384 BIOLOGY OF THE LABORATORY MOUSE 



Cameron, Delafield, and Wilson (43) have recently demonstrated that a toxic 

 substance obtained from 6'. typhimuriiim by tryptic digestion produces 

 congestion, disappearance of glycogen, and focal necrosis of the liver, and 

 early necrosis of Malpighian bodies and of lymphoid follicles in the lymph 

 glands. 



The mortality in spontaneous and in experimental epidemics varies from 

 20 to 80 per cent, and is influenced by the strain of organism, dosage or 

 multiple exposures, resistance of the stock, age of animals, season, and other 

 factors (159, 308, 316, 329, 206, 207, 211, 277, 279, 181). 



Pathology. — The pathology of this infection has been studied in mice 

 dying of the spontaneous disease, but, more satisfactorily, in mice experi- 

 mentally infected by mouth under controlled conditions (154, 177, 190, no, 

 247, 87, 26, 196). In this way it has been possible to compare the findings 

 in acute and chronic infections, and to follow the course of chronic disease 

 by daily examinations (247). 



In very acute infections such as result from massive doses, the patho- 

 logical findings are not characteristic but resemble those of any septicemic 

 disease. Gross examination reveals congestion of all blood vessels and 

 viscera, some enlarge nent of liver and spleen which are usually dark red in 

 color, occasionally serosanguineous fluid in the peritoneal cavity, slight to 

 moderate enlargement of the lymph nodes, and redness, injection, and 

 swelling of the intestinal mucous membrane. Microscopically, the findings 

 are those of hyperemia and congestion of all the organs, fatty degeneration 

 in the liver, and severe catarrhal inflammation of the intestinal mucous 

 membrane. Bacteria may be found in large numbers in the blood, peri- 

 toneal exudate, and the various tissues. Focal lesions are infrequently 

 found in animals dying before the fifth day. 



Animals living i or 2 weeks or longer show more typical lesions. Ema- 

 ciation is usually pronounced and the abdomen appears enlarged due to 

 increase in size of the liver and spleen and to intestinal distention. On 

 opening the body, the vascular congestion is seen to be less pronounced 

 than in the acute infection. The liver is enlarged and the spleen may extend 

 down to the level of the pelvic bones. The peritoneal and thoracic cavities 

 may be free from fluid or contain smafl amounts of bacilliferous serous, 

 serofibrinous or sanguineous (154) exudate. The intestinal serosa is usually 

 reddened and injected, and the content of the bowel varies from thin, watery, 

 yellowish material containing mucus to soft or normal scybalae. 



The pathology of the gastro-intestinal tract can be correlated quite well 

 with the stages in the pathogenesis of the infection given above. During 



