48 THE LUNG PLAGUE OF CATTLE. 



with a particular air tube and its accompanying blood vessels, and the artery leading 

 to such lobules is as constantly blocked by a tirm blood-clot. The mode of causation 

 is this : The artery being in the center of a diseased mass, becomes itself inflamed. As 

 soon as the inflammation reaches its inner coat the contained blood coagulates; the 

 vein is usually blocked in the same way. The blood formerly supplied by the artery 

 to certain lobules is now arrested ; that in the capillary vessels of these lobules stag- 

 nates; nutrition of the walls of the capillaries ceases, and these losing their natural 

 powers of selection allow the liquid parts to pass freely out of the vessels, leaving the 

 globules only in their interior. More blood continues to enter them slowly from ad- 

 jacent capillaries supplied from other sources, and as this is filtered in the same way 

 by the walls of the vessels, these soon come to be filled to repletion by the globules 

 only, and hence the intensely dark color assumed. The color is often heightened by 

 the escape of blood from the now friable vessels into the surrounding tissue, and it is 

 by this means that the interlobular tissue is usually stained. " This black hepatiza- 

 tion, or as it is technically called, infarction, is an almost constant occurrence in the 

 disease as seen in New York, and the death and encysting of large portions of lung is 

 therefore the rule. If too extensive, of course the patient perishes, but not unfro- 

 quently a mass of lung measuring four or six inches by twelve is thus separated with- 

 out killing the animal. " 



If at a later stage we open an animal which has passed through the above condi- 

 tion, the following may be met with: A hard, resistant mass is felt at some portion 

 of the lung, usually the lower and back portion, and on laying it open it is found to 

 consist of dead lung tissue in which the hepatized lobules and interlobular tissue, 

 the air tubes and blood vessels are still clear and distinct, but the whole is separated 

 from the still living lung by a layer of a white pus-like liquid, outside which is a 

 dense, fibrous sac or envelope, formed by the development of the surrounding inter- 

 lobular exudation. From the inner surface of this dense cyst, the firm, thick bron- 

 chial tubes and attending vascular systems project in a branching manner like dirty 

 white stalactites, and these, with the interlobular tissue thickened by its now firmly 

 organized exudation, may form bands extending from side to side of the cavity. 



At a still more advanced stage the dead and encysted lung tissue is found to have 

 been entirely softened and the sac contains but a mass of white liquid debris, or, still 

 later, a caseous mass of its dried, solid matters, upon which the fibrous covering has 

 steadily contracted, so as to inclose but a mere fraction of its original area. In'hnn- 

 dreds of post rnortems we have only once seen the dead and encysted lung the seat of 

 putrid decomposition, and never found the cavity opening into a pervious air tube. 



There remains to be noticed the condition of the air tubes and accompanying ves- 

 sels in the diseased lungs. In all cases where we see the starting point of the disease 

 we find in the small tubes leading to the affected lobules, a loss of the natural bril- 

 liancy of the mucous membrane, which has become clouded and opaque, and the tis- 

 sue beneath it infiltrated and thickened. In more advanced cases, and above all, in 

 those showing the dropsical condition of the interlobular tissue, we find a similar in- 

 filtration into the connective tissues around the air tubes and their accompanying 

 vessels, and in the hepatized lung this is always seen as a ^hick, firm, resistant 

 white material, having the compressed and contracted and often plugged air tubes 

 and vessels in the center. (See Heliotype. ) These thickened masses have already 

 been referred to as standing out in stalactite form from the inner wall of the sac in 

 which the dead (necrosed) lung is undergoing solution. (Lung Plague, Law.) 



It is worthy of notice that though the connective tissue in the walls 

 of the air tubes is invariably the seat of extensive thickening, and 

 though the clear brilliancy of the epithelial layer is usually impaired, 

 yet absolute degeneration of the epithelium is exceptional, the cells re- 

 maining in columnar ranks around the lumen of the tube in place of 

 showing any transformation into rounded or lymphoid cells, or breaking 

 down into granular debris, as in active disease. When the smaller 

 tubes are plugged with exudate, the epithelium may be removed as 

 claimed by Professor Yeo, but when the lumen is still clear and pervious 

 the epithelial covering retains its normal condition of columnar cells, as 

 has been demonstrated by Drs. Porter and Hegeman, of New York. 

 In other words the extensive disease changes are found in the con- 

 nective tissues, and the lymphatic system in the walls of the tubes and 

 substance of the lungs, rather than in the cellular lining of the tubes. 

 The disease is an inters titial lobular pneumonia, rather than a croupous 

 pneumonia. 



