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JAMA. 1932;99(18):1489-1494. doi:10.1001/jama.1932.02740700029006.
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Although research workers in the field of arthritis have rightfully come to suspect the streptococcus to be a causative factor in so-called rheumatoid or atrophic-deformans arthritides, there has not been a sufficient consensus on the subject to correlate divergent findings and allow general acceptation of the streptococcus as the main etiologic factor in this widespread and disabling disease.

My own clinical and research work has steadily made me more confident that the streptococcus is the sine qua non of what is generally termed nonspecific infectious arthritis. My co-workers and I have attempted to complete the etiologic proof of this theory in every way possible and the recent experimental findings of Hadjopoulos have forcibly confirmed our original contentions.

In our early work with complement-fixation reactions in the arthritides, we regularly found antibodies against various strains of streptococci in the blood serums of afflicted persons.1 Since the presence of an antibody


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