Research Article| Volume 76, ISSUE 2, P322-332, August 1970

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Streptococcal group A carbohydrate antibody in rheumatic and nonrheumatic bacterial endocarditis

  • Elia M. Ayoub
    Reprint requests should be sent to Dr. Ayoub at the address given below.
    From the Department of Pediatrics, University of Minnesota School of Medicine Minneapolis, Minn., USA
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  • Burton A. Dudding
    From the Department of Pediatrics, University of Minnesota School of Medicine Minneapolis, Minn., USA
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  • Author Footnotes
    ∗ Present address: Department of Pediatrics, University of Florida College of Medicine, Gainesville, Fla. 32601.
    ∗∗ Present address: Department of Virus Diseases, Walter Reed Army Institute of Research, Washington, D. C. 20012.
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      The persistence of elevated levels of antibody to the streptococcal group A polysaccharide (A-antibody) in patients with chronic rheumatic valvular heart disease was previously reported. Other studies have shown that valvular glycoproteins share common antigenic determinants with the streptococcal polysaccharide. The possibility that valvular damage per se contributes to the elevated antibody levels was examined in the present study by measuring the levels of A-autibody in the serum of patients with congenital heart disease and in patients with chronic rheumatic valvular heart disease. The results show that in the absence of evidence for antecedent group A streptococcal infection, the levels of the A-antibody in patients with congenital heart disease are normal, in contrast to the elevated levels found in patients with rheumatic heart disease. To test whether acute valvular damage would affect the A-antibody levels, similar determinations were performed on patients with bacterial endocarditis superimposed on rheumatic or congenital heart disease. The A-antibody levels obtained on these two groups of patients with bacterial endocarditis were not significantly different from the values obtained for the corresponding group of patients without endocarditis. These findings suggest that valvular damage does not contribute to the elevated A-antibody levels in patients with chronic rheumatic valvular disease.
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