Rheumatic fever

Overview rheumatic fever (rheumatic fever) is a common recurrent episodes of acute or chronic suffer Guitar Associating inflammation, mainly involving the heart, joints, the central nervous system, skin and subcutaneous tissue. Clinical manifestations carditis and arthritis mainly associated with fever, shock, skin rash, subcutaneous nodules, chorea, and so on. Acute arthritis usually to the more obvious, but at this stage of rheumatic carditis can cause a patient's death. Huai attack after radical left often ranging from the severity of heart damage, particularly valve disease most significantly, chronic rheumatic heart disease (rheumaticheart disease) or rheumatic disease (rheumatic valvular disease). Group A Streptococcus causes of rheumatic fever wind heart disease etiology, is a clinical, epidemiological and immunological aspects of some indirect evidence support. A number of clinical and epidemiological studies of group A streptococcal infection and is closely related to rheumatic fever, immunology study also confirmed that Acute rheumatic fever attack existed before the early history of streptococcal infection; Prospective long-term follow-up of antibacterial treatment and prevention of streptococcal infection, rheumatic fever prevention of primary and recurrent; In addition, route is also essential, streptococcal throat infection pathogenesis of rheumatic fever is a necessary condition. Nevertheless, the group A streptococcus cause rheumatic fever since the mechanism is not fully understood. Rheumatic fever is not the direct streptococcus infection caused. Rheumatic fever because the incidence is not the time streptococcal infection, but the infection after 2 ~ 3 weeks onset. Rheumatic fever in the blood of patients with heart tissue has never been found Group A streptococcus. Suffering from the after streptococcal pharyngitis, and only 1% ~ 3% of the patients developed rheumatic fever. In recent years, the group A streptococcus was found on the cell wall with a layer of protein, M, T and R composed of three proteins, M protein with the most important of all, can hinder phagocytosis, and type of bacteria is the foundation, also known as "cross-antigen reaction." In addition, the cell wall polysaccharide composition, there is a specific antigen, known as "C substances." Streptococcus infection by the human body, that some people can produce antibodies, not only in the role of Streptococcus itself, but also the role to heart valve thus leading to valvular disease. Mucopolysaccharidosis heart valve components and variation with age, thus interpreted young adults with heart valve disease incidence different. Immunological studies suggest that acute rheumatic fever regulate the immune deficiencies. Characterized B cells and helper T cells increased and inhibition of T cell relative decline lead to the humoral and cellular immune enhancement. Although there is no chronic rheumatic heart disease, rheumatism, but the persistence of B cells increased, suggesting immune inflammatory process is still ongoing. Streptococcal infection after the occurrence of rheumatic fever with human reaction, the response level, on the one hand with the Streptococcus antigen antibody correlated parallel relationship, antibody volume occurred long allergic opportunities; and other nervous system function of change. Pathological changes of systemic rheumatic fever is the inflammation of connective tissue, joints and in the early cardiac involvement of the most common, Then damage to the heart of the most important. According to the occurrence of disease process can be divided into the following three. (1) exudative degenerative connective tissue collagen fiber splitting, swelling and formation of the glass and cellulose-like degeneration. Variability lesions around lymphocytes, plasma cells, eosinophils, neutrophils, and other inflammatory cell infiltration response. A sustainable current ~ 2 months, to restore or to enter the second and third phases. (2) proliferation current period is characterized by the lesions on the basis of the emergence of rheumatic or rheumatoid granuloma body (Ascho ff body), which is characteristic of rheumatic fever disease, Histopathological diagnosis of rheumatic fever and rheumatic the basis for the activities of the indicators. A central body fibrinoid necrosis, the margin of lymphocytes and plasma cells infiltration, and rheumatoid cells. Rheumatoid cells were round, oval or polygonal, was basophilic cytoplasm rich nuclei space, and they have marked the nucleolus, sometimes two or more nuclei formation of giant cells, and entered the hardening phase. This period lasted about 3 ~ April. (3) Phase rheumatoid sclerosis upper central necrosis material gradually being absorbed, causes inflammatory cells decreased, fibrous tissue hyperplasia, in granuloma formation of scar tissue site. Because the disease often repeated attack, the development of these three processes can be staggered existence, which lasted about 4 ~ 6 months. The first period and the second period accompanied the serous exudates and inflammatory cell infiltration, Such infiltration to a large extent determines the clinical symptoms of various notable for the selection. In the joints and pathological changes of pericardial effusion in the main, and the scar formation is largely confined endocardial and myocardial. In particular valve. Rheumatic fever of systemic inflammatory disease involving the connective tissue collagen fibers, with joints and early involvement of the heart, Later main damage to the heart. Lesions in the period of organ involvement focus, as in joints and pericardial exudate to form arthritis and pericarditis. After exudation be completely absorbed, a small number of pericardial exudate absorption is not complete, of the plane caused some adhesions, in the myocardium and endocardium mainly proliferative lesions, scar formation after proliferation. Heart valve disease proliferation and adhesion often leads to chronic rheumatic valvular heart disease. All organs and tissues of the pathological changes are summarized as follows : 1. Heart almost every one of rheumatic fever patients had heart damage. Mild heart damage may not become chronic rheumatic heart disease. Acute rheumatic carditis center endometrium, myocardium, pericardium, etc. can be sorrow and create fully-yim, and myocarditis and endocarditis most important. Myocardial showed typical changes of rheumatism, widely distributed, mainly in myocardial interstitial adjacent to the vascular connective tissue. Endocarditis sorrow and the main valve, the valve congestive inflammation, swelling and thickening on the surface of a small vegetation, Formation valve regurgitation. The valve closure Department fibrin can calmly flap leaves adhesion; Valve change with the tendons and papillary muscle adhesion shortening, cardiac valve deformation, which could later be produced valve stenosis. Pericardial cavity can produce fibrin or fibrin to sexual fluid exudation. Activities after a period of less patients may fully restored, but in most patients, caused heart valve and the deformation within the myocardium or pericardium scar formation, resulting in chronic non-active heart disease, and to heart valve disease as the most significant. Early the main valve defects have closed, the formation of mitral stenosis need about 2002 more Aortic stenosis require a longer period of time. 2. And arthritis synovial tissue edema, synovial connective tissue under a mucinous change, cellulose-like changes and inflammatory cell infiltration, and sometimes not typical of rheumatoid body. As the exudation of cellulose is usually not more, susceptible to absorption, generally do not cause adhesions. After a period of activity will not produce strong joint deformity or other consequences. 3. Subcutaneous nodules subcutaneous connective tissue degeneration and necrosis, the collagen fibers split, basal cell and lymphocyte infiltration. granuloma formation, integration into nodules, rheumatoid to suggest an important sign, but only in 10% of patients seen. 4. Artery lesions involving the arterial wall layers, prompted artery wall thickening can lead to thrombosis. Was particularly prevalent in the coronary and kidney, pancreas, mesenteric, lung and brain and other parts of the artery. 5. Pulmonary lung lesions can occur irregularly mild real change, real change pulmonary interstitial and alveolar cells are inflammatory exudation, more lesions in small vessels around. 6. Brain lesions in small brain vascular congestion, lymphocytes, plasma cells, such as infiltration, have formed around the small blood vessels in the summary of the trend; Summary of this distribution in the striatum and substantia nigra and cerebral cortex and other places. Striatal lesions in significant, often Chorea clinical performance. If other rheumatic pleurisy, peritonitis may occur occasionally.