ABSTRACT-The biochemical and histopathological changes in rats experimentally infected with T. evansi isolated from camels in El-Gadarif State, Sudan, were studied. A number of 18 adult male outbred albino rats, weighing between 133-137g were used in the study. The rats were divided into 3 groups of 6 animals each (A,B and E). Group A and B were intraperitoneally infected with T. evansi (Showak stabilate) with 1×10 4 trypanosoma for the inoculum. Group B was given quinapyramine sulphate (20 mg/kg bwt) after parasitaemia was evident. Group E was left healthy uninfected controls for the stabilate. There was significant reduction in serum glucose and phosphorus; compared to significant increase in Glutamate Oxaloacetate Transaminase (GOT), Glutamate Pyruvate Transaminase (GPT) and total protein in groups (A and B). Microscopically, the brain tissues of the infected rats revealed acute congestion of the meningeal capillaries, perivascular oedema, neuronecrosis (vaculation), gliosis and trypomastigotes in dilated capillaries. The lung revealed oedema, congestion, multifocal alveolar emphysema, hyperplasia of the peri-bronchiolar lymphoid tissues and haemorrhages. The spleen showed extensive haemorrhages, haemosiderosis and aggregation of histiocytes resulting in multinuclear giant cells formation. The kidneys showed acute congestion of the glomerular tufts. All tissues obtained showed exactly the same histopathological changes. No significant histopathological alterations were observed in the liver and heart. The most consistent histopathological changes were seen in the brain, lungs, spleen and kidneys. These changes were consistent with trypanosome infection and were confirmed by the presence of trypanosomes in most of the tissue sections examined.

A number of 18 adults male outbred albino rats, weighing between 133-137g were used to investigate the drug susceptibility of Trypanosoma evansi strain isolated from naturally infected dromedary camels in Umbadir area, North Kordofan State, Sudan. The rats were divided into 3 groups (C, D and F) of 6 animals each. Group C and D were infected intraperitoneally with T. evansi (Umbadir stabilate) with 1×10 4 Trypanosome for the inoculum. Group D rats were given quinapyramine sulphate (20 mg/Kg bwt) after parasitaemia was evident. Group F was left as healthy uninfected control for the stabilate. When parasite counts were one or more parasites per field, counting in haemocytometer were used for exact number of parasite per cubic millimeter using Neubaeur's counter. Parasites from tail blood were first fixed, stained and diluted in trypanosome diluting reagent. The parasites were diluted to the level that can be easily counted in WBC counting chamber in the haemocytometer. The total number of parasites was expressed as log 10 number of parasites per ml of blood. The presence and degree of parasitaemia were determined daily for each rat by examining tail blood. The identity of the local stabilates of Trypanosoma evansi was confirmed through adopting PCR where primers that target the internal transcribed spacer one (ITS1) of the ribosomal DNA were used. There was significant reduction in serum glucose and potassium as well as significant increase in total protein, urea, calcium, albumin and cholesterol in group C. The Umbadir stabilate showed low mortality and high sensitivity to quinapyramine sulphate.