A number of diseases of unusual nature and uncertain aetiology have affected black rhinoceroses (Diceros bicornis) in captivity. These diseases have played a significant role in limiting the growth of the captive black rhinoceros population. Haemolytic anemia is one example; in one survey of captive black rhinoceroses, it accounted for 40% of all adult deaths. A syndrome of mucocutaneous ulcers has had a similar impact and other poorly understood conditions include an apparently increased incidence of fungal pneumonia, haemosiderosis and encephalomalacia. Although there are few, if any, reports of these syndromes in the wild, there are reports of similar diseases occurring in black rhinoceroses shortly after capture, and thus, these syndromes may have significance for black rhinoceroses maintained in even semi-captive situations. In contrast to the black rhinoceros, the diseases reported in captive white rhinoceroses (Ceratotherium simum) in North America are of a more routine nature and an apparently lower incidence.
In maintaining black rhinoceroses in captivity, it is advisable to avoid exposure to creosote and other phenolic compounds. Exposure to these and possibly other chemicals may induce and/ or contribute to a syndrome of liver necrosis and failure. Epidemiology suggests that several recent black rhinoceros deaths in North America have been associated with exposure to creosote. Initial clinical signs are related to liver failure, including marked hyperbilirubinemia (both direct and indirect bilirubin are elevated). Terminally, mucocutancous ulcers and haemolytic anaemia may develop (it is unclear if these signs are from the toxic exposure or simply agonal events as has been noted in other black rhinoceroses with chronic diseases). The signs of liver necrosis and skin ulcers are similar to those previously reported in black rhinoceroses exposed to creosote in North America and southern Africa.
Black rhinoceroses are susceptible to tuberculosis. Recommendations for the most effective testing regimens for this disease have been limited by a lack of positive individuals. In the past, two black rhinoceroses infected with Mycobacterium bovis and one exposed to those individuals were positive on intradermal testing with MOT (mammalian old tuberculin) and ELISA. More recently, a black rhinoceros at the Detroit Zoological Park who was culture-positive for Mycobacterium tuberculosis, was positive when 0.1ml of USDA bovine tuberculin was administered intradermally in the eyelid, and this animal was also positive on ELISA testing. It has been our recommendation that any suspicious or positive tuberculin test be followed by acid-fast culture of gastric lavage or tracheal wash samples.
Encephalomalacia has been reported in three black rhinoceros calves and one 2-year-old animal. All were female. Clinical signs varied from somnolence and hyperthermia to hyperexcitability. Three died during their episodes and one was euthanized subsequent to becoming a 'dummy' calf. Histologically the lesions were notable for massive white matter necrosis (leucoencephalomalacia), and in some areas, adjacent gray matter was also affected. Evidence of inflammation was evident only in the older lesions where presumably it was a reaction to necrosis. It is believed that the variable neurological signs may simply reflect which areas of the brain in each individual were most severely affected. Histology or specific diagnostic tests were not supportive of vitamin E-induced malacia, polioencephalo-malacia, or viral infections (eg., encephalomyocarditis virus or equine encephalitis). The histologic pattern most closely resembled that of leucoencephatomalacia due to ingestion of food contaminated with the mould Fusarium moniliforme, however, feedstuffs ingested prior to the onset of the neurological symptoms were not available for analysis. The variable clinical presentation of this disease emphasizes the importance of collecting brain and spinal cord tissues from all rhinoceros deaths, particularly those in which a diagnosis is not readily evident. It is possible that this syndrome is under-diagnosed due to the difficulties in removing a rhinoceros brain.
Diceros bicornis. HAEMOLYTIC ANAEMIA. Our investigations centred on possible causes for the hemolytic anaemia. A fatal case of haemolysis at the St. Louis Zoo led to subsequent surveys that noted 47 episodes of haemolysis in 39 individual black rhinoceroses. Cases can be classified as 'primary,' i.e., those haemolytic events that occur without other obvious underlying disease, and 'secondary,' those cases that occur as agonal events in rhinoceroses dying of other causes. Although several familial groupings of affected rhinoceroses exist, no sex, age, or captive-bred vs. wild-caught patterns were evident. Early reports suggested that many of the acute cases of haemolysis were associated with leptospirosis. Indeed, with the advent of the fluorescent antibody (FA) test for Leptospira interrogans, many cases that were not evident by titres were positive. At the present time, biannual vaccination of all black rhinoceros with leptospiral bacterins that contain the serovars icterohemorraghiae and grippotyphosa (serovars that have elicited elevated titres in two reports of rhinoceroses surviving haemolysis) has been recommended. (Author's note: Leptospire interrogans has also been identified in the tissues of an aborted greater one-horned Asian rhinoceros (Rhinoceros unicomis) calf at the Bronx Zoo.) However, not all of the cases of haemolysis could be accounted for by leptospiral infection, and a series of investigations was initiated to determine if other aetiologies or properties inherent in the black rhinoceros red blood cell (RBC) increased their susceptibility to haemolysis from a number of causes (drug exposure, bacterial infection, etc.). Various studies indicated that the anemia was unlikely to result from autoimmune disease, uncomplicated vitamin E deficiency, nor an unstable haemoglobin. The most significant findings resulted from investigations into the metabolism of the black rhinoceros RBC. Initial studies focused on RBC levels of glucose-6-phosphatase dehydrogenase (G-6 PD) and other enzymes commonly recognized to cause haemolysis in man, but those levels were either normal or elevated compared to human normals . However, on a more fundamental level, the black rhinoceros RBCs were noted to be markedly deficient in energy (ATP), when compared to other mammalian species. The RBCs of white rhinoceroses, a species which has been apparently healthy in captivity, were also low in ATP, but they also had significantly higher levels of the enzyme catalase than black rhinoceroses. The full significance of this is unknown, but further metabolic studies are underway. Interestingly enough, Dr. Paglia has hypothesized that the energy deficiency of the black rhinoceros RBC could be an adaptive characteristic for haemic parasitism in the same manner than G-6-PD deficiency is considered adaptive in man. Dr. Paglia, is presently on sabbatical in the laboratories of Dr. Eric Harley at the University of Cape Town. At the present time, suggested treatment of acute cases of haemolysis is supportive and includes penicillin and possibly dihydrostreptomycin (in the event that it is leptospirat-induced), parenteral vitamin E (to assist in the maintenance of membrane stability), enteral andlor parenteral phosphorus supplementation (as many of the chronically haemolytic individuals have become hypophosphataemic)', and possibly blood transfusion. The latter has been attempted in two black rhinoceros as preliminary findings suggest that rhinoceroses do not have inherent antibodies to other blood groups of their species.
Haemosiderosis. Accumulation of iron has been noted in tissues of captive black rhinoceroses and has been shown to be positively correlated with length of time in captivity. At the present time it is uncertain if this may represent a chronic stage of haemolysis or nutritional deficiencies/ excesses in the captive diet.
