Serum Biochemical Changes in Experimental Gambian Trypanosomosis. II. Assessing Hepatic and Renal Dysfunction

Serum biochemical changes were assessed to determine hepatic and renal function in 4 vervet monkeys experimentally infected with Trypanosoma brucei gambiense, the causative agent of sleeping sickness in West and Central Africa. Parameters examined included serum bilirubin, blood urea nitrogen (BUN), and cholesterol levels. Significant increases in the total bilirubin and BUN levels occurred from the second week post-infection (PI) (P ≤ 0.05) and remained so until the monkeys died of infection, at 12 to 15 weeks PI. Serum cholesterol levels increased from the fourth week to the eighth week of infection. These changes suggested early hepatic and renal pathology, and dysfunction in the monkeys, which were thought to be associated with the early death of the primates. These observations were at variance with the typically mild and chronic nature of T. brucei gambiense in humans. It was concluded that early hepatic and renal damage in trypanosomosis is an important obstacle to the success of chemotherapy of sleeping sickness in humans, as the drugs themselves are thought to be hepatotoxic and nephrotoxic. Furthermore, characterisation of atypically virulent T. brucei gambiense stains may be necessary in distinguishing such strains from T. brucei rhodesiense and preventing the spread of Rhodesian sleeping sickness.