While, then, we cannot as yet admit that acute miliary tuberculosis is always and only set up by a contagium, it is unquestionably true that it is in a large majority of instances caused by an infective material, which, however, does not come from without, but is produced within the system. This material is the purulent detritus resulting from the softening and breaking down of the inflammatory and other cellular hyperplasias which have undergone the caseous degeneration. It seems to make little difference whether the caseous product was derived from scrofulous glandular hyperplasia, catarrho-pneumonia, inflammation of serous membranes with a cellular exudation, or ordinary cellular inflammation; the only essential prerequisites being that there shall exist a cellular exudation or proliferation, and that these cells shall undergo the caseous degeneration.
The inoculation of this material into certain species of the lower animals or its absorption into the blood of a human being predisposed to tuberculosis will, as a rule, produce tuberculosis. Koch and his disciples add to the foregoing another prerequisite—viz. that the caseous matter must contain the bacillus tuberculosis. But as the bacillus is generally found in all the cheesy inflammatory products we have mentioned, they have (ignoring Virchow's definition of tubercle) declared that all these are tubercle, thus very much enlarging the hitherto accepted doctrine upon this subject. But if any of the cheesy products are found not to contain the bacillus, then such product is not tubercle, whatever may be the apparent identity or dissimilarity in their etiology, microscopical appearances, or clinical history. This seems to us to be a begging of the whole question of the relation of the bacillus to tubercle, and in the absence of fuller experimentation and investigation involves an assumption which cannot yet be admitted.
While the absorption of caseous pus is undoubtedly by far the most frequent cause of miliary tuberculosis, it cannot be inferred that all who may happen to have foci of caseous degenerations will necessarily be attacked by tuberculosis. On the contrary, a vast majority escape, and it is almost surprising how few of those who suffer from scrofulous inflammation of glands, joints, etc. become the subjects of miliary tuberculosis. Many cases of pulmonary phthisis also, originating as a cheesy pneumonia, run their course without any distinct tubercular complication. We can only explain these exemptions from the tubercular process by supposing that in such cases the predisposition to tuberculosis does not exist—they do not have the tubercular diathesis—or that such persons possess a peculiar means of resistance to the entrance of the infecting material into their blood.
Other diseases are supposed to favor the tubercular process, either by directly exciting or increasing the predisposition to it. Among others, measles, whooping cough, and typhoid fever have been regarded as specially liable to be followed by tuberculosis. Bad air, poor or insufficient food, onanism or other forms of sexual excess, severe study with insufficient exercise, and, in short, anything which impairs the strength or lowers the vitality, have been heretofore considered as excitants or predisposers of the disease. Admitting all these causes as effective in either exciting it or increasing the predisposition to it, there still remains quite a large residuum of cases in which the disease can be traced to none of these causes, and which, for the want of more accurate knowledge, we are compelled to call idiopathic or spontaneous. Such are those cases of tubercular meningitis occurring in young children heretofore in apparent good health, and in whom no traces of caseous degeneration can anywhere be found. It is true that it may be asserted that these children may have been infected through kissing by persons suffering from pulmonary consumption; but if this were so the disease ought to be far more frequent than it is, since the habit of kissing babies is universal and consumption the most prevailing of all diseases. In the absence of any proof to the contrary, we think that we are justified in believing that these are cases of spontaneous tuberculosis, occurring in consequence of intensity of the diathesis, either inherited or acquired.
Miliary tubercles are found in the form of small roundish nodules ranging in size from 1/500 to 1/250 inch (submiliary tubercles), up to the size of a millet-seed or even of a pea. When of the latter size they are always made up of a number of submiliary tubercles. Much larger masses are found usually in the lungs and in the mesentery, but these will generally be found to consist not of miliary or submiliary tubercles alone, but of cellular new formations derived from endothelial or lymphatic proliferations excited by the presence of tubercles, and therefore mixed with them. When first formed they are grayish in color, somewhat translucent, and tolerably firm to the touch (gray granulations). They soon, however, undergo partial fatty degeneration (this degeneration usually commencing in the centre of the mass), and subsequently are converted into a dry, yellowish-white, and somewhat crumbly mass which from its resemblance to cheese is called caseous. This sooner or later softens (the softening process beginning also in the centre), and the mass breaks down into a fluid detritus—tubercular pus. In some situations they never reach the caseous and purulent stage (notably in the cerebral meninges), because the interference with the organs or nerve-centres of animal life excited by their presence destroys the patient before there is time for the accomplishment of these changes. The subsequent history of tubercle depends upon the condition of the patient, his powers of resistance, the intensity of the tubercular diathesis, the injury inflicted by the first eruption, and the appearance of secondary eruptions. If all conditions are favorable, the patient placed under proper hygienic conditions and properly treated, the first eruption will also be the last, and the tubercle dries up into an earthy mass (calcareous degeneration), or it may remain for months, and even years, in its caseous stage without undergoing the softening process.
If we examine a fresh tubercle under the microscope, we find, according to Woodward2 and Zeigler,3 that it is usually made up of three different kinds of cells: first and most abundantly, lymphoid cells (Woodward) or white blood-cells (Zeigler); second, endothelioid cells; and third, embryonic cells. In addition to these there is often found (but not always) a few so-called giant-cells, generally occupying the centre or circumference of the tubercle, and sometimes both. These cells, which usually contain two or more nuclei and are much larger than the ordinary lymphoid cell, were thought at one time to constitute an essential histological feature of tubercle, and have been named tubercular cells. But the frequent absence of these cells in genuine tubercle has led to the conclusion that they do not possess any special significance and are purely accidental. Each submiliary tubercle is usually surrounded by a proliferating zone in which multinuclear (giant) cells and fibro-plastic or spindle-form elements can be distinguished (Cornil and Ranvier4). According to Rindfleisch,5 Woodward,6 and Zeigler,7 the cellular elements of tubercle are always found included in a trabeculum of fine fibrillar (connective) tissue, while Cornil and Ranvier deny the existence of any such trabeculum, maintaining that its appearance is due to the action of hardening agents used for preparing it for microscopic examination. Virchow and Woodward believed that tubercle always takes its origin in a lymphatic vessel, while Rindfleisch, partially agreeing with this view, maintains that they most generally occur in the lymphatic sheaths of the blood-vessels and follow the course of the latter, and that the cells which compose the tubercle are formed by proliferation of the endothelia of the lymphatics.
2 Medical and Surgical History of the War of the Rebellion, Part 2, Medical Volume, p. 593.
3 General Pathological Anatomy, London, 1883, p. 171.
4 Pathological Histology, Philadelphia, p. 116.
5 Textbook of Pathological Histology, Philadelphia, 1872, p. 125.