The following conclusions are sub mitted: 1. That the primary and sec ondary broncho-pneumonias have a dif ferent bacteriological origin. 2. That secondary broncho-pneumonia is, for the most part, due to streptococcic infection derived from some source in connection with the air-tubes, throat, and mouth. 3. That primary broncho-pneumonia is of pneumococcic origin. 4. That pneu mococcic inflammation occurs with al most equal frequency in the child and the adult. 5. That pneumococcic inflam mation takes a different form in each,— in the adult producing massive consoli dation, and in the child disseminated patches of consolidation. Samuel West (Brit. Med. Jour., May 28, 'OS).
In the acute pneumonia of childhood bacteriology demonstrates that the pneu monia of infancy can in no sense be considered a specific disease, in the sense that it is due to any special organism, as similar, if not identical, pathological changes are produced in the lung-tissues by various organisms. The reason why the same infection that produces a catarrhal pneumonia ::n infants should produce a fibrinous pneumonia in adults or in children over five years of age is explained by the fact that the alveoli of the lung are not fully developed until about the fifth year of extra-uterine life.
Catarrhal pneumonia is essentially the pneumonia of infancy. Carmichael (Edinburgh Med. Jour., Aug., '98).
Morbid Anatomy.—The appearances presented by the lungs in cases of bran cho-pneumonia are complex, consisting in inflammatory changes in the bronchial tubes, and in pulmonary consolidation, both lobular and more extended. Some of these pulmonary changes in both varieties are due to collapse and some to vesicular inflammation, lesions which are at times difficult to distinguish from one another, and they also give rise to con siderable diversities in the aspect of the lungs.
The mucous membrane of the bron chial tubes is swelled, reddened, and thickened, at times materially diminish ing the calibre of the tube. It is usu ally, but not always, covered with a thick, tenacious, or puriform mucus. In cases of some standing this mucus may become inspissated, so that the course of the bronchi is marked out by yellow lines. Fibrinous concretions are sometimes ob served. The other coats of the bronchi are also thickened and swelled, so that their cut extremities stand out promi nently from the pulmonary tissue to an extent which is more marked in the child than in the adult. The anterior branches are sometimes less affected than the posterior, particularly in diphtheria. The
inflamed tubes tend to become dilated, owing to the loss of resistance of their wall, which is infiltrated with inflamma tory products. In the larger tubes the dilations are commonly fusiform and cylindrical; in the smaller they are globular, and the terminal dilations may attain the size of a millet-seed or hemp seed. They may stand out prominently on the pleural surface, and yield a yel low fluid when punctured, or they may, when distended by inspissated pus, strongly resemble tubercles. They may also rupture into the pleura and give rise to pneumothorax. In the more marked dilations the thickening of the walls dis appears and they may be almost mem branous. Dilation is more commonly marked in the broncho-pneumonia of whooping-cough.
The extension of the inflammatory process to the lung is intimately asso ciated with the process of collapse. The extent of collapse in infantile bronchitis is largely due to the obstruction of the bronchial secretion. It may occur both in lobular and disseminated and also in diffused form. In its early stages it is capable of insufflation, which distin guishes it in either form from lung-tis sue filled with inflammatory products; but this capability for insufflation may be lost. It is generally distinguishable from pneumonic infiltration by being sunk below the level of the surrounding tissue, by its glistening smooth section, and by the fact that, when occurring at the surface of the lung, the pleura shows no sign of exudation and still maintains its transparency. Its areas are harder and resist pressure more than inflamed portions of the lung, and when scattered thickly throughout the organ may give to the finger the sensation of shot-grains. In these collapsed portions of lungs pneu monia tends to occur. Hyperaemia en sues, owing to the impeded circulation arising from defective respiratory move ment; and this is followed by cedema. The collapsed portions become more bulky, of a deep-purple color, and softer than before. Under the name of "splen ization" the condition has often been confounded with inflammation, as also has the condition which has preceded it, to which the name of "carnization" has been given. In neither of these states, however, has a true inflammatory exuda tion occurred. On pathological as well as clinical grounds it is important that the distinction should be maintained.