In the last two posts, we established that macroparasites are pretty much always aggregately distributed among hosts, and this aggregation can result from several ecological processes (e.g., variation in infection rates among hosts). This week, we will answer the next obvious question: who cares?! Why is macroparasite aggregation important enough to study? There are many reasons, but we’ll focus on these three things:
- Individual host fitness
- Parasite transmission – superspreaders!
- Regulation of host populations
As we’ve already discussed, the more parasites that a host is infected with, the more likely that host is to suffer negative fitness consequences. Highly infected hosts might have lower fecundity, slower growth rates, or higher mortality rates, for instance. So, when we’re considering individual-level fitness, we need to consider individual-level parasite loads. That is, assuming that all hosts harbor some mean number of parasites is probably not going to cut it.
Having a bunch of parasites might also make a host more susceptible to future infection – the “vicious circle” of disease where having parasites leads to lower body condition which leads to higher susceptibility to parasites which leads to MORE parasites, etc. Once upon a time, I made a cartoon about that. Parasite transmission – superspreaders!
Say you’re about to go eat some delicious sushi, and the chef lets you decide between a fish with just a few parasites and a fish with tons of parasites. Which one do you pick? (Yes, I know, I’m evil.) Obviously, you’re more likely to get infected by the parasites – assuming that they’re trophically transmitted and you can serve as the next host – if you eat a huge dose of parasites. This brings us to the topic of superspreaders, which we have discussed once or twice on this blog already. If we’re talking about just one host species, superspreader hosts are responsible for a disproportionate amount of the parasite/pathogen transmission. For instance, superspreaders may be individuals that 1) are heavily infected, 2) are shedding more ‘infectious particles’ (i.e., parasites) than other hosts, or 3) both. (Other options exist – like individuals with normal infection levels who have many social contacts and thus transmit more infectious particles than others). These individuals are the ones that exist in the tail of the negative binomial distribution: Superspreaders are important because if we can identify which individuals are the superspreaders, we can target them for disease management. For instance, if we can easily recognize the wormiest hosts – by doing fecal egg counts, etc. – then we can target those individuals with anthelmintic drugs.
Regulation of Host Populations I could talk about regulation of host populations by parasites all day. Like here. But let’s just focus on how aggregation of parasites affects host populations. And for that, let’s visit the very important Anderson and May (1978) paper. I was originally going to make this post very mathy, but instead, I’m just going to summarize one main point of Anderson and May (1978), and you guys can check out the PDF here for the beautiful details.
If you start with a host population that has exponential growth in the absence of parasites, no parasite aggregation, no affects of parasites on host mortality or fecundity, etc., you can get two basic kinds of population behavior – damped oscillations to a constant population sizes or population cycles. The potential problem with this basic, simplified model is that it is neutrally stable – meaning that if you perturb the system from an equilibrium, it shifts to a different equilibrium. And that means that the model is structurally unstable: a small change in parameters (e.g., infection rate) can cause the model to shift from one qualitative behavior to another, and that may not be biologically realistic.
Even though the basic model has some less than ideal characteristics, we can use it as a baseline model to see what happens when we add complications to the model. In a series of two papers, Anderson and May (1978) added a bunch of complications: overdispersion of parasites, underdispersion of parasites, parasite-induced host mortality, density-dependent parasite population growth, and other things. Some of these things made the model dynamics more stable, and some of them make the model dynamics more unstable. And the relevant point for this post is that aggregation of parasites is a stabilizing force in host population dynamics.
So, aggregation of parasites among hosts is important because individual-level parasite loads determine individual host fitness and transmission potential, and the individual-level impacts scale up to affect transmission in host populations and also the stability of host population dynamics. Next week, we’ll talk about how to model macroparasite aggregation. Stay tuned!!
References: Anderson, R. M., and R. M. May. 1978. Regulation and stability of host-parasite population interactions. I. Regulatory processes. Journal of Animal Ecology 47:219-247.