Scudamore referred its prevalence at these particular seasons to their attendant vicissitudes of heat and cold (the strongest of all the exciting causes of gout). Trousseau states that “gout with successive paroxysms shows itself early or late in the year, at the beginning of spring or late autumn, the wherefore I know not.” This tendency on the part of acute gout to seasonal rhythm is ultimately lost. For, once the disorder is established, no period of the year confers absolute immunity. Whatever be the explanation of the vernal and autumnal incidence of gout in its early stages, this peculiarity is at any rate not incompatible with its _infective_ origin. In this connection it may be recalled that it was once described as “a tertian fever terminating in fourteen days.” Again, further evidence may be obtained from the action of colchicum, our sheet-anchor in the treatment of gout. Thus, Dixon and Malden have shown that _colchicine_ has no action on the metabolism of _purins_ or on the _kidney_. On the other hand, it causes a primary diminution followed by a _marked increase_ in the number of _leucocytes_, which suggests the possibility that it exerts its beneficial effects by combating _infection_. Lastly, turning our attention to the anatomical changes as disclosed after death during an acute articular paroxysm, these present appearances quite compatible with their infective origin. Dr. Munro, in one of my examples of _acute gouty polyarthritis_, aspirated the knee joint. The results of _cytological_ examination were precisely such as are deemed characteristic of arthritides of infective source. The results of our analysis of the component elements of an acute paroxysm of gout are, for the following reasons, strongly indicative of the intrusion of an _infective_ element:— (1) The onset, temperature curve, the character of the local phenomena, and course of the disorder. (2) The presence of _leucocytosis_ with secondary anæmia, and exceptionally of _leucopenia_. (3) Enlargement of the lymphatic glands, and possibly of the spleen. (4) Occasional complication of the acute articular disorder by _lymphangitis_ and _phlebitis_. (5) The paroxysmal nature and periodicity of the disorder. (6) The compatibility of the morbid anatomical changes and the cytological content of aspirated joint fluid with their genesis by infection. THE EVOLUTION AND LIFE HISTORY OF GOUT If the onset, phenomena, and course of acute gout are reminiscent of infection, so, also, does a review of the life history of the disease, as a whole, carry with it the same inference.