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
If we reflect on the general features and local characters of an initial outbreak of gout they are precisely such as would, did they occur anywhere but at the classic site, the big toe, suggest an infection. The abrupt onset, the local signs, the crisis, and no less the subsequent swift restoration to health, how strikingly reminiscent of an exanthematous fever! Moreover, does not this outward clinical resemblance seem to predicate an inward pathological similarity? And now to scrutinise more narrowly the component elements that make up the content of a paroxysm of gout.
Its fulminant onset, with shivering, if not a definite rigor, in a person in sound and sometimes exuberant health, irresistibly reminds one of the sudden onfall of an infective disorder. Doubtless, as Duckworth says, “the conditions leading up to the attack have been some time previously in operation.” But, as he rightly contends, “some determining factor must now be invoked to explain how, as it were, the train is fired.” Quite so, and what more likely to call into the open these latent morbid potentialities than an infection?