Adult Oesophagostomum columbianum populations were larger in sheep fed low-protein diets than in adequately fed animals. Diet did not influence the numbers of larva which became established in sheep. Sheep fed high-protein diets eliminated more worms and were more immunologically competent than poorly fed animals. More encapsulated larvae, showing arrested development, were found in adequately fed sheep than in those fed low-protein diets. Adult O. columbianum produced eggs at an earlier time after infection in poorly fed sheep than worms in well fed sheep. More eggs/female worm were produced in sheep on a low-protein diet compared with the number of eggs produced in well fed hosts over the last week of the infection. The effects of immunity on the behaviour of the worm in both host diet groups is discussed.
There was a greater cellular proliferation in the intestines of infected adequately fed sheep than in infected animals on low-protein diets. These changes were most pronounced in the large intestine where the adult parasites were found. The macrophage-lymphocyte series of cells underwent hyperplasia in well fed animals but these changes were reduced, particularly among the plasma cells, in sheep fed low-protein diets. Increased mucin and mast cell counts were observed in sheep on high-protein, but not in hosts on low-protein diets: the intestinal populations of eosinophil and globule leucocytes were also reduced in poorly fed sheep.
The relationship of these various cellular reactions and their effect on the protective immunity of sheep to O. columbianum is discussed. It was concluded that the increased susceptibility of protein deprived sheep to O. columbianum infections was associated with malfunctions of the innate immunity of the gut, involving decreased peristalsis and failure of the mucin cell response, and with reduction of the adaptive immune response which was reflected by impoverished lymphocyte and plasma cell reactions, and possibly with poor cooperation between sensitized lymphocytes, antibodies and the mast cell-granulocyte effector mechanisms in protective immunity.