1883 The Lancet  
tubercle. That there is a definite product, an entity with peculiar and distinguishable characters, with invariable results, and that the disease of phthisis is a pathological unity, have become more and more the doctrine of the day. Be tubercle what it may, it is now more defined than ever; and if we can assign to it an unvarying cause of production, an origin constant and unique, in a germ-producing bacillus, we have certainly receded from some late teaching. If tubercle, or those small
more » ... seen on the lung and prone to cheesy degeneration, be only common products of ordinary inflammation, as some have taught, we must believe that ordinary pulmonic inflammation, if it affect the walls of the alveoli and the interlobular tissue, has its origin in the parasitic germ. Koch attributes miliary tubercle and all cheesy degenerative nodules to the bacilli. He has inoculated with them all, and found the same result. Since Koch's observations have been published there have of course been many experimenters anxious to prove or to disprove them, and we have already numerous records of their experience. In Germany, Flänkel found bacilli in 120 cases of phthisis, which were all he examined, and Heron in sixty.two case9. Dr. Dreschfeld of Manchester has contributed most valuable observations. He found the tubercle bacilli in all cases (forty-six) of phthisis where the physical signs were well marked. He has also examined six cases of bronchitis and emphysema, one of bronchiectasis, and two of fibroid phthisis, without finding bacilli. Of catarrhal pneumonia he had three cases with the same result. In two well-marked cases of lung disease there were no bacilli. Taking cases of tubercular disease of organs other than the lung, Frankel found bacilli in fifteen out of sixteen cases in the secretion covering laryngeal ulcers, and Crudeli found them always in the stools of tubercular enteritis. Rosenstein also found bacilli in the urine of a patient who had tuberculous dis. ease of the epididymis, the lungs being free from disease. Frankel also in the pus of a scrofulous joint. We thus seem to have it proved that bacilli are present in all tuberculous disease, and absent in non-phthisical lung affections. As regards the stage of lung disease in which they are most prevalent, observations show that it is rather in the later stages that they are in greatest quantity. Our evidence hitherto also seems to prove that their greater number is accompanied by a higher degree of pyrexia, and signifies a more acute form of disease. On this point further observations are necessary, and the same may be said of acute miliary tuberculosis, about which we have hitherto no eyidence. My colleague, Dr. Williams, has examined the sputa in 130 cases at Brompton Hospital. Of these, 109 were cases of phthisis, cavities in eighty-one; nine were cases of early consolidation. Bacilli were found in all of them, excepting three. There were twenty-one cases examined of other lung affections-bronchitis, bronchiectasis, pleurisy, empyema, and pulmonary congestion from heart disease, but no bacilli were found in any of them. Of the 109 cases of phthisis, there was pyrexia in fifty-one, the temperature ranging from 100° to 105'. Taking the fact of Koch's discovery as sufficiently established, and that, bacilli being found in all cases of phthisis, they stand in the position of a causative agent, and taking also into due estimation that all persons exposed do not get the disease, we have to inquire whether there are not antecedent conditions-that is, conditions prior to the introduc-tion of the germs-which favour their development. There is, we may assert, a state of health, or of constitution, or of lung, which is a main factor in the induction of disease. It is here that the old pathology meets the new, and we imagine that it will be found that in all instances there is a pre-existing state which prepares the way for such germs as shall be accidentally introduced. This consideration demands our earnest attention. The period to which we allude is as much a first stage period as is the manured and prepared bed in the garden to the crop which is to grow in it. It is probable, nay certain, that germs daily enter the air-passages and take no root. The two factors of I eredity and inflammation are those which all recognise as d i Ili culties in the way of accepting off-hand the bacillus theory. But they seem to be the agents which exactly prepare the way for the reception of infective germs. In the first lecture we dwelt on the evidence for the presence of inflammatory products in all cases of phthisis, and it is so proved that it cannot be omitted in any theory of the disease. Let us examine what heredity and inflammation do and how they are supposed to act. Heredity may mean not only a germ conveyed by the parent or more remote ancestor, but may, and in fact often is, a weakness of constitution, a tendency to disease, an especial vulnerability of lungs, and proneness to their inflammation. As Dr. Green has remarked, the tendency to retention and accumulation of inflammatory products is a leading character of scrofulous inflammations. An inherited proclivity to phthisis favours congestion. It is also conceivable that a want of tone of the bloodvessels is inherited, with a general deficiency in the power of products of the circulation, which no doubt favours transudation of low vitality. On the whole, then, a want of resistance to such attacks is held to be the most likely preparation of a bed which will grow bacilli. A mere exposure of the bronchial membrane is not considered sufficient for their development, but their entrance to and impaction in the alveoli. Another question which has been dwelt on by Dr. Green and others is the condition of the apex of the lung. Tne common localisation of tubercle in the apex has been referred to a diminished range of movement tending to stagnation in the pulmonary capiltaries, a state which is closely allied to congestion and the formation of inflammatory products. In this manner a nidus or bed is formed fit for the reception of germs, and ready to reproduce them. Thus the old pathology joins on to the new, and we carry the idea of inflammation as a necessary preparation for the reception of the bacilli. It is indeed essential to conceive some such preparation for the elaboration of the germ into an established disease of specific character, and it also accounts for the innumerable cases of exposure to contagion where no disease results, for we must uphold that clinical experience is against the contagious nature of phthisia, and that something more is required than the mere presence of the organisms. Again, we would say that the recognised observation that the walls of the alveoli are essentially engaged in true tubercular disease favours the bacillus theory, the germs being found in that position. We seem, then, to have advanced from one pathological view to another, and, if Koch's observations turn out to be co rect, he has discovered that specific element of disease to which all advancing pathology pointed, and which the best observers were expecting. It is not a contradiction of their observations, but an addition, which is not out of harmony with their results, and may even account for phenomena for which all previous reasoning had failed to find an adequate cause. It is in these subtle causes which influence the constitution as heredity and sexual transmission of tendencies to disease, and even of particular forms of disease bearing the same name, that we shall find ground for referring the germ theory to some deeper line of argument than can be resolved by a chemical experiment. Whole families are liable in a peculiar degree to phthisis, to rheumatism, to typhoid, to diphtheria, or to scarlet fever poisons. They seem to have been born with a proclivity which others have not. Is phthisis always the result of contact with diseased persons ? 1 Is the seed always sown at a given time, and can we gather more than one kind of fruit from a defiui!e germ ? Again, is it not possible to account for the phenomena of phthisis in another way? Granted.that a given cause has originated a local deposit in the lung, do we see more in the symptoms of irritative fever so initiated than can be accounted for by the local cause of impacted alveoli, with compressed and strangled walls, pressure on the nutritive and pulmonary vessels, and resulting necrosis? Only last year we should
doi:10.1016/s0140-6736(02)26238-8 fatcat:dpsb4o3oijeqblanvpqstdbjx4