The assumption gathers weight in light of the experimental proof adduced by Adami that not only tubercle bacilli, but _streptococci_ and other organisms, _taken orally_, can gain an entrance into the system. Upon this basis we get a clear conception of the possible relationship of gout to _local foci of infection_. Thus, whether it be a condition of oral sepsis—pyorrhœa alveolaris, tonsillar sepsis, sinus disease, intestinal disorders, constipation, and so forth—we see that it is highly probable that organisms at any one of such infective foci may gain access to the blood-stream with subsequent installation of local lesions in _joints_ or other structures. Now, as pointed out, inflammatory states or _functional_ derangements of the _alimentary_ tract, whether focal or diffuse, favour the ingress into the tissues of organisms. Is it not reasonable, therefore, we ask, to suppose that the functional derangements which so commonly precede or accompany gout may modify the character of the _intestinal flora_, and promote their migration inwards in greater numbers? The inevitable swiftness with which relapses or exacerbations of this disorder follow even venial dietetic indiscretions distinctly favours this assumption, one, moreover, substantiated by the amelioration or immunity which follows abstention from the offending foodstuffs. The often prolonged course, too, of gout, and its marked liability to periodic recurrence, would be explicable as the outcome of a continued or intermittent series of sub-infections. My conclusions then are that:— (1) The majority of cases of gout are marked by the presence of _local foci of infection_, pyorrhœa alveolaris, tonsillar, pharyngeal or nasal sepsis, etc., or by gastro-intestinal derangements, constipation, etc. (2) The said local foci should be regarded not as symptomatic of, but _etiologically_ related to, gouty arthritis, and that the same is strongly indicated by the fact that (3) Acute _glandular_ affections of undeniably _infective_ source—tonsillitis, pharyngitis, etc.—frequently and immediately _precede_ acute paroxysms of _articular_ gout, and, lastly, (4) The gastro-intestinal defects, secretory or motor, which chequer the course of gout, enhance the pathological activities of the intestinal flora, and incidentally the liability to infection, at various sites of the alimentary tract. CHAPTER XV GOUT AS AN INFECTION (_continued_) ANALYSIS OF THE ACUTE PAROXYSM