Although there are, no doubt, tuberculoses purely local, a tuberculosis extending through several organs, or even through one entire organ, is invariably the offspring of a tuberculous dyscrasis.

The latter is for the most part developed out of a fibrin-crasis. In the dead subject, a hyperinosis of the blood may not be ostensible. Nay! owing to the frequent and voluminous processes of exudation attendant upon the course of a tuberculosis, a poverty in fibrin is perhaps more likely to reveal itself after death. Excess of fibrin has, however, been demonstrated, in such cases, by the chemical examination of blood withdrawn during life, and it may also be inferred from the extent of the tuberculous deposition. Still the hyperinosis is far from being adequate to account for the disease. It is the qualitative anomalies of the fibrin that must determine its tuberculous nature, - anomalies of quite a peculiar kind, which, as we shall see, may modify every one of the fibrin-erases referred to into the tuberculous.

The gray tubercle answers to the character of the simple jibrin-crasis. [See "Gray Tubercle."]

The opaque, yellow, lardo-caseous tubercle, marked by its proneness to undergo softening, answers to the character of the croupous-crasis. [See "Yellow Tubercle."]

We have remarked of the products of the fibrin-crases that they are seldom unalloyed. The same observation applies to the products of the tuberculous crasis. The products of the one always occur intermingled with elements of the other; and tuberculous products may even include more or less of organizable elements which form into textures in the ordinary way.

Again, the transitions of the individual tubercle-crasis from one to another are obviously brought about step by step. The croupous tubercle appears but rarely as the primitive tubercle. It is generally based upon a pre-existent gray tubercle, and the croupous tubercle appears as an aggravation of the simple form.

In the fibrin-erases a minimum of fibrin suffices for the groundwork of a qualitative impairment, and this in its amplest sense applies to tubercle. The smallest proportion of fibrin present in the blood takes on the taint and becomes expended, up to the point of complete defibrination, in the deposition of tubercle.

Still these said erases by no means serve to throw much light upon the nature of tuberculosis. They must needs involve a peculiar - a tuberculous - modification, the existence of which is indeed proved by the tuberculization of extra-vascular fibrin in hemorrhage, and also of intravascular fibrin-coagula. In this modification must be rooted:

(a.) The surpassing proneness of the fibrin to deposition, so frequently brought about in quite an insensible manner;

(b.) The assumption by the deposited fibrin of the particular form of tubercle. The granulation of tuberculous products of inflammation upon serous membranes might indeed be ascribed to a separation of the tuberculous portion, due to its great coagulability. Still the very localization of the tubercle-crasis, in such minute and sharply-defined areae that little granule-shaped exudates are the result, constitutes a peculiarity - a remarkable peculiarity, seeing that the same form of separation - the same form of tuberculization - attaches to the fibrin of hemorrhage and to endogenous vascular coagula.

(c.) The fact that blastemata resulting from the tuberculous fibrin-erases do not undergo the metamorphoses - proper to the pure fibrin-exudates - of textural formation on the one side, and of rapid purulent liquefaction on the other; but throw off their exudate-water in the act of firm coagulation, and tarry for a while in this crude state of consolidation. This respite is of various duration, but at all events exceeds both that proper to textural conversion, and that common to disintegration, in corresponding, purely fibrinous exudates.

As the most marked and obvious phenomena connected with tubercle must be specified its high grade of coagulability, and its surpassing prone-ness to deposition, - to the localization of its crasis. In these are without doubt centred the peculiarities of the fibrin-crases in their tuberculous modifications.

If, in relation to these peculiarities of tuberculous fibrin, we take into account:

(a.) The consummate coagulability of arterial fibrin generally;

(b.) Its supreme sensitiveness towards heterogeneous substances, such as inflammatory products, whose reception, for example, in arteritis, occasions locally so rapid an obstructing coagulation of the blood-column, as to obviate any infection of the general blood-mass from that point. [See "Arteritis," vol. iv].

(c.) The ready deposition of fibrin out of arterial blood, as stratiform coagula upon the inner arterial surface, a disease, in its consummate form, peculiar to arteries.

(d.) The very common localization both of the fibrin-erases, whether spontaneous or determined by infection, in the shape of exudate, or of endogenous coagulation within the capillaries of the arterializing organs [the lungs], and again the still more marked relation of the tuberculous crasis to these viscera.

(e.) On the one side, the pre-eminent development of the pulmonary organ as predisposing to the fibrin-erases in general, and to their tuberculous modification in particular;

(f.) On the other side, the pre-eminent immunity afforded by exquisite venosity and cyanosis, against fibrin-erases, more especially the higher (croupous) grades, and most particularly against the tuberculous crasis, - taking, we say, all these circumstances duly into account, we are forced on to the momentous conclusion that arteriality, that is, the arterial development of the fibrin, pre-eminently constitutes the cardinal character of tuberculosis.