Abstract:
This work was designed to study the effects of Trypanosoma brucei and Trypanosoma congolense infection on the renal function of mongrel dogs. Also, the effects of treatment of the infection with diaminazene aceturate were evaluated. Sixteen (16) male mongrel dogs aged between 3 and 6 months, and weighing between 2.5 and 5.2 kg were used for the study. The dogs were acquired, numbered, tagged and weighed. The dogs were kept in clean metal cages in a fly proof house and were fed once daily with either rice and beans , or garri with soup and water given ad libitum. The 16 dogs were randomly assigned with a bias for even weight distribution into four groups (A-D). Groups A and B had five dogs each, while groups C and D had three dogs each. The five dogs in group A were infected with Trypanosoma brucei while the five dogs in group B were infected with T. congolense. On establishment of parasitaemia, all the dogs were treated with 7mg/kg of diminazene aceturate. Groups C and D dogs were uninfected. Group C was treated with 7mg/kg of diminazene aceturate whereas the three dogs in groups D were untreated. Parameters monitored were prepatent period, parasitaemia, body weight, rectal temperature, packed cell volume (PCV), hemoglobin concentration and total white blood cell counts (TWBC). Urinalysis and serum biochemical analysis were equally performed. The results of the study showed that parasitaemia occurred in the T. brucei infected dogs (group A), 4-6 days post infection (PI) while it occurred in the T. congolense infected dogs (group B) 7-10days post infection (PI). Following treatment with diminazene aceturate, parasites cleared from the T. brucei and T. congolense infected dogs within (3) days. No relapse of infection was recorded following clearance of the parasites. Trypanosoma brucei infected group had 20 % mortality while T. congolense infected group had 80 % mortality. The T. congolense infected dogs before they died manifested some forms of aggression like biting the metallic rods that were used in constructing the house suggesting cerebral involvement. However the T. brucei group was apparently healthy and did not manifest any change in behaviour as observed in the T. congolense. Trypanosomosis caused significant (p<0.05) reduction in the packed cell volume and haemoglobin concentration of the infected dogs. However treatment with trypanocide was able to reverse these haematological alterations. Serum concentrations of creatinine, urea nitrogen (BUN), potassium and calcium as well as urine specific gravity and pH were not altered by the infections. However, mild levels of protein (30 – 100 mg/dl) were detected in the urine of both T. brucei and Trypanosoma congolense infected dogs during the course of the infection. There was also significant (p < 0.05) decrease in the levels of protein in the serum of T. brucei but not in the T. congolense-infected dogs. This is probably caused by protein loss in the urine and possibly tissue invasiveness of the parasites and damage of organs such as liver which affected albumin synthesis . The total protein of T. brucei infected group was significantly ( p< 0.05 ) lower than that of T. congolense group at week one post infection. At week three post treatment, the infected groups recorded significantly (p<0.05) higher total protein levels than the control group. The protein loss in the urine was isolated and minimal post treatment with diminazene aceturate. The hypoalbuminaemia that occurred in the T. brucei infected dogs persisted throughout the study irrespective of treatment. It was concluded that T. brucei and T. congolense infections in dogs produced mild proteinuria, with concomitant hypoalbuminaemia in T. brucei infected dogs which did not clear on trypanocidal administration.