This disease occurs most frequently in children, and is in them, as in adults, associated with catarrh of the finer bronchi. The bronchi are first affected, and so it may be said that the pneumonia springs out of a Capillary bronchitis, the tubes affected being those of the finest calibre. In a large proportion of cases the bronchitis originates in measles, or it may occur in diphtheria, or small-pox, or whooping-cough. In adults it may follow typhoid or other infectious fever, or it may be the result of the inhalation of irritating gases.

It is to be noted that an ordinary bronchial catarrh, such as was described in the section on bronchitis, seldom goes on to a catarrhal pneumonia, but that for the most part the latter is due to the existence of some special irritant such as the virus of measles.

As the disease begins in the bronchial tubes, and is propagated to the lung tissue, it follows in its distribution the arrangement of the bronchial tubes; that is to say, it occurs in a lobular form, hence the name Lobular pneumonia which is frequently used. Although the disease is thus primarily lobular, it is clear that it will often occur in several neighbouring lobules, and so a considerable tract of lung may be involved.

The inflammation manifests itself by the production of an exudation mingled with cells, so that the fine bronchi and the connected alveoli become filled. There is thus brought about a lobular condensation. The cells produced are partly leucocytes and partly catarrhal cells, the derivatives of the epithelium. The proportion of each of these will -depend somewhat on the acuteness and nature of the irritant, but in acute cases each minute bronchus will often contain a small drop of pus. In addition to these cells fibrine and red blood-corpuscles are frequently present in the lung alveoli. The affected pieces of lung are firm and reddish brown or grey, and on the cut surface stand above the general level. Even when a considerable district is affected the lobular appearance is usually visible.

As the disease begins in a catarrh of the finer bronchi, there is often Collapse of the corresponding portion of lung even before any actual inflammatory process has occurred. The obstruction of the tubes with tough secretion sufficiently accounts for this collapse (see p. 747). It is a lobular collapse, and, as seen from the surface, areas of larger or smaller size are depressed and of a bluish red colour. These are mostly to be found, in the first instance, at the posterior and inferior parts of the lung. In other parts, and especially in the upper lobes, we may have emphysema.

The inflammation does not confine itself to the bronchi and alveoli, but may extend to the connective tissue of the lung generally. In such cases the exudation in the bronchi is composed of leucocytes, and cells of a similar character infiltrate the bronchial wall and neighbouring structures, the bronchi evidently forming centres of irritation.

In many cases Acute pleurisy accompanies the process in the lung.

The inflammatory products in the air vesicles may after a time undergo fatty degeneration, break down, and be discharged, some part of them being probably absorbed by the lymphatics. In some cases, however, the result is not in every part of the lung so fortunate. For one thing, the collapsed portions may remain uninflated, and, as considerable tracts of lung may be affected, marked shrinking of the lung and deformity may result. Or, again, the catarrh may become chronic, and, being associated with an interstitial inflammation, result in a permanent induration, the alveoli being encroached on by the growing connective tissue, as in the case of chronic pneumonia. In this way, the person, though recovering, emerges from the disease with a damaged lung; according to the extent of the permanent damage will be the shrinking of the lung and possible displacement of organs. Again, phthisis pulmonalis may develop out of an acute catarrhal pneumonia, but this is fortunately an unusual result.

It has already been mentioned that the disease begins in the bronchi, and it has been asserted by Buhl that, throughout, the inflammation remains confined to the bronchi, the inflammatory products found in the alveoli being simply insufflated from the bronchi. This view, however, can hardly be maintained, as evidence of acute changes can actually be observed in the epithelium of the alveoli.