He thinks it at least as probable that the gastro-intestinal disorders are due to an alteration in the intestinal secretions from an internal cause as that they are due to bacteria in the formation of toxins, or, he suggests, to some alteration in the epithelial cells, so that they take up chemical compounds of different nature from the ordinary. To him it does not seem at all probable that gout will ever be found affiliable to any specific micro-organism, inclining rather to the belief that a solution of the riddle will only be found in a closer and more extended study of that most difficult subject, the actual chemistry of the cell protoplasm.
CHAPTER XIV
GOUT AS AN INFECTION
“The old order changeth, giving place to new,” and the uric acid theory having failed us, it is essential that we cast round for some other solution of the problem, carrying with us, however, this guiding principle, that uric acid, having lost its etiological status, be viewed in its right perspective as not the cause, but the consequence, of gout.
Happily, with the advent of bacteriology our views, or rather our hazards, as to the nature of joint diseases underwent profound modification. But, strange to say, though quick to apprehend the significance of infection, its causal relation to other joint disorders, we still seem unaccountably loth to discard our time-worn conception of “gouty” arthritis as of purely metabolic origin. This, to my mind, is the more remarkable in that the onset, clinical phenomena, and course of acute gout, and no less the life history of the disorder as a whole, are emphatically indicative of the intrusion of an infective element in its genesis.
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.