186 FAMILY: AMCEBID^ 



the digestive fluids the cyst ruptures. From the work of Chatton (1917a), 

 who fed cats with material containing cysts, and that of Penfold, Woodcock, 

 and Drew (1916), who treated cysts with liquor pancreaticus, it appears 

 that it is the secretions in the small intestine which cause the cyst wall 

 to dissolve. 



Chatton stated that the cyst liberated a four-nucleated amoeba, while 

 the other observers merely noted that a single amoeba escaped from the 

 cyst. Whether this happens in the human intestine or not cannot be 

 stated. Dobell and Stevenson (1918) and the writer have failed to bring 

 about any escape of amoebae from cysts by means of liquor ]Kmcreaticiis. 



From experiments on cats, there can be no doubt that human beings 

 are infected by the ingestion of cysts. Whatever may be the exact method 

 of escape of the encysted amoebae and their development after this, it is 

 a fact that invasion of the intestinal wall by the amoebae quickly takes 

 place. In the earliest condition the amoebae make their way into the 

 glands of the large intestine, and crawl to the bottom of these. Here they 

 multiply, and partly by pressure, and possibly by the secretion of a toxin, 

 the gland cells degenerate and separate from one another. By this time 

 the tubule of the gland has probably become blocked, and if the adjacent 

 glands over a small area of surface are all similarly involved, as is usually 

 the case, a slightly raised yellowish nodule is produced. Meanwhile, the 

 amoebae have made their way into the interglandular connective tissue, 

 and a certain amount of necrotic material from broken-down cells has 

 collected. In this condition the yellow nodule is in reality a small 

 amoebic abscess of the mucosa. Very soon this abscess bursts into the 

 lumen of the intestine, and the contents are discharged, with the result 

 that a small undermined ulcer is formed (Figs. 93, 94). The amoebae which 

 thus escape invade other glands, causing the condition to spread, or they 

 are passed in the faeces with a certain amount of blood and mucus, which 

 represents the discharge from the abscess. The infected portions of the 

 intestine may be very limited, so that only a few scattered nodules are 

 formed, or there may be a more or less continuous infection of all the 

 glands. After rupture of the primary abscess the ulcer so formed becomes 

 gradually larger, the amoebae multiplying in the base of the ulcer and 

 extending over a wider area. They break through the muscularis mucosae, 

 and extend into the submucous tissues, producing eventually ulcers which 

 may reach an inch or more in diameter. These ulcers, like the small ones 

 originally formed, have undermined edges, and become filled with mucoid 

 material, debris of cells, and amoebae. It is probable that the plugs of 

 mucus admixed with blood, which occur in the stools of amoebic cases, 

 represent the evacuations from these ulcers. These masses of mucus 

 may contain enormous numbers of amoebae. 



