Experimental concomitant toxoplasma and malaria infection in rats.

The effect of concomitant toxoplasma and malaria infection on the reticuloendothelial system was investigated in rats. This was evaluated by the level of plasmodial parasitaemia; humoral antibody response; effect on splenic weight; histopathological changes in thymus and spleen; histopathological and histochemical changes in liver. The parasitaemia appeared after 2 days in single malaria and concomitant infections. The peak was reached after 6 days with single and precedent malaria, and after 10 days with precedent toxoplasma. The clearance of parasitaemia was delayed to 30 days with concomitant infections instead of 14 days with single malaria. Higher than normal malarial antibody levels were reached with precedent toxoplasma, while the toxoplasma antibodies were lower than normal in both concomitant infections. There was a significant increase in splenic weight in both precedent malaria and toxoplasma, followed by a decrease which did not return to normal in case of precedent malaria. The thymus was packed with thymocytes in precedent malaria, while depletion in the cortex occurred in precedent toxoplasma. In the liver, there was glycogen depletion and decrease in succinic dehydrogenase activity in both concomitant infections. Choline esterase activity in precedent malaria was decreased and returned to normal on day 40 while in precedent toxoplasma the activity was normal all through the period. The alkaline phosphatase activity was decreased and returned to normal on day 40 in both concomitant infections.

Effect of Toxoplasma gondii on histopathology and histochemistry or reticuloendothelial system in experimental animals.

The effect of acute and chronic infections by Toxoplasma gondii on the spleen, thymus and liver of mice and rats, and on their antibody response has been studied. In acute infection while the splenic weight increased the thymic weight decreased. The histopathological studies demonstrated lymphocytic depletion of splenic follicles and thymic cortex. Numerous phagocytes and plasma cells were seen in the red pulp and thymic medulla. Vascular congestion and haemorrhages were marked. The liver cells showed degeneration which progressed from hydropic to fatty. The succinic dehydrogenase activity of damaged cells was decreased, while the phosphatase activity was increased. The parasites were seen in some liver cells. Marked cellular infiltration was observed around the blood vessels in the form of granulomata. The reticuloendothelial cells, Kupffer cells and phagocytes showed higher alkaline phosphatase activity. In chronic infection the thymus showed early lymphocytic depletion then returned to normal. The splenic weight was increased and the follicles were enlarged with the presence of immunoblasts in the germinal centres. The cords of the red pulp were thickened and contained numerous plasma cells. Most of the liver cells were normal with normal enzymatic activity but small foci of necrosis were seen. There was a gradual increase in antibody response in both acute and chronic infections. It was concluded from the results that acute infection mainly produced toxic effects, whereas chronic infection produced immunological responses.