“Dr. Ruhling, of Gottingen, writing in 1774, of the disease in animals, says: ‘The malady is transmitted to sound animals by direct contact of animals standing side by side in the stall, and licking each other, and breathing the expired air direct from the diseased lungs; the frequenting of the same pastures will also serve to propagate it.’ In Krunitz’s encyclopedia, published in Berlin, in 1787, is the following: ‘The heifers show an ardent desire for the male, and remarkably enough, do not become pregnant, but part with the fruit of conception. When opened these animals show the first stomach, kidneys and surface of the lungs, covered with pustules like dried mulberries or in suppuration. The affection is contagious, and communicates itself from one animal to another by contact.’
“Fromage, in the Dictionaire de Rozier, Article Phthisis, says: ‘Men of art are very much in accord that this malady is not contagious, but some stock owners think differently.’
“Huzard, who saw much of tuberculosis in the Parisian dairies in the concluding decade of the last century, said that most of the veterinarians looked upon the disease as contagious, and that some of the physicians believed the same of the phthisis of man.
“Dewar, speaking of his experience in Scotland in 1839, and succeeding years, in a particular herd, says: ‘The proprietor agreed to remove partition walls, and to make openings opposite one another in the outside walls, so that there might be a current of fresh air passing through. These alterations combined with cod liver oil, tonics and stimulants, may have prolonged life but yet no cure was effected, and that herd died out. I resorted to every precaution when new cattle were purchased to prevent infection; as I had an idea, even at that time, that the disease might be communicated from one to another when in immediate contact. The precautions adopted when fresh cattle were purchased had the desired effect, for in a few years afterward, they were as good a lot of cattle as any in the district. That herd left an impression on my mind that never can be effaced, and made me always dread the evil consequences of tuberculosis. Having practiced in the same locality, which is an extensive breeding and rearing district, I have seen several herds decimated. Though I have sometimes foretold the owner what he might expect, yet he did not believe me until so many were infected that the byres were infested with the fearful malady, and your remarks in regard to nose contamination are so true that I do not think it possible any can escape that are so exposed. I have also seen, as Grad has, the same stall infecting beast after beast until a thorough cleaning and disinfecting, with plenty of fresh air had removed all infection.’
“Spinola, writing in 1858, of bovine tuberculosis, gives contagion as a possible cause, and Lafosse, in 1867, says: ‘Physicians begin in imitation of Morgagni to believe in the contagion of phthisis. The facts published by Villemin appear to support this opinion, which has been held by our colleague, Dupont, of Bordeaux, for several years.’
“Cruzel in his work of date, 1868, is much more positive; he says: ‘This fœtid expired air, inhaled immediately by another cow upon a sound lung, gives the latter tuberculous infection. It is a matter of every day experience to the veterinarian. Two oxen or cows are kept in the same stable, take their food from a common rack or manger, lie in the same stall, and respire nose to nose. The one is, to all appearances, perfectly sound, the other is in as good a condition, and is vigorous, but it coughs from time to time, and its breath is foul. Soon we notice that the animal that does not cough, eats with less appetite, he loses flesh and soon he is unequivocally affected with the same malady as the first.’ The foregoing quotations show clearly that in spite of the misleading teachings of Broussais and others, the doctrine of contagion in tuberculosis could not be overcome, and that up to the time of the remarkable experiments of Villemin, in 1865, it maintained its hold upon the minds of extensive and careful observers. In animals, especially, the evidence was so frequent and clear, animal following animal in the same stall, and eating from the same infected manger, only to be infected in turn, and two animals stalled together, and licking the same manger with their prehensile tongues, transmitting the infection with certainty the one to the other, were facts that could not possibly be ignored. Other cattle in the same building might escape for a length of time, but the eating in common from the same fatal manger, by a tuberculous and a healthy animal, quickly sealed the fate of the latter.
“Physicians, too, who were compelled to investigate the causes of the extraordinary fatality from tuberculosis in the armies and navies, could not shut their eyes to the fact notwithstanding that they came to the task strongly prejudiced through education against the acceptance of contagion. Thus, Dr. Bryson, in his report to the Epidemiological Society, in 1860, on consumption in the several ships of the English navy on the Mediterranean station, says distinctly that the disease appeared to be propagated by contagion. Dr. Parkes, quoting this in his Practical Hygiene, says: ‘It may be inferred that pus cells were largely thrown off during coughing, and floating through the air, were received into the lungs of other persons. The production of phthisis in animals confirms this view. The case of monkeys in the zoological gardens, narrated by Dr. Arnot, is a striking instance. Cows in close stables frequently die of phthisis. But not only phthisis may reasonably be considered to have one of its modes of origin in the breathing of an atmosphere contaminated by respiration, but other lung diseases, bronchitis and pneumonia, appear also to be more common under such circumstances.’
Villemin in 1865, published his investigations in which he had produced tuberculosis in a great number of animals, by inserting particles of fresh tubercle or injecting the tuberculous sputa of man into the subcutaneous connective tissues, the peritoneum and the trachea. There resulted in nearly every case a chronic disease, the marked phenomena of which were caseated centers devolving from firm inflammatory nodules in the seat of inoculation, in the adjacent lymphatic glands, in the lungs, serous membrane, liver, spleen and kidneys. The centers of such nodules were at first transparent and grayish, but soon the center underwent necrobiosis, forming a soft cheesy mass the size of a pin’s head, and gradually enlarging to that of a pea, a bean, a hazel nut or larger. After a period of about 14 days the lymphatic gland nearest the seat of injection could be felt as a firm pea-like nodule, and in two weeks more a second gland on the line of the lymph circulation, had become enlarged and nodular, while the first, now the size of a large bean, had probably undergone distinct softening. This became adherent to the skin, burst and discharged continuously or at intervals with little or no tendency to heal. If killed at this date, the animal showed only the open sore and a chain of nodular pea-like caseated lymphatic glands leading up from it. The lungs might be apparently sound, but the spleen and liver usually showed miliary elevations on the surface, with clear grayish centers, as viewed under a magnifying glass, opaque patches were found on the omentum, and the lymphatic glands of the mesentery, of the portal fissures of the liver and of the Hilus of the spleen were distinctly enlarged and resistant. If not killed, the subject usually died 100 to 120 days after inoculation, and then the lungs were found studded with tubercles miliary or larger and more or less caseated; the bronchial mediastinal, subdorsal, pectoral, prepectoral, phrenic, mesenteric, hepatic, and splenic lymphatic glands were more or less enlarged and caseated, while the liver and spleen were enlarged and studded with multiple tubercles. Guinea pigs give the most extensive and intensive lesions, rabbits much less so, but in both emaciation and wasting are very marked. In short the lesions are essentially and unmistakably those of generalized tuberculosis.
“At first, however, incredulity prevailed and experiments on a large scale were inaugurated all over Europe and America to put the question to crucial test. Martin, Conheim, Burdon-Sanderson, Simon, Wilson, Fox, Lebert and Wyss, Fraënkel, Waldenbourg, and others inoculated with all sorts of non-tuberculous organic materials (bronchial mucus, foul pus, cancer juice, diseased liver, simple cotton setons, etc.) and from these in Guinea pigs there resulted local caseated foci, and implication of the adjacent lymphatic glands. It was found that the liquids from low types of pneumonia produced these apparently tubercular deposits, while that from acute sthenic pneumonia did not; that the cotton thread seton failed to produce the disease if it were first steeped in carbolic acid, and that the lesion caused by breaking a bone without injury to the skin failed to produce the characteristic lesions even in the very susceptible Guinea pig. It became evident, therefore, that the morbid results in these cases, were due to accidental inoculations with the poison of the tubercle, which is widely distributed, or with some pyæmic or other germs.
“Gradually the truth triumphed, and those who had at first been loudest in their opposition were led by their own experiments to become the firmest supporters of the new truth.