Ingestion.— For years it was thought that tuberculosis of the lungs was the result of in halation of the germs, and abdominal tuber culosis the result of ingestion with food or otherwise. The argument favoring this view appeared plain ; namely, tnat primary mesenteric gland tuberculosis is almost limited to children, especially the bottle-fed. Living as they do en tirely on cows' milk, and considering the sus ceptibility of horned cattle to tuberculosis, the inference seemed so justified that scarcely any exception was taken to it. In addition, adults who live as a rule on cooked food scarcely ever show mesenteric gland tuberculosis as a primary infection, but practically always tuberculosis of the lungs, which would readily seem to be the result of contact with the disease in their occu pation, sleeping-rooms, etc. This plain view of the matter has, however, undergone a change. The majority of clinicians and pathologists of our day believe that children manifest the mesenteric form more frequently simply be cause these glands are more susceptible at that age, and adults the pulmonary form for an analogous reason. For several years at the end of the 19th century considerable was writ ten to prove that practically all cases of tuber culosis were the result of ingestion of the germs. It was contended that even in tuber culosis of the lungs the germs entered through the digestive tract, passed into the chyle-vessels with the fat, were carried through the thoracic duct to the heart and took up lodging in the lung on account of its non-resistive power. The experiments about this time demonstrating the infectivity of cows' milk became so numer ous (Gerlach, Bang, Bollinger, Ernst) that the question of the digestive tract as a probably common route (if not actually the most com mon) seemed practically settled. At the British congress on tuberculosis in 1901, however, Koch threw a shell which scattered scientific physicians and left them in two hostile camps. Coming from any one else the opinion (for it was scarcely more than an opinion, being based on a small number of experiments) would have been scoffed at, but coming with Koch's au thority it could not fail to arouse interest and even advocates. Koch affirmed that the differ ence between the bovine tubercle-bacillus (that is, the bacillus causing disease in cattle) and the human tubercle-bacillus was such that one was not contagious to the other species, or was so slightly contagious that the number of case's of tuberculosis thus produced might be left out of consideration without impairing statis tics. During the past 18 years the efforts to disprove Koch's statement have been numerous, but the question is not yet absolutely settled. Our investigations are conclusive enough, how ever, to lead us to believe that about 5 per cent of the cases in human beings are due to the bovine bacillus. Practically all of these are in the lymphatic glands of children, or in other extra pulmonary locations; the number in the lungs of adults is negligible.
Primary and Secondary The belief is gradually gaining ground that the ordinary manifest tuberculosis of the lungs is a result not of primary but of secondary in fection. Inoculation experiments on animals have always shown primary inoculation to pro duce tuberculosis of the nearest lymphatic glands with no lesion at the site of inoculation, and secondary inoculation to produce no lesion of the lymphatic glands with definite tubercu losis at the site of inoculation. It would ap pear, therefore, that pulmonary tuberculosis is the result of secondary rather than primary in fection and occurs in one of the following ways: The individual ingests tubercle bacilli, which pass through the intestinal wall without producing a lesion, but cause tuberculosis of the mesenteric, and later the bronchial glands.
The disease of the bronchial glands produces stasis of the lymphatic circulation in the lung, with a consequent retrograde flow of lymph, which carries the tubercle bacilli from the glands to the lung tissue. Or after the lymphatic glands have become involved an en tirely new Infection by inhalation or ingestion produces the pulmonary manifestation. A num ber of investigators (prominent among them Bushnell) believe that the primary infection practically always occurs in childhood and that adult infection is extremely rare.
Pathology.— When the tubercle bacilli are deposited in a tissue they proceed to multiply. Like other plants in growth, they take from their surroundings the chemical elements neces sary. The living cells from which this material is taken die. In addition, the growing bacilli throw off waste products containing a poison (toxin) which kills other cells. We soon, therefore, have the tubercle bacilli in a mass of dead debris. A reaction now occurs on the part of the healthy tissue to prevent extension —the cells of the part multiply, and white blood cells wander in from the blood for the pur pose of consuming the organisms. It is this mass of bacilli, debris and new cells which constitutes the tubercle described first by Baillie in 1794, and which is the specific lesion of the disease no matter in what organ it occurs. The debris looks like a soft cheese, and is called caseous material or caseation. The new cells are called epithelioid. Usually a tubercle also shows what we call a giant cell, a cell three to eight times larger than the epithelioid.
The question of the cure of the tubercle seems to depend on whether the epithelioid cells or the tubercle-bacilli obtain the upper hand. If the epithelioid"cells are manufactured more rapidly than the tubercle-bacilli destroy them they form a dense wall about the tubercle bacilli, elongate, become fully formed fibrous connective-tissue cells, thus shutting the bacilli up in a capsule, and the bacilli die, while the caseous material calcifies or is absorbed and re placed by scar-tissue or fibrous tissue. When the amount of fibrous tissue in the lung is large we speak of fibrosis of the lung. If, however, the bacilli are victorious the tubercle may grow larger and, coming in contact with other tuber cles, form what is known as a conglomerate tubercle, and so continue until even a whole organ is involved. Again, the caseation may advance so rapidly, especially in the lung, that there is never any sharp demarcation between healthy and diseased tissue. This is generally called diffuse tuberculosis, and in the lungs is known as caseous or tuberculous pneumonia.
Finally, as the tubercle advances, other micro-organisms (particularly streptococci or staphylococci) may gain entrance to the caseous material and break it up. If now the tubercle, in growing, reaches a surface its liquid con tents may be expelled, leaving behind an ulcer or a cavity. This happens most frequently in the lungs, and the resultant cavity may be of any size from a pea to that of a whole lobe of the lung.
The cavity is usually within the lung, or if at the margin, is limited by the pleura, which thickens about it. Sometimes, however, it breaks through the pleura, allowing pus into the pleural cavity, which is called pyothorax or empyema; occasionally both pus and air are ad mitted producing pyopneumothorax.