Life cycle of Frenkelia. IV. Pathomorphological findings in the organs of experimentally infected bank voles]

In 1975 the buzzard (Buteo buteo) was found to be the final host of Frenkelia clethrionomyobuteonis. After this discovery it became possible to investigate systematically the pathomorphology of the infection in the intermediate host, the bank vole (Clethrionomys glareolus). Fifty bank voles were infected orally with a suspension of sporocysts recovered from the faeces of experimentally infected buzzards. Each rodent receive 7000 sporocysts. Six controls each were given a faecal suspension from a non-infected buzzard. The voles were killed between 1 and 140 days after infection and examined histologically. Between the 5th and 8th day of the infection during the schizogonic multiplication of the parasite a focal necrosis of liver cells and of the liver parenchyma is observed followed by a reversible resorptive inflammation associated with siderophagia and the occurrence of giant cells. The spleen was spodogenously enlarged up to twice its normal size. There also was haemosiderosis of the bone marrow, the liver and the spleen up to 25 days after infection. At the same time the erythropoiesis in the bone morrow, the spleen and in the lymph nodes increased; there also was a lymphoid hyperplasia in spleen and lymph nodes. About 10 days after infection a reversible infiltration with lymphocytes and plasma cells developed in the liver, heart and brain. This infiltration was again detectable as perivascular and meningeal reactions in the brain after the 49th day after infection. The second asexual multiplication of the parasite was seen histologically in the grey and white matter of the central nervous system after the 18th day of infection. The developing cysts increased in size continuously thereby compressing the surrounding nervous tissue. Disseminated focal necrosis with resorptive inflammatory components was prominent in the parenchyma of the brain after the 49th day of infection. It was possible to differentiate between damage in single organs and systemic pathological lesions. The lesions in single organs were directly connected with the development of parasitic stages in the liver (schizonts) and in the brain (cysts). The generalized lesions occurred in the haemopoietic system after an impairment of the blood during the first asexual multiplication. They also occurred in the immunocytic systems after the first and during the second asexual multiplication and during the relatively late cystic phase of the parasite in the brain. The pathogenesis of the disintegration of blood cells is not clear. The immunocytic reaction can be considered an immunological response of the host against the parasite. The effect of the development of the cysts on the function and structure of the central nervous system is expected to lead to an increasing impairment of the motility of the intermediate host.