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perivascular sheaths, and from both these sources of origin a rapid extension ensues into the surrounding walls of the alveoli and smaller bronchi. A thickening of these is thus produced apparently by a double mode of growth— by a rapid development of fusiform cells at the margins, clusters of which are seen passing among the capillaries, and by an increase of rounder cells which are seen nearer the centre of the new formation; coincidently with this growth a change of great importance occurs in the neighbouring capillaries of the lungs: their nuclei enlarge, and the vessels otherwise apparently unchanged, contain no blood—that is to say, no injection will pass into them; and yet their outline is still marked by lines of nuclei. This obstruction of the capillaries takes place through very much wider areas than the space apparently occupied by the tubercle. So also with the thickening of the walls of the alveoli. Around the grey granulations, and for a space of three or four times their area, there is a circumference of thickening affecting the walls of both the alveoli and the smaller bronchi. This appearance is more distinct in the guinea-pig than in many specimens of tubercle in the human lung; but it can sometimes be distinctly seen in the latter, and is a fact of great pathological importance, explaining the increase of density and loss of elasticity in the lung, which occurs in the early stage of tuberculosis, and which cannot be satisfactorily accounted for by the mere presence of the grey granulations.'1

In his second paper, Dr. Sanderson confirms his conclusion that the tubercles and consolidations artificially produced in the various organs of animals consist essentially in overgrowth and induration of the adenoid tissue naturally existing in various parts of the textures; but as regards the semi-transparent and iron grey nodules in the 1 Dr. Wilson Fox, op. cit., p. 10-12.

lungs, that they comprise also an accumulation of the bodies commonly found in the alveoli, and which have been generally but erroneously considered epithelial. These alveolar cells are nucleated bodies consisting of a solid envelope of transparent substance collected round a more refractive central part, and contain pigment and other granules. The true alveolar epithelium cells are much smaller, and are very difficult to demonstrate; but those in the terminal bronchi can be made evident by nitrate of silver, and appear as oval plates, with spherical nuclei about half their width. 'In animals killed at an early stage of tuberculosis, that is to say about four weeks after inoculation, no change is observed except that the peribronchial adenoid pulp is increased, or in other words that true miliary granulations are formed in the neighbourhood of the terminal bronchioles.' Subsequently the alveolar cells become multiplied, and, filling the aveoli, complete the mass of iron grey nodules. 'Whether the choking up of the air-cells is merely a mechanical result of the accumulation of adventitious matter around the bronchioles, or of a catarrhal process, there can,' Dr. Sanderson thinks, 'be little doubt that the granulation stands to the block of lobular pneumonia in the relation of cause to effect, and that when a kernel of adenoid pulp occupies the centre of a nodule, the fact signifies that the nodule originated from it.'1

Dr. Wilson Fox also denies the epithelial character of the alveolar corpuscles, and, as a true disciple of Virchow, considers them to be derived from the connective tissue.

It is not necessary for our object to enter into the details of the process of artificial tuberculisation in other organs. Suffice it to say that they correspond in character with those in the lung, having their origin and chief seat in the adenoid tissue, naturally existing in mem1 Dr. Burdon Sanderson, 11th Report, <Jr., p. 115.


branes or textures, appear first as a rapid multiplication of lymph cells or corpuscles, with a fibrous network, all of which increase and harden, and eventually caseate and break up by fatty degeneration and disintegration, with variations in course and concomitants, according to the structure and functions of the parts.

The perfect resemblance of tubercle thus artificially produced to human miliary tubercle, in seat, general distribution, intrinsic structure, and in course and effects, removes all doubt as to their identity. But as regards their modes of origin, and comparative power of affecting different animals or species, there may be yet a great difference; and we must be cautious, therefore, before we apply all the facts of an artificial tuberculosis to the spontaneous occurrence of tubercle in man. The closest analogy lies with those cases of tubercle which are of constitutional nature, not arising from a visceral inflammation or any local cause, nor affecting one organ in particular, but scattered through several in the form of miliary granulations, and having their origin in the circulating lymph or blood. We comprehend them, therefore, under the second division of the Table of Elements of Consumptive Disease (p. 60).



Nature and Conditions of InfectionCausation of PhthisisSpecific or Common Septic ?—Parallel between Experimental and Clinical Origin of TuberclesPredisposition necessaryDefective Vitality of Sarcophytes, and corrupting Influences in the AirAnalogy between Pyremia and Acute TuberculosisThe latter developed by Heat and DampInflammatory and Chronic Phthisis produced more by ColdThe former more diffusive, the latter more circumscribedInfluence of Climate and Altitude on different forms of Consumptive Diseases.

We may sum up the chief facts of the process of the production of tubercle by inoculation in the following conclusions:—

1. With regard to the material necessary for inoculation, it is no specific form of tubercle, nor even tubercle at all; for some non-tuberculous matters are equally successful, and, in a minor degree, matters formed in an open wound in the same animal. But those materials are most sure to produce tubercle which either resemble it in its tendency to decay, or show a septic character, as foul pus, putrid muscle, carious bone, and the like. On the other hand, healthy pus or other product of acute inflammation, has no effect; and although a seton or other open wound sometimes produces tubercles, yet setons dressed with an antiseptic, and wounds secluded from the septic influence of the air, have no such result.

2. The local effect of successful inoculation is not active inflammation, suppuration, or sloughing, for these always

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prevent the tuberculisation; but either low inflammation, slowly producing a slight abscess, often offensive or cheesy; or the direct formation of little nodules at the point of inoculation, consisting of adenoid indurations, and which may be considered a primary tuberculisation. And what are these but sarcophytes or bioplasts, proliferating and hardening in their fibrous network, and tending to early death and decay by caseation?

3. The next effect is found in the lymphatic glands supplied by the absorbents proceeding from the seat of inoculation. These are enlarged, indurated, and soon become cheesy in points, but never suppurate (in the guinea-pig), even where there may have been partial suppuration in the primary wound. Most natural is it that the lymphaties should convey injured sarcophytes (lymph corpuscles) to their usual receptacles, and with them that deteriorating influence on the myriads of sarcophytes contained therein, which take on the same degenerative course of rapid proliferation and induration, ending in early decay.

4. After the lymphatic glands, various organs and membranes of the body become invaded by the indurations, chiefly in the granular form of grey tubercles, but some, as the liver, in larger masses. But in all forms and sites the careful examinations of Drs. Sanderson and Fox have detected the same structure, that of the adenoid or lymphatic glandular tissue, hypertrophied and indurated by multiplication of corpuscles and fibrous reticulum; tending to obstruct and irritate the natural structures, and to infect them with their own degeneration and decay. The channel of dispersion may be both the lymphaties and blood-vessels, communicating, as they do, not only through the thoracic duct, but more directly in the spleen, and probably also in the lymphatic glands, in which the blood and lymph corpuscles are either intermingled or


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