Friday, February 22, 2013

The Impact of Multiple Stressors On the Evolution and Survival of Natural Populations



With outbreaks of diseases and increased pollution in our environments, many natural populations just cannot get a break. These organisms are exposed to many different stressors, whether biotic (such as predation or parasites) or abiotic (such as chemical pollution or losses of habitats). These stressors can yield genetic adaptations in organisms due to strong selection pressures from their local habitat, of course if gene flow is negligible. (Coors et. al. 2009) When threats such as parasites, pollution, or predation, are present in an environment alone, populations are able to react to each in a different induced specific adaptation. However, when it comes to multiple stressors, evolution has been proven to play a part.
One recent experiment highlights what happens when organisms are exposed to multiple threats and its effect on an individual’s fitness. In this experiment, when the model organism Daphnia magna is introduced into an environment with both parasites and pesticides, the populations either adapt to one set of conditions or the other. D. magna has been chosen as the model organism due to its ability to produce latent egg stages that can be conserved. The D. magna clones from these latent eggs are exposed to Pasteuria ramosa (parasite) and diazinon (insecticide). After the exposure, each organism was tested for infections, survival rate, and the number of offspring for 21 days. The results showed that both of these stressors caused higher mortality rates in the D. magna populations together than if they were in contact with just one. Moreover, it was found that the evolution to repel one stressor, such as the diazinon, lowered resistance against another stressor, such as P. ramosa. However, it must be noted that by the end of the 3 weeks of the experiment, there were no observable signs of parasitic infection within any of the population, but there was a drastically higher mortality rate when the D. magna were exposed to both the pesticide and the parasite simultaneously instead of one stressor by itself. (Jansen et. al. 2011)
This evolutionary catch-22 could be due to a number of factors. For example, the P. ramosa could be causing an immune suppression within the population that allows other disturbances, in this case the diazonin, to easily infiltrate the populations. On the other hand, the increased mortality due to multiple disturbances could be a result of the accumulation of the increasing demand for energy by each of the stressors.  In addition, there are three different reasons for why there were no visible signs of parasitic infections even though it still played a huge part in the survival rate of the hosts. First, it could be that the hosts were infected by certain spores that were not virulent for these set of clones. Secondly, it could be that the specific strain of P. ramosa chosen was not infectious for the hosts. This could be because the infectiousness of a parasite, its influence on the host’s ability to survive and reproduce, is dependent on how a specific host and parasite interact and can also be impacted by the conditions of its environment. (Coors et. al. 2008)  Last, there is a possibility that due to unknown causes the amount of viable spores declined. Nevertheless, infected or uninfected, the parasites caused a lot of stress on the survival rates of these hosts. (Buser et. al. 2012)
Diazonin, often used for agricultural and domestic purposes, can cause death, immobilisation, delay in reproduction, and less offspring yield, because of its ability to suppress acetylcholinesterase, a crucial enzyme of the nervous system.  Toxic pollutants such as diazonin can cause genotoxicity or genetic bottlenecks and can therefore have long term effects on the genetic structure of a population. P. ramosa, the parasite, was a great parasite to use because detection of its infection was clear. Once D. magna was infected by the parasite, the individuals would become infertile, and its body would change in appearance – it would grow larger and darker. This parasite would be released after the death of its host in the form of spores and could remain inside the sediments of its aquatic environment and continue being infective for many years after. Thus, having to deal with two such strong population disturbances has led to an adaptation struggle as it is difficult to keep defences against both. . (Buser et. al. 2012)
In conclusion, our society’s tendency to contaminate our environment is having a dramatic impact on the natural populations that habituate them. Each population of organisms already have their own natural predators and problems that they have to surpass in order to survive and reproduce, not counting the ones humans impose on them. Such as in the experiment above, adapting to combat parasitic or predation threats is lowering population’s resistance against pollution and causing very low survival rates. The anthropogenic stressors that humanity inflicts on these populations are the last and ultimate blow that is making it difficult for them to progress and flourish in today’s world.

Word Count: 826

References

Buser, C.; Jansen, M.; Pauwels, K.; de Meester, L.; & Spaak, P. (2012). Combined exposure to parasite and pesticide causes increased mortality in the water flea Daphnia. Aquatic Ecology. DOI: 10.1007/s10452-012-9397-9

Coors, A.; Decaestecker, E.; Jansen, M.; & de Meester, L. (2008). Pesticide exposure strongly enhances parasite virulence in an invertebrate host model. Oikos DOI: 10.111/j.1600-0706.2008,17028.x

Coors, A.; Vanoverbeke, J.; de Bie, T.; & de Meester, L. (2009). Land use, genetic diversity and toxican tolerance in natural populations of Daphnia Magna. Aquatic Toxicology. DOI: 10.1016/j.aquatox.2009.08.004

Jansen, M., Stoks, R., Coors, A., van Doorslaer, W., & de Meester, L. (2011). Collateral damage: Rapid exposure-induced evolution of pesticide resistance leads to increased susceptibility to parasites. Evolution DOI: 10.1111/j.1558-5646.2011.01331.x

3 comments:

  1. Your argument makes sense but I think it's very general. Also, I believe the manner in which biotic factors affect organisms is different from how abiotic factors affect them.

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  2. You mention that the D. magna populations were evolving to repel a stressor. What exactly does this mean? Did the experimenters observe an allele frequency change? Was there actually visible evolution of adaptations in these populations? I agree that it's important to consider abiotic influences in evolutionary relationships, though.

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  3. What are the different roles do biotic vs abiotic factors play in this case? I am a little confused by the exact mechanism that the D. magna repel evolutionary stressors

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