Hungry hungry (hygienic) ibex

Alpine ibex (Capra ibex) is a wild goat species that lives in the European Alps. Like other ungulates, it eats plants, defecates, eats more plants, and continues on its merry way. The ibex, unlike contemporary humans, does not have access to a toilet, latrine, or other location designated specifically for feces. Some of us might cringe at the ibex’s corresponding lack of hygiene – depositing previously eaten food near where it is now eating food does not seem like a good idea. However, the ibex does have certain behaviors that make it more hygienic.

poop pictureA recent study by Brambilla et al. (2013) investigated the foraging behaviors of ibex in their natural habitat. The authors recorded foraging locations of marked individuals, and counted the fecal pellets in foraging areas vs. patches in which the ibex did not feed (“avoided” patches). “Avoided” patches were chosen as the midway point between two foraging patches. While admittedly arbitrary, such a measure seems practical, since one cannot ask an ibex why it fed in one spot versus another. The authors compared the number of fecal pellets in the first foraging patch to the “avoided” patch. The authors discovered that grazed plots had a lower density of fecal pellets than avoided plots, and that individuals consistently differed in their avoidance behavior, but that such differences did not correlate with individual age or infection status (infection status was assessed from feces obtained from marked individuals).

poop travels

These results are interesting for a variety of reasons. For example, while ibex do not have toilets, they do avoid feces, a behavior analogous to our own feces-avoidance behaviors. Further, individual ibex vary in their feces avoidance behaviors, just as humans vary in their hygiene. Some people, for instance, are more likely to eat food off the floor, or more regularly wash their hands. These differences can be attributed to personality. Someone’s hygiene can thought of as part of their personality. Likewise, ibex have hygiene personality too. Interestingly, such personality does not seem to correlate, in the ibex, with their infection status or age. Apparently infected or older ibex are no more or less cautious around feces than uninfected or younger ibex. Thus, just as for humans, how the consistent ibex behavioral differences arise remains unknown.


Brambilla, A., von Hardenberg, A., Kristo, O., Bassano, B. & Bogliani, G. (2013). Don’t spit in the soup: faecal avoidance in foraging wild Alpine ibex, Capra ibex. Animal Behaviour, 86, 153-158.

Snails are Snowflakes

Have you ever heard someone say, or thought to yourself, “You are unique”? Of course you have. It’s a pretty common phrase. We’re all snowflakes. Among other sources, our personalities create this variation. No one behaves the same as someone else in all circumstances. Perhaps some individuals will behave similarly in some circumstances, but even then, their behavior would not be exactly the same. Such a statement likely surprises no one, but would it surprise you to hear that snails have personality?

They do! People who study animal behavior often define personality as consistent individual differences in behavior, meaning that individual A behaves in a consistent way that differs from the consistent behavior of individual B. For example, if one were to test the response of individuals to a new object (say, by measuring how close the individual would get to the object), over the course of repeated tests, one individual might consistently get closer to the object than another individual, who consistently stayed farther away. These individuals would be said to have personality.

In a recent study with a marine snail, the common periwinkle (Littorina littorea), and one of its parasites, the authors found that their snails displayed personality, which also varied with infection. Specifically, after removing a snail from the water and poking it, then placing the snail back in the water, the authors timed how long until the snail reemerged from the shell. Interestingly, the authors found that individual snails (each measured three times) differed consistently in how long they remained inside their shell. Snails, furthermore, differed by infection status, with infected snails remaining inside their shells for longer on average than uninfected snails. So all snails had a different and relatively consistent hiding time, but on average, infected snails remained inside their shells for longer periods. Snails are snowflakes too!

But what about those infection results? Did infection change the behavior of snails, or were uninfected snails with certain personalities more likely to acquire infection? Because the study design did not implement controlled infections, testing behavior before and after infection, the authors noted that they could not answer that question. However, either answer would be interesting, and relevant for humans. For example, if personality influences whether an individual acquires infection, then studying such processes in a snail could inform epidemiology of human diseases (studying disease transmission in snails, or the many other non-human animals that have been shown to display personalities, also circumvents the obvious ethical issues with controlled infections in humans). If infection influences personality, then investigating that process in a snail or other animal could likewise inform disease transmission in humans.


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.

The War of the Parasites

Hey all: Firstly, sorry for the large absence since my last post. Interestingly, I had my own parasite (pneumonia), which put me out of action for a while.

Anyway, to the post!

Hosts often have multiple parasites at a time, and what is good for one parasite may not be good for another parasite.

A real-life example.

The cestode parasite Schistocephalus solidus has a three host life cycle. It first infects copepods (Macrocyclops albidus). Then, three-spined sticklebacks (a fish) acquire the parasite through eating infected copepods. Finally, birds acquire the parasite by eating infected fish. The parasite reproduces inside the bird, releasing further parasites into the environment, which will infect copepods. The circle of life.

life cycle

Such a transmission cycle, in which the parasite moves through consumption of one species by another, is referred to as trophic transmission.

The predictions.

Trophically-transmitted parasites often manipulate the behavior of one of their earlier hosts to facilitate transmission to the final host (see, for example, Moore 2013, Poulin 2010). Normally, we think of these behavioral alterations as making hosts more susceptible to predation by the next host in the life cycle (e.g., Lafferty 1992). Parasites, however, often have development times inside their hosts. By development times, I mean that parasites are not typically infective to the next host in the life cycle immediately upon infecting the current host. Once in a host (say, the copepod), a parasite needs some time before it can successfully infect the next host (the fish). If the parasite’s host were to be eaten before the parasite was infective to its next host, then the parasite would die, even it were eaten by the correct next host. For this reason, many authors have hypothesized that before the parasite is infective, it should reduce its host’s susceptibility to predation (e.g., by increasing host hiding behaviors). Other authors have further noted that if a host is infected by parasites at different developmental stages (parasitized by both infective and uninfective stages), then the different parasites may attempt to sabotage the manipulation of the other. For example, the infective parasite may prevent the uninfective parasite from reducing the host’s susceptibility to predation. Crazy (cool), right?

Hypothesis Tested

Hafer and Milinski (2015) tested this idea with S. solidus in its copepod host. Just ignoring all the details about statistics and experimental design (who cares about that anyway?), here are their results: Hafer and Milinski found that copepods infected with different stages of parasite experienced sabotage of behavioral manipulation. When copepods were infected with two parasites, which were both infective, then the copepods displayed reduced anti-predator behaviors. Likewise, when both parasites were uninfective, the copepods exhibited increased anti-predator behaviors. But when copepods were infected with one infective and one uninfective parasite, then the copepods still demonstrated reduced anti-predator behaviors. The uninfective parasites lost out! The manipulation by the infective parasites prevented that by the uninfective parasites.

only one


Hafer, N. and M. Milinski (2015). “When parasites disagree: Evidence for parasite‐induced sabotage of host manipulation.” Evolution.

Lafferty, K. D. (1992). Foraging on prey that are modified by parasites. American Naturalist.

Moore, J. 2013. An overview of parasite-induced behavioral alterations – and some lessons from bats. Journal of Experimental Biology.

Poulin, R. 2010. Parasite manipulation of host behavior: an update and frequently asked questions. Advances in the Study of Behavior.

Sex Matters

Because of the differences between male and female physiology, males and females can have different reactions to the same parasite. These variable responses can have important consequences for parasite-host interactions and the overall transmission of the parasite. Take, for example, a relatively recent study of great tits (Parus major, a bird).

Dunn et al. (2011) explored the effect of malarial infection on the behavior of male and female great tits. While the differences between males and females are obvious in many species, sex-specific differences in behavior due to infection are not often investigated. Anyway, in their study, the authors captured wild birds, and compared the behavior of infected and uninfected birds, as well as a number of physiological measurements. A quick summary of the results: Infected males were more likely to problem solve (in this case pulling a lever to release food) than uninfected males, but infected females were less likely to problem solve than their uninfected counterparts. Infected females were more exploratory (exploration of a novel room) than uninfected females, but infection did not influence male exploratory behavior. Infected males were more risk averse (retreating from a disturbance – noise caused by stick movement) than uninfected males, but infection did not affect females.

What does all this mean, exactly? Well, one of two things: One, males who get infected differ from females who get infected. Or two, infection changes the behavior of males and females differently. The first scenario argues that infection does not change behavior, that certain behaviors instead make individuals more or less likely to become infected. According to Dunn et al. (2011), for example, problem solving males should be more adept at using different food resources, and exposure to those different food resources should expose the birds to more parasites than males who are less capable at problem solving and therefore use fewer food resource types. The second scenario asserts that infection itself changes behavior, either as a host response to the parasite or direct manipulation by the parasite. While one can generally use information about the biological system to hypothesize whether behavior causes infection or vice versa, the truly definitive way to test this question would be to do controlled infections and monitor behavior before and after infection.

Such distinctions, as well as male vs. female behavioral differences, can be important for a number of reasons. They might, for instance, affect species management programs. If one had a species infected with a parasite, and one thought that bold individuals were more likely to acquire and spread that parasite, one might imagine a culling or vaccination program that focused on bold individuals to decrease future parasite transmission. However, if infection makes individuals bold, this program could be relatively pointless. If one of the two sexes, moreover, is predominantly responsible for transmission of the parasite, one might focus isolation, vaccination, or culling efforts on that sex. One could probably list many other examples in which sex differences and the direction of causality in behavior-infection connections matter.

Or, one could end the blog. To finish, then: Sex matters.


Dunn, J.C., Cole, E.F. & Quinn, J.L. (2011). Personality and parasites: sex-dependent associations between avian malaria infection and multiple behavioural traits. Behavioral Ecology and Sociobiology, 65, 1459-1471.

Parasites and the Benficial Predator?

Parasites and predators, generally speaking, negatively affect the organisms that they use (i.e., parasites hurt their hosts, and predators are obviously deleterious for prey). However, as I mentioned in the last blog, in ecology everything depends (on the details). Here, I will focus on some of the complications that can arise when one considers the effects of parasites and predators together.

First off, parasites can be eaten. They can be eaten when they are inside a host, and that consumption can put the parasites in the right or wrong host (the right host would be the one in which the parasite can complete its life cycle). For example, improperly cooked pork can contain parasites (e.g., Taenia solium). These parasites do not “want” to get into humans; they cannot complete their life cycles inside humans, and instead tend to cause huge problems. Parasites can also be eaten when they are outside the host. Many parasites have free-living stages in the environment, and they need to be consumed in order to continue their life cycle. Such consumption can also lead the parasite to the right or wrong host (Johnson et al. 2010).

Both of the above consumptive scenarios (a parasite being eaten when it is in or outside of the host) contribute to parasite population dynamics (how large is the parasite population, how many hosts are infected, what proportion of hosts is infected). One could thus imagine that predation could facilitate or hinder parasite transmission. For instance, if hosts acquire more energy from eating parasite-infected prey than they lose from the infection, hosts might do better if they ate parasite-infected prey, and therefore predation could increase parasite transmission. But if non-host predators eat parasites in the environment or prey with parasites, then these predators might reduce transmission to the host species (Johnson et al. 2010, Lafferty & Morris 1996).

Importantly, predators also affect their prey by more than just killing the prey. As any hunter can tell you, prey tend to run or fight back when encountered with a predator. If prey survive a predation attempt, they tend to alter their behavior to reduce predation risk (e.g., increase hiding time and reduce foraging time). Such behavioral changes can happen even if the prey never experienced a direct predator attack. Simply exposure to the smell/sight/etc. of a predator, or the smell/vision/etc. of other dead prey, can elicit behavioral changes in prey. These behavioral changes may also affect that prey’s exposure to parasites. If, for example, prey are more likely to encounter parasites by staying in one place and reducing activity, predators may indirectly increase parasitism among prey. The opposite may occur, however, if prey activity increases exposure to parasites.

In a recently published paper, a group of authors attempted to discern whether the combination of these factors – predators eating parasites and predator effects on host behavior – sum to positively or negatively affect parasite transmission to hosts. Orlofske et al. (2014) found that in the presence of a predator (a dragonfly larvae), tadpoles reduced activity and acquired more parasites. Other authors have previously demonstrated that active tadpoles acquire fewer parasites than anesthetized tadpoles, so activity was the key factor driving the increase in parasitism in this study. Interestingly however, the authors also discovered that the purported predator (damselfly larvae) of the free-living form of the parasite in question (a trematode) did not actually eat the parasite in a more realistic experimental setting (but it did in previous laboratory studies). Further, damselfly larvae caused the same reduction in activity among the tadpoles as the dragonfly larvae, even though the damselflies are not predators of the tadpoles.

\While this study did not reveal that parasite predators reduce infection intensity (contrary to expectation), it did validate the idea that host predators should be expected to increase parasitism when predator behavioral responses work against anti-parasite behaviors. It also highlights the notion that everything in ecology depends on the details, and concepts that bear fruit in lab settings may not do so in the field for a variety of reasons.



Orlofske, S.A., Jadin, R.C., Hoverman, J.T. & Johnson, P.T.J. (2014). Predation and disease: understanding the effects of predators at several trophic levels on pathogen transmission. Freshwater Biology 59(5): 1064–1075

Johnson, P.T.J., Dobson, A., Lafferty, K.D., Marcogliese, D.J., Memmott, J., Orlofske, S.A., Poulin, R., & Thieltges, D.W. (2010). When parasites become prey: ecological and epidemiological significance of eating parasites. Trends in Ecology and Evolution 25(6): 362-371

Lafferty, K.D. & Morris, A.K. (1996). Altered behavior of parasitized killifish increases susceptibility to predation by bird final hosts. Ecology 77:1390-1397.