 Reference Base  Mortalities associated with the capture, translocation, t... |
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McCulloch, B.; Achard, P.L., 1969. Mortalities associated with the capture, translocation, trade and exhibition of black rhinoceroses, Diceros bicornis. International Zoo Yearbook 9: 184-191
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| Location: |
Africa - Eastern Africa - Tanzania |
| Subject: |
Diseases |
| Species: |
Black Rhino |
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Capture in Tanzania. Grumeti, 1964. Eight rhinoceroses were caught between February and August. As a prophylactic treatment against trypanosomiasis, 1.5 to 3.0 gm of diminazine aceturate were administered subcutaneously to all of them.
Lamai, 1964. Seventeen rhinoceroses were captured between the beginning of October and the end of November. They were treated with a prophylatic dose of 1.5 to 3.0 gm of diminazine aceturate.
Two rhinoceroses (5789 and 5645) died after 17 and 13 days in captivity. These animals were less aggressive and more lethargic than usual. Although there was only some slight loss of appetite, loss of weight was rapid and a marked deterioration was followed by death. Post-mortem examinations were carried out and showed marked pulmonary oedema, with froth exuding from the cut bronchioles. Stomachs and intestines contained normal ingesta but the small intestines showed catarrhal inflammation. The carcasses were emaciated, with depletion of the cardiac, omental, perirenal, intermuscular and subcutaneous fat deposits. Post-mortem examinations suggested that active trypanosome infections were involved. Blood smears from 5645 showed trypanosomes of the brucei subgroup. No haematozoa were seen in slides from 5789.
Lamai, 1965. In the first group (5 rhinoceroses: diminazine aceturate 3.0 to 10.0 g) all died. One animal (4675) died on the day of capture. 4674 died after 15 days in captivity and post-mortem examination indicated trypanosome infection. Blood smears were positive for brucei subgroup and Trypanosoma vivax.
At the Lamai blood smears were prepared from 15 rhinoceroses at the time of capture. Trypanosomes were seen in the slides from three young animals. Brucei subgroup and T. vivax were seen in blood smears from 4769 and T. vivax in smears from 4678 and 3401. Small piroplasms, probably Theileria spp. were seen in slides from one young rhinoceros, 4678, and one mature, 3509.
Discussion
Systematic protozoal infections in domestic animals are usually diagnosed by an assessment of clinical and/or post-mortem observations, in relation to microscopical findings. Biological and serological examinations provide only limited assistance in this respect. For instance, subinoculation of trypanosomes into rats is an aid to trypanosome identification, but is of no help in differentiating active from latent infection. As latent trypanosome infections are widespread in game animals in general, the diagnosis of active infection is difficult. It has to be based largely on clinical and/or post-mortem findings in relation to the characteristic features of active trypanosomiasis in domestic animals, described, for example, by Hornby (1952).
In our work with rhinoceroses the presence of latent trypanosome infection was established. Blood smears were prepared from 15 rhinoceroses at capture. Trypanosomes of the brucei subgroup and T. vivax were seen in blood smears from one young rhinoceros, and T. vivax in smears from another two young animals. The extent of latent infection was not established as blood slide examination is an unreliable method of assessment and latent infection in adults may have been overlooked.
At the Lamai, the deaths of five rhinoceroses were attributed to active trypanosomiasis. Three showed post-mortem features which were in accord with active infection with brucei subgroup. Two showed trypanosomes in blood and tissue smears, one showing brucei subgroup and the other mixed brucei subgroup and T. vivax. Nevertheless, we could not be sure that trypanosomes were the cause of the disease syndrome as there was no way of differentiating between primary infection, reinfection, latent infection and exacerbating latent infection. However, active trypanosome infection in wild-living game animals may be more widespread than is generally supposed. McCulloch (1967) drew attention to what he thought was probably natural and active infection of the brucei subgroup in wild and free- living zebras Equus burchellii. Nevertheless, the apparent problem of active trypanosomiasis at the Lamai was alleviated when the prophylactic cover was; increased by about four to six times that initially provided at the Grumeti. Diminazine aceturate/pyrithidium bromide and homidium bromide/pyrithidium bromide appeared equally efficient.
Tsetse fly density was low at the Grumeti compared to the Lamai where flies were seen in the holding pens, in the tents and all about the immediate vicinity of the camp. In both areas G. swynnertoni, G. pallidipes and G. brevipalpis were seen although G. smynnertoni was the dominant species. Weitz (1963) reported on relevant tsetse feeding habits as follows: G. swynnertoni: 5531 meals, 65.4% from warthog, 6.7% from rhinoceros. G. pallidipes: 2688 meals, 19.2% from warthog, 0.6% from rhinoceros. G. brevipalpis: 1151 meals, nil from warthog, 1.8% from rhinoceros. At the Lamai, where warthogs Phacochoerus aethiopicus were fewer and rhinoceroses were more numerous than at the Grumeti, G. swynnertoni particularly may have been forced to feed to a large extent on rhinoceroses. It is probable that the apparent breakdown of the Grumeti prophylactic cover when used at the Lamai was associated with the disparity in tsetse fly density, and with the difference in the availabilities of warthogs and rhinoceroses as sources of fly food.
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