REPORT OF THE BUREAU OF ANIMAL INDUSTRY. Ill 



ation is without doubt caused by the packing of the respiratory tis- 

 sue with cells, by which the capillaries are compressed and all food 

 supply cut off. The caseous foci vary from the size of a small pea 

 to that of a marble or horse-chestnut. (Plate IV, fig. 1.) They are 

 usually round, rarely irregularly elongated. They are occasionally 

 present in such numbers that the affected lobe feels like a bag filled 

 with small marbles. It is highly probable that now and then the 

 pathologic process may go a step farther. The caseous mass may be 

 separated by secondary suppurative processes from the living tissue, 

 soften, and be discharged through a bronchus, leaving an irregular 

 cavity. We have seen but once what appeared to be cavities in a 

 piece of lung sent to us from the West. 



A few lungs have come to our notice in which this process of slow 

 necrosis was not limited to groups of a few or more lobules, but had 

 involved the entire lobe uniformly. The tissue was completely air- 

 less and bloodless, of a homogeneous consistency, cutting like cheese, 

 yellowish, with a semi-translucent, waxy luster. 



In distinction from the acute type of this disease, the process end- 

 ing in caseation may be regarded as essentially slow and chronic, It 

 may either be due to a diminished virulence of the bacteria or to a 

 greater resistance on the part of the lung tissue. The former suppo- 

 sition seems to us nearer the truth, and there is much other evidence 

 which points to a rapid attenuation of this specific virus. 



The pathological process may be briefly summarized as follows : 

 The bacteria, which have somehow entered the air tubes, begin their 

 destructive activity in the alveoli and ultimate bronchi. A copious 

 exudate, consisting chiefly of desquamated epithelium and round 

 cells or leucocytes, fills them completely. Although the bacteria are 

 finally destroyed by the exudate, the latter impairs by pressure the 

 nutrition of the lung tissue proper, and the whole becomes involved 

 in necrosis. The covering of the lungs is secondarily affected. In 

 acute cases the pleura of the hepatized lobes may be covered with a 

 fibrinous exudate of a spongy texture, containing a considerable num- 

 ber of round cells and bacteria. It may become several millimeters 

 thick, and tends to unite the lungs with the chest wall. The adhe- 

 sion is at first broken without injury to the lung substance and is 

 quite easily peeled from the pleura itself, as shown in Plate I. Not 

 infrequently the diaphragm is more or less firmly glued to the base 

 of the principal lobe when that is diseased, as is shown in Plate II. 

 The pulmonary pleura and adherent costal pleura may sometimes 

 form cavities between them, containing a yellowish- white, very tur- 

 bid liquid crowded with bacteria. The adhesions are sometimes very 

 close, the costal pleura having its minute vessels much injected at 

 such spots. In older cases there are bands of fibers, of various 

 lengths and density, bringing about the adhesion. In most cases the 

 pleuritis is dry, with no adhesions. Over the dead lung tissue the 

 pleura may be opaque and thickened or quite transparent, as in 

 health. In several cases in which gangrenous processes were indi- 

 cated by putrid odors, a generalized pleurisy was found gluing the 

 entire lungs to the chest wall by means of a pasty exudate. In this 

 various bacteria were found, which, very likely, had a share in the 

 inflammatory changes. The pericardium occasionally is involved 

 with the pleura and is subject to similar changes. In but one of the 

 cases (No. 366) .thus far examined was the<epicardmm covered with 

 a fibrinous exudate. 



