The microbic theory fast gained ground. Thus Luff, who in the first edition of his work advocated the renal origin of gout, subsequently renounced the same in favour of its infective origin. To sum up, the opinion generally was that it was more than probable that _gastro-intestinal derangements_, with their altered secretions, exert an influence on the intestinal flora with resultant formation of toxins, and that these same, acting chiefly on the liver, put in motion those obliquities of metabolism which eventuate in gout. Sikes, however, in 1907, discussing the _rôle_ of gastro-intestinal disorders, expressed a doubt as to whether the same are primarily or secondarily related “to the actual chemical processes at the base of the disease.” He thinks it at least as probable that the gastro-intestinal disorders are due to an alteration in the intestinal secretions from an internal cause as that they are due to bacteria in the formation of toxins, or, he suggests, to some alteration in the epithelial cells, so that they take up chemical compounds of different nature from the ordinary. To him it does not seem at all probable that gout will ever be found affiliable to any specific micro-organism, inclining rather to the belief that a solution of the riddle will only be found in a closer and more extended study of that most difficult subject, the actual _chemistry of the cell protoplasm_. CHAPTER XIV GOUT AS AN INFECTION “The old order changeth, giving place to new,” and the uric acid theory having failed us, it is essential that we cast round for some other solution of the problem, carrying with us, however, this guiding principle, that _uric acid_, having lost its _etiological_ status, be viewed in its right perspective as not the cause, but the _consequence_, of gout. Happily, with the advent of bacteriology our views, or rather our hazards, as to the nature of joint diseases underwent profound modification. But, strange to say, though quick to apprehend the significance of infection, its causal relation to other joint disorders, we still seem unaccountably loth to discard our time-worn conception of “gouty” arthritis as of purely _metabolic_ origin. This, to my mind, is the more remarkable in that the onset, clinical phenomena, and course of acute gout, and no less the life history of the disorder as a whole, are emphatically indicative of the intrusion of an _infective_ element in its genesis.