Dr. Murai Éva szerk.: Parasitologia Hungarica 20. (Budapest, 1987)
quently within the blood-vessel wall, attached to the endothelial cells. In the killed voles trypanosomes were demonstrable only infrequently. By haemalaun-eosin (HE) staining there was pronounced cell proliferation in the Malpighian corpuscles (Fig. 4) and reticulumcell hyperplasia with the presence of dividing reticulumcells, plasmoblasts, plasma cells and, here and there, phagocytosed trypanosomes (Fig. 5) in the red pulp of the spleen. In HE-stained sections of the 18-fold enlarged spleen we observed pronounced cell proliferation (Fig. 3), reticulu mcells, plasmoblasts , immature stages of red blood cells, and a large haemorrhage in the red pulp. In that spleen no trypanosomes were demonstrable by Giemsa staining. Histologically no appreciable difference was found between the spleen of voles challenged two weeks after infection and that of the unchallenged litter mates. At the peak of immunity, in the still 2 to 3 times larger spleen of the challenged voles, and those infected only once, cell proliferation (reticulumcells,plasma cells) was found by HE staining. In the spleen of the voles challenged 3 months after infection cell proliferation (hyperplasia) was much more pronounced than in the killed controls. In the latter voles cell proliferation had started to regress. The course of infection, together with the gross pathological and histopathological findings obtained for the killed voles, have proved that the vole is resistant to T. equiperdum infection. Voles can mobilize their macrophages and other T cells to an extent that the considerable splenomegaly and macrophage activation occurring from PI days 3-4 result in a gradual decrease of trypanosomal counts. In most cases trypanosomes are no more demonstrable microscopically on day 5. At the same time, in the blood of susceptible mice trypanosomal counts keep increasing up to death. Therefore, the splenomegaly found in mice dying of the infection does not even come close to the temporary splenomegaly developing in voles surviving the infection. The remarkable ability of voles to develop splenomegaly and to activate their other macrophages rapidly are, thus, life-saving properties in T. equiperdum infection. The response of the spleen is of decisive importance in determining the course of infection in other trypanosomoses as well (ACKERMANN and SEED, 1976; ANOSA and KANEKO, 1983; CLAYTON et al., 1980; LLENDE et al., 1983; MOU LTON and COLEMAN, 1977; MOU LTON et al., 1974; REGENDANZ and KIKUTH, 1927). IMMUNOLOGICAL STUDIES Antibodies to T. equiperdum persisted in the convalescent voles' serum for 2-3 months (Fig. 6). Parallel with time, antibody levels tend to decline and finally disappear from the blood of voles, proving that the infected voles no longer harbour living trypanosomes (antigen stimulus), as opposed to such resistant rodents which can carry trypanosomes in their blood for months. Legend to the figures Fig. 2: Spleen from voles killed in litter A (a, b, c= controls; d, e= infected, with 5- to 7-fold splenomegaly) (x 1). Fig. 3: Spleen from voles killed in litter D (f= histological picture of a spleen, 18-fold splenomegaly, two cross-sections ; g= spleens of control litter mates, two cross-sections) (x 5). Fig. 4: Pronounced cell proliferation in a Malpighian corpuscule and the red pulp of an enlarged spleen) (x 200). Fig. 5: Proliferation of reticulocytes and plasma cells in the red pulp of the spleen (x 460).
