Small hemispherical elevations of the overlying mucosa mark the location of the deeper-lying necrotic process. With the multiplication of the amoebae and the extension of the necrotic process in the submucosa we have thrombi formed in the terminals of the portal vein and possibly in those of the mesenteric arteries, which in the former case may result in emboli being swept up the portal vein to lodge in the liver and form a starting point for a similar necrosing process there or, as the result of interference with the blood supply of the overlying mucosa, cause this to undergo necrosis and be cast off as a slough, leaving an oval or irregular ulcer with deeply undermined edges and a floor formed by the muscular coat. The ulcers may be no larger than a pin’s head or they may be 1 or 2 inches in diameter or by coalescence be still larger. The gelatinous necrosis in the submucosa always extends beyond the limits of the necrosis of the mucosa, thus explaining the undermining. At times the muscular coats of the intestines are involved thus leading to a slough which involves all coats except the serous one. Bacterial infection, with coagulation necrosis of the mucosa overlying the amoebic process, is also responsible for some of the tissue destruction. The amoebic ulcerations rarely extend above the ileo-caecal valve but may involve the entire large intestine. Rogers and Lafleur found the lesions most often in the caecum and ascending colon, often limited to this area. The appendix was involved in 7% of the Manila autopsies. Often mild cases may only show lesions in the caecum. When there is a tendency to perforation the omentum will often be drawn over to the location of the threatened perforation. There is often thickening of the intestine in one place with cicatricial contraction of the lumen and thinning in another, so that there is an appearance of great irregularity. SYMPTOMATOLOGY The great majority of cases of amoebic dysentery run a chronic course with periods of improvement alternating with recurrences of pains and dysenteric stools. From Walker’s experiments the period of incubation would appear to be from one to three months. The onset in such cases is very insidious and the patient may complain more of diarrhoeal than dysenteric manifestations. Such patients often give a history of passing three or four pultaceous stools daily and complain of tenderness in the region of the caecum or along the course of the large intestine. One may determine some thickening of the colon in a thin subject.