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Cheetah genetics and disease

The Cheetah (Acinonyx jubatus) has long been considered a paradigm of disease vulnerability due to loss of genetic diversity (Munson et al. 2005). O’Brian et al. (1983, 1985 & 1986) performed much of the initial genetic work on Cheetahs. These initial studies utilised methods that can be considered outdated by today’s standards and found that the Cheetah had extremely low levels of genetic variation. Menotti-Raymond and O’Brien (1992) predicted that the global Cheetah population experienced¬† a bottleneck event near the end of the last glacial period or ice age (late Pleistocene, approximately 10,000 years ago). The global Cheetah population was thought to have been reduced to a few individuals and these survivors were supposedly the ancestors of all Cheetah currently found in Africa and Asia today.¬† For more than two decades the Cheetah was a classic text book example of a species that is particularly vulnerable to disease due to low genetic diversity (Castro-Prieto et al. 2010). Recent genetic analyses using more robust methods and a larger sample size suggest that Cheetah have considerably more genetic variation than previously thought (Charruau et al. 2011). The bottleneck theory has been completely refuted and the split between the two African subspecies of Cheetah is predicated to have taken place approximately 66 000 years ago. A second split between one African subspecies and Asian Cheetah is thought to have taken place approximately 49 000 years ago (Charruau et al. 2011).

The supposed lack of genetic diversity in Cheetah has been suspected to be the basis for their general poor health and reproductive failure in captivity (Castro-Prieto et al. 2010). Captive populations have high prevalence of hepatic veno-occlusive disease, glomerulosclerosis, gastritis, and systemic amyloidosis, diseases that are rare in other species (Munson et al. 2005). Unusually severe inflammatory reactions to common infectious agents have also been documented in captive cheetahs. More recent studies carried out on free roaming Cheetah suggest that that they have considerably lower prevalence of disease than captive populations (Castro-Prieto et al. 2010). For example, despite heavy Helicobacter bacterial colonisation in wild Cheetahs, only 3% of free roaming Cheetahs were found to suffer from moderate to severe gastritis whilst, in contrast with 64% of captive Cheetahs (Munson et al. 2005). Additionally no incidents of inflammatory reactions to viral infections have been detected in free roaming Cheetah. These findings demonstrate the importance of extrinsic factors in wildlife health and caution against attributing loss of fitness solely to genetic factors (Munson et al. 2005).

Many of the effects of inbreeding depression such as increased susceptibility to disease, reduced litter sizes and infertility are limited to captive Cheetah and may be explained by physiological or behavioural artefacts, particularly chronic stress suffered by Cheetah in captivity (Terio et al. 2004). Carnivores exhibit significantly lower levels of genetic variation than other mammals and the genetic constitution of the Cheetah does not appear to compromise its survival. Conservation efforts should be more effectively aimed at real and more immediate threats to Cheetah such as the loss of their natural habitat (Merola 1994).