INTESTINAL LESIONS ASSOCIATED WITH AMEBIC AND BALANTIDIAL INFECTION IN MAN AND LOWER ANIMALS*

Abstract

Pathogenic spp. of Endamoeba and Balan-tidium have identical effects upon the mucosa of the large intestine of susceptible hosts. The primary and perhaps the total effect of the organisms is merely necrosis. They enter the tissue only after necrosis has taken place, except as a postmortem or late antemortem change. The protozoa apparently elaborate a cytotoxic or necrotizing substance that causes tissue degeneration. Lesions are invaded by intestinal bacteria also. Hence extension of tissue necrosis may be due to a combination of factors, and the inflammatory response may not be attributed to the parasites alone. Resistance of the host must be impaired before the intestinal tissues are subject to necrosis. In either balantidiasis or amebiasis lesions of the intestinal wall originate in the mucous surface. Surface and deep ulcers are genetically the same, except when the latter result from bacterial abscesses of the follicles. The lymphoid tissues of the gut wall, because of their anatomic position and make up, are important foci for extension of the disease to the sub-mucosa. Postmortem penetration of tissue by Balan-tidium and Endamoeba account for the fact that isolated organisms and groups of organisms are found deep in the intestinal wall. Balantidia also can invade cut edges of the large intestine at autopsy.