In this chapter, we discuss the diseases and related pathologic alterations that may be encountered in the gastrointestinal tract and associated organs of various species of laboratory animals, birds, fish, reptiles, and amphibians. Diseases of various segments of the gastrointestinal tract, the salivary glands, liver, and pancreas are discussed and categorized as inflammatory, parasitic, neoplastic, or miscellaneous. The latter category includes developmental anomalies and metabolic lesions. Due to space limitations, this presentation is not an all-inclusive review, but it does provide a rather extensive review of these lesions. We have also included a rather comprehensive literature review, with a list of references for those readers who want more detailed information with respect to specific diseases.

The Digestive System

Acanthamoeba interactions with human brain microvascular endothelial cells.

We studied the adherence of [3H]thymidine-labeled axenic Entamoeba histolytica (strain HM1-IMSS) to in vitro preparations of rat and human colonic mucosa. Studies were performed with fixed or unfixed rat colonic mucosa, unfixed rat mucosa exposed to trypsin, unfixed rat submucosa, and fixed human colonic mucosa. Twenty percent of the amebae adhered to fixed rat colonic mucosa; adherence was specifically inhibited by N-acetyl-D-galactosamine (GalNAc), galactose, and asialofetuin. The adherence of amebae to fixed human colonic mucosa was also GalNAc inhibitable. Greater adherence was found with unfixed rat colonic mucosa (40.9%) and was not GalNAc inhibitable unless the tissue was first exposed to trypsin. However, GalNAc did inhibit the adherence of amebae to unfixed rat submucosa. Glutaraldehyde fixation of amebae inactivates known amebic adhesion proteins; there was a markedly decreased adherence of fixed amebae to trypsin-exposed mucosa or fixed rat colonic mucosa. However, fixed or viable amebae had equal levels of adherence to unfixed rat colonic mucosa, suggesting the presence of a host adhesion protein that binds to receptors on amebae. Human (10%) and rabbit (5%) immune sera reduced the adherence of viable amebae to fixed rat colonic mucosa. We concluded that the GalNAc-inhibitable adhesion protein on the surface of E. histolytica trophozoites mediated adherence to fixed rat mucosa, fixed human colonic mucosa, trypsin-exposed unfixed rat mucosa, and unfixed rat submucosa. The surface of unfixed rat colonic mucosa contained a glutaraldehyde- and trypsin-sensitive host adhesion protein, perhaps in the overlying mucus blanket, which bound viable or fixed E. histolytica trophozoites.

Adherence of Entamoeba histolytica trophozoites to rat and human colonic mucosa.

Amebiasis, a significant cause of morbidity and mortality on a global scale, is caused by invasion of the colonic mucosa by the cytolytic protozoan parasite Entamoeba histolytica. A review of the investigations into the mechanisms by which the parasite causes invasive disease is presented, including the relevant history, epidemiology, and pathology of amebiasis, the biology of the parasite, in vivo and in vitro studies of the pathogenesis of disease, the host immune responses, and possibilities for prevention and biologic control. New insights into the cell biology of E. histolytica, especially its adherence and cytolytic properties, offer several new approaches to biologic control of this invasive, destructive parasitic infection.

A Review of the Parasite Cellular Mechanisms Involved in the Pathogenesis of Amebiasis

Amebiasis is due to invasion of the colonic mucosa by the enteric protozoan Entamoeba histolytica. The biology of the parasite and the pathogenic mechanisms of E. histolytica have been extensively studied. Recent studies provide new insights into the mechanism by which amebas colonize the gut, interact with bacterial flora, adhere to and lyse tissue, and combat the host's inflammatory response. Elucidation of the biochemical and cellular bases of the pathogenesis of disease caused by E. histolytica may lead to the development of an immunologic or pharmacologic means of prophylaxis.

Pathogenesis of Disease Caused by Entamoeba histolytica: Studies of Adherence, Secreted Toxins, and Contact-Dependent Cytolysis

Weanling rats given protein deficient diets for 2 to 4 weeks and then infected intracaecally with Entamoeba histolytica trophozoites showed a greater susceptibility to infection compared with controls. The proportion of infected animals that developed caecal ulceration was also increased. Supplementation of the low protein diet with extra carbohydrate produced an even greater infection rate but the likelihood of caecal ulceration was lower. No relationship between amoebic infection and the bacterial flora or pH of the caecum was noted, however the redox potential was lower in those animals that developed ulceration. The possible mechanisms involved are discussed together with the relevance of these findings to human amoebiasis.

G.W. Ross

Papers

Dietary factors affecting the pathogenicity of Entamoeba histolytica in rats