686 



Dysentery- 



will be remembered are actively motile, to penetrate between the 

 epithelial cells of the intestinal mucosa to the lymph-spaces of the 

 submucosa below. Here the amebas multiply in large numbers, 

 and by the enzymic action of their metabolic products produce 

 necrosis of the suprajacent tissues with resulting exfoliation and 

 the production of round, oval, or ragged ulcerations with markedly 

 infiltrated and undermined edges. As the amebas continue to in- 

 crease and fill up the lymphatics, and as bacteria add their effects 

 to those occasioned by the amebas, the ulcers increase in extent and 

 depth until the mucosa and submucosa may be almost entirely 





- 0/ 



.4 



Fig. 272. — Entamoeba histolytica. Section of the human intestinal wall 

 showing the amebas at the base of a dysenteric ulcer: A, A, A, Amebas, some of 

 which are in blood-vessels, Gf (Harris) . 



destroyed, leaving the entire large intestine denuded, except for 

 occasional islands of much congested, inflamed, and partly necrotic 

 mucous membrane. The diseased intestinal wall is the seat of much 

 congestion and is much thickened. The amebas not only occur in 

 great numbers in the interstices of the tissues about the base of the 

 ulcers and in the lymphatics, but also enter the capillaries, through 

 which they are carried to the larger vessels, and eventually to the 

 liver, where their activities continue and give rise to the amebic 

 abscess. The first expression of their injury to the liver parenchyma 

 is shown by focal necroses. In each of these the organisms multiply 

 and the lesion extends until neighboring necroses are brought into 

 union, and eventuate in great collections of colliquated necrotic 



