Says Duckworth, “The pyrexia proper to acute gout is paroxysmal with remission, and the pain of gout is likewise paroxysmal. One is reminded of the influence of marsh poison upon the nervous centres. This paroxysmal no less than periodic element in gout stamps a nervous character upon the malady and binds it in alliance with other well-recognised neuroses.” How interesting these reflections by this distinguished physician in light of latter-day revelations! For, in so far as these features in gout are reminiscent of _malaria_, they disclose an affinity, not for a malady of nervous, but one of established _infective_, origin. Simultaneously with the onset of _pyrexia_ the pulse quickens. The blood shows that increase in fibrin characteristic of inflammation, a fact noted by Gulland, Cabot, Buchanan and others. But more significant is the presence of _leucocytosis_. It may be of high grade. In a case of acute gouty _polyarthritis_ recently under my care the leucocyte count reached 27,000. Even in a _subacute_ example of the classic _monarticular_ type the leucocyte count attained 25,920. It was of _leucoid_ type and attended by moderate anæmia due to deficiency of red corpuscles. Nor is leucocytosis restricted to the periods of exacerbation, but it may be met with in the _inter-paroxysmal_ stages. In my experience, even in cases of definitely _chronic_ type it may reach 14,000. The higher grades of leucocytosis are obviously very suggestive of an _infection_, and that lesser degrees should be encountered in examples of definitely chronic type seems to point to gout being of the nature of a _chronic_ or _serial_ infection. I would here add also that the converse of leucocytosis, viz., _leucopenia_, is sometimes met with in chronic cases. Dr. Munro and I have met with two instances of such in chronic gout in the intervals between paroxysms. This decrease in the number of leucocytes (leucopenia) is, of course, deeply interesting and, needless to say, quite compatible with infections, _e.g._, enteric, malaria, tuberculosis. In fact, it suggests that gout may be the outcome of divers infections, and not due to any specific organism. _Enlargement of the lymphatic glands_ was, by older authors, believed not to occur in gout. But obviously the lack of macroscopic evidence does not exclude the possibility of microscopic changes in these structures. The likelihood of such, moreover, is enhanced by the occasional occurrence of _lymphangitis_ in connection with the inflammatory articular lesions. Buzzard, indeed, long since claimed that there was “clinical evidence of subacute gouty inflammation of lymph spaces in certain regions due to uratic deposit and influence.”