A closer look at our research on invasive parasites |
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What is the underlying mechanism behind the demographic patterns of the invasive bopyrid isopod Orthione griffenis? |
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The mud shrimp Upogebia pugettensis (above) develops extensive burrows in intertidal mud flats that may be very dense and can extend up to a meter in depth (left). This ecosystem engineer plays a crucial role in estuarine processes because of its burrowing that increases bioturbation and greatly extends the sediment-water interface, and because of its filtration activities. |
While conducting studies on the feeding ecology of Upogebia in Yaquina Bay, Oregon during the late 1990s, I discovered a bopyrid isopod parasite that lives within the branchial chamber of the shrimp. The parasite, named Orthione griffenis by bopyrid isopod expert John Markham, is an invasive parasite that apparently was introduced to the Pacific Northwest in the 1980s. After remaining at relatively low prevalence for some time, then quickly became very abundant and by 2002 was found in the majority of shrimp within the Yaquina Bay population. The parasite shows a curious pattern of prevalence in its host (part A in figure below). At the same time that the parasite increased in abundance, its shrimp host has declined in abundance throughout much of its range. It is presumed that the parasite is responsible for this decline. |
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Figure from Griffen 2009 demonstrating the observed prevalence of the parasite across different sizes of male and female shrimp and the sex ratio of shrimp of different sizes. To understand the mechanism underlying these patterns, and therefore to hopefully better understand why the host population is declining, I constructed a family of 6 individual-based, stochastic simulation models to explore the ability of several potential mechanisms to reproduce the observed patterns of changing parasite prevalence and shrimp sex ratio with shrimp size shown in part A of the figure to the left. I first developed a null model in which mortality rate of infected and healthy shrimp were constant, in which no parasite mortality occurred (i.e. parasites remained with the host until host death), in which infection rates were the same for male and female shrimp and no feminization occurred (Model 1, part B of figure). I then modified this null model in various ways for each of the subsequent models to explore 5 different potential mechanisms, as follows. The first explored higher background mortality in male than in female shrimp (Model 2, part C of figure). Second, higher infection-induced mortality in male than in female hosts (Model 3, part D of figure). Third, higher infection rate in female than in male shrimp (Model 4, part E of figure). Fourth, mortality of parasites in male hosts (Model 5, part F of figure). And fifth, feminization of male hosts (Model 6, part G of figure). Comparing each to the observed patterns, it is apparent that feminization of male hosts is best capable of reproducing observed patterns and is therefore the most parsimonious mechanism. Combinations of other mechanisms are also capable of reproducing the observed patterns, but no other single mechanism is capable. These results suggest that the parasite causes feminization of male hosts. Feminization has been observed for other burrowing shrimp-isopod parasite pairs. |
| Together with Michele Repetto, then an undergrad in my lab, I recently tested the hypothesis that feminization of male hosts is responsible for the patterns shown above. We collected ~400 shrimp from throughout the intertidal regions of a mud flat in Yaquina Bay, Oregon. For each of these crabs, we determined their infection status and physiological condition and looked for evidence of feminization using gonopores, modified pleopods, and claw morphology. To do this we made morphological measurements and also dissected each shrimp and measured the size of the gonad+hepatopancreas as well as the lipid content within the hepatopancreas. We did not find any evidence that feminization is occurring. Thus, the most parsimonious explanation does not appear to apply in this case. While feminization does not appear to be the underlying mechanism, parasites do appear to exert a strong energetic burden on hosts, as evidenced by smaller gonads+hepatopancreas of infected compared to healthy shrimp. It also appears that parasites have different physiological impacts on male and female shrimp. | |
| Change in the gonado-hepatosomatic index, a measure of physiological condition, as a function of tidal height and infection status. Shows that energetic state was negatively correlated with tidal height, likely because individuals higher up on the shore are covered with water for less time each day and so have less opportunity to filter feed. Figure from Repetto and Griffen 2011. |  |
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Lipids play an important role in long term energy storage. This figure shows that lipid storage decreases with tidal height and with parasite infection, supporting the hypothesis that parasites withdraw energy from their shrimp hosts. Figure from Repetto and Griffen 2011. |
| The influence of the parasite on host energetics appears to be specific to the sex of the host. As shown in the figure to the right, we found no difference in the effect of the parasite on immature male and female hosts. However, once sexual maturity in the host was reached, we found that the parasite had much larger impacts on energetics of male shrimp hosts than on female shrimp hosts. Figure from Repetto and Griffen 2011. |  |
Clearly there is more work to do in this system to determine just what impacts this invasive parasite has on its shrimp hosts. Determining just what the impacts are will be essential to understanding the affect of the parasite on the host shrimp population. Currently, the extent to which host populations are declining remains unclear. And if they are in decline, the role of the parasite in that decline remains to be demonstrated. |
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