الفهرس 
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Abstract
Rheumatic fever is a multi—system disease with joint, heart, skin & neurological manifestations. The development of acute rheumatic fever and rheumatic heart disease is generally held to involve some reactions of the immune system to group A streptococci or their
products. The development of antibodies cross—racting with streptococcal cellular constituents and with components of cardiac cells C Zabriskie 1969) as well as alterations in various aspects of the celluler immune response
( Marie and Berkal,l979 ) is, at least, presumptive evideace for immune mechanisms in the pathogenesis of rheumatic heart disease
The changes in the cellular immune function are diene and intriguingly complex, Leukocyte migration inhibition in response to streptococoal membrane is increased in acute rheumatic fever and may persist for at least 5 years after the initial attack C Read et al, 1974 ). The one — way mixed lymphocyte culture response of acute rheumatic fever cells to allogeneic lymphocytes may be depressed ( fluëker and Williams 1972 ). Several reports indicated altered lymphocyte transformation response to streptococcal antigens in post—Streptococcal disease. Using either whole organisms or streptococcal substances in various stages of impurity,
a depressed lymphoproliferative response has generally been observed in the acute rheumatic fever and in the rheumatic heart disease ( Cuppari et aL’ 1972 ).However Sapru et al (1977) and Gray et al (1981) have reported an elevated blastogenic response in acute rheumatic fever and rheumatic heart disease. The complexity of the streptococcal preparation used in these various studies makes it difficult to interpret the results. Gray (1979) reported that studies with purified substances might resolve some of these discrepancies
The development of acute rheumatic fever and rheumatic heart disease is apparently a consequence of group A streptococcal infections.:of the upper respiratory tract. Infections with group A streptococci at other sites e.g. skin, do not lead to these complications (Wannamaker , 1970 ). The role of the tonsil in this process is unknown, but Drucker, at &j1979) reported that local factors could be important in the pathogenetic process leading to heart damage, for example, tonsilar lymphocytes may be a different subpopulation (s) and/or may respond to streptococcal antigens in a different manner than the lymphocytes of peripheral blood. Abo—Ilussein et al (1981) recited that the uiajor immunologic features of. rheumatic fever are :
(1) presence of circulating antibodies directd against cardiac tissues and group A streptococcal antigens
(2) Deposition of immunoglobulin and complement in the myocardial and valvular tissues
(3) Presence of antibodies against various group A streptococcal toxins.
Aim Of Work
The present work aims at :
1— Isolation and typing of B—haemolytic streptococci if present in pMtients suffering from acute, chronic active and chronic inactive rheumatic fever and in normal healthy individual as a control group
2— Estimation of serum antistreptolysin’O’ and antihyaluro— nidase levels in those patients of acute, chronic active and chronic inactive rheumatic fever and in the control group.
3— Estimation of imcnunoglobuljn G, immu.noglobulin M, immanoglobulin A and complement 3c C 03c ) in the same previous groups of patients and in the control group
4— Detection of serum autoanticardiac antibodies in the previous groups of patients and in the control group.