Several immunologic diseases result from infection with S. pyogenes, the group A streptococcus. Acute glomerulonephritis, characterized by hematuria, proteinuria, hypertension and edema, may appear 6-14 days after infection caused by a limited number of group A streptococcal serotypes. Attack rates are related to the magnitude of the immune response, with high levels of antibodies to streptococcal cell membrane antigens being found in the serum of affected patients. Electron microscopic demon stration of subepithelial lumps in renal biopsy specimens, along with hypocomplementemia, suggests that the renal injury is due to deposition of preformed immune complexes. The identity of the streptococcal components involved in this disorder remain unknown.
Acute rheumatic fever, a syndrome of migratory arthritis, carditis and/or chorea appears about 18 days after pharyngitis due to a group A streptococcus. Several theories regarding the pathogenesis of this disorder exist, but most widely accepted is that autoimmune phenomena are responsible, based on the similarity of streptococcal antigens to various human tissue antigens. Strains of group A streptococci that cause rheumatic fever appear to have in common M proteins with an antigenically conserved surface-exposed domain. Epitopes of these M proteins have been shown to share antigenic determinants with cardiac muscle myosin or sarcolemmal membrane antigens.
Guttate psoriasis is a well-described form of psoriasis characterized by the abrupt appearance of small psoriatic lesions over much of the skin; it occurs primarily in children and young adults a few weeks after streptococcal pharyngitis. This disorder appears to be a result of superantigenic stimulation of T cells by streptococcal pyrogenic exotoxin C with subsequent selective accumulation of V|32+ T cells in the areas of the skin lesions.
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