The causes which tend to originate a pulmonary weakness or encourage a natural delicacy of lung ate all those which in any way help to lower nutrition and depress the natural vigour of the body. In childhood—a period of life in which nutrition is only maintained at a healthy standard by the continual influx of nutritive .material—any interference with the digestive or assimilative processes has an exceptional influence in diminish ing resisting power. It is for this reason, probably, that in unwholesome conditions of living slight febrile attacks, such as are incidental to many of the less serious ailments of early life, may start an enfeebling process which ultimately determines phthisical changes. In this way unsuitable food and close rooms, a damp residence, mental depression from unkind treatment, over-exercise of the immature brain, and any other like agency may have an influence in exciting the mischief in the lung.
Certain diseases have an undoubted tendency to be followed by phthisis. On this account measles and whooping-cough are justly dreaded for the injurious influence they are known to exercise upon scrofulous and weakly subjects. These affections not only encourage a special lung weakness, but also by promoting enlargement and caseation of the lym phatic glands, may set up a focus of infection by which, through the medium of the blood-vessels or lymphatics, secondary inflammatory pro cesses of a more or less acute character may be excited in the lung. Scarlatina, too, is sometimes a cause of phthisis, acting by similar means ; empyema may induce the pulmonary mischief through absorption of infective material from the pleura ; and the disease not uncommonly arises in children who suffer from scrofulous joints and old-standing caries of bone. The influence of catarrhal pneumonia in inducing the disease has been already referred to.
Since the discovery of the bacillus the question of the infectiveness of phthisis from person to person has again assumed considerable prominence. The presence of bacilli has been discovered in the air expired by con sumptive patients ; and if this microphyte be indeed the agent by which the infection is conveyed, it would seem to follow as a logical conclusion that the disease must be continually communicated by this means. Whether, however, it be that a predisposition of rare intensity is required for the ready reception and development of the bacillus, or that the im portance of this organism as an infecting agent has been overestimated, the fact remains that the disease is practically not communicable by thir:, means.
Morbid all cases of pulmonary phthisis the lungs after death are found to be more or less consolidated by a cheesy-looking sub stance which is in various stages of softening and disorganization. Whether the disease has begun by a chronic process of tuberculisation, or has originated in a catarrhal pneumonia and epithelial accumulation in the alveoli, the degeneration of the morbid material gives rise to caseons solidification of very similar character. Even when the primary patho
logical change consists in a chronic formation of grey tubercle in the lung tissue, a secondary catarrhal pneumonia is usually set up sooner or later ; and the resulting caseous infiltration materially contributes to the enlargement of the area of solidification. Again, when the form of phthisis is originally catarrhal, softening of the cheesy material which infiltrates the lung may be a source of infection. By this means a second ary formation of miliary tubercle is excited, at first in the immediate neighbourhood of the affected region, afterwards more generally over both the lungs. Consequently, in most cases, the pathological changes are not simple, but tend to complicate one another, so that the lung is at the same time the seat of different morbid processes. 'We often find grey or yellow granulations combined with masses of yellow infiltration of various extent. In these masses the tissue is soft and friable, and on section is found to be clryish, of a straw or grey colour, and streaked or spotted with black pigment. The surface is commonly marked with intersecting lines which indicate the position of the interlobular septa. At the borders of the con solidated region is usually a zone of reddish-grey glutinous infiltration. Often many of these caseous masses are seen scattered over the lung, the pulmonary tissue between them being (edematous or congested, and partially collapsed.
If the phthisis has reached an advanced stage, cavities from breaking down of the consolidating material are usually found. Cavities are not uncommon in the young subject, and are probably met with less frequently in the child than in the adult, only because the disease in early life often proves fatal from a secondary tuberculosis or other exhausting complica tion before the stage of excavation has been arrived at. When softening begins, it always occurs first in the centre of the caseous mass. The dead shrunken cells and molecular debris lying around them are loosened by the imbibition of watery fluid, and the cheesy material is converted into a soft purulent pulp. The wall of the bronchus, which lies in the centre of the nodule, then becomes perforated, and the cheesy matter is coughed up, leaving a ragged excavation. The softening may attack the cheesy masses generally through the lung, as happens in the more acute form of the disease ; or may begin in those situated in the upper part. of the lung, and thus pass gradually from apex to base. The expectorated matter in these cases contains particles of elastic tissue and shrunken cells, and often under the microscope exhibits bacilli in large quantities.