User:Wagner.925/sandbox

EDIT: I posted the following edit to this page: https://en.wikipedia.org/wiki/Talk:Cheetah

I suggest creating a subtitle about captive cheetahs with under the relationship with humans section of the article with the following text:

Recent research has suggested that cheetahs in captivity actually experience more illness and have lower reproductive success than cheetahs in the wild[4]. For example, a recent study found that the Helicobacter species, a bacterium that often causes disease in cheetahs, that was so prevalent in the captive species actually does not typically cause as much harm to cheetahs in the wild, suggesting that cheetahs are not actually predisposed for this diseases, but rather that some factor of being in captivity is the cause. One suggestion as to why there is such a marked difference between the health of captive and wild cheetah populations is that cheetahs are maladapted to captivity. It has been hypothesized that captivity can lead to increased stress levels which in turn causes poorer health and lower reproductive ability. In a study comparing the adrenal cortices and corticoid concentrations in captive and native cheetahs, it was found that captive cheetahs had larger adrenal cortices and higher corticoid concentrations[5]. This strongly indicates that stress is a factor in the lower health of captive cheetahs. Although it is still unknown as to why exactly cheetahs in captivity experience such increases stress levels as compared to their wild counterparts, one theory suggests that the stress is due to the fact that cheetahs are designed to run, but in captivity they do not have room to do so. Another theory as to why captive cheetahs are so much worse off than wild cheetahs invokes the red queen hypothesis in order to explain the discrepancies between wild and captive cheetahs. Wild cheetahs are exposed to a number of parasites whereas captive cheetahs are routinely given medication to ensure that they are not infected by parasites. However, these parasites may actually aide in the suppression of the inflammatory response in wild cheetahs, a trait which the parasites evolved in order to survive within the host, thereby making them less susceptible to certain types of diseases[6].

Wagner.925 (talk) 00:30, 17 November 2014 (UTC)

FINAL DRAFT:

The effects of low genetic diversity on cheetah populations. Genetic variability is crucial to the survival of a species. It provides a species with the means necessary to evolve beneficial traits due to natural selection. The cheetah is a remarkable species in that it has an extremely low degree of genetic variability but still continues to survive as a species. This lack of variability is thought to have been caused by a population bottleneck that occurred roughly 10,000 years ago, from which current cheetah populations are still continuing to recover. Due to lack of study on wild cheetah populations it was thought for years that the cheetahs’ susceptibility to certain diseases was caused by lack of genetic diversity. However, more recently it has been found that although wild and captive cheetah populations are genetically almost identical, captive populations suffer from disease much more often than wild cheetahs indicating that factors other than genetics may be the cause of increased disease susceptibility. There are a number of theories about why this occurs, the most prevalent of which is that stress negatively affects the health of captive cheetahs. As previously stated, evidence suggests that the extreme lack of genetic variability within cheetah populations is due to a population bottleneck followed by a period of inbreeding, both of which worked to lower genetic variability. This was proven upon examination of mitochondrial DNA and hypervariable minisatellite loci, which are two rapidly evolving DNA sequences found in cheetahs. By using known mutation rates of these sequences, it has been hypothesized that the bottleneck occurred near the end of the last ice age around 10,000 years ago (Menotti-Raymond et. al, 1992). When a population bottleneck occurs, much of the genetic variance is lost from the population because the population size is drastically decreased. Over time, it is possible for populations to reestablish variance, however in the case of the cheetah, populations were unable to grow back to their previous population size due to excessive hunting. In fact, cheetahs were hunted so much that they were eventually declared and endangered species. Because of their continuously low population sizes, cheetahs were unable to successfully reestablish variance and therefore stayed extremely genetically similar over many generations. This lack of genetic diversity has often been attributed to causing lower reproductive success and higher susceptibility to disease in cheetah populations throughout the world. A consequence of the lack of genetic diversity in cheetahs that is often sited is that cheetahs have a relatively low reproductive success. In 1983, a study took place in which semen samples were collected from eighteen different male cheetahs and compared to previously reported values in semen samples obtained from domestic cats. Upon examination, it was found that sperm concentration, percent motility, and normal morphology were less than those in domestic cats (Wildt et. al, 1983). These abnormalities often lead to decreased fertility. It was first suggested that because development of sperm is under genetic control that the lack of genetic variation in cheetah populations is to blame for these abnormalities. While this may be the case for some infertility in regards to male cheetahs, a recent study has shown that in female cheetahs lack of genetic variability may not be as important a factor. The reproductive success of female cheetahs was measured by observing the survival rate of heir cubs. For each cheetah, its age and reproductive history were determined. The findings showed that age and reproductive history both have larger effects on reproductive health than do genetic variance or stress. 75% of cubs survived their first year in north Namibia where predator density is low. This shows that where there is low predator density, genetic variation is not as important to reproductive success which makes sense in the context of natural selection as selection is much lower in areas without predators and therefore less genetic diversity is required for survival. It is important to remember that although the wild is not predator-free, cheetahs that live in captivity are in fact in predator-free environments and therefore should have high reproductive success. The fact that this is not the case suggests that perhaps it is not low genetic variance but actually some other practice of caring for cheetahs in captivity that causes lower reproductive success in captive animals (Wachter et. al, 2011). The cheetah’s increased susceptibility to infection is attributed to lack of genetic variation quite often. A study that took place over the course of twenty years and ending in 1999 surveyed 69 captive cheetahs in South Africa. In each animal, the cause of death was examined. It was found that the same diseases, specifically diseases caused by Helicobacter-like organisms, glomerularsclerosis, which causes kidney problems, and veno-occlusive disease, in which some of the small veins within in the liver become obsturcted, that were most prominent in captive cheetahs in South Africa were also prominent in cheetahs in the United States. Due to the distance between these populations as well as the variation in environments it was concluded that cheetahs must have some genetic predisposition to these diseases (Munson et. al, 1999). However, more recent studies have found that an abundance of other factors may actually play a bigger role in determining disease susceptibility. A new study found that the Helicobacter species that was so prevalent in the captive species actually does not typically cause as much harm to cheetahs in the wild, suggesting that cheetahs are not actually predisposed for this diseases, but rather that some factor of being in captivity is the cause (Terio et. al, 2005). Another example is a study conducted on the similarities of MHC genes in cheetah populations. MHC genes help to control resistance to pathogens through their connection to the adaptive immune response. They code for proteins which bind foreign bodies to T-cell receptors in order to elicit an immune response. High diversity of MHC genes indicates that an organism is able to quickly detect and deal with a large variety of different pathogens and is therefore highly beneficial in environments where and organism could potentially come into contact with any number of unknown pathogens. Cheetahs have been found to have remarkably low diversity within their MHC gene loci. In a study on Namibian cheetahs living in the wild, it was found that despite low genetic variability in MHC genes, their immune system is not compromised by infectious diseases at a higher than average rate. In fact, many of the cheetahs actually tested seropostive for a number of infectious diseases but did not show any signs of actually being adversely affected (Castro-Pietro et. al., 2010). In a final example, it has actually been found that cheetahs that lived in areas with higher human population densities were more often to be found seropositive, meaning that they tested positive for a virus, than cheetahs that lived in areas where there were not as many people. This is because areas with more people have more feral dogs and cats which can transmit diseases to wild cheetahs (Thalwitzer et. al, 2010). The reason for the presence of disease in these wild populations is not due to lack of diversity, but simply because there are more organisms available to transmit diseases to the cheetahs. One suggestion as to why there is such a marked difference between the health of captive and wild cheetah populations is that cheetahs are maladapted to captivity. It has been hypothesized that captivity can lead to increased stress levels which in turn causes poorer health and lower reproductive ability. In a study comparing the adrenal cortices and corticoid concentrations in captive and native cheetahs, it was found that captive cheetahs had larger adrenal cortices and higher corticoid concentrations (Terio et. al, 2004). This strongly indicates that stress is a factor in the lower health of captive cheetahs. Although it is still unknown as to why exactly cheetahs in captivity experience such increases stress levels as compared to their wild counterparts, one theory suggests that the stress is due to the fact that cheetahs are designed to run, but in captivity they do not have room to do so. Another theory as to why captive cheetahs are so much worse off than wild cheetahs invokes the red queen hypothesis in order to explain the discrepancies between wild and captive cheetahs. Wild cheetahs are exposed to a number of parasites whereas captive cheetahs are routinely given medication to ensure that they are not infected by parasites. However, these parasites may actually aide in the suppression of the inflammatory response in wild cheetahs, a trait which the parasites evolved in order to survive within the host, thereby making them less susceptible to certain types of diseases (Tiero et. al, 2005). While genetic variation is usually incredibly important within populations, it does not seem to adversely affect cheetahs. A population bottleneck that occurred years ago caused the lack of variation that we see in cheetahs today. For years, it was thought the this lack of variation was the cause of multiple issues for cheetahs, but recently it has come to light that perhaps genetic variation does not play as big a role in cheetah populations as we had once thought. One of the most interesting observations about cheetahs is that many of the adverse effects that were once attributed to lack of genetic variation are present in captive populations of cheetahs but not in wild populations. It has been proven that reproductive success in areas of the wild where there is low predator density is actually relatively high and therefore shouldn’t be affected by genetic diversity. It has also been shown that although wild cheetahs can test seropoistive for infectious diseases, they often don’t show any symptoms whereas cheetahs in captivity will often get seriously ill when they contract a virus. Theories as to why this phenomena occurs include that cheetahs in captivity experience higher levels of stress than those found in the wild, perhaps because they are unable to run, and that wild cheetahs are exposed to parasites that suppress the inflammatory response which lets them live healthy lives while carrying a virus or bacteria. With all of this in mind, it may be interesting to next examine the ways in which cheetahs have evolved that make them maladapted to living lives in captivity because perhaps these traits, rather than simple lack of diversity can help us to explain the maladies of captive cheetahs.

References Castro-Prieto, A., Wachter, B. and S. Sommer. 2010. Cheetah paradigm revisted: MHC diversity in the world’s largest free-ranging population. Molecular Biology and Evolution 28:1455-1468.

Menottiraymond, M., and S.J. O’Brien. 1993. Dating the genetic bottleneck of the African cheetah. Proceedings of the National Academy of Sciences of the United States of America 90:3172-3176.

Munson, L., Nesbit, J.W., Meltzer, D.G.A., Colly, L.P., Bolton, L., and N.P.J.Kriek. 1999. 	Diseases of captive cheetahs (Acinonyx jubatus jubatus in South Africa: A 20-year	retrospective survey. Journal of Zoo and Wildlife Medicine 30:342-347.

Terio KA, Marker L, and L. Munson. 2004. Evidence for chronic stress in captive but not free- ranging cheetahs (Acinonyx jubatus) based on adrenal morphology and function. J Wildl Dis 40:259-266. Terio, K.A., Munson, L., Marker, L. Aldridge, B.M., and J.V. Solnick. 2005. Comparison of 	Heliobacter spp. in cheetahs (Acinonyx jubatus) with and without gastritis. Journal of        	Clinical Microbiology 43:229-234.

Thalwitzer, S., Wachter, B., Robert, N., Wibbelt, G., Muller, T., Lonzer, J., Meli, M.L., Bay, G., Heribert, H., and H. Lutz. 2009. Seroprevalences to Viral Pathogens in Free-Ranging and Captive Cheetahs (Acinonyx jubatus) on Namibian Farmland. Clinical and Vaccine Imunology 17:232-238.

Wachter, B., Thalwitzer, S., Hofer, H., Lonzer, J., Hildebrandt, T. B., and R. Hermes. 2011. Reproductive history and absence of predators are important determinants of reproductive fitness: the cheetah controversy revisited. Conservation Letters 4:47-54.

Wildt, D.E., Bush, M., Howard, J.G., O’Brien, S.J., Meltzer, D., Vandyk, A., Ebedes, H., and D.J. Brand. 1983. Unique seminal quality in the South African cheetah and a comparative evaluation in the domestic cat. Biology of Reproduction 29:1019-1025.

Proposed Suggestions and Edit:

https://en.wikipedia.org/wiki/Cheetah:


 * Because this was a locked page, I added my edit to the talk page of this article.

Suggestions
It might be helpful to add a citation about the dating of the population bottleneck or about specific evidence of the bottleneck.

It could also be useful to provide a citation that highlights the lack of genetic diversity in cheetahs. I know I have read studies where multiple microsatellites in the cheetah genome have been mapped and it has been shown that there is little to no variance in these microsatellites.

There have been recent studies to show that free-ranging populations of cheetahs are relatively healthy, whereas captive populations are more likely to suffer from infectious diseases. It could be beneficial to discuss this in the article.

In the conservation status section of this article, it is noted that the decline of the cheetah is most likely due to factors other than genetics. It might be helpful to support this by adding that captive cheetahs tend to have higher susceptibility to diseases than cheetahs in the wild despite the fact the cheetahs in the wild stem from the same gene pool, suggesting that conditions in captivity are the cause of vulnerability of these cheetahs.

Evolution Topic and Bibliography

For my evolution topic, I would like to talk about the low genetic variation in cheetahs and how this affects their overall fitness. Due to a genetic bottleneck, cheetahs have very low genetic variability as a species. This causes them to be more susceptible to certain diseases and causes them to have lower reproductive success than other feline species. I will be using the following sources:

Menottiraymond, M., O’Brien, S.J. (1993). Dating the genetic bottleneck of the African cheetah. Proceedings of the National Academy of Sciences of the United States o America, 90(8), 3172-3176.

Genetic diversity of mitochondrial DNA and hypervariable minisatellite loci was examined in two different species of cheetahs. Based on the extent of genetic diversity and the current mutation rate of these genes, it has been determined that an ancient bottleneck occurred around 10,000 years ago that caused the lack of genetic variation in cheetahs.

Munson, L., Nesbit, J.W., Meltzer, D.G.A., Colly, L.P., Bolton, L., & Kriek, N.P.J. (1999). Diseases of captive cheetahs (Acinonyx jubatus jubatus in South Africa: A 20-year	retrospective survey. Journal of Zoo and Wildlife Medicine, 30(3), 342-347.

In order to determine the basis for the high rate of mortality from glomerulosclerosis and chronic lymphoplasmactyic gastritis archived pathology materials from 69 captive cheetahs that died in the Republic of South Africa were examined. It was found that cheetahs in South Africa had the same chance of developing these rare diseases as captive cheetahs in the USA, suggesting that a genetic predisposition to these diseases and a lack of genetic diversity is what causes such high mortality rates from these diseases.

O’Brien, S.J., Wildt, D.E., Bush, M., Caro, T.M., Fitzgibbon, C., Aggundey, I.,& Leaky, R.E. (1987). East African cheetahs: Evidence for two population bottlenecks. Proceedings of The National Academy of Sciences of the United States of America, 84(2), 508-511.

A population of East African cheetahs and a population of South African cheetahs were examined and the genetic distance between the two was determined. From the results, it was determined that two bottlenecks occurred: an ancient bottleneck as well as a more recent bottleneck that led to changes in the South African populations of cheetahs.

Wayne, R.K., Modi, W.S., & O’Brien S.J. (1986). Morphological variability and asymmetry in in the cheetah (Acinoyx-jubatus), a genetically uniform species. Evolution, 40,(1), 78-85.

Sperm samples from 18 different cheetahs were collected and examined. It was found that cheetah ejaculates contained 71% morphologically abnormal spermatozoa whereas the domestic cat only has about 29% of abnormal spermatozoa. The reason for this is likely to be genetic and can be attributed to the lack of genetic variation in cheetahs.

Wildt, D.E., Bush, M., Howard, J.G., O’Brien, S.J., Meltzer, D., Vandyk, A., Ebedes, H., & Brand, D.J. (1983). Unique seminal quality in the South African cheetah and a comparative evaluation in the domestic cat. Biology of Reproduction, 29(4), 1019-1025.

Sperm samples from 18 different cheetahs were collected and examined. It was found that cheetah ejaculates contained 71% morphologically abnormal spermatozoa whereas the domestic cat only has about 29% of abnormal spermatozoa. The reason for this is likely to be genetic and can be attributed to the lack of genetic variation in cheetahs.