Abstract
The rôle of Streptococcus hemolyticus in scarlet fever is generally admitted to remain as unsettled as the question about the actual cause of this disease. 1 Both Ciuca 2 and Satake 3 failed consistently to produce experimental scarlet fever in a large series of Dick positive human volunteers by swabbing or injecting their tonsils with freshly isolated cultures of scarlet fever streptococci or scarlet fever blood. Specificity of the Dick toxin has not been granted by Bürgers, 4 Cooke, 5 von Gröer and Redich, 6 Friedemann, 7 Meyer, 8 Molkte, 9 Parish and Okell, 10 Smith, 11 Wheeler, 12 Wadsworth, 13 Zlatogoroff and Derkatsch 14 and numerous other investigators. Serological specificity of Streptococcus scarlatinae has not been conceded by Bürgers and Wohlfeil, 15 Ciuca, 2 Friedemann, 7 Maclachlan and Mackie, 16 Smith, 11 Wadsworth, 13 Williams, 17 Zlatogoroff and Derkatsch 14 and many others. Failure of the scarlet fever antitoxin to abate septic complications is now generally admitted. This apparent lack of agreement with the group adhering to the streptococcic etiology of scarlet fever recently prompted Zlatogoroff 18 to review the filterable virus theory of the disease. In an extensive series of experiments on rabbits, monkeys and man he claims to have proven that during the incipient stages of scarlet fever a filterable virus is present in the faucial exudate which is capable of activating the otherwise ubiquitous and avirulent hemolytic streptococcus to assume toxigenic and pathogenic properties by which the clinical picture of scarlet fever is produced. When injected either intravenously or subcutaneously in rabbits, monkeys and man the filtered and sterile scarlatinal exudate almost constantly produces the scarlet fever syndrome, with subsequent typical histopathological lesions, as well as changes in the blood-picture, analogous to the epidemic form of the disease. The experimental disease bestows immunity for over 2y2 years against reinfection.
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