Inflammatory Tuberculosis, like the foregoing species, is rarely primary. It generally accedes to antecedent, insensibly generated tubercle, invading either the organ already diseased, or a structure intimately connected with it. Thus pneumonic tubercle and tuberculous pleurisy associate themselves to pulmonary phthisis; tuberculous peritonitis, to abdominal tuberculosis of the lymphatic glands. Or else tuberculoses become consecutively developed according to the same scheme, each fresh one bearing more and more decidedly the impress of its inflammatory origin.

The ordinary succession of the different fibrin-tubercles, and their different modes of exudation, partly deducible from the preceding statements, are highly interesting. Generally speaking, the gray tubercle, insensibly effused into an organ, leads the way. The yellow tubercle is less frequently the primitive one. Nor is the hypersemic or the inflammatory oftener the primary source of the effusion in either case. Upon the primitive, insensible deposition of gray tubercle follows, with increasing dyscrasis, the exudation of combined gray and yellow tubercle, the yellow progressively assuming the ascendant, until it ultimately exudes alone. Step by step the exudatory process becomes more and more acute in character; hyperaemia, inflammation, and, at the same time, the quantity of tubercle thrown out, more and more pronounced.

Under certain conditions there exudes, in the sequel of inflammation, more particularly in a new growth naturally prone to tuberculization (pseudo-membranes upon serous tunics), a tubercle reddened and pigmented by adherent haematin and embodied blood-corpuscles. It might be suitably denominated the pigmented or hemorrhagic tubercle.

The increment of tubercle, as a consolidated, non-vascular exudate abiding in its rude, primitive condition, can only take place through adjacency and blending with a mass recently exuded in its immediate vicinity. It is doubtless thus that many bulky, lobulated, stellate masses have become aggregated out of individual tubercles, dating from various periods.

But, whereupon does it depend that the product of the said processes, and, in particular, that the product of inflammation, in other cases reabsorbed or transformed into textures, is here precisely tubercle?

We do not consider the standing explanation of this phenomenon, namely, of the persistence of the exudate in its primitive rude state, satisfactory. It is to this effect:

(a.) The lack of an adequate vitalizing influence in the surrounding textures, and in the entire organism, upon the exudate (blastema). To this, it may be objected that the tubercle-blastema remains crude, however scanty its proportion, and however unimpaired the energies of the surrounding textures and of the entire organism. On the other side, we find in the vicinity of diseased parts, and this in persons altogether debilitated and cachectic, bulky blastemata forming into textures both homceoplastic and heteroplastic; even into textures whose development is, generally speaking, very easily arrested; for example, bone-callus in individuals affected with osteo-malacia, cicatrix in, and in the proximity of, ulcerating textures. We might with propriety ask, wherefore does not the portion of an exudate farthest removed from the living textures and their influence, - wherefore, for example, in exudates upon membranous expansions, does not an entire layer uniformly, - why, in the midst of exudates, do only little scattered portions abide crude, that is tuber-culize, whilst the remaining major part of the exudate becomes developed into textures?

(b.) The lack of sufficient moisture, of water, in the blastema, is alleged as the condition upon which tuberculization depends.

To this we reply that tubercle-blastema exudes under all conditions, and, not at all rarely, with a considerable amount of water, of blood-serum. A primitive lack of moisture in the entire exudate cannot therefore determine the tuberculization, the tuberculous nature, of its coagu-lable, solidifying portion. If perfected tubercle be poor in water, it is so obviously in consequence of the high degree of solidification of its blastema. This, therefore, namely, its high degree of coagulability, might be the cause of the tuberculous nature of the exudate, - of its persistence at its primitive stage of crudity. This, again, might be the reason why the tuberculous exudate takes the form of granulation. Inflammatory products, like blastemata generally, seldom exude pure. Inflammatory products of a tuberculous nature are, therefore, ordinarily alloyed with others of a different kind. Hence, portions of the former emerging, by reason of their transcendent coagulability, from their combinations with the latter, appear to the eye in the shape of roundish coagula, in a word, of tubercle.

But, again, it will be necessary to ask, whereupon does this high grade of coagulability depend?

It can but be founded in an as yet unknown dyscrasial constitution of the fibrin, as tubercle-blastema. There are blastemata dry from primitive poverty in serum; and also others which, parting with their serum and passing into a high degree of condensation, nevertheless do not tuberculize, but become developed into textures, in the plenitude of their mass. It would appear evident, therefore, that the tuberculous nature of a blastema must be indwelling, be acquired either during the local process (inflammation) or in the general blood-disease which preceded and prepared its exudation. Accordingly, tubercle would, as once before stated, have to be interpreted, now as a local, now as a general affection.

This general character of tubercle is the more marked in proportion as its mass as an exudate is considerable; as its diffusion through the organism is extensive; as its characters are impressed upon any spontaneous coagula formed within the vascular system; and, lastly, as the organism in its totality reflects and manifests the tuberculous habit.