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  Non suppurative sequelae

Non suppurative sequelae or post streptococcal diseases:

Two serious diseases might develop as sequelae to Str. Pyogenes infections. Following an acute Str. pyogenes infection, there is a latent phase of 1-4 weeks. After this period seldom nephritis or rheumatic fever develops. Such conditions are not due to the direct effect of the organisms, though due to hypersensitivity response. Nephritis is more general after skin infections. Rheumatic heart disease is ordinary after respiratory infections.

a. Acute glomerulonephritis (AGN):

This condition builds up 3 weeks after streptococcal infections. It is related with certain M antigenic kind mainly M types 2,4,12,49. Some strains are nephritogenic. Glomerulonephritis might be initiated by antigen-antibody complexes on the glomerular basement membrane. In acute nephritis, there is protein and blood in the urine. Oedema, high blood pressure, and urea nitrogen retention are also seen Serum complement levels become low. Few patients might die. Some build up chronic glomerulo nephritis with ultimate kidney failure. The majority of the patients recover totally.

b. Rheumatic fever:

Rheumatic fever is a main cause of acquired heart disease in young people. It is a situation in which inflammation of joints (i.e., arthritis), heart (i.e., Carditis), central nervous system (i.e., Chorea), skin (i.e., erythema marginatum) and /or subcutaneous nodules take place. Poly articular arthritis is the most common manifestation. Carditis is a most serious condition since it leads to permanent harm to heart valves. Rheumatic fever is autoimmune in nature. Theories to elucidate the pathogenesis of rheumatic fever have focused on tissue harm caused by streptococcal products (that is, streptolysins), or antigen-antibody complexes (as in serum sickness). Lately it is proposed that rheumatic fever might be due to molecular mimicry and autoimmunity.

Different streptococcal cellular components have been revealed to mimic the structure of molecules found in human tissue. Antibodies directed against streptococcal products are considered to cross-react with host tissue, generating autoimmune damage. Similarities in structure and ensuing serological cross-reactivity of streptococcal cell constituents (i.e., M-protein, membrane antigens, group carbohydrate) with human heart, joint and brain tissues have been explained. Patients exhibiting rheumatic fever are found to harbor antibodies which cross-react with both streptococcal products and human tissue components. The main antigens included are tropomyosin, myosin, laminin and keratin in the human tissues and the group A, Str. pyogenes antigen that is polymer of N-acetyl glucosamine. Repeated episodes of Str. Pyogenes infection raise the severity of the disease.

 

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