REPORT OF T1IE BUREAU OF AMIMAL INDUSTRY. 81 



Besides the fibrin in the alveoli there may or may not be one or 

 several large cells, round, with much protoplasm inclosing a vesicular 

 nucleus. The bronchi are all patent, the epithelium intact. The alve- 

 olar walls are not changed, nor is there any round-cell infiltration to 

 be seen. In circumscribed areas the capillary net- work is distended 

 with blood corpuscles, while all the larger vessels are similarly filled 

 with these elements. 



In the alveolar ducts there is now and then considerable fibrillar 

 fibrin well brought out by Weigert's stain. 



In about 15 per cent, of the animals examined one of the smaller 

 ventral lobes was airless throughout, moderately enlarged. Viewed 

 from the surface the diseased lobe is bright red, dotted with minute 

 pale grayish or yellowish points of a diffuse hazy outline, each not 

 more than 1 micromillimeter in diameter. They are usually arranged 

 in groups of four and represent the ultimate air cells filled with cellular 

 exudate. The larger bronchi are also occluded. The exudate is yel- 

 lowish white, so firm that it is possible to tear away the lung tissue 

 with needles without necessarily breaking up the inclosed exudate. 

 It may thus be teased out in the form of branching cylinders, becom- 

 ing smaller and finally dwindling down to the size of a coarse hair. 

 Microscopic sections reveal the alveolar walls beset with distended 

 capillaries. The alveoli are filled up with cellular masses, fibrin ap- 

 pearing very rarely. In most alveoli the cells are large, round, with 

 vesicular nucleus, evidently derived from the alveolar epithelium. 

 In some alveoli and in the smallest air tubes the cell mass is so dense 

 that individual elements can only be seen with difficulty. But they 

 appear to be identical with the cells just described. The process 

 seems to be accompanied with but little inflammation. The desqua- 

 mation and proliferation go on in the alveoli and smallest air tubes 

 until they are occluded by the casts described. 



Of the 49 animals of the same herd, 17 were found with collapse 

 and 8 with lobular broncho-pneumonia; more than one-half, there- 

 fore, had some defect of the lungs. 



It might be questioned whether such lesions as those of broncho- 

 pneumonia are not due to swine plague bacteria since they closely 

 resemble the appearance found in many swine plague lungs. This 

 question is effectually disposed of by the inoculation of lung tissue 

 into rabbits. From 16 lungs, 16 rabbits were inoculated. Of these, 

 8 lungs were involved in simple collapse, 8 in broncho-pneumonia. 

 Of these 16 rabbits 4 survived; the remainder died of hog cholera. 

 Of the 4 survivors 3 had been inoculated from collapsed lung tissue; 

 1 from a broncho-pneumonia. It is interesting to note that of these 

 rabbits, 1 died in six days, 4 in seven days, 3 in eight days, 2 in ten 

 days, 1 in thirteen, and 1 in fifteen days after inoculation. Plate 

 cultures from the corresponding bit of lung tissue showed a variable 

 number of colonies almost invariably non-liquefying, and in many 

 cases identified as hog cholera bacteria. 



To determine, if possible, whether lung disease can be produced by 

 innoculation, the following instructive experiment was made: 



Two pigs (460, 461), about ten weeks old, received into the right 

 lung, December 21, 3 cubic centimeters each of a beef infusion peptone 

 culture, two days old, inoculated from a single colony growing in a 

 roll cultiire. This had been made from a bit of spleen tissue from pig 

 No. 46 of the outbreak described in these pages. There were about 

 fifty colonies in the tube, all alike. To test the culture a rabbit re- 

 12057 A I 6 



