Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig

The development of histolytic lesions of acute amebic colitis was studied by light (LM) and electron (EM) microscopy and by histochemistry (HC) in the germ-free guinea pig inoculated intracecally with amebae and the enteric flora derived from patients with acute amebic colitis. Between 7 and 12 days after inoculation the animals had developed focal amebic ulcerations ranging from microscopic in size to large ulcers. The ulcerated areas were covered with gray to gray-red exudate and were surrounded by edematous and hyperemic areas. The smallest ulcerations involved only the epithelium and the immediate underlying lamina propria, while the more extensive ulcerations with histolysis involved the whole thickness of the mucosa. The lytic areas consisted of amorphous material, which was intensely and diffusely alkaline phosphatase positive, while the intraepithelial enzymes were completely lost. By EM this material was identified as cellular debris from degenerating PMN, epithelial and other host cells and as fibrin. Although intact PMN’s were present adjacent to the histolytic lesions, PMN’s within the lytic area showed active degranulation and severe alteration. The vascular structures were extensively altered and showed lysing endothelial cells and thrombosis. The areas surrounding the ulcers were edematous, hyperemic and infiltrated by numerous PMN’s. The crypts were elongated and the epithelium cuboidal and showing degenerative changes when in contact or in close vicinity to amebae. Goblet cells were depleted. The activity of intracellular enzymes of epithelial cells was depressed, while the alkaline phosphatase activity in the PMN was greatly increased. The influx of PMN’s in the lesions and their massive degeneration in the lytic areas, may well explain contradictory reports of leukotaxis into amebic lesion as well as of absence of PMN’s in amebic colonic exudate. These observations suggest that lysis of colonic mucosa in amebic infection is due in part to tissue ischemia caused by vascular thrombosis, and in part, to the lytic action of degenerating PMN’s, possibly through the discharge of their lysosomal enzymes into the intercellular spaces.