In developing this hypothesis I purpose devoting the present chapter to consideration of the frequency with which local foci of infection are met with in gout, the frequency, too, with which exacerbations of the disorder are presaged by acute glandular affections of undeniably infective source. The latter part of the text will concern itself with the rival claims of _auto-toxæmia_ and _infection_ or _sub-infection_. In the subsequent chapter we shall analyse critically the component elements of the acute paroxysm of gout, their compatibility or not with an infective origin. The affinities between gouty arthritis and the specific infective arthritides will then be noted, and, finally, an endeavour made to link up the specific stigmata of gout—its uratic deposits—with the postulated infective element. LOCAL FOCI OF INFECTION The extreme frequency with which _infective foci_ are met with in the victims of gout is by no means adequately realised. Moreover, we are only now beginning to appreciate the grave significance of such “nests” of infection and how devious are the ways in which they work their malign influence. For our forefathers gout began, and, forsooth, often ended, in the “stomach,” or it was the “liver” that was impeached. But the portal to the alimentary canal was for them only a cavity, the contained structures of which, albeit, to their mind often betrayed evidences of a “gouty diathesis.” They distinguished “gouty” teeth, “gouty” tonsillitis, “gouty” pharyngitis, even “gouty” parotitis; but all these they classed as tokens or sequelæ of gout—not possible causes or excitants thereof. Nevertheless, their observations on “gouty” teeth are of deep interest, though their significance was misinterpreted. Thus, Duckworth, for example, wrote: “The tendency to shed sound teeth has been noted with some frequency in middle or later life in goutily disposed persons, and they are more than others liable to occasional and fugitive attacks of pain in several sound teeth at a time, with a sensation as if these were starting from their sockets, being tender to bite upon.” In truth, a succinct picture of _pyorrhœa alveolaris_, of unprejudiced source, hence the more valuable. Garrod again tells us that he saw an initial attack of gout supervene after extraction of a tooth, a sequence attributed by him to loss of blood. How interesting this, in light of the fact that exacerbations of joint disease have frequently been seen to follow the removal of septic teeth. The same authority also noted the incidence of a primary attack of gout following _epistaxis_, and the same after copious _hæmatemesis_, and Todd several times observed such articular outbreaks after _venesection_.