Dr. Murai Éva szerk.: Parasitologia Hungarica 23. (Budapest, 1990)

Guinea pigs that had died of chronic trypanosomosis were subjected to detailed gross and histopathological examination. For histopathology, the organs were fixed in 10 % neutral formalin. The paraffin-embedded sections were stained usually with haemalun-eosin, Giemsa solution and by the PAS reaction. Impression smears of the bone marrow and subcutaneous connective tissue were stained with Giemsa solution. The guinea pigs were weighed weekly to check whether infection caused a reduction in their body mass. These data are shown in Fig. 1. RESULTS At 2-3 weeks PI the blood of 21 out of 30 guinea pigs proved to be positive for trypanosomes by microscopy. Nine groups of mice were inoculated, each with one of the 9 blood samples judged negative by microscopy. Two groups of mice died of acute trypanosomosis. Mice of the other 7 groups survived. Mice surviving the infection consistently died of acute septicaemia after challenge, indicating that no protection developed in any of them. The spleen of 5 out of the 9 guinea pigs that had been negative by microscopic examination of the blood proved positive by inoculation of mice. At 5-6 weeks PI 3 guinea pigs died of subacute trypanosomosis. The guinea pigs showed a lack of appetite, gradually lost weight (Fig. 1) and were reluctant to move. From the blood taken from two dying guinea pigs a few motile trypanosomes were demonstrable. The spleen of all guinea pigs proved positive for trypanosomes by the inoculation of mice. At 8-12 weeks PI 9 out of the 18 surviving guinea pigs had trypanosomes detectable in the blood. The spleen homogenate of 3 out of the 9 guinea pigs killed and found negative for trypanosomes by microscopic examination of the blood was positive by inoculation of mice: the mice inoculated with their spleen homogenate died of septicaemia (Table 1). At 20-22 weeks PI 3 guinea pigs died of chronic trypanosomosis. The guinea pigs were without appetite, reluctant to move and showed oedematous swelling of the thoracic and abdominal wall, genital region and, in one animal, the eyelid. The most severely affected guinea pig was exsanguinated, the other two died. No trypanosomes could be demonstrated from the blood of the exsanguinated guinea pig even by inoculation of mice. Trypanosomes were detectable only in the oedematous lesions and the spleen of that animal. Spleen homogenates from the other two animals were also positive. The surviving 6 guinea pigs were killed by bleeding at 38 weeks PI. No trypanosomes could be demonstrated from their blood, spleen and other organs even by inoculation of mice (Table 1). Guinea pigs that died of subacute or chronic trypanosomosis had lost weight in the days preceding their death, as compared to the surviving inoculated and the uninoculated control guinea pigs that appeared to be healthy throughout (Fig. 1). The gross pathological lesions seen in the three guinea pigs that died or were killed at 20-22 weeks PI resembled that of dourine in horses. The animals were cachectic and showed severe oedema of the subcutaneous connective tissue (anasarca) all over the body (Fig. 2). The spleen had undergone a 3- to 5fold enlargement and was hyperplastic. The kidneys were swollen, pale brown, and in some cases their cortex contained punctiform haemorrhages. The testicles were atrophic.