To other interesting features of these researches of Watson’s we shall allude later, but, concerned here more with tracing the evolution of the infective theory of gout, we would hasten to add that in September of the same year Ringrose Gore, discussing the inadequacy of the uric acid theory, boldly avowed and ably propounded his belief in the _infective_ origin of the disorder. Thus he writes: “I consider a toxin to be the cause of this disease. If so, such toxin must be formed in the intestine. As the symptoms of gout are constant, it must be a definite toxin, the product of a definite bacillus acting upon the intestinal secretion. As gout is capable of being caused in any subject, it must be one of the bacilli normally found in the intestinal canal.” Nor did Gore lack supporters in his suggestion that the alimentary tract was the primary source of the changes in the metabolism of gout. For in the same year Minkowski, Le Gendre, and in this country Watson, hazarded the view that intestinal derangements, through the medium of their resultant toxins, initiate disturbances in the liver, and these in turn determine those obliquities of metabolism typical of gout. At the same time their contentions derive colour from the researches of Grübe, who, despite traditional views, maintained that in gout the hydrochloric acid of the gastric juice, far from being increased, was in most cases _diminished or wholly lacking_, while, on the other hand, lactic acid was present in some instances. In 1903 Woods-Hutchinson ably contended that “gout and lithæmia are mere symptom names for a miscellaneous group of _chronic toxæmic processes_ of widely varied origin, characterised by the production of uric acid and the urates.” He held that the uric acid in gout as well as the associated phosphoric acid are merely a criterion of the measure to which the nucleins of the body cells (chiefly probably of leucocytes) have undergone destruction in consequence of their invasion by a toxin or toxins of organic or inorganic nature. He furthermore contended that the _rôle_ of the _liver_ in gout was purely negative, consisting in its inability “to absorb or transform into harmless excretory substances the excess of toxins brought to it by the portal vein.”