PART II. CHARACTKRS AND DIAGNOSIS 57 



The development of liver abscess in cases which give no history 

 of dysentery is far from uncommon, and it seems justifiable to 

 assume that these cases must have been carriers of E. histolytica 

 and must have suffered from unrecognized ulceration of the large 

 intestine. 



Taking all these points into consideration it seems safe to assume 

 that the E. histolytica in the intestine of the carrier case is not 

 comparable with the perfectly harmless E. coli, but that it is the 

 cause of a certain amount of ulceration, and we know that this 

 ulceration may be quite extensive without giving rise to any definite 

 dysenteric symptoms. 



Another argument in favour of this view is the remarkable action 

 of emetin on the E. histolytica infections and its comparative 

 inaction on those of E. coli. It seems difficult to understand why 

 the drug should be more toxic to one than another amoeba if they 

 were both living under similar conditions in the large intestine. 

 Yet administered by injection to a healthy carrier showing infec- 

 tions of both E. histolytica and E. coli, it causes the former to 

 disappear, while the latter, as a rule, persists. It seems most prob- 

 able that the drug given in this manner reaches the E. histolytica 

 more easily than the E, coli, and the only way in which this could 

 occur would be if the E. histolytica had a different habitat from the 

 E. coli. This difference can be readily explained if we assume 

 that, in the carrier, the E. histolytica is living in or about intes- 

 tinal ulcers while the E. coli is more uniformly distributed over the 

 healthy gut. The injected drug would thus reach the.E. histolytica 

 through the circulation, while the E. coli would escape. This view 

 is supported by the fact that emetin administered by the mouth 

 generally causes temporary disappearance of both E. histolytica and 

 E. coli. Though we assume that infection with E. histolytica 

 means ulceration of the large intestine it still remains a fact that 

 the type of ulceration in a carrier case must be different from that 

 in an acute dysenteric. The ulcer in the carrier is probably of a 

 more indolent nature without there being active destruction of 

 tissue or outpouring of exudate from its surface. Living in the 

 deeper tissues of the ulcer are large amoebae, while towards the 

 surface of the ulcer, and possibly to a large extent over the surface 

 of the gut around the ulcer, are smaller amoebae which have been 

 produced by successive divisions of the larger forms. Here on the 

 surface these small amoebae, the minuta forms, become encysted 

 and produce the typical cysts of E. histolytica, which escape in the 

 stool. If, for some reason, such an indolent ulcer becomes acute 



