Rheumatic fever - RAA

Rheumatic fever is an inflammatory disease of connective tissue caused by beta-hemolytic streptococcus, pathogenic infectious, immunologic, pathologic substrate aviind Aschoff node exacerbation of chronic evolution and tend to cause aviind released during acute myocardial injury and potentially fatal injuriesvalve with fibrous scars.
The mortality and morbidity rheumatic fever is a major public health problem in developing countries, rheumatic cardiopathy forcing 35-40% of hospital admissions, representing the most frequent indication for cardiac surgery and heart causing death prindipala group 5-25 years.
The incidence varies with socio-economic level. Even in developed countries, rheumatic fever remains a major health problem, although in the 60s and 80s has dropped dramatically morbimortalitatea by:-Improving the sanitary conditions of housingNurse-level risePenicillin-effective in the treatment of streptococcal angina and secondary prevention.In recent years the U.S. has been a recrudiscenta of rheumatic fever which was explained by:-The emergence of new strains of beta-hemolytic streptococcus-Relaxation of prevention programs-Wave of immigrants from Third World countries.
The disease is characterized by inflammation of connective tissue in joints, heart, skin, brain, after upper respiratory tract infection: angina strep or scarlet fever. Those affected will develop acute or late phase after infection arthritis, carditis, Sydenham choreea, erythema marginatum.
Treatment is aimed at eradicating strep bacteria with antibiotics, immune therapy with salicylates and corticosteroids and cardiac therapy. V Penincilina preferred oral antibiotic for the treatment of streptococcal angina. If this is not available or the patient may be given intramuscularly injectable penicillin is used benzatin. For those allergic to penicillin may be given other antibiotics.
When medical therapy fails to opt for the surgery. Approximately 40% of patients will develop mitral stenosis as adults. This inflammatory sechela streptococcal infection different techniques valve replacement, or mitral valvuloplasty.
Clinical manifestations of rheumatic fever usually resolves in 12 weeks in 80% of cases. After-effects are limited to heart disease and depend on the severity of the attack carditei infarction.
Pathogenesis
Rheumatic fever develops in children and adolescents who had a history of streptococcal angina, after 14 days, scarlet fever, 21 days ago. Beta-hemolytic streptococcus cells attack the upper respiratory tract and produces numerous toxins and enzymes that allow invasion of host cells. After an incubation period of 2-4 days bacteria cause inflammatory response, after another 3-5 days following pharyngeal erythema, fever, malaise, headache and leukocytosis. In a small number of patients the infection leads to rheumatic fever from strep throat a few weeks after that deal. Only throat infections initiated or reactivated rheumatic fever.
Direct contact with respiratory secretions or oral is contagious.Patients remain infected for several weeks after resolution of streptococcal angina and reserved by infecting other people.Penicillin treatment shortens the clinical course of ulcerative and prevents the major sequelae.After solving the throat without treatment streptococii8 remain stationed in the pharynx and nasopharynx, without going into the blood and determine the complex immunological reaction that will lead to chronic rheumatic heart disease, glomerulonephritis poststreptococica and reactivation of streptococcal angina.
Infectious-immune mechanism.It is a complex and incompletely understood.
Exotoxinele streptococcal toxic hypothesis considers that the traffic would be issued in the cardiotoxic effect, but rather experimental cardiac causes exudative and necrotic lesions, can not reproduce garnulomatosi Aschoff nodules.
Immunological hypothesis is suggested by the latent period between the occurrence of angina and the occurrence of cardio-articular manifestations. It considers that the conditions of a genetic predisposition streptococcal antigens responsible for triggering antibody specific for cardiac lesions due to cross-reactions between streptococcal components and the infarctions.
As M protein is found in:Strep protoplasm-membraneSarcolemei myocardial-membrane.
C polysaccharide is composed of fractions present in:Streptococcal cell-membrane-Glycoproteins from valvular endocardium, synovial fluid and cartilage.
Anti-myocardial antibodies appear not cross react with streptococcal antigens, but may occur through the components of myocardial damage. These anti-myocardial antibodies present in 80% of cases of carditis will be found in complezele Ag-Ac-C on myocardial rheumatic exudative-necrotic lesions, but not in Aschoff granulomas.
The role of the autoimmune mechanism.Endomyocardial granulomatous lesions were produced by cellular immune mechanisms by streptococcal antigen sensitization of T lymphocytes with cytotoxic effect on cardiac miofibrilelor.