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.

Are the majority of human EIDs really zoonotic?

 In 2001, Taylor et al. reviewed more than 1415 pathogens that infect humans. They found that 61% of those pathogens were zoonotic, meaning that they are transmitted between animals and humans. Furthermore, 75% of the pathogens classified as causative agents of emerging infectious diseases of humans were considered zoonotic. Clearly, if we want to understand pathogen transmission in human populations, we need to understand how these pathogens are spilling over from wildlife populations. But here’s a sensational question for you: are the statistics that I just summarized accurate?

Before I speculate further, I need to introduce a category of pathogens that may be commonly overlooked: sapronoses. Unlike ‘typical’ pathogens (whatever that means), sapronoses do not need a host to survive. While sapronoses might replicate in a host or even be transmitted among hosts, they can also reproduce and flourish in the environment outside of the host indefinitely. In contrast, pathogens with free-living stages eventually need a host to complete their life cycle.

Brain eating amoebas are one example of a sapronosis. These amoebas typically live in the environment, but they can accidentally enter the human body through the nose. For instance, this might occur when a human is swimming in water containing the amoebas. From there, the protist feeds on nervous tissue, and the human host almost always dies due to infection. Because the amoebas don’t really need a host for reproduction or transmission among environments, there is no selection pressure for the amoebas to keep their hosts healthy for longer periods by evolving reduced virulence. And because the amoebas aren’t transmitted directly among hosts, treating or quarantining infected people won’t reduce the probability that other humans become infected. Instead, limiting human contact with contaminated environments or treating contaminated environments to eradicate the sapronotic agent are the only ways to reduce transmission to other hosts.  Some other examples of sapronoses are anthrax, cholera, and tetanus.

Ok, back to my sensational question:

Kuris et al. (2014) reviewed a subsample of the human pathogens that Taylor et al. (2001) reviewed previously, and Kuris et al. (2014) found that one third of the subsampled pathogens were sapronoses. Cool! When they broke down the percentages by taxa, almost 100% of the fungi that they examined were sapronotic/saprophytic, as well as ~29% of the bacteria and ~13% of the protists. When Taylor et al. (2001) classified the pathogens, they found 113 zoonotic fungi. But Kuris et al. (2014) argue that their subsample suggests that almost all of the fungi should be saprophytic, not zoonotic. It may be that Taylor et al. (2001) classified saprophytic pathogens as zoonotic pathogens, leading to an overestimate of the proportion of human pathogens that are zoonotic.

I think it’s still safe to say that most human pathogens have an environmental and/or animal reservoir. Additionally, even though the proportion of human pathogens that are zoonotic might be less than “the majority” (i.e., <50%), a large proportion of the human pathogens would still be classified as zoonotic, even after reclassifying the potentially sapronotic pathogens. But Kuris et al. (2014) bring up a subtle point that deserves more attention: just because animals can be infected by a human pathogen doesn’t mean that there is transmission of the pathogen between animals and humans. Neat stuff!


Kuris, A.M., K.D. Lafferty, and S.H. Sokolow. 2014. Sapronosis: a distinctive type of infectious agent. Trends in Parasitology 30(8): 386-393.

Taylor, L.H, S.M. Latham, and M.E. Woolhouse. 2001. Risk factors for human disease emergence. Philos. Trans. R. Soc. Lond. B: Biol. Sci. 356: 983–989.

Will Tasmanian devils soon go extinct?

Last week, we talked about Tasmanian devil facial tumor disease, which is caused by an infectious cancer that is transmitted after a susceptible devil bites a tumor on an infected devil. After becoming infected, devils almost always die within several months. As the disease has spread through their range, devil populations have drastically declined, and there is great concern that the devils will go extinct in the near future. But not all infectious diseases that cause high host mortality will lead to host extinction, so what is special about Tasmanian devil facial tumor disease?

A while ago, I posted about the difference between pathogens with density dependent and frequency dependent transmission dynamics. To recap: when transmission is density dependent, the rate of host contacts (and thus pathogen transmission) increases with host density. When transmission is frequency dependent, the rate of host contacts (and thus pathogen transmission) does not change with host density. This means that as a host population crashes due to high mortality from an infectious disease, the transmission rates of pathogens with density dependent transmission will decline, but the transmission rates of pathogens with frequency dependent transmission will not change. Therefore, it isn’t possible for pathogens with density dependent transmission to be the cause of host extinction, because the pathogen will go extinct due to low transmission rates before the host goes extinct. (Note, however, that pathogens with density dependent transmission might cause declines in a host population that make the host population more susceptible to local extinctions due to stochastic events, like bad breeding years.)

Historically, only sexually transmitted pathogens and vector transmitted pathogens were thought to have frequency dependent transmission. And we know that Tasmanian devil facial tumor disease is not sexually transmitted or vector transmitted. However, McCallum et al. (2009) found that models with frequency dependent transmission fit mark-recapture data for devil disease dynamics better than models with density dependent transmission. How can that be? Well, it might that the number of aggressive encounters between individuals is not dependent on host density; for instance, if confrontations at carcasses continue to be likely to occur even as populations decline.

When pathogens utilize frequency dependent transmission, we know that unselective culling to reduce the number/density of susceptible hosts won’t stop a pathogen from invading a naïve host population. That’s because no matter how many individuals you cull, you won’t reduce the actual pathogen transmission rate, which is independent of host density. But what if instead of unselective culling, we try to stop the spread of Tasmanian devil facial tumor disease by selectively culling infected individuals? A culling program was undertaken to try this, but it was not effective (Lachish et al. 2010). Beeton and McCallum (2011) used epidemiological models to show that while selective culling might be effective, the rate of culling that would be necessary is just too high to be logistically possible given current resources.

Tasmanian devils have been the largest extant marsupial carnivore since the thylacine went extinct. What will happen if the Tasmanian devil goes extinct? Well, there are already documented changes in the animal communities in Tasmania that might be caused by devil declines, where the abundances of some species (e.g., feral cats) have increased and the abundances of other species (e.g., eastern quoll – so cute!) have decreased (Hollings et al. 2014). But the long term changes that will result from devil population declines (or full extinction) are hard to predict.

It’s a rough time to be a marsupial.


Beeton, N. and H. McCallum. 2011. Models predict that culling is not a feasible strategy to prevent extinction of Tasmanian devils from facial tumour disease. Journal of Applied Ecology, 48: 1315–1323.

Hollings, T., M. Jones, N. Mooney, and H. McCallum. 2014. Trophic cascades following the disease-induced decline of an apex predator, the Tasmanian devil. Conservation Biology 28(1): 63-75.

Lachish, S., H. McCallum, D. Mann, C.E. Pukk, and M.E. Jones. 2010. Evaluation of selective culling of infected individuals to control tasmanian devil facial tumor disease. Conservation Biology 24(3): 841-851.

McCallum, H., M. Jones, C. Hawkins, R. Hamede, S. Lachish, D. Sinn, N. Beeton, and B. Lazenby. 2009. Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction. Ecology 90(12): 3379–3392.

Transmission of Tasmanian devil facial tumor disease

Tasmanian devils are threatened by one of the craziest pathogens I’ve ever heard of: an infectious cancer. You might be wondering, “How the heck can a cancer be infectious? Shouldn’t the host’s immune system recognize the parasitic cells as foreign and kill them?” Well, yeah, it should. But Tasmanian devils have very low genetic diversity in their Major Histocompatibility Complex (MHC) genes, a group of immune system genes associated with recognizing foreign/non-self materials. As a result, Tasmanian devil immune systems can’t tell that the parasitic cell line is different from the animals’ own cells. Major bummer!

So, how is this infectious cancer transmitted among Tasmanian devils? Well, you’ve probably heard that devils are very aggressive: males fight over females during the breeding season and females will fight to defend their dens. There is also fighting over carcasses. So, there’s lots of biting happening among devils, and many of these bites occur on the devils’ heads. And guess what? The infectious tumors usually occur on the faces of devils, which is why the disease is called Tasmanian devil facial tumor disease. So, people suspected for a long time that biting and transmission were linked.

Ok, now for the cool part! Hamede et al. (2013) hypothesized that the devils with the most bites on their heads would be the most likely to become infected by Tasmanian devil facial tumor disease. However, they found the opposite trend! The devils with the most bites on their heads were less likely to become infected. Hamede et al. (2013) suggested that instead of an infected biter transmitting the infectious cells to an uninfected bite recipient (more bites on devil = higher infection probability), it may be that uninfected biters become infected after biting the tumors of infected bite recipients (more bites given to other devils = higher infection probability). Devils often have open mouth wounds and the tumors often start growing inside the oral cavity, and these observations support the idea of infection resulting from biting tumors.


Dominant individuals are probably more likely to do lots of biting (as opposed to receiving many bites), so it may be that dominant individuals have higher risk of infection. This is a really cool possibility, because it suggests that some hosts (in this case the dominant individuals) in a population are “super receivers” of infection. A lot of attention has been given to disease super spreaders, like Typhoid Mary, and the super receiver concept is a neat addition to our understanding of heterogeneity in pathogen transmission rates.

Finally, I just want to point out that not all infectious cancers are transmitted by biting. For instance, there’s an infectious cancer of canines that is sexually transmitted. Crazy!


Hamede, R.K., H. McCallum, and M. Jones. 2013. Biting injuries and transmission of Tasmanian devil facial tumour disease. Journal of Animal Ecology 82: 182-190.

Biological control of schistosomiasis: prawn terminators

Schistosomiasis is the second most common parasitic disease infecting humans. (The first is malaria.) According to The Global Network for Neglected Tropical Diseases, 240 million people in 78 countries are infected by schistosomes at this moment. This disease kills hundreds of thousands of people each year.

Of course, most of the people afflicted by schistosomiasis live in tropical and subtropical regions, especially in poor regions with limited water availability and inadequate water sanitation. Therefore, the average US citizen probably hasn’t even heard of schistosomiasis. So, briefly, schistosomiasis is a disease caused by a parasitic worm, called a trematode. Schistosome trematodes have complex life cycles, as depicted by the CDC diagram here. When infected humans urinate or defecate in bodies of water, the eggs of the parasite are released and hatch in the water. A free-living larval parasite, called a miracidium, swims around until it finds a snail to infect. Later, the infected snail releases more free-living larvae, called cercariae, and these swim through the environment until they find a human to infect. In water bodies with infected snails that are releasing cercariae, humans can get infected whenever they contact water for swimming, bathing, or water-collecting purposes.

The global burden of schistosomiasis is huge, so there is great imperative to figure out a way to control transmission of schistosomes to humans. The most common control strategy is an antihelmentic drug for humans (praziquantel). When entire communities of people are treated, the health of the treated individuals improves, and the chain of transmission from humans to snails is broken. Another control method involves using chemicals (molluscicides) to kill the snails in particular water bodies. However, those chemicals can have unintended adverse effects on non-snail organisms living the same water bodies. Additionally, both control methods tend to be temporary in nature – if the treatments aren’t kept up, snails can be reintroduced into the water bodies and/or humans can become infected with new adult parasites.

This brings me to the topic of this post: biological control of schistosomiasis as a supplement to existing control strategies. As far as I know, biological control of schistosomiasis isn’t being used in a major way in any control programs. But there is a lot of interest in this type of control, and I’ve seen several recent papers on this topic that I wanted to share:

  • Introduce snail parasites: Duval et al. (2015) recently discovered a bacterial pathogen of snails (Paenibacillus glabratella) that causes high snail mortality. The pathogen is also transmitted from adult snails to eggs, and infected eggs are less likely to hatch successfully. So, this bacterium might be a promising biocontrol option! However, it’s unclear at this point whether the bacteria are specific to the snails that are intermediate hosts for schistosomes, or if the bacteria would infect many invertebrate species.
  • Introduce snail competitors or predators: There has been interest in using competing snail species and predators of snails to control snail populations for a long time. Of course, these biocontrol agents need to have a strong enough effect on the target snail species that they greatly reduce or eliminate populations of the target species. And ideally, the biocontrol agents won’t wreak havoc on any other species, even after the target species has been eliminated. Sokolow et al. (2014) recently showed that river prawns are voracious predators of snails when the two are maintained together in the laboratory. Furthermore, Sokolow et al. (2014) point out that prawns are nutritious, delicious, and sell for high prices, and local people could harvest the larger prawns for food while leaving the small and medium prawns to do their snail terminating. WIN-WIN.
  • Introduce parasite predators: The free-living larvae that trematodes use for transmission between hosts are susceptible to predation by all kinds of animals: fish, dragonfly and damselfly larvae, filter-feeding invertebrates, etc. My personal favorite is an oligochaete worm (Chaetogaster limnaei) that lives symbiotically on the snail and eats both miracidia and cercariae. People often suggest that these parasite predators could control trematode transmission, including the transmission of the trematode species that cause schistosomiasis and the related trematodes that cause Swimmer’s Itch. Cool stuff!


(Added to the list of things I cannot draw: motorcycles.)


Duval D, Galinier R, Mouahid G, Toulza E, Allienne JF, et al. (2015) A Novel Bacterial Pathogen of Biomphalaria glabrata: A Potential Weapon for Schistosomiasis Control? PLoS Negl Trop Dis 9(2): e0003489.

Sokolow, S.H., K.D. Lafferty, and A.M. Kuris. 2014. Regulation of laboratory populations of snails (Biomphalaria and Bulinus spp.) by river prawns, Macrobrachium spp. (Decapoda, Palaemonidae): Implications for control of schistosomiasis. Acta Tropica 132: 64–74.