Pathogenesis 597 



The bacilli enter the solitary glands and Payer's patches, and 

 multiply slowly during the incubation period of the disease — one to 

 three weeks. The immediate result of their activity in the lymphatic 

 structures is an increase in the number of cells, the ultimate effect 

 is necrosis and sloughing of the Peyer's patches and solitary glands. 

 From the intestinal lymphatics the bacilli pass, in all probability, 

 to the mesenteric nodes, which become enlarged, softened, and 

 sometimes rupture. They also invade the spleen, liver and some- 

 times the kidneys, and other organs where they may be found 

 in small clusters in properly stained specimens. 



Mallory* found the histologic lesions of typhoid fever to be wide- 

 spread throughout the body and not limited to the Peyer's patches of 

 the intestine, where they are most evident. His conclusions regard- 

 ing the pathology of the disease are briefly: "The typhoid bacillus 

 produces a mild diffusible toxin, partly within the intestinal tract, 

 partly within the blood and organs of the body. This toxin pro- 

 duces proliferation of the endothelial cells, which acquire for a 

 certain length of time malignant properties. The new-formed cells 

 are epithelioid in character, have irregular, lightly staining, ec- 

 centrically situated nuclei, abundant, sharply defined, acidophilic 

 protoplasm, and are characterized by marked phagocytic properties. 

 These phagocytic cells are produced most abundantly along the line 

 of absorption from the intestinal tract, both in the lymphatic ap- 

 paratus and in the blood-vessels. They are also produced by dis- 

 tribution of the toxin through the general circulation, in greatest 

 numbers where the circulation is slowest. Finally, they are pro- 

 duced all over the body in the lymphatic spaces and vessels by 

 absorption of the toxin eliminated from the blood-vessels. The 

 swelling of the intestinal lymphoid tissue of the mesenteric lymph 

 nodes and of the spleen is due almost entirely to the forma- 

 tion of phagocytic cells. The necrosis of the intestinal lymphoid 

 tissue is accidental in nature and is caused through occlusion 

 of the veins and capillaries by fibrinous thrombi, which owe 

 their origin to degeneration of phagocytic cells beneath the 

 lining endothelium of the vessels. Two varieties of focal lesions 

 occur in the liver: one consists of the formation of phagocytic cells 

 in the lymph-spaces and vessels around the portal vessels under 

 the action of the toxin absorbed by the lymphatics; the other is 

 due to obstruction of liver capillaries by phagocytic cells derived 

 in small part from the lining endothelium of the liver capillaries, 

 but chiefly by embolism through the portal circulation of cells 

 originating from the endothelium of the blood-vessels of the in- 

 testine and spleen. The liver-cells lying between the occluded 

 capillaries undergo necrosis and disappear. Later the foci of cells 

 degenerate and fibrin forms between them. Invasion by poly- 

 morphonuclear leukocytes is rare." 



* "Journal of Experimental Medicine," 1898, vol. m, p. 611. 



