| dc.description.abstract | The aim of this experiment was to study the pathology of the disease in goats, due T. congolense infection, with a special emphasis on the mechanism of the anaemia.
The experimental animals were bought from KISIMA FARM, in Rumuruti, and the experiment was conducted in the University of Nairobi, at the Faculty of veterinary Medicine, Kabete.
The age of the experimental animals ranged from 1-4 years. They were kept in stalls and fed on hay, wheat bran and lucern throughout the course of the experiment, with free access to water.
T. congolense (Kiboko strain), obtained from the Kenya Veterinary Laboratories was used in the experiment. Initially, an infected mouse from the Kenya veterinary Laboratories was bled from the heart, and 2 ml of the blood injected into the jugular vein of a reservoir goat.
As soon as it developed parasitaemla, the reservoir goat was bled from the jugular vein and the experimental goats injected with infected blood into their jugular veins.
Daily rectal temperatures were then taken throughout the course of the experiment, and the clinical signs observed. Blood smears were collected frequently, from the superficial ear veins for the estimation of preparasitaemic period and the degree of parasitaemia.
Blood from the jugular veIn was collected atleast once a week for the routine haematology. The red blood cells, packed cell volume, haemoglobin and
leukocytes were determined using the coulter counter.
Bone marrow specimens were collected from the
sternum, and air dried cover slip smears were prepared and stained. A total of 1000 cells were counted and identified from each smear.
Four ml. of serum were collected weekly from each goat to enable the estimations of serum bilirubin protein, alkaline phosphatase and the transaminases.
The post-mortem examinations were done as soon as possible following death of the animals and the gross lesions observed and recorded.The histological sections were fixed and the sections were cut 6 microns thick and stained with H & E, Prussian blue and
Giemsals tecrilliques.
The clinical signs observed were:- progressive weakness,progressive emaciation, pale mucous membranes,rough and harsh coats, swelling of superficial lymph nodes,oedema of the face and submandibular regions. However, the animals continued eating throughout
the course of the infection, giving the impression that the appetite was not severely affected. The rectal temperatures were not very high compared to those of the
controls, with the exception of occasional peaks. The degree of parasitaemia fluctuated f'rom day to day, showing no apparent relationship with the temperature.
The red blood cells, packed cell volume and haemoglobin dropped significantly starting from the second week post-infection and persisting at low levels throughout the course of the infection.
The mean corpuscular volume and the mean corpuscular haemoglobin concentration remained fairly constant.The total leukocyte counts revealed a slight elevation
during the intermediate stage of the infection. The erythrocyte sedimentation rate showed a significant increase in the infeeted animals, while no alteration was observed in the erythrocyte osmotic fragility.
Total serum bilirubin, conjugated bilirubin and unconjugated bilirubin, all showed significant elevations during the intermediate stages of the disease.
The serum total protein levels remained unchanged throughout while the globulin showed a significant elevation and the albumin became significantly depressed towards the terminal stages of the infection.
The alkaline phosphatase and the transaminases showed no consistent change which could have been associated with the disease.
The bone marrow counts showed an apparent initial stimulation, followed by a terminal depression. An apparent maturation arrest was observed at the prorubricyte/rubricyte cell stage.
The gross pathological lesions observed were:- enlargement of the spleen, oedematous Lympnodes , serous fat atrophy in subcutaneous, coronary, perirenal, and perinodal fat, emaciation, increased serous fluid in the body cavities, liver congestion,pulmonary oedema, pink bone marrow, flabby and contracted testicles.
Histologically, in the liver, there was swelling of the Kupffer cell nuclei and an increased number of leukocytes in the sinusoids. In the spleen, there was hyperplasia of both red and white pulp,with an increased number of plasma cells, macrophages and lymphocytes in the red pulp. Heavy deposits of haemosiderin were observed in the macrophages in the spleen.
In the kidney, some glomeruli appeared slightly swollen and hypercellular,and protein casts were observed in the tubules.
In the testes, there was a complete degeneration of the seminiferous tubular epithelium, and the epididymis was empty and shrunken.
In the bone marrow there was an accumulation of the immature cells and there were many small erythropoietic foci.
Trypanosomas were observed in the blood vessels of the myocardium, brain, kidney and a few in the liver and none in the spleen. Tryrpanosomes were never observed outside blood vessels.
The increase in the serum unconjugated billirubin, together with the heavy haemosiderin deposits in the spleen suggest a haemolytic component in the pathogenesis of the aaemia.
The drop in the percentage of the nucleated red blood cells in the bone marrow towards the terminal anaemlc stage of the disease, and the maturation arrest at the prorubricyte/rubricyte cell stage indicate a bone marrow hypoplasia component in the
pathogenesis of the anaemia.The anaemaa in try-panosomlasis is therefore due to both an increased destructlon of red blood cells from the peripheral blood and due to bone marrow inhibition. | en |
