Indeed, the great Boerhaave avowed his belief that gout was _contagious_—a forecast, we may take it, of the modern theory of _infection_. Subsequently his pupil, Van Swieten, went a step further, maintaining that sometimes wives, while nursing husbands afflicted with gout, contracted the malady! Passing now to relatively modern times, it will be noted that in 1864 Laycock classed acute gout with rheumatic fever as an “excretory fever,” while Parkes even prior to this, in 1860, wrote: “I define gout after Garrod as a febrile infection with inflammation about the joints leading to a deposition of urate of soda.” But it must be freely acknowledged that, subsequent to Garrod’s discovery of _uric acid_ in the blood in gout, the spell exercised by the _uric acid theory_ was such that it dominated medical thought almost to the exclusion of all other possibilities. All energies were forthwith centred upon endless laborious researches into possible modes of uric acid formation, but which, alas, did little to purge men’s minds of their obsession that _uric acid_ was the _proximate cause_ of gout. Still it would be unfair to infer that the disabilities attaching to the uric acid hypothesis were wholly unrealised. Indeed, it may be fairly said of Duckworth’s reflections on the pathogeny of gout that they definitely foreshadowed the _infective_ theory. His views postulated what may be termed a _toxic tropho-neurosis_, wherewith to explain the paroxysmal nature, the periodicity and protean symptomatology of the disorder. But in the early part of 1900 we may, I think, discern in some words of Chalmers Watson a change coming over our thoughts as to the pathology of gout, this as the result of some studies of a series of examples of _acute gouty polyarthritis_. The results of his researches were such that he challenged the accuracy of Garrod’s original observations as to the lowered alkalinity of the blood during acute attacks, also his claim that the uric acid content of the blood was increased and the uric acid excretion diminished during the paroxysm. If these points be accepted, he says we must start _de novo_ in search of the cause of the acute paroxysm. He noted also the interesting fact that during acute attacks of gout a very marked _leucocytosis_ was present. Another outstanding feature was the presence in large numbers of peculiar myelocyte-like cells, half as many in number as the ordinary finely granular oxyphil leucocytes. Reflecting on these findings, he observes: “It would, I think, be well if much less attention were centred on the excretion of uric acid alone as the all-important factor in the disease, whether in its acute or chronic form. The results obtained by the line of investigation here followed suggest the advisability of more attention being devoted to the histo-chemical characters of the blood, the ratios of uric acid to other important products of metabolism, and, if opportunity be afforded, an examination of the bone marrow.”