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.