The study was carried out on a game ranch in Chisamba located approximately 45 km north of Lusaka, Zambia. In October 2005, blood samples were collected from 14 wildlife species captured during a translocation exercise using M99 (etorphine hydrochloride) and reversed using M5050 revivon (diprenorphine) at standard capture dosages (Novartis SA Ltd, Animal Health, Johannesburg, South Africa). The buffaloes included in the study were immobilized for foot and mouth disease surveys, while 4 zebras (Equus burchelli) and 4 kudus were sacrificed for feeding lions. The general body condition of the animals was good. The numbers of animals sampled on the ranch are shown in Table 1. Thin blood smears were made from the ear vein on site. Second sets of blood smears were made from Buffy coats from blood collected in EDTA soon after arrival at the laboratory at the School of Veterinary Medicine in Lusaka. All the slides were examined after staining with Giemsa under a light microscope. The number of positive animals is shown in Table 1, while Fig. 1 displays the trypanosomes detected in a greater kudu. The length of the trypanosomes (= trypomastigote stage) averaged 28.7 µm (n = 100, SE = 2.3 µm). All trypanosomes observed showed presence of pronounced free flagella, a pointed posterior end and conspicuous undulating membranes as shown in Fig. 1 and were identified as T. brucei as described elsewhere [5-7].

In Zambia, T. brucei has been reported from warthogs (Phacochoerus aethiopicus), hyaena (Crocuta crocuta), waterbuck (Kobus ellipsiprymnus), lion (Panthera leo), hippo (Hippopotamus amphibius), and other wildlife species in the Luangwa valley [8-11]. The ecological habitat of the Luangwa valley supports the survival of wildlife reservoirs found in the North and South Luangwa National Parks. These animals provide a wide host range for vector tsetse flies [3,8,9,11]. However, T. brucei has not been reported from wildlife on game ranches thus far.

As shown in Table 1, only the kudu out of the 14 species examined showed presence of T. brucei. In the absence of serological testing and screening using more robust diagnostic tools like PCR [12], it is difficult to establish the prevalence of the disease on the game ranch. Considering that wild ungulates have been reported to asymptomatically maintain transient infections of trypanosomes for a long time in their blood [13], it is likely that T. brucei detected in kudus in the present study might have been present in these animals for a long time. It is not known whether these animals got the infection on the game ranch or they could have carried the infection from another source when they were brought on the game ranch. Given the fact that most of the animals sampled in the present study were for the purpose of translocation to other game ranches, these findings suggest that translocation of game animals to new habitats could serve as a disease dispersion mechanism. This is particularly true when disease carriers are translocated into ecological habitats that support co-existence of wildlife reservoirs and vector species. Hence, new ecological niches that support sylvatic cycles of wildlife diseases could easily be established outside the commonly known endemic areas. The findings obtained in the present study are particularly important in promoting active surveillance and designing effective disease control strategies aimed at preventing the transmission of wildlife diseases to domestic animals and humans.