Cheetahs have been tamed, used for hunting and kept in zoos in countries across Asia, Europe and Africa for centuries. However, they have never really thrived under captive conditions.
Between 1829-1952 there were 139 wild-caught cheetahs displayed at 47 zoological facilities. Most of these animals survived less than a year with 115 deaths and no births recorded during this period.
Despite improvements in husbandry conditions in zoos and other captive facilities around the world, cheetahs continue to suffer from a number of unusual diseases that are rarely reported in other captive cats. These include gastritis, various kidney ailments, liver abnormalities, fibrosis of the heart muscle and several ill-defined neurological disorders.
Post mortem findings in cheetahs housed at captive facilities in both North America and South Africa found that over 90% had some level of gastritis when they died. Similarly, the incidence of kidney disease affected more than two-thirds of captive cheetahs. In contrast, these diseases are extremely rare in wild free roaming cheetahs.
We set out to find out why so many die in captivity.
Several factors have been put forward. One theory that’s been around since the 1980s is that low genetic diversity of the cheetah increased their vulnerability to disease because of inbreeding depression. But captive and wild cheetahs have comparable genetic variation. To date no heritability (degree to which characteristics are transmitted from parents to offspring) has been demonstrated for any of these diseases.
Other factors such as chronic stress and a lack of exercise have also been suggested.
More recently investigations have started to focus on what captive cheetahs are fed.
Wild cheetahs predominantly hunt small antelope, consuming almost the entire carcass, including the skin, bones and internal organs. Captive cheetahs are often fed only the muscle meat and some bones from domestic species such as cattle, horses, donkeys or chickens.
Recent studies, show that if cheetahs were fed whole carcasses, their stool consistency improved, the production of beneficial fatty acids increased and the production of some toxic compounds in the colon reduced. But this is an expensive way to feed cheetahs in captivity.
It’s become clear that what’s needed is a better understanding of cheetah metabolism. Metabolism is the sum of all the chemical processes that occur in a living organism to maintain life. When some of these processes are abnormal they often result in disease.
In my PhD research, which is ongoing, I turned to the emerging field of metabolomics - the scientific study of the set of small molecules present within an organism, cell, or tissue - to evaluate various small molecules in the serum and urine of cheetahs. I was looking for any differences in the molecule profiles of samples from captive versus wild cheetahs. I also wanted to see if these profiles were different to those of humans and other species.
We measured the concentrations of hundreds of amino acids, fatty acids, acylcarnitines, sugars and other products of metabolism.
In the first part of the study, we compared the fatty acid profiles of captive cheetahs to those of wild cheetahs. Abnormal fatty acids levels have been linked to a variety of disease processes in humans and other animals.
We found very low levels of polyunsaturated fatty acids in the blood samples of wild cheetahs compared to those from cheetahs in captivity.
There are at least three potential reasons for this:
Wild cheetahs typically hunt and consume small antelope. These species have a high saturated and low polyunsaturated fatty acid content in their tissues. Captive cheetahs, on the other hand, tend to be fed meat from animals, like horses, donkeys and chickens, which have high polyunsaturated fatty acid content.
The abdominal organs and fat stores consumed by wild cheetahs are high in saturated fats and low in polyunsaturated fatty acids when compared to the fats stored in and around the muscle tissues typically fed to captive animals.
Wild cheetahs eat less often than those in captivity. During periods of fasting, the body uses its stored polyunsaturated fatty acids for energy, thus leading to lower levels.
Polyunsaturated fatty acids are very sensitive to oxidative damage when compared to the more stable saturated fatty acids. I suspect that cheetahs may not have effective antioxidant capabilities to cope with higher levels of damaged polyunsaturated fatty acids and this may contribute to their ill health in captivity.
In the second part of the study, we analysed the urine organic acids in the urine of captive cheetahs. Urine organic acids are the end-products of the breakdown of amino acids, fatty acids and sugars.
We found that the cheetahs were excreting a numbers of particular compounds known as phenolic acids. They form because proteins arrive in the large intestine undigested. Some amino acids from these proteins are changed by gut bacteria into potentially toxic compounds that are then absorbed into the bloodstream and either directly excreted or detoxified by the liver before being excreted. This is a problem because studies suggest that phenolic acids may have a negative effect on the production of dopamine. Dopamine plays an important role in gut and kidney function.
We also discovered that cheetahs use a particular chemical process to detoxify the phenolic acids. Known as glycine conjugation, it requires large quantities of a different amino acid: glycine.
Glycine levels are low in the muscle meat diets of captive cheetahs since they don’t often get fed skin, cartilage or bones that contain much higher amounts. Together with an increased demand for glycine for detoxification, these animals are likely to end up with a deficiency of this amino acid. Glycine is very important in several body functions and a deficiency could therefore have many negative health effects.
Although our research hasn’t provided all the answers, it’s focused attention on several potential issues, opened up avenues for future research and provided some guidelines about what cheetah’s in captivity should be fed.
This article was originally published on The Conversation.
Adrian Tordiffe, Veterinarian, Senior Lecturer, Researcher - Department of Paraclinical Sciences, University of Pretoria