The Coevolution Continues


A while back, I made a post about parasite-host coevolution.

Here’s a cartoon, because my posts are too often filled with text.

Image

Anyway, to continue on the topic. In the last article about coevolution, I covered the idea of host and parasite coevolution leading to continual and reciprocal evolutionary changes – the hosts and parasites are constantly running, but they stay in the same place relative to each other. The (excellent) cartoon makes sense now, right?

In the article about coevolution, I also touched on the issue of multiple parasites infecting multiple hosts, and how this can complicate host-parasite coevolution. Here, I’m going to further complicate matters by talking a little about environmental heterogeneity and other species that interact with host-parasite associations.

Harrison et al. (2013) dealt with the issue of environmental heterogeneity. They conducted an evolutionary experiment with bacteria and their viral parasites, varying the bacterial habitat over time. They found that varying the habitat prevents coevolutionary dynamics between the bacteria and their viral parasite.

Conversely, Friman and Buckling (2013) experimented with bacteria, their viral parasites, and protist predators of the bacteria. These authors found that the bacteria tend to coevolve to either the viruses or the predator, not both. The presence of the bacterial predator also constrained the coevolution between the bacterial and virus.

So where does this leave us? It seems that when we consider only single host-single parasite systems, we may find the treadmill coevolutionary pattern seen in the cartoon above, but the likelihood of this situation breaks down when we consider other factors like habitat heterogeneity and multiple natural enemies (i.e., predators and parasites). However, one could reasonably argue that the discussed experiments with bacteria are not relevant for all organisms, and systems in which parasites and hosts do engage in treadmill (aka arms race) coevolution could exist. Whether such coevolution does or does not occur, though, will likely be system specific.

Citations
Friman, V. P. and A. Buckling (2013). Effects of predation on real-time host-parasite coevolutionary dynamics. Ecology Letters 16(1): 39-46.

Harrison, E., A. L. Laine, M. Hietala and M. A. Brockhurst (2013). Rapidly fluctuating environments constrain coevolutionary arms races by impeding selective sweeps. Proceedings of the Royal Society B-Biological Sciences 280(1764).

When Sharing is Caring: A Parasite’s Perspecitve

We’ve all heard of Influenza A, or Flu. It’s a viral parasite that can and has caused massive pandemics in humans. However, Influenza A does not infect only humans. It also parasitizes birds, particularly waterfowl, and other mammals. Many parasites have this diverse infection ability, i.e., many parasites infect multiple host species.

For such parasites, questions regarding their transmission dynamics become more interesting (and complicated). Instead of considering the interaction between only one parasite and one host species, one has to consider how different host species contribute to the parasite’s population. One host species may be the parasite’s main host, adding more parasites to the parasite population than any other host species. On the opposite side of the spectrum, the parasite may have no main host; each host species may contribute equally to parasite numbers in the community at large. In all likelihood, most parasites probably fall somewhere in the middle of this range; the parasites do not have a single main host, but the host species also contribute unequally to the parasite population.

In the cases where a parasite has a few (or one) main hosts, those hosts are called reservoirs. By producing most of the parasite population, reservoirs maintain that population. Reservoirs are thus important research areas for parasite population control, and therefore wildlife and human health. For example, many parasites that infect humans have non-human animal reservoir hosts. These parasites, ones that spillover into humans from other species, are called enzootic parasites. If one can determine their specific wild reservoirs, then one can eliminate parasite transmission to humans in a number of ways, including: limiting human-reservoir contact and preventing successful transmission among the reservoir species members (which itself can be accomplished through different mechanisms such as: vaccination, culling, habitat modification). However, such tools and goals are not simple, even when managing only a few host species.

More than the practical and financial considerations in appreciably affecting even a few host species, the different types of reservoir hosts complicate management efforts. Not all reservoir hosts are so for the same reasons. Streicker et al. (2013) argue three main mechanisms create reservoir host species: 1) The host species can be super abundant and have high population density; 2) The host species can be very susceptible to infection; 3) The host species can be highly infectious, producing numerous new parasites when infected. In the first mechanism, the host maintains the parasite simply by being so numerous. While a small percentage of the host population is infected, the host population is so large that it produces many parasites and maintains the parasite population. In the second mechanism, because hosts are so susceptible, a very high proportion of the host population is infected and can maintain the parasites at relatively lower host population sizes. In the third mechanism, hosts are highly infectious, so even though few hosts are infected, a single infected host produces many new parasites and has a high chance of infecting another host. These three situations are not mutually exclusive, but Streicker et al. argue that which one mostly applies to a particular reservoir species should affect management practices regarding that species. For example, the authors analyzed the effect of targeted removal of infected hosts and random removal of hosts from populations where a host species was either only super abundant, only super susceptible, or only super infectious. For super abundant hosts, random removal of hosts did not efficiently decrease the host’s contribution to parasite population because there was a small chance of removing an infected host. Targeted removal of infected hosts resulted in a moderate reduction, however. For super susceptible hosts, where a large proportion of the host population is infected, both random and targeted removal of hosts efficiently reduced the host’s contribution to parasite numbers. Because so much of the host population is infected, the chance that a random removal gets an infected host is not much less than targeted removal of infected hosts. For super infectious hosts, random removal finds infected hosts in proportion to their frequency in the population, and since each infected host contributes a large parasite number, each removal of an infected host will noticeably decrease the host’s contribution to the parasite population. Targeted removal of infected infectious hosts will decrease the host contribution to parasite population much more than random, although. This occurs because when there are few infected individuals, and each produces a large number of parasites, specific removal of the infected hosts will remove a large proportion of the parasite population pool. These results indicate that – for removal of hosts as a management tool – the different mechanisms creating reservoir hosts affect the outcomes of management actions.

Citations

Streicker, D.G., A. Fenton, and A.B. Pedersen, Differential sources of host species heterogeneity influence the transmission and control of multihost parasites. Ecol Lett, 2013. 16(8): p. 975-84.

Behavior and Parasite Transmission Risk

What determines parasite risk for a host? We often focus on factors such as the host’s immune system and the parasite’s ability to find or infect hosts. However, host behavior can determine a large proportion of infection risk. Take the 10-second rule for example. Some people like to say that food that has been on the ground for less than 10 seconds is safe to eat. That may or may not be true, but it is likely a riskier behavior (in terms of possible food contamination) than not eating food that has fallen to the ground. Engaging in such risky behaviors could thus make 10 second rule followers more likely to obtain parasites than people who do not eat food that has touched the ground. Importantly, this logic applies beyond humans and the 10 second rule. Within a species, one might predict that individuals that are more bold would be more likely to obtain parasites. One might predict this assuming that bolder individuals would be more likely to engage in risky behaviors, such as eating obviously bad meat. A recent study analyzing the contribution of host behavior to parasite transmission, for example, discovered that bold behavior (assessed through number of aggressive interactions and a few other measures) predicted Hanta virus infection in deer mice [1]. Specifically, bold deer mice were much more likely to show positive infection status for Hanta virus than shy deer mice. Cool, right? There are a few qualifications to point out here though. A significant percentage of shy mice were infected with Hanta, meaning there are other factors that need to be researched in the Hanta virus-deer mice system. This study did also not illuminate whether bold deer mice are bold because they were infected with Hanta (Hanta made them bold), or whether deer mice are more likely to obtain Hanta if they are bold (deer mice are bold prior to Hanta infection). Lastly, conclusions about the role of behavior in parasite transmission need to be relatively host and parasite specific. In the Hanta virus and deer mice system, for example, aggressive interactions lead to virus transmission because the virus is spread through bodily fluids. Aggressive interactions in which deer mice wound each other thus promote transmission of Hanta virus. However, for parasites that spread through other means, more sedentary or shy individuals could be more beneficial to parasite transmission.
Literature Cited

1.    Dizney, L. and M.D. Dearing, The role of behavioural heterogeneity on infection patterns: implications for pathogen transmission. Anim Behav, 2013. 86(5).

Parasite extinctions. A new hope?

So, first off, sorry that I did not post anything last month.

But let’s not dwell on the past. Instead, let’s focus on the future, and the role of current massive extinction rates on future biodiversity – and how parasites fit in to this picture.

Extinctions can occur through numerous mechanisms. Common ones include habitat loss, species invasion, overkill, climate change, and coextinction (Dunn et al. 2009). Regarding coextinction, it is easy to understand how the extinction of prey species could lead to the extinction of predators (for example, the extinction of krill could cause the extinction of baleen whale species). In a similar fashion, coextinction can apply to parasites. If a host species has species-specific parasites (and many hosts species do), then those parasites may go extinct along with the host species (Dunn et al. 2009). Furthermore, coextinction can include cascades of extinctions. If an insect species goes extinct, a bird species that uses that insect as prey may go extinct, and the parasites of that bird may then become extinct also. Whether such processes occur depends primarily on the host specificity of the parasite (Dunn et al. 2009). Host specificity, importantly, is very difficult to measure – for a variety of reasons, including that it is infeasible to expose all possible hosts to a particular parasite. In addition, because individuals within a parasite population likely have varying host specificities, the frequency of each host specificity level is probably more important than the average host specificity level (for example, knowing that 80% of the parasite population is highly general and 20% highly specific would be more important than knowing that the average parasite is moderately host specific) (Dunn et al. 2009). These considerations beg the question: If a host goes extinct, how likely is it that the parasite (or mutualist) will become extinct also or adapt to another available host? While studies often indicate that parasite are more general than previously assumed (Dunn et al. 2009), whether a parasite survives will depend highly on the specific parasite species in question; generalizations seem inadvisable.

But why should we care? Parasites are bad, right? Well, if we care about biodiversity for the sake of biodiversity, then we should protect parasites, which are often more diverse than their hosts (Dunn et al. 2009), implying that parasite species may outnumber host species. Furthermore, a common hypothesis for the evolution of diversity within sexual organisms relies upon parasites – to escape their parasites, hosts diversify. Without parasites, the force to diversify could thus decline, resulting in declines in host biodiversity (Dunn et al. 2009). Additionally, as stated above, host-specific parasites are more likely to become extinct than generalist parasites; generalist parasites are also often more pathogenic than host-specific parasites (Dunn et al. 2009). Zoonoses, parasites that infect humans but are maintained in the wild by non-human animal reservoirs, are by definition generalists. Therefore, as host-specific parasites become extinct, we should ask ourselves whether pathogenic zoonoses will become more common, filling the gaps left by the specific parasites, and whether such a result will negatively affect human health.

Literature Cited
Dunn, R. R., N. C. Harris, R. K. Colwell, L. P. Koh, and N. S. Sodhi. 2009. The sixth mass coextinction: are most endangered species parasites and mutualists? Proceedings of the Royal Society B-Biological Sciences 276:3037-3045.

Parasites are Always Late to the (Range Expansion) Party

Looking back at my previous posts, they are all pretty long. So I’m going to shoot for brevity here.

Two kinds of factors determine where one can find an organism, or its range: Abiotic factors, or how often it rains, soil mineral content, etc.; and biotic factors, or what other organisms are around, what they eat, what they defecate, what they do, etc. For a parasite, which needs a host to survive, biotic factors play a dramatic role in determining the parasite’s range. Abiotic factors contribute a great deal as well, but focusing on the biotic side is more than enough for a short blog article.

Take host range effects on parasites as an example. Due to the nature of parasitism, parasites can only exist where their hosts do. This restriction poses a problem for parasites because host ranges can shift over time, and hosts that can shift ranges quickly (mobile animals, for example) can move beyond their parasites (Phillips et al. 2010). How could a host “out-run” its parasite though? Parasites are typically tightly connected with their hosts (e.g., often physically attached to or within the host), and so should move with their hosts.

According to Phillips et al. (2010), hosts can move away from their parasites through range shifts because of chance. Before I go any further, I should say that hosts do not often permanently escape their parasites through range shifts; rather, the parasite shifts its range more slowly than the host, so the host experiences a parasite-free lag time before the parasite catches us. Now, chance can create parasite range shift lag times through two mechanisms. The authors contend that low host population size at the leading edge of range shifts increases the chance that parasites will not be present in that subsample of the population. The authors also argue that the parasites will be less able to maintain successful transmission in the smaller host population at the range edge. These two chance mechanisms are called founder effects, and they rely on probability. In any range, the population on the edge of the range is much smaller than that in the center of the range. Because of its smaller size, the range population has an increased chance of not having parasites that are found dispersed among the larger parent population (Say you have a large bag of marbles, and most are black and a few are red. If you grabbed a few out of the bag, representing your range edge population, the chances that that group would have a red marble are pretty low). Further, the few parasites that are represented within the range edge population have an increased risk of local extirpation because the fewer number of hosts at the range edge mean the parasites may not be able to maintain transmission – by chance the parasites may not encounter a host when their life cycle dictates they must. However, this second mechanism only applies to parasites with density-dependent transmission (the number of hosts present in an area affects the success of parasite transmission). Because of these chance, or founder, effects, parasites will be more likely to die or never have been present at the range edge, allowing the host population at the range edge to expand with fewer parasites than the host population in the center of range. Such a lack of parasites at the range edge creates the lag time between host range expansion (which occurs at the range edge) and parasite range expansion.

Citation
Phillips, B.L., et al., Parasites and pathogens lag behind their host during periods of host range advance. Ecology, 2010. 91(3): p. 872-81.