Suggestion of a Specific Infection
It will have been noted that, despite the growing number of adherents to the infective theory, no attempt had been made to saddle any particular organism with the responsibility of initiating gout. But in 1905 Trautner, holding mucous colitis to be one of the initial manifestations of gout, affirmed his belief that the bacillus coli communis was the responsible microbic agent.
He claimed that this particular organism, during its passage through the system, gives rise to a reducing agent which is subsequently transmuted into xanthin and uric acid. This is, of course, but a variant of Gore’s original view that the toxin of gout is a product of certain bacteria normally present in the intestine, but which under certain conditions take on a pathogenic action.
The microbic theory fast gained ground. Thus Luff, who in the first edition of his work advocated the renal origin of gout, subsequently renounced the same in favour of its infective origin. To sum up, the opinion generally was that it was more than probable that gastro-intestinal derangements, with their altered secretions, exert an influence on the intestinal flora with resultant formation of toxins, and that these same, acting chiefly on the liver, put in motion those obliquities of metabolism which eventuate in gout.
Sikes, however, in 1907, discussing the rôle of gastro-intestinal disorders, expressed a doubt as to whether the same are primarily or secondarily related “to the actual chemical processes at the base of the disease.”
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.