Effects of melarsamine hydrochloride (Cymelarsan) and diminazene aceturate (Berenil) on the pathology of experimental Trypanosoma brucei infection in red fronted gazelles (Gazella rufifrons).

An experimental infection of red fronted gazelles (Gazella rufifrons) with Trypanosoma brucei strain MKAR/84/NITR/6 was carried out. Two waves of parasitaemia which corresponded with a significant decline (p<0.05) in packed cell volume (PCV) was encountered in the infected untreated controls and those treated at day 8 post-infection with a sub-optimal dosage of diminazene aceturate (Berenil) at 3.5 mg/kg body weight. At postmortem, hepatomegally, splenomegally, lymphadenopathy, nephritis, myocardial degeneration with pulmonary oedema was observed in the two groups. Similarly, histopathological studies of some organs revealed interstitial haemorrhages, severe degenerative changes with cellular infiltrations. On the other hand, those treated by day 8 post-infection with melarsamine hydrochloride (Cymelarsan) at 0.3 mg/kg, 0.6 mg/kg or diminazene aceturate (Berenil) at 7.0 mg/kg body weight had apparently normal organs at the end of the experiment. These results suggest that, T. brucei can cause severe pathological changes in untreated red fronted gazelles (Gazella rufifrons). However, treatments at the onset of parasitaemia, by day 8 post-infection with melarsamine hydrochloride (Cymelarsan) at 0.3 and 0.6 mg/kg or diminazene aceturate (Berenil) at 7.0 mg/kg body weight ameliorated the deleterious effects of the infection in the gazelles.

The clinico-pathology and mechanisms of trypanosomosis in captive and free-living wild animals: a review.

Reports on the clinico-pathology and mechanisms of trypanosomosis in free-living and captive wild animals showed that clinical disease and outbreaks occur more commonly among captive than free-living wild animals. This is because the free-living wild animals co-exist with the disease until subjected to captivity. In exceptional cases however, draught, starvation and intercurrent diseases often compromised trypanotolerance leading to overt trypanosomosis in free-living wild animals. Meanwhile, in captivity, space restriction, reduced social interactions, change in social herd structure, reduced specie-to-specie specific behaviors, altered habitat and translocation were the major stressors that precipitated the disease. The cumulative effect of these factors produced severe physiological and somatic stress leading to diminished immune response due to increased blood cortisol output from adrenal cortex. The major symptoms manifested were pyrexia, innapetence, increased respiration, anaemia, cachexia and death. At necropsy, pulmonary oedema, splenomegally, hepatomegally, lympadenopathy and atrophy of body fats were the gross changes encountered. At the ultra-structural level, the tissues manifested degenerative changes, haemorghages, necrosis and mononuclear cellular infiltrations. The mechanisms of cellular and tissue injuries were primarily associated with physical and metabolic activities of the organisms. From the foregoing, it is evident that stress is the underlying mechanism that compromises trypanotolerance in wild animals leading to severe clinico-pathological effects.