Back in 1985, Stephen O’Brien and colleagues at the National Cancer Institute in Maryland reported extremely low levels of genetic variation in cheetahs – so low in fact, that skin grafts from one animal were not rejected by another, a sign that their immune systems are genetically identical. This lack of genetic variation was attributed to a decline in population numbers at end of last ice age, plus more recent declines that have led to inbreeding. The species appeared to be highly susceptible to feline infectious peritonitis (FIP), a disease which had decimated some captive populations, and attempts to breed cheetahs in captivity were hampered by poor reproductive success and apparently high levels of sperm defects. O’Brien and colleagues attributed these problems to their extremely low levels of genetic variation, and the species quickly became a classic example of the perils of inbreeding.
However, in the early 1990’s, field studies questioned whether the cheetah’s survival in the wild was being compromised by their lack of genetic variation. In a commentary in Science in 1994, Caro and Laurenson pointed out that disease susceptibility and breeding problems only appeared to be an issue for captive cheetahs, and that predation of cubs, habitat destruction and persecution by humans were greater threats to the species.
Still, a lack of variation at immune genes is still an important potential threat to any species, as shown by the case of the Tasmanian devil, where low variation at Major Histocompatibility Complex, or MHC genes, has allowed Devil Facial Tumour Disease to spread unchecked throughout the population. MHC genes are key part of the immune system in vertebrates as they code for the molecules that distinguish self from non-self, and instruct the immune system to respond when foreign proteins (i.e. from a pathogen) are detected. High diversity at MHC genes plays an important role in protecting populations from disease epidemics as it allows wide array of foreign pathogens to be resisted, and means that some individuals are likely to be more resistant to new diseases than others (instead of all individuals being equally susceptible).
The skin graft experiments of the mid-1980s indicated that cheetahs have virtually no MHC variation, because of the absence of an immune response when skin from one cheetah was grafted onto another. However the disease susceptibility seen in captive cheetahs doesn’t seem to extend to cheetahs in the wild – a recent study on wild cheetahs in Namibia found that the population was generally in good health, and that many individuals carried antibodies to a range of diseases (suggesting they had been exposed to those diseases) but no clinical symptoms of acute disease. These results suggest that wild cheetahs may have more MHC diversity than the captive population, and that their immune systems work just fine.
Somewhat surprisingly, only a couple of studies in the 26 years since the skin-graft study was published have actually attempted to quantify cheetah MHC diversity. These studies found low diversity and seemed to corroborate the skin-graft results, but either used low resolution methods to measure MHC diversity or had small sample sizes, so weren’t particularly conclusive.
This latest study, by Aines Castro-Prieto, Simone Sommer and colleagues at the Leibniz Institute for Zoo and Wildlife Research in Berlin, takes a much more comprehensive approach to measuring genetic variation. Castro-Prieto and colleagues determined how many different alleles are present at two types of MHC genes in 149 Namibian cheetahs. They found more variation than was previously described for the first type (Class I MHC), but not for the second type of gene (Class II MHC). The number of different MHC alleles counted in the Namibian cheetahs is still quite low compared with what is seen in other big cat populations, so it appears that cheetahs have lost a fair amount of variation as their numbers have declined. However, the amount of DNA sequence variation among the alleles is fairly high – that is the different alleles code for proteins that are quite different from one another in their sequence, so overall they can probably recognise a wide array of foreign proteins.
Castro-Prieto and colleagues also found hallmarks of selection on the MHC sequences, and speculate that selection, driven by exposure to a range of pathogens over thousands of generations, has led to highly divergent alleles being retained. However, they point out that although wild cheetahs appear to have enough MHC variation to respond to common infectious diseases, they may still be at risk from new emerging diseases, as the few remaining alleles might not be sufficient to be able to recognise and ward off an entirely new pathogen.
This study provides some much-needed data on immune variation in cheetahs, and it seems that the idea of the cheetah being a classic case of disease vulnerability associated with low genetic diversity is looking a little shaky. As Castro-Prieto et al point out, “the long term survival of free-ranging cheetahs in Namibia seems more likely to depend on human-induced rather than genetic factors”.
Reference: Castro-Prieto A, Wachter B, & Sommer S (2010). Cheetah paradigm revisited: MHC diversity in the world’s largest free-ranging population. Molecular biology and evolution PMID: 21183613
For an excellent write-up on why genetic diversity is important (and more stuff about cheetahs), see this (fairly old) post on Mauka to Makai .
O’Brien SJ, Roelke ME, Marker L, Newman A, Winkler CA, Meltzer D, Colly L, Evermann JF, Bush M, Wildt DE (1985) Genetic basis for species vulnerability in the cheetah. Science 227: 1428-1434
Caro TM, Laurenson MK (1994) Ecological and genetic factors in conservation: a cautionary tale. Science 263: 485-486.
Thalwitzer S, Wachter B, Robert N, Wibbelt G, Muller T, Lonzer J, Meli ML, Bay G, Hofer H, Lutz H (2010) Seroprevalences to Viral Pathogens in Free-Ranging and Captive Cheetahs (Acinonyx jubatus) on Namibian Farmland. Clin. Vaccine Immunol. 17: 232-238.