Bigger is Better

Population size impacts host-pathogen coevolution (2021) Papkou et al. 2021, Proc B,

Image credit: Kbradnam, CC BY-SA 2.5, via Wikimedia Commons

The Crux

Host-pathogen interactions are maybe best characterized as a battle – a pathogen (a parasite that causes disease) doing what it can to maximize how much it can get from a given host organism, and a host doing what it can to defend itself from this endless attack. As a result, hosts and pathogens are locked in an endless evolutionary battle, whereby hosts evolve to better defend themselves and pathogens evolve to better attack the host. A key factor in this battle is population size, as this affects the evolutionary potential of a given population of organisms to respond to selection.

The larger a population of hosts, the more novel genetic variants there are, which are simply organisms with different genetic make-ups, which can be the result of mutations popping up or through combinations with other genetic variants within the population. The more variation there is, the more diverse the population is, and the more chance it has of carrying the genes that could help it respond to a new threat, like a pathogen.

This means that a larger host population is more likely to have a genetic variant that is able to defend itself from these pathogens. That variant will then be selected for and the host population will become more resistant to that pathogen over time. While a lot of theory has been dedicated to understanding these coevolutionary battles, actual experimental evidence is lacking. Today’s authors used a model system to conduct evolutionary experiments to test the effect of host population size on host-pathogen coevolution.

What They Did

The authors conducted a number of tests and comparisons to understand how host population size affect host-pathogen coevolution, but I’ll be focusing on the coevolutionary dynamics aspect of this experiment.

The authors used the nematode Caenorhabditis elegans as their host and the bacterium Bacillus thuringiensis as their pathogen. Hosts and/or pathogens were tracked over a period of 23 host generations, with host and/or pathogen individuals transferred to new plates for each new host generation after a period of seven days. For their population size treatments, the authors had with small populations (100 nematodes), large populations (3000 nematodes), and large populations with a bottleneck event (3000 nematodes, but every fifth transfer the authors only transferred 100 nematodes, similar to a natural bottleneck where the majority of a population is killed/removed).

To test for coevolution of the host and pathogen, the authors used three different evolutionary treatments: coevolution, host adaptation, and host control. For the coevolution treatment both the nematodes and bacteria were transferred to new plates for the new host generation, allowing both the host and pathogen to evolve in response to the other. For the host adaptation, only the nematodes were transferred to new plates where they were exposed to the ancestral bacteria, which allowed only the host to evolve to the pathogen. For the host control, nematodes were alone in the plates, and they were transferred to new plates like the other treatment, giving the authors an evolutionary “baseline” to compare the other treatments to.

Fitness of the host was measured via the host fertility (mean number of eggs produced per host) when infected with the ancestral bacteria. If host fitness increased over time, that would show that they were evolving in response to the selection imposed by the pathogen. Pathogen fitness was measured as the competitive ability of the evolved bacteria compared to the ancestral (the bacteria that they started the experiment with, absent any evolutionary changes). To measure the competitive ability of the bacteria, the authors infected the ancestral nematode population with a 1:1 mixture of ancestral and evolved bacteria, then measured the frequencies of the two bacteria strains after a 7-day infection period. If most of the bacteria after 7 days was the evolved strain, that would show that it was more competitive and therefore more fit.

Did You Know: Genetic Drift

Genetic drift is the change in gene frequencies over time due to random sampling. Random chance determines which individuals survive and reproduce, so if there are many copies of a given gene within a population the chances are good that there will be copies of that gene in the next generation. However, in small populations there is less genetic diversity (i.e., fewer types of genes), so random losses mean that a gene could be lost entirely from the population very quickly.  

While not the nematodes from this study, the above image shows what the C. elegans in the experimental treatments would look like (Image credit: snickclunk, CC BY 2.0).

What They Found

The fertility of nematodes from both the coevolution and host adaptation treatments increased as time went on, indicating that the host populations adapted to the pathogen. This happened for both the large and small host populations, but the hosts from the large populations had more eggs than those from the small populations, meaning the smaller population size limited the ability of those nematode populations to adapt as well as the larger populations. For the pathogens the authors found that only the pathogens from the coevolution treatment had higher fitness than the ancestral population.


This experiment was very well designed and allowed the authors to tackle their main question from a variety of angles, but I wish they had also investigated how changes in pathogen population size affected the coevolutionary dynamics between hosts and their pathogens. Obviously logistics are always a concern, and sometimes it just isn’t possible to look at every possible combination of treatments, but given the effect of population size that they found, and the fact that population size is variable in nature, I am very interested in knowing how changes in pathogen population size further affect these evolutionary relationships.

So What?

I have talked about papers like this before, where authors attempt to test a well-established theory using an experiment. I personally love these papers, as they can support theory and provide solid experimental evidence for a concept. What’s more, the results of this paper provide more evidence for why fragmentation and habitat loss is so dangerous for wildlife the world over. Smaller populations from fragmentation means less genetic diversity, which means that species are less able to respond to a given, harmful environmental factor (like the pathogens in this study).

Dr. Adam Hasik is an evolutionary ecologist interested in the ecological and evolutionary dynamics of host-parasite interactions who is beyond excited to do these kind of evolutionary experiments in his own work. You can read more about his research and his work for Ecology for the Masses here, see his personal website here, or follow him on Twitter here.

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