tained from Toussaint, and injected them into twelve animals; of these, seven were under observation for a sufficient length of time without the development of tubercle in any of the animals. Thus, thirteen animals were inoculated with the micrococci with which Toussaint works, obtained from Toussaint himself, and in no case did tuberculosis follow. From these and other facts, Cheyne concludes that the micrococci described by Toussaint do not cause tuberculosis, and therefore his results must be due to some other agency. Toussaint produces true tuberculosis very often, not by means of his micrococci, but from some fault in experimentation, such as contamination of his fluids with Koch's bacilli, or from the presence of these organisms in the air of the room in which the experiments are done. Toussaint also depends largely on carbolic acid as a disinfectant, an agent which is quite ineffectual against the spores of bacilli, unless it acts for a long time.

"In Koch's research, the results are much more definite than any previously obtained. He also cultivates micro-organisms from tubercle, but now it is no longer the fact that he only sometimes succeeds in causing tuberculosis, and that the tuberculosis thus produced occurs as slowly as, or more slowly than, from inoculation of tuberculous material. The result of the inoculation of his cultivations is certain, and the disease is more rapid in its commencement than after inoculation of tuberculous matter. The fact that the inoculation of the cultivated bacilli is so certain and rapid in its effects can only be explained on the supposition that in these cultivations we have the virus of the disease in a more or less pure state, and in large amount. But as the only things which we see multiplying on the serum are these bacilli, and as they are also constantly present in tubercles, it is difficult to see what other conclusion can be come to than that they constitute the virus.

"Professor Klebs makes two objections to Koch's facts, and apparently still upholds his views that a micrococcus and not a bacillus is the real cause of tuberculosis. The first of his objections is that these bacilli may be crystals. This objection is not a formidable one; for any one acquainted with micro-organisms can tell on examination that this is an organism and not a crystal. Its appearance, the apparent presence of spores, its variable lengths, its frequent curved form, its arrangement, its behaviour with staining agents, and above all its growth on serum, demonstrate its living nature. It is difficult to conceive that a few crystals put on serum will grow and extend from one point with the rapidity and in the mode that these bacilli spread, and I know of no better test, in spite of Klebs' assertion to the contrary, for a living organism than its increase

and multiplication when placed on a suitable soil. They are not any kind of fat crystals, for they are not found in cheesy matter which is not tubercular; and they vary greatly in number in tubercular material itself, sometimes only one being present in two or three fields of the microscope, sometimes a large number.

"All that has as yet been absolutely proved is that a variety of materials in man which we class together as tuberculous, produce, when inoculated into rabbits, guinea-pigs, and other animals, acute tuberculosis, and that this also occurs from the inoculation of bovine tuberculosis. Koch's researches further demonstrate that this result is due only to the tubercle bacilli which were present in the materials inoculated. We may say definitely that the tubercle bacillus is the cause of acute tuberculosis, and that scrofulous glands, degenerated (strumous) synovial membranes of joints, phthisical lungs (in short, all those materials obtained from man which, inoculated into animals produce acute tuberculosis), contain in them bodies (bacilli) which, if they entered the circulation in sufficient numbers, would give rise to acute tuberculosis. It has been demonstrated by several observers that probably in all cases of acute tuberculosis a place can be found where these bacilli get into the circulation.

"Two distinct structures have been described, and may be readily recognised in a tuberculous lung-viz., nodules of lymphatic tissue in close proximity to the vessels and bronchi, and nodules which are largely made up of epithelioid cells. If a case of commencing tuberculosis of the lung be examined, it will be found that bacilli are only present in the latter nodules; and, indeed, it is rare, even in the later stages, to find them in the former, and in that case epithelioid cells will be found as well. The bacillus being the cause of this disease, only the nodules containing epithelioid cells are tubercles. Surrounding the epithelioid cells, which are always in the central portion of the tubercle, and make up the greater part of it (though after a time leucocytes penetrate among them), we have what I consider to be simply inflammatory tissue, but what is sometimes spoken of as lymphatic tissue. As the tubercle gets older, it is found that the epithelioid cells at the centre undergo cheesy degeneration, and they can only be seen, if present at all, at the margin. In tubercle we also find giant cells in which bacilli are generally present, sometimes in considerable numbers. These giant cells I have distinctly traced to epithelioid cells, especially to epithelioid cells containing bacilli; for where several bacilli are present in cells, all gradations may be found.

between the single nucleated cell and the multinucleated giant cell.

"As to the origin of these epithelioid cells, I can only speak from a study of the process in the lungs and the liver. In the lungs, I am satisfied that the great majority are derived from the alveolar epithelium. The bacilli escape from the blood-vessels or lymphatics, and get into the alveolar epithelium, where they grow and cause multiplication of the epithelial cells, till the alveolus becomes completely filled with these cells and infiltrated leucocytes. Around this mass the walls of the alveolus become inflamed and thickened, and form the granulation tissue surrounding the epithelioid mass.

"The structural definition of a tubercle must run somewhat as follows:-A nodule, composed of a central mass consisting in the main of epithelioid cells, or in its place a cheesy mass, surrounded by more or less inflammatory tissue, with or without the presence of giant cells. The absolute diagnostic mark is, however, the presence of the tubercle bacillus. group of granulation cells without epithelioid cells, or without cheesy matter or giant cells to indicate the previous presence of epithelioid elements, is not a tubercle. On the other hand, I know of no morbid structure except tubercle which contains the same histological elements, arranged in the same way, and possessing the same tendencies.

"The following is what the foregoing facts lead me to suppose to be the sequence of events in phthisis. The tubercle bacilli which reach the lung by inhalation develop in the epithelial cells lining an alveolus, this alveolus becomes filled. with cells, neighbouring alveoli become infected, and the same process goes on in them. The further result will depend on the number and rapidity of growth of the bacilli, and on whether the patient is a good soil for their development. If they develop well, we have caseous pneumonia, if they grow slowly and with difficulty, we have fibroid phthisis. In the former case the alveoli become distended early with epithelioid cells, this leads to inflammation of the walls of the alveoli, the cells soon undergo cheesy degeneration, and the pressure of the masses leads to atrophy or sloughing of the walls of the alveoli. (In the latter case elastic tissue will be found in the sputum.) Infection of neighbouring parts of the lung occurs both by continuity, and also by partial coughing up and reinhalation of the bacilli into other parts of the lung. In this rapid phthisis, fibrous formation around the alveoli only takes place imperfectly, and the lung rapidly breaks down. In the case of fibroid phthisis the bacilli are few, and grow only with difficulty. Thus fibrous formation occurs extensively, and

giant-cells are caught in this fibrous tissue in the manner formerly described. Nevertheless, in parts the process may be more rapid, and there cheesy masses are formed which may lead to breaking down of the lung and the formation of cavities. On this view we have an explanation of several facts. First, we have the rarity of acute general tuberculosis in connection with phthisis, even though bacilli are present in the lungs One reason of this is probably that the bacilli can hardly be said to enter the body: they are separated from the circulation by the layer of granulation and fibrous tissue. This is a fact which can be readily observed. Secondly, we have the explanation of their presence in the sputum even before physical signs are marked, or, indeed, have become evident at all It is now stated that the number of bacilli in the sputum is a means of forming a prognosis as to the rapidity of the disease. According to the views I have just stated, this would be a very likely thing, for the presence of large numbers in the sputum would indicate either an affection of numerous alveoli, or a large amount of caseous material-i. e., extensive affection of one part of the lung, and hence rapid death.

A consideration of all the facts has led me to the conclusion that tuberculous processes in the lungs are due to the tubercle bacilli, and, so far as I know, to them only. By a tuberculous process I mean one where there is proliferation of epithelium, caseous degeneration of this proliferated epithelium, and inflammation round about, these changes being progressive. It has been supposed that inhalation of dust of various kinds may give rise to phthisis. That the inhalation of dust will lead to inflammatory changes is very likely, that it may lead to proliferation of epithelium which may subsequently degenerate is possible, but that the process will be progressive and extend beyond the seat of irritation is not probable. That the changes set up by the presence of gritty particles may, however, prepare the lung and render it a fit soil for the implantation of bacilli is very probable, and in this way a true tuberculous process may supervene, not due to the original gritty substances, but to the bacilli which came afterwards. It has often been urged that the milk of tuberculous cows is infective. This may be the case when the mammary glands become tuberculous."

Mr. Cheyne is to be congratulated on the production of this very able monograph; it is well worked out, and we commend it to the attention of our readers.

BY ROBERT MUNRO, M.A., M.D., KILMARNOCK.

PART II.

THE splendid success of these researches of Pasteur could not fail to throw much light on the general pathology of epidemic diseases among the higher animals, and the immediate result was that the germ theory, formerly only occasionally mooted as a mere speculation, now again came to the front. A disease known under the various names of splenic fever, charbon, anthrax, &c., was then causing much animal loss in several countries in Europe. In its most malignant form horses, cattle, and sheep, were killed in 24 hours. Even man himself was not safe from its attacks, as we find from the statistics of the district of Novgorod in Russia, where no less than 56,000 animals and 528 human beings are said to have died of its effects during the three years preceding 1870.

As early as 1850 two French pathologists, MM. Davaine and Rayer, noticed, in the blood of animals which had died of splenic fever, certain little rod-like bodies, but no causal connection between these microscopic organisms and the disease was thought of till the publication of Pasteur's memoir on the fermentation of butyric acid in 1861, when it occurred to Davaine that splenic fever might also be a kind of fermentation set up in the living body. It was then that the life

No. 6.

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