Those who favour the view that _direct infection viâ_ the blood from foci of oral sepsis is the more probable _modus operandi_ are wont to produce the following points in support of their view. Arthritis, they say, is relatively rare in _enteric fever_. In yet another disorder, _dysentery_, which gives every chance of absorption from the intestine, arthritis when it occurs is seldom very acute, while in _appendicitis_ it is distinctly uncommon. On the other hand, we must recall that even in normal animals the alimentary and respiratory tracts, and alike the liver and kidneys, constantly afford cultures of pathogenic and non-pathogenic bacteria. Such was established by Adami and his co-workers, who moreover found that such organisms, through the agency of leucocytes, continually pass into the system, where subsequently in the healthy animal they as constantly undergo destruction. If, however, inflammatory processes are at work, their migration into the tissues is favoured. For under such conditions leucocytes aggregate at the reactive focus, and concurrently, their migration being more active, larger numbers of bacteria achieve entry into the system. The subsequent course of events is determined by the number and virulence of the organisms that effect a lodgment in the tissues, where under favourable conditions they originate other foci of infection or sub-infection. By _sub-infection_ is understood the fact that microbes carried into the system undergo slight, if any, numerical increase, and do not set up _foci of suppuration_. Here we may note that “gouty” inflammation, however intense, never ends in _pus formation_. But, to resume, the bacteria, instead of multiplying, undergo lysis, and, their endo-toxins being released, the more highly specialised tissue cells in the vicinity are destroyed. Coincidently the lower grade connective tissue elements are by the self-same poisons stimulated to proliferate, and an area of _chronic interstitial fibrosis_ is formed. Incidentally this is interesting, inasmuch as the _visceral_ organs in gout evince a tendency to _fibrosis_. But, as Gideon Wells observes, “the actual increase of uric acid in the blood and tissues in gout is so slight that we are not warranted in saying that the usual tendency to sclerosis in all the organs in gout is due to the action of uric acid rather than to some other unknown agent or agents.” In view of these revelations, is it not infinitely more likely that the chronic interstitial fibroses in gout are the outcome of such _sub-infection_?