How noteworthy the well-established proclivity of gout to involve bursæ, tendon sheaths, and fasciæ, especially the plantar! Is not this exactly paralleled in certain _infections_? Note the predilection of post-scarlatinal rheumatism for bursæ and tendon sheaths; that of the gonococcus for these structures as well as fasciæ, not to mention the frequency with which bursal enlargements are traceable to syphilitic, tuberculous, and other infections. We see, therefore, that in virtue of its tendency, not only to _arthritic_, but also to _muscular_ and _nerve_ disorders, gout falls into line with the _specific infections_. Its predilection for bursal and fascial structures is but another evidence of affinity with this group of disorders. In view of these similitudes, one may well ask, Are not these _gouty_ manifestations, all of them, susceptible of a like explanation, viz., that they are the outcome of an _infection_? For, in reviewing the foregoing analogies, it cannot, we think, be denied that in the aggregate they are emphatically suggestive of an infective origin. CORRELATION OF THE METABOLIC PHENOMENA OF GOUT WITH THE POSTULATED INFECTIVE ELEMENT In essaying this difficult task, we must recall to the mind of the reader our findings or deductions from the data disclosed in preceding chapters. The outstanding conclusions that we felt justified in formulating were that:— (_a_) Uric acid is not the cause but the _consequence_ of gout. (_b_) _Inflammatory reaction_ is, we believe, an invariable precursor in all gouty processes. In other words, we suggest that, although abnormalities of metabolism form an integral part of gout, they are of themselves inadequate to achieve its efflorescence. Thus, when we came to consider the elemental manifestations of gout, _i.e._, uratic deposits or _tophi_, we saw that neither the purely physical nor the purely chemical theory of their origin would suffice, nor, for that matter, could any solution of this complex problem be gleaned from even a blend of the twain. In short, such hypotheses are too _mechanical_. The intrusion of some other factor, “some vital something biological,” seems essential for the elucidation of _uratosis_, _i.e._, uratic deposition. For this, _not uricæmia_, is the specific characteristic phenomenon of gout. If we cannot explain uratosis on physical or chemical grounds, then how much less, in view of the _non-toxicity_ of _uric acid_, can we, on this basis, account for the _inflammatory_ phenomena of the disorder?