Abstract

In many cases of scarlet fever the symptoms of the infection have passed and recovery has apparently been established, when acute nephritic symptoms without fever appear about the third week. Of these, the signs of glomerular nephritis are the most prominent. It is generally thought that the new symptoms are not those of a secondary infection or late manifestations of scarlatina. In this connection Longcope and his co-workers indicate that the late nephritis following scarlet fever is the result of existing foci of streptococci in the throat and other parts of the upper respiratory tract. They could not obtain evidence that the streptococci caused the glomerular nephritis by actual invasion of the kidney, as cultures of the blood and urine were negative. These authors suggest that toxin from streptococcal foci in the throat, sinuses, etc., is eliminated by the kidney, thus causing the acute glomerular nephritis. Our experiments with 17 healthy young dogs support Longcope's contention and furthermore prove that the late acute glomerular nephritis (at least in the dog) is not the result of retained viable streptococci in the body but is due solely to the in vivo prepared streptococcal lysate (endotoxin) of Duval and Hibbard. In the recovered experimental dogs which had been infected with living cultures of scarlatinal streptococci, a second or a third dose of “lysate” (toxin in vivo prepared) produce a severe and often fatal acute hemorrhagic glomerulo nephritis which in every way corresponds to the afebrile post-scarlatinal nephritis of man. These animals tested before administrating the “lysate” showed more or less lytic immunity; that is, a specific streptococcal lysin was demonstrable in the blood serum and the animals could not be infected with the same dosage of living culture that infected them originally.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call