Social spiders and hilarious field equipment

Before I even explain the topic of today’s post, I have to tell you that the papers that I’m blogging about today use the best and most hilarious piece of field equipment that I have ever seen. Project budgets may never be the same. I may even need to change study systems. Read on, if you dare.

The literature on parasites and animal personalities is ever-growing, perhaps because personalities have palpable consequences for transmission dynamics: the likelihood of direct transmission between infected and susceptible hosts often depends on host behavioral tendencies and their impacts on social interactions. I’ve blogged about this in the past: aggressive Tasmanian devils are more likely to transmit facial tumor disease to non-aggressive conspecifics and house finches that dominate the use of artificial feeders are more likely to acquire and transmit conjunctivitis. Similarly, in a world (er, Africa) where spiders live together in a shared web and cooperatively capture and share prey, bold spiders are more likely to transmit cuticular bacteria to shy spiders than shy spiders are to bold spiders (Keiser et al. 2016a). And what’s more, spider social networks are behaviorally disassortative, where bold spiders were more likely to rest in contact with shy spiders than they are with their own personality types. Thus, it appears that this system might be poised for rapid transmission of microbes, depending on the personality composition of the susceptible spiders in the colony.

These South African social spiders (Stegodyphus dumicola) live in colonies of a few dozen to over a thousand individuals. The ability to capture a large amount of large prey items is key to a colonies’ success, and colonies attack faster when they contain a mixture of bold and shy personality types in the group (Keiser et al. 2014). Furthermore, the execution of this important collective behavior is often based on the behaviors of one or a few important “keystone individuals” or leader spiders (Pruitt & Keiser 2014). These keystone individuals are so important in this system – and probably in many other systems, too – that we have to wonder: what happens when the keystone individuals take a sick day or even die from infection?

It turns out that increased bacterial load on colonies’ keystone individuals can impair the collective behavior of their entire society (Keiser et al. 2016b). Specifically, groups whose keystone individual are exposed to bacteria attack prey stimuli more slowly, and fewer individuals participate in the attack. Interestingly, the keystone’s participation in the task is not altered, suggesting that increased bacterial load alters the way keystones influence their colony-mates’ behavior.

Perhaps you find yourself wondering how, exactly, one might measure a spider group’s response to prey stimuli. Do you sit around and wait all night for some prey to get caught in the web? Boring. Do you try to throw a moth into the web and watch what happens? Rude. No, what you do is you attach a “hand-held vibrator” (Model: Flamenco Purple no. 4, Golden Triangle; do not Google if you’re at work) to a wire and then attach a piece of paper to the other end of that wire, and you use that vibrating piece of paper as your simulated prey. This is brilliant, and I HAVE SO MANY QUESTIONS. Why that model? How awkward is international travel for field work? I must know!


Anyways, social spiders are awesome, their personalities influence pathogen transmission, and their pathogens influence the role that individuals’ personalities play in colony behavior. Cool stuff!


Keiser, C.N., Jones, D.K., Modlmeier, A.P. & Pruitt, J.N. (2014) Exploring the effects of individual traits and within-colony variation on task differentiation and collective behavior in a desert social spider. Behavioral Ecology and Sociobiology, 68, 839-850.

Keiser, C.N., Pinter-Wollman, N., Agustine, D.A., Ziemba, M.J., LingranHao, J.G.L., and Pruitt, J.N. (2016a). Individual differences in boldness influence patterns of social interactions and the transmission of cuticular bacteria among group-mates. Proceedings of the Royal Society B, 283, 20160457.

Keiser, C.N., Wright, C.M. & Pruitt, J.N. (2016b) Increased bacterial load can reduce or negate the effects of keystone individuals on group collective behaviour. Animal Behaviour, 114, 211-218.

Pruitt, J.N. & Keiser, C.N. (2014) The personality types of key catalytic individuals shape colonies’ collective behaviour and success. Animal Behaviour, 93, 87-95.

Slugs ruin everything

Mutualisms are important; we’re sure about that. Here’s something we don’t know as much about: are mutualisms resilient? As species go extinct or species appear in new places, as nutrient cycles change, and/or as the global climate changes, will the mutualisms that ecological systems rely on keep functioning?

Errbody knows that I like ant-plant mutualisms, including seed dispersal mutualisms where ants take seeds with juicy eliaosomes back to their nests, eat off the eliaosomes, and then dump the seeds. I also loooove snails and their close relatives: SLUGS. Today, we shall combine them, and see what happens to ant-plant dispersal mutualisms when invasive slugs get thrown into the mix. Below is the short version, and you can read all of the details in Meadley Dunphy et al. (2016).

Slugs eat elaiosomes, just like ants. But unlike ants, slugs eat the elaiosomes without moving the seeds, so the seeds aren’t dispersed. Furthermore, when slugs eat the elaiosomes off seeds, ants won’t disperse the seeds anymore, so the mutualism is disrupted. Moral of this story: Slugs. Ruin. Everything.



Meadley Dunphy, S.A., K.M. Prior, and M.E. Frederickson. 2016. An invasive slug exploits an ant‑seed dispersal mutualism. Oecologia 181:149–159.

Food provisioning and wildlife disease dynamics

Humans change environments in many different ways, including accidentally or purposefully provisioning wildlife with novel food resources. For example, bird feeders, salt licks, ecotourism feeding stations, and dumpsters all provide concentrated food resources for wildlife. Does this food provisioning influence disease dynamics?

First, let’s consider how food provisioning might influence disease dynamics for parasites with any given transmission mode. The big rates that we care about here are the transmission rate (a function of contact rate and transmission success), birth and death rates, and immigration and emigration rates. If resource provisioning increases host population density via increased aggregation of individuals, increased birth rates or decreased death rates, and/or increased immigration or decreased emigration rates, then transmission rates for pathogens with direct contact density-dependent transmission should increase. In the same scenarios, pathogens with frequency-dependent transmission may not be affected by provisioning, or transmission rates may even decline if high birth rates dilute the prevalence of infection in the population. For pathogens that are transmitted via environmental stages, environmental stages may build up at resource provisioning sites when high densities of animals hang out there for long periods, increasing transmission. For pathogens that are transmitted via intermediate hosts, transmission may be reduced if hosts switch from foraging on intermediate hosts to foraging on human-provided resources.

Factors besides transmission mode might also be important. For instance, regardless of transmission mode, if resource provisioning increases host resistance – for instance, by increasing body condition – then transmission rates should decrease. Conversely, if resource provisioning decreases host resistance – for instance, if the provisioned food is nutritionally poor or there is high competition at sites with provisioning and body condition is reduced – then transmission rates should increase. Resource provisioning might also alter host tolerance to infection, so that hosts aren’t as sick but continue shedding infectious agents longer than they would if they didn’t have supplemental resources.

Ok, I think that covers most of the possibilities. Back to our question: does food provisioning influence disease dynamics? Yes, sometimes. Most of the mechanisms listed above were supported by at least one study in a recent review by Becker et al. (2015). Based on the long, messy list above, you can probably guess that sometimes food provisioning increases transmission, sometimes it decreases transmission, and sometimes nothing notable happens. The big take-home message is that there isn’t just one universal outcome when we provision wildlife with supplemental resources, and it’s important that we conduct more and better studies aimed at elucidating the epidemiological mechanisms underlying the observed relationships. Cool stuff!

Have you read this post about house finch conjunctivitis yet?



Becker, D.J., D.G. Streicker, and S. Altizer. 2015. Linking anthropogenic resources to wildlife–pathogen dynamics: a review and meta-analysis. Ecology Letters 18: 483–495.

My new favorite symbiosis: boxer crabs!

I can’t believe that I only just learned about the glorious symbiosis between boxer crabs and anemones. The crabs hold one tiny anemone in each claw, and they use the anemones to defend themselves from predators. The anemones benefit from increased access to food because they’re constantly being waved about.



And look at these dance moves!

That tiny cheerleader’s got game.

I’m in love.


Which cartoon would you rather see?

I couldn’t decide which paper to cover this week. Instead, I’m going to summarize two neat papers that I read recently, and then you can vote on which cartoon you would like me to make.

Option 1: Life in the fast lane

Social insects vary in their worker turnover rate, with some species having workers who live very short lives and some species having workers who live relatively long lives. Buechel and Schmid-Hempel (2016) manipulated worker pace of life in bumblebees and found that there were fewer infected workers in fast-paced colonies, because parasites couldn’t spread fast enough to keep up with turnover. The cartoon would be something like: parasite invades bumblebee and bumblebee immediately grows gray hair and drops dead amidst much parasite cursing.

Option 2: Rapping, rocking hermit crabs

This paper actually has nothing to do with parasites, but it cracks me up, so I’m including it. Hermit crabs compete for gastropod shells, where attackers use two behaviors to try to evict defenders from their shells: shell rapping and shell rocking. Edmonds and Briffa (2016) put a thin layer of aquarium sealant on defenders shells to reduce the efficacy of shell rapping by the attacker, and found that attackers continued to rap but also rocked more, suggesting that they evaluate their own attack efficacy. Obviously, this cartoon would involve a hermit crab rap star turning into a rock star when his rap career wasn’t successful enough.

Refugia, connectivity, and transmission

When populations become small, their probability of extinction typically goes up, because demographic and environmental stochasticity are more likely to set the population on an irreversible decline. However, when one population goes locally extinct, a species is not necessarily lost; the area might be re-colonized by migrants from a different population later, if other populations exist. Metapopulation theory tells us that a balance between population extinctions and re-colonizations in heterogeneous patches that are linked by dispersal can allow a species to persist regionally, even when it goes extinct locally.

What happens when we add infectious diseases into our host metapopulation model? Connectivity might be detrimental to regional persistence when infectious diseases are introduced, because pathogens in one population can invade the other populations via host dispersal, whereas pathogens are limited to a single population when populations aren’t linked via dispersal. Or…not?

Heard et al. (2015) recently published a quite complicated and fancy metapopulation model that suggests that connectivity actually increases the probability of metapopulation persistence in an Australian frog species endangered by the fungal pathogen (Bd), which causes the disease chytridiomycosis. From survey work, they knew that the prevalence of Bd in growling glass frogs was lower in warm and/or salty wetlands. They could also show that the probability of a local extinction in any given frog population increased with the prevalence of Bd in the frog population. By linking local extinction risk to Bd prevalence and microclimate, they could create metapopulation models using known dispersal distances for the growling glass frog, and they could run simulations regarding metapopulation persistence under scenarios where they eliminated frog dispersal among populations or not. They had two important findings. First, if you ignore the fact that Bd prevalence varies with microclimate, the probability of metapopulation persistance is predicted to be much lower than it actually is. The warm and/or salty wetlands act as important low Bd prevalence frog population refugia that can seed the other populations in a metapopulation when they go locally extinct, such that microclimate variability increases persistence. Second, “re-seeding” can only happen if dispersal occurs among populations, so connectivity increases metapopulation persistence in this system.

One lingering question is whether this system is a good example of the role of connectivity in all host metapopulations plagued by infectious diseases. Heard et al. (2015) argue that Bd is basically everywhere already – and there to stay – because it can be maintained in both environmental reservoirs and reservoir hosts. Therefore, they suggest that for growling glass frogs, dispersal of hosts among populations doesn’t really play a role in disease dynamics. In systems where the pathogen is not yet widespread (i.e., regions currently being invaded), where reservoirs are less likely to provide long-term maintenance of the pathogen, or where dispersal of reservoir hosts is particularly important to pathogen spread, host dispersal could start to have detrimental impacts on long-term metapopulation persistence. This is cool stuff that deserves more attention!


Heard, G.W., C.D. Thomas, J.A. Hodgson, M.P. Scroggie, D.S. Ramsey, and N. Clemann. 2015. Refugia and connectivity sustain amphibian metapopulations afflicted by disease. Ecology Letters, 18: 853–863.