci are sensitive to it!The prevention from the recurrence of the symptoms is also made with penicillin preparations and should continue over 10 years, up to age 25. Removing the tonsils (tonsillectomy) should be done under the protection of penicillin! Extraction of teeth too!

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