Antistreptolysin Titre of the Serum in Acute Glomerular Nephritis

Abstract

Todd 1 has demonstrated that the serums of animals immunized with S. hemolyticus develop a significant amount of an antibody which inhibits the activity of the streptococcal hemolysin. The serums of animals immunized to a number of other bacteria (pneu-mococcus, hemolytic staphylococcus, non-hemolytic streptococcus, and B. diphtheriae) do not contain appreciable quantities of this antihemolysin.

In subsequent studies Todd 2 working in conjunction with Coburn and Pauli 3 showed that there was a consistent increase in the anti-streptohemolysin titre (termed antistreptolysin by Todd) in human serums after hemolytic streptococcus infections. This antibody did not appear in significant amounts in the serums of patients convalescing from such other infections as lobar pneumonia, hemolytic staphylococcus osteomyelitis, joint tuberculosis and measles. The presence of high antistreptolysin titres in the serums of patients with rheumatic fever was additional immunological evidence leading to Coburn and Pauli's hypothesis that S. hemolyticus initiates the rheumatic process.

Todd found that at least 0.01 cc. of the serum of a normal individual without a recent hemolytic streptococcus infection was required to neutralize the hemolysin unit he utilized. He observed that as little as 0.0008 cc. of the serum of patients convalescing from hemolytic streptococcus disease contained the same neutralizing dose of antistreptolysin. Todd has described the antihemolysin titres of serums by recording the reciprocals of the fractions of the neutralizing doses of the serums as units. Thus a neutralizing dose (N.D.) of 0.01 cc. is equivalent to 100 units of antistreptolysin. He considers this value the upper limit of normal in the serums of healthy individuals without a preceding hemolytic streptococcus infection.

The accompanying table shows the degree of the antistreptolysin titre∗ of the serum 6-57 days after the onset of acute glomerular nephritis in 22 unselected cases. A throat or upper respiratory infection preceded the onset of acute nephritis in 21 of these patients. Fifteen of these infections were associated with the presence of the hemolytic streptococcus in the pharynx.

Twenty of the 22 serums from this group of cases contain a sufficiently high antistreptolysin titre to be indicative of a recent hemolytic streptococcus infection. The remaining 2 serums contain 100 units each of the antibody. These data offer strong additional evidence to the concept that acute glomerular nephritis in New York City is chiefly related to a preceding hemolytic streptococcus infection.