growth into the alveoli of fibrous tissue. The latter eventually converts portions of lung tissue into a resisting, flesh-like mass carnification, or chronic fibrous pneu monia. In sections of this kind (chiefly when stained especially for elastic fibers) there will be seen shoots of spindleshaped, connective-tissue cells (fibroblasts) breaking through the alveolar walls and passing in a wreath-like manner from alveolus to alveolus, filling up and distending the lumens. The connective tissue is moderately cellular, especially in the central portions of the shoots, in which are seen richly protoplasmic, epithelioid cells, as well as dark, small, round cells. An increase in the thickness of the alveolar walls does not usually take place. The rather scanty vascular connective tissue does not, therefore, originate from the alveolar walls, but rather from the scanty connective tissue surrounding the end bronchioles. Sometimes the shoots also penetrate into the finer bronchioles. The unresolved fibrin seems to play the rôle of bridges, which the connective tissue follows in passing through Cohn's spaces, which become dilated. Polypoid connective-tissue plugs are seen penetrating into smaller bronchioles, and finally occluding them. Detached alveolar epithelium may still be found within the alveoli and near the connective-tissue shoots. Occasionally, these shoots become lined with extensive rows of cuboid epithelium. Quite frequently, there is seen a proliferation of the remaining epithelium of the alveoli not altogether filled with the connective-tissue plugs. These new cells do not remain flat and low, but become higher, cuboid, oftentimes cylindric in shape, so that adenoma-like structures result (Friedländer's atypical proliferation of the alveolar epithelium). This atypical proliferation occurs in all those processes in which the lung tissue becomes indurated, including tuberculosis and syphilis, and depends undoubt edly on the removal of the pressure of the air on the walls of the partially occluded alveoli. Naturally, such fibrous, "carnified" portions of the lung are rendered useless for respiratory purposes. In such areas are sometimes found glistening, concentrically lamellated, globular bodies, the so-called corpora amyloidea. (See General Part.) Bronchopneumonia. All the remaining forms of pneumonia (with the exception of the tuberculous) are macroscopically distinguished, in the early stages, by the appearance of circumscribed areas of inflammation, usually affecting single lobules. Through confluence of many lobules it may lead to larger areas of infiltration: sometimes a whole lobe may in this manner become solidified. When this occurs, it is known as "pseudolobular" extension. All All these forms of pneumonia are most commonly the result of extension from a primary infection of the smaller bronchioles. A simple catarrhal inflammation of a bronchiole may spread to the surrounding lung tissue, which the bronchiole supplies. Usually, the bronchial stem becomes occluded by the accumulation of cells and increased mucous secretion, as a result of which the alveolar area that it supplies collapses and becomes atelectatic. Later, these collapsed alveoli become distended, not with air, but with cellular elements, especially with alveolar epithelium. The latter find their way into the lumen partly through desquamation and, on the other hand, as a result of active proliferation. Some of the cells are still flat and polygonal in shape, while others have become swollen, vesicular, or globular, and may easily be distinguished from other cellular elements by their vesicular nuclei. Around tuberculous areas in the lung similar forms of pneumonia may develop (desquamative pneumonia of Buhl, see Tuberculosis). In the later stages these cells become mixed with a variable number of leukocytes as well as red bloodcorpuscles which have passed out from the alveolar capillaries. Fibrin is not found in the purely catarrhal forms of bronchopneumonia; if present, it is only met with in limited amount. Macroscopically, the cut surface of such inflammatory areas is always smooth. Resolution takes place through fatty degeneration of the cells that fill the alveoli. pneu A form of consolidation that resembles catarrhal monia very much in structure is the so-called marantic splenization of the lung. It is usually found in connection with long-standing, hypostatic congestion, especially when edema is also present. (Plate 36, Fig. II.) Complicated in structure as well as in genesis is the so-called lobular pneumonia that occurs secondarily to various other diseases, and especially in children after the acute infections, such as diphtheria, measles, scarlatina, smallpox, whooping-cough, influenza, etc. These forms of pneumonia are also of bronchiogenic development, but the inflammation, instead of extending along the long axis of the bronchial tube into the corresponding lobule, spreads into the bronchial walls and the surrounding peribronchial tissue, whence it passes over into the neighboring groups of alveoli. Since the latter do not belong to the lobule supplied by the affected bronchus, the typical lobular arrangement of the consolidation is disturbed, and there are produced variously sized, rounded, elongated or circular, infiltrated areas, which surround a bronchus and are not confined to the lobular limit or border. Transverse sections through a bronchus and its surrounding lung tissue will show, even macroscopically, the central yellow-stained portion-namely, the bronchus-filled with the purulent exudate, and its infiltrated wall, while the periphery of the nodule is deeper in color. Microscopically, the bronchus is filled with pus-cells |