MORBin ANATOMY 



38- 



tains immense numbers of them and the denuded mucosa fur- 

 nishes a favorable place of entr}-. It is otherwise difficult to 

 explain the continued increase in thickness of the walls of the 

 cecum after the mucous membrane has been shed. This con- 

 tinued increase in thickness is due to an extensive infiltration 

 of small round cells and the presence of some giant cells. 

 Parasites in this advanced stage are scarce and usually recog- 

 nizable only as vacuole-like bodies within the giant cells. 



The thickening of the wall is associated in some cases 

 with an extension of 

 the inflammation to 

 the contiguous wall of 

 the intestine, which 

 becomes firmlj^ at- 

 tached to the cecum. 

 Yellowish exudates 

 are sometimes found 

 outside of the diseased 

 cecum on its serous 

 covering and they 

 bind it inextricably 

 to the other cecum or 

 to the intestine or at- 

 tach it to the abdom- 

 inal wall. In these 

 stages, the micropara- 

 site is not found. It seems to have done its work by destroy- 

 ing the mucous membrane and to have left the field for 

 mi.scellaneous bacteria. 



Other portions of the digestive tract are not affected. 

 The secondary lesions are found in the liver, although in some 

 cases they do not appear. The organ itself is enlarged to 

 probably twice the normal size. Over the surface are distrib- 

 uted roundish, discolored spots, distinctly demarcated from 

 the surrounding tissue. These may be distributed uniformly 

 over the whole surface of the liver or they may be limited in 

 number to a few. They vary from 3 to 15 mm. in diameter. 



Fig. ioi. Liver s/i07uiiig diseased foci. 



