Protozoa of the Digestive and Urogenital Tracts 557 



a small portion of the cytoplasm emerges through a pore in the mem- 

 brane. Eventually, the organism surges back and forth until it squeezes 

 out as a multinucleate stage (33). The details of growth, nuclear division 

 and plasmotomy vary somewhat, but eight uninucleate amoebae are 

 usually produced from each excysted stage before the normal cycle of 

 fission is resumed (33, 46). 



Invasion of tissues by E. histolytica 



Invasion of the wall of the colon is heaviest in regions where 

 stasis of the contents occurs most frequently (31, 125) — cecum, ascending 

 colon, rectum, sigmoid flexure, and the appendix. In very severe infec- 

 tions the colon may be attacked throughout its length, but no single 

 region is invaded invariably. Consequently, the proctoscopic finding of 

 no rectal ulcers cannot guarantee freedom from amoebae in other parts 

 of the colon. 



It is generally assumed that invasion of the tissues may involve me- 

 chanical penetration by pseudopodial activity and the destruction of 

 tissue cells by cytolytic enzymes. The relative importance of these two 

 factors has been disputed. Epithelial necrosis with no apparent mechan- 

 ical penetration has been seen in kittens (118), whereas penetration in 

 monkeys has been attributed primarily to mechanical activities (69). 

 Meleney and Frye (121) concluded that in kittens as well as man, lysis of 

 tissue cells and mechanical penetration are both significant factors, 

 whereas Craig (41) has stressed the cytolytic activity of E. histolytica in 

 human amoebiasis. The interpretation of cytolytic activity is based upon 

 the histological appearance of invaded tissues and upon the reported ex- 

 traction of an active cytolysin from E. histolytica in cultures (37). 



Development of the amoebic ulcer has been discussed by various 

 workers (41, 52, 69, 136, 137, 140, 178). The amoebae apparently may in- 

 vade the tissues by crawling into the crypts of Lieberkiihn or by attacking 

 the more superficial mucosa. As pictured by Wenyon (178), invasion of 

 an intestinal gland and multiplication of the amoebae is followed by de- 

 generation of gland cells and loosening of the tissues so as to block the 

 duct, and there may be a slight nodular elevation of the mucosa. The 

 earliest lesions reported in human autopsy material are inconspicuous 

 "pinpoint" lesions in individuals reporting no symptoms of amoebiasis 

 (58). The early lesion, if it does not open into the intestinal lumen, may 

 be considered an amoebic abscess which will later rupture to form a 

 small flask-shaped ulcer. After penetrating the epithelium, the amoebae 

 may migrate along the basement membrane or may pass through into 

 the underlying connective tissue. Increase in number of amoebae is ac- 

 companied by local necrosis of tissue cells and rupture of capillaries, and 

 the margin of the ulcer is gradually undermined. This ulcer of the colon 

 differs from the typical bacterial ulcer in that there is no tendency for 



