58 HUMAN INTESTINAL PROTOZOA IN THE NEAR EAST 



there is a greater activity and multiplication on the part of the 

 deep-seated large amoebae and a greater outpouring of exudate with 

 blood and mucus. In this process the small amoebae and cysts on 

 the surface of the ulcer are washed away and will only be found 

 in the stool at the commencement of the dysenteric attack, while 

 the now active large amoebae escape from the ulcer in the exudate, 

 and appear in the blood and mucus stool where they are seen actively 

 crawling about with included red blood corpuscles. When the 

 dysentery abates the ulcer returns to its more indolent state, while 

 the small amoebae are again produced and the cysts reappear. 

 An acute attack of dysentery may arise, however, not from an 

 increase in the activity of an existing indolent ulcer, but by a 

 fresh attack on some still healthy part where a new ulceration 

 is being established. 



The above conception, admittedly somewhat theoretical, fits in 

 well with what we know of the history of many of the carrier cases 

 of E. histolytica, and affords a possible explanation of the difference 

 in the action of emetin on E. histolytica and E. coli. 



(d) How does E. histolytica establish itself in the Human Intes- 

 tine? Individuals become infected with E. histolytica by ingesting 

 the well-known four nuclear cysts. This has been experimentally 

 proved in cats by many observers, and by Walker and Sellards 

 (1912-1913) in the case of human beings. As there occur so many 

 carriers who have never suffered from dysentery it is clear that 

 many become infected with E. histolytita without showing any 

 signs of their infection, at any rate, for some time. In their experi- 

 mental infection of human beings Walker and Sellards found that 

 only a small percentage (four out of eighteen) of those who became 

 infected actually developed definite dysenteric symptoms. It would 

 seem probable that in nature too the majority of those who become 

 infected acquire at first a benign infection which can only be recog- 

 nized by an examination of the stool, and that it is only later that 

 the ulcerative process becomes acute or extensive enough to give 

 rise to dysenteric symptoms. In other words, the cases become 

 first of all healthy carriers and then only later lapse into a condi- 

 tion of amoebic dysentery. It is but rarely that one has an oppor- 

 tunity of obtaining evidence to support this view. Case Kushforth, 

 already referred to above, was seen at the commencement of his 

 first attack of dysentery, and in his case cysts of E. histolytica were 

 found as well as active amoebae with included red blood corpuscles. 

 It would seem that the case had been a carrier of E. histolytica 

 without showing any symptoms, and was just then lapsing into a 



