An Ode to Quantifying Infection Risk in Addition to Prevalence

When you’re studying parasites (or symbionts or pathogens), the prevalence of the parasite in the host population is one of the easiest response variables to measure. That’s not to say that it is easy; there are certainly a variety of methodological difficulties that crop up, and it can be expensive to run lots of blood tests if you’re looking at seroprevalence. But getting a prevalence estimate is certainly a lot easier than pinpointing when each host becomes infected (e.g., via mark-recapture methods) and/or calculating the actual risk of infection (i.e., the rate that susceptible hosts become infected = force of infection). For that reason, we often use prevalence as a response variable, and hope that we can infer things about parasite transmission based on those data. Sometimes, it works out great! For instance, in 1854, John Snow (the physician, not the Brother on the Wall) mapped the locations of Cholera cases in London. By pinpointing an area of high incidence on the map, he found a water pump that was probably an important source of infection in the epidemic. But do areas of high disease incidence or prevalence always occur in areas of high disease exposure?

Littorina littorea, the common periwinkle, is an abundant and widespread marine snail that hangs out in the intertidal zone (various levels of exposure to the air with the tides) and the subtidal zone (almost never exposed to air). Periwinkles are hosts for a few different trematode species, but for today, we’ll just focus on Cryptocotyle lingua, which infects snails, then fish, then shorebirds. Snails get infected when they consume trematode eggs from shorebird feces. ‘Loitering’ shorebirds are 6-20 times more likely to hang out in the high intertidal zone than the low intertidal zone, and as a result, the density of shorebird feces in the high intertidal zone is 70 times higher than in the low intertidal zone (Byers et al. 2005). Therefore, it is not surprising that when uninfected ‘sentinel’ snails were placed in field cages in the high and low intertidal zones, snails were four times more likely to become infected in the high intertidal zone (Byers et al. 2005). In fact, the probability that an uninfected snail would become infected in the low intertidal zone was effectively zero. That makes sense, because bird guano was almost never found in that zone.

So, when Byers et al. (2005) went out and sampled periwinkles in the high and low intertidal zones, they found way higher prevalences of infection in the high intertidal zone, where infection risk was high, right? WRONG! The prevalence of infection was much higher in the low intertidal zone, even though snails do not become infected there! How could that be?

First, let’s back up and talk about an important selection pressure in the low intertidal zone: predation. There are extreme size-dependent predation pressures in that zone that pretty much prevent small/young snails from living there. So, the only snails in the low intertidal zone are bigger/older snails. Big/old snails are much more likely to be infected by trematodes than small/young snails, because they have had longer to be exposed and become infected. But we know that the big snails aren’t becoming infected in the low intertidal zone, so where are they coming from? It may be that young snails hang out in the high intertidal zone, escaping predation but experiencing high infection risk, until they are big enough to safely live in the low intertidal zone. Once big enough, the snails migrate to that low zone, which provides better foraging opportunities, and the high density of big, infected snails results in high prevalences of infection (76% infection!) in an area that has effectively zero risk of infection. Isn’t that neat?!

So, as Byers et al. (2005) point out, “disease risk and prevalence patterns need not be tightly coupled in space.” I think that’s important to remember when we’re deciding what response variables we want to consider in ecological and epidemiological studies.



Byers, J.E., A.J. Malek, L.E. Quevillon, I. Altman, and C.L. Keogh. Opposing selective pressures decouple pattern and process of parasitic infection over small spatial scale. Oikos.

World’s coolest vector of infectious pathogens

If you weren’t born before the 1980s, you probably don’t know what an entire street lined with elm trees looks like, because Dutch Elm Disease spread through both Europe and North America in the early and middle 1900s and decimated elm populations. Pockets of elms still persist in places like Amsterdam and Winnipeg, but it is a never-ending battle to keep those trees disease free.

So, which highly virulent pathogen is responsible for totally reshaping temperate tree communities? The culprit is a fungus (well, a few fungal species, actually) that is vectored by a tiny and totally adorable beetle (well, a few beetle species, actually). Ladies and gentlemen, I present to you the horrible, terrifying, death-spreading elm bark beetle:


Joking aside, these beetles are completely amazing. They have symbiotic relationships with fungi, where the fungi range from weak parasites to commensalists to mutualists depending on the beetle species, the fungus species, and perhaps environmental conditions. In the simplest cases, bark beetles act as transport vessels for the fungi, without getting anything in return for their dispersal services. In contrast, ambrosia beetles cultivate fungus gardens in the galleries that they excavate in dead trees, and the beetles consume the fungus as their sole source of nutrition. When the young beetles emerge from their natal galleries to disperse, they take fungal spores with them to their new galleries. Isn’t that cool?! Whereas fungus farming has evolved just once each in ants and termites, it has evolved many times in the ambrosia beetles (Hulcr and Dunn 2011). And get this: at least one species of ambrosia beetle is eusocial!

If bark beetles and ambrosia beetles typically only excavate in dead trees, why did the elm bark beetle go rogue and start attacking live elms? Well, it turns out that it wasn’t an isolated event. There are more than a dozen examples of the beetles shifting from dead to live trees in recent history, with catastrophic results for some of the tree species that are being attacked (Hulcr and Dunn 2011). Humans are unintentionally shipping these beetles and their fungal associates to novel regions around the globe. And in novel regions, bark beetles searching for dead trees by following volatile cues might mistake living trees for dead trees. Or, as Hulcr and Dunn (2011) put it, some living trees might smell dead. Even if the beetles realize their mistake and don’t completely excavate a gallery in a living tree – choosing instead to go search for a dead tree – their initial boring activities might inoculate the tree with the fungal symbionts.

But here’s a conundrum: if a fungal symbiont transported by bark beetles doesn’t really affect trees in the beetle’s native range, why should the fungus be highly virulent in the introduced range? After all, the beetles can only introduce a little fungal innoculum into a giant living tree. Well, it may be that the majority of the tree pathology is caused by the tree’s response to the pathogen, rather than the direct actions of the fungus, just like the animal immune response to pathogens is often worse for the host than the actual damage caused by the pathogen. It may be that trees wildly overreact to the novel fungal pathogen by expanding the walls of the xylem so much that the tree ends up dying.


Anyways, bark beetles are really cool vectors, and I think disease ecologists should pay more attention to them.


Hulcr, J., and R.R. Dunn. 2011. The sudden emergence of pathogenicity in insect–fungus symbioses threatens naive forest ecosystems. Proceedings of the Royal Society B 278: 2866–2873.

How fast can pathogen epidemics spread?

Everyone dreads the idea of a pathogen that can rapidly spread across vast distances, especially if that pathogen causes high host mortality or morbidity. For today, I’m going to ignore host mortality/morbidity part, and just focus on the first part: how fast can pathogens spread across space, and what affects their rate of spread?

To start answering this question, we need to dig backwards in the literature more than a decade to an Ecology Letters paper by McCallum et al. (2003). They searched the literature for estimates of the rate of pathogen spread across space in marine or terrestrial systems, while excluding any pathogens whose spread was mostly facilitated by human activities. The pathogen with the fastest rate of spread was a herpes virus that infected pilchards (fish) in Austrailia. The virus spread at rates of up to 11,000 km per year!!

In general, pathogens in marine environments tended to spread faster than pathogens in terrestrial environments. Pathogens might spread more quickly in marine environments because marine habitats tend to be more connected (or more “open”), with higher dispersal rates among patches than in terrestrial environments. However, there was a lot of variation in the rates of pathogen spread in both environments, where some terrestrial pathogens spread rapidly and some marine pathogens spread very slowly. Some of that variation can be explained by host mobility: pathogens that infect sessile (or at least very slow) host species spread more slowly than pathogens that infect highly mobile host species. Neat!

I want to see this analysis done again with the data that have accumulated since 2003. Someone get on that!



McCallum,H., D. Harvell, and A. Dobson. 2003. Rates of spread of marine pathogens. Ecology Letters 6(12): 1062-1067.

Unofficial ESA 2015 Parasite Ecology Cartoon Contest

ESA 2015 is just one month away! Last year, I had tons of fun judging a parasite ecology cartoon contest that no one knew they were participating in. I posted the results here. This year, I’m announcing the (technically second annual) Unofficial ESA Parasite Ecology Cartoon Contest.

Here’s how it works: myself and a top secret team of judges will be watching your symbiont-related talks and taking notes on your use of cartoons. Our favorite cartoonist will be awarded an almost entirely worthless prize (i.e., snail mail from yours truly, some publicity for your cool science, and bragging rights for a year). The cartoons don’t need to be funny! We’re just looking for cartoons that help communicate your work to the audience. That being said, anything punny is worth mega bonus points.

My minions and I should be able to make it to the majority of the parasite-related talks, but it’s logistically impossible for us to see them all. If you know you’re going to have some rocking cartoons and you want in on this highly prestigious contest, let me know in the comments or via email and I’ll make a special effort to come to your talk. This is particularly important if you’re in a session that isn’t parasite-themed.

To anticipate some questions:

Will the judges be participating in the contest? No!

Can I use cartoons from this site, if I use proper attribution? Yes!

Can the judges be swayed by offers of free beer or tenure-track faculty positions? No! (Except yes. So much yes.)

Good luck!!

Parasites and Snail Personality

When individual animals show consistent behavioral responses in different scenarios or in similar scenarios across time, and individuals vary in their responses, we can say that there are behavioral ‘types’ or personalities in that animal population. For instance, some animals might have aggressive personalities, where those individuals are consistently more aggressive than other individuals in the population. Personality is getting a lot of attention in disease ecology right now because particular animal behavioral traits (or suites of personality traits = behavioral syndromes) might increase an individual’s risk of becoming infected by a pathogen or the probability that an infected individual transmits a pathogen. For instance, I recently blogged about how Tasmanian devils that receive many head wounds in aggressive encounters (=lower social rank individuals) are less likely to become infected by Tasmanian devil facial tumor disease than individuals with fewer head wounds (=more aggressive/higher social rank individuals).

In a recent study, Seaman and Briffa (2015) set out to determine (1) whether snails have personalities and (2) whether snail personality traits are related to trematode infection status. The personality trait that they considered was “re-opening” time, which was a measure of how reluctant the snail was to re-open it’s operculum after being poked by the investigator. I’m not ashamed to say that this reads like an excerpt from the description of my dream job: “All observations were carried out by a single observer who had practised touching snail’s feet with a consistent level of pressure.”

Seaman and Briffa (2015) found that snails did have consistent responses to the mock predation encounters, where individual snails took consistently more or less time than average to re-open their operculum. Additionally, snails that were first intermediate hosts for trematodes (i.e., castrated snails) had longer re-open times, on average.

Because Seaman and Briffa (2015) used uninfected and infected field snails – as opposed to experimentally infecting their snails – it is unclear whether the differences in snail opening times is driven by infection, or whether the differences in opening times somehow affects the probability of becoming infected. Even if infection is driving the different mean response times, it doesn’t mean that the parasites are manipulating the snails. For instance, it might just be that infected snails are showing a sickness response, which makes them act sluggish. (Heh, get it?) Or it could be that the trematodes are manipulating the snails to make them behave more cautiously, thereby decreasing the probability that the host (and parasites!) gets eaten by a predator.

Because there are multiple potential mechanisms at work, I couldn’t decide on the dialogue of this cartoon. So, pick your favorite!





Seaman, B., and M. Briffa. 2015. Parasites and personality in periwinkles (Littorina littorea): Infection status is associated with mean-level boldness but not repeatability. Behavioural Processes.

Why are caterpillars hairy?

Why is it advantageous to be a hairy caterpillar? One answer can be found in a beautiful paper by Sugiura and Yamazaki (2014). They put five species of caterpillars with various amounts of hairiness in containers with carabid beetles that naturally prey on caterpillars. The carabid beetles were always successful when attacking the smooth/hairless caterpillar species, and it usually only took beetles one try to successfully catch the caterpillar. When attacking a short-haired caterpillar species, the carabid beetles were still always successful, but it took them more tries. And when attacking a long-haired caterpillar species, the carabid beetles were only successful ~50% of the time. Even when they were successful, it took beetles more attempts to catch the caterpillars. Therefore, it looked like long hair protected caterpillars from beetle attacks. To test that idea, Sugiura and Yamazaki (2014) gave the long-haired caterpillars haircuts, so that the hairs were shorter than the beetles’ mandibles. The beetles were then way more successful at attacking the caterpillars with haircuts than the long-haired caterpillars! Now that is sexy science.

So, long-haired caterpillars are out there multiplying like crazy while their short-haired neighbors are getting mown down by beetles, right? Actually, having hairs may be a trade-off. Hairy caterpillars are more likely to be attacked by parasitoids, and a higher diversity of parasitoids attack hairy caterpillars than smooth caterpillars (Stireman and Singer 2003)! It might be beneficial for parasitoids to stick their eggs in hairy caterpillars because the eggs+caterpillars will be less likely to be eaten by a predator before the parasitoid emerges than if the caterpillar is smooth. Or it may be that hairy caterpillars – which are usually not cryptic – are easier for parasitoids to find. Either way, these papers have changed my life.



Stireman, J.O., and M.S. Singer. 2003. Determinants of parasitoid-host associations: insights from a natural tachinid-lepidopteran community. Ecology 84(2): 296-310.

Sugiura, S., and K. Yamazaki. 2014. Caterpillar hair as a physical barrier against invertebrate predators. Behavioral Ecology 25(4): 975–983.

ASP Teaching Parasitology Symposium

Sadly, I’m not going to the American Society of Parasitologists conference this year. I’m bummed, because I’m missing the awesome talks in the Teaching Parasitology Symposium and the Science Outreach in the Classroom and Beyond session. The talks include:




And because nothing is quite as beautiful as the marriage of math and parasites, my personal favorite:


If you’re going to ASP 2015 and you’d like to do a guest post about the things you learn from these cool talks, let me know! I’m sure I’m not the only person who would like to live vicariously through you.