Streptococcal neuraminidase and acute glomerulonephritis.
We examined the hypothesis that streptococcal neuraminidase may alter host serum immunoglobulin G so that autoantibodies are formed which lead to immune complexes and acute glomerulonephritis. We confirmed the observation that T-type 4 and T-type 12 streptococci (both associated with acute glomerulonephritis) are the most likely of many types studied to produce neuraminidase. However, we did not find this enzyme to be produced by any of 23 streptococcal strains isolated from patients with nephritis, whereas it was produced by two strains from patients with rheumatic fever and by one strain from a patient with scarlet fever. Also, we were unable to find direct or indirect evidence of increased neuraminidase activity in the sera of six patients with acute glomerulonephritis when they were compared with the sera of six patients with acute rheumatic fever and with those of six normal subjects.
D000208:Acute Disease; D005921:Glomerulonephritis / Q000201:enzymology / Q000209:etiology* / Q000382:microbiology; D006801:Humans; D009439:Neuraminidase / Q000097:blood / Q000378:metabolism*; D012794:Sialic Acids / Q000097:blood; D013290:Streptococcal Infections / Q000201:enzymology / Q000382:microbiology; D013291:Streptococcus / Q000201:enzymology*
D012794:Sialic Acids; D009439:Neuraminidase