Electron microscope studies of experimental Entamoeba histolytica infection in the guinea pig. II. Early cellular and vascular changes accompanying invasion of the lamina propria.
Early cellular and vascular changes in response to invasion of lamina propria by Entamoeba histolytica were studied sequentially, at the ultrastructural level, in germfree guinea pigs inoculated intracecally with amebae and enteric flora derived from patients with acute amebic colitis. Approximately one week post-inoculation the animals developed acute colitis with mucosal invasion by trophic amebae. Although epithelial cells at the sites of amebic invasion showed progressive cytoplasmic changes and desquamation resulting in microerosions, most mesenchymal elements in the lamina propria appeared normal without cytopathic changes even when in direct contact with invading amebae. Only the polymorpho-nuclear leukocytes (PMN) apposed or topographically close to amebae exhibited degenerative changes which were characterized by condensation of nucleoplasm and cytoplasm, extra-cellular release of cytoplasmic components including granules, and, finally, lysis of cell membranes. Capillaries and venules in the lamina propria showed a variety of changes such as swelling and gap formation at the intercellular endothelial junctions and more rarely at the fenestrae. Blood vessels physically close to amebae showed formation of endothelial cytoplasmic blebs which pinched off into the vascular or extravascular space. Platelet and fibrin thromboses were common in the more severely damaged capillaries and venules. Fragments or clumps of fibrin-like material were found also in the extracellular spaces. Amebic invasion of the lamina propria, then, is accompanied by continued epithelial shedding, PMN degeneration, and changes in both capillaries and venules consisting of endothelial damage and occlusive thrombosis. The vascular changes appeared to be closely related to PMN degeneration resulting from interaction of PMN with invading amebae.
D000562:Amebiasis / Q000473:pathology*; D000818:Animals; D002432:Cecum / Q000648:ultrastructure; D004727:Endothelium / Q000648:ultrastructure; D004847:Epithelial Cells; D004848:Epithelium / Q000648:ultrastructure; D004912:Erythrocytes / Q000648:ultrastructure; D005856:Germ-Free Life; D006168:Guinea Pigs; D007249:Inflammation; D007365:Intercellular Junctions / Q000648:ultrastructure; D007413:Intestinal Mucosa / Q000098:blood supply / Q000648:ultrastructure*; D007962:Leukocytes / Q000648:ultrastructure; D008833:Microcirculation / Q000648:ultrastructure; D013927:Thrombosis