Are you super?

Disease ecology often uses the term, “super-spreader,” which describes an individual responsible for a disproportionate amount of disease transmission. For example, in the diagram below, each circle or triangle represents an infected individual. Each circle infects four more circles, but each triangle infects only one. After only a few rounds of infection, there are far more circles than triangles, and the circles would be called super-spreaders.transmission

However, the spread of infection depends on more than the transmitter. Some individuals may be far more likely to receive an infection than others (these individuals could be called “super-receivers”).

super receivers

As one might guess, if an individual were both a super-spreader and a super-receiver, they would greatly impact disease spread in a population. Whether such individuals exist, however, remains an open question.

Adelman et al. (2015) recently investigated this question in house finches (Haemorhous mexicanus) and their bacterial parasite, Mycoplasma gallisepticum, which causes conjunctivitis. The authors performed two studies. In the first, they monitored the presence of tagged birds at feeders in order assess feeder use, aggressive interactions at feeders, and aspects of sociality (such as local bird group size, number of birds with which a focal bird usually feeds, and a few others). The authors then compared these measures with the presence of infection. Interestingly, the authors found limited connection between a bird’s aggressive or social interactions and whether that bird was infected. But feeder use did strongly associate with infection. Birds that spent more time foraging at feeders were more likely to be infected.

However, because this study did not manipulate infection, it was unclear whether spending more time at feeders led to infection, or whether infection led to increased time at feeders. Consequently, in a second study, Adelman et al. created artificial bird groups in captivity, where each bird had a known foraging propensity. Then, the authors introduced the infection to each group, but to a bird of different foraging propensity each time. In this experiment, the infection spread faster in groups in which the initial infection was on a bird that spent more time at feeders. Although, because groups for which the initial infection was on a “high time forager” also had higher average foraging times than groups for which the initial infection was on a “low time forager,” the result that the parasite spread faster in the “high time forager” groups could be due to the initial individual infected or the high average foraging of the group. Foraging clearly affects transmission of the disease, but it is still unclear whether foraging does so through super-spreaders, super-receivers, or both.


Adelman, J.S., Moyers, S.C., Farine, D.R. & Hawley, D.M. (2015). Feeder use predicts both acquisition and transmission of a contagious pathogen in a North American songbird. Proceedings. Biological sciences / The Royal Society, 282.


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.

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.

Does your behavior influence your immune system?

I previously wrote an article about how behavior can influence transmission. In that piece, I focused on behaviors that can increase transmission (in some cases, bolder individuals can be more likely to contract a particular parasite because their boldness may lead them to make risky decisions, such as fighting with infected individuals). However, to provide a fuller picture of host behavior in parasite transmission dynamics, I decided that I should now talk about how behaviors can influence parasite infection in a way that benefits the host.

I cannot speak with authority for disease ecologists as a group, but generally speaking I think we all realize that host behavior is very important for parasite transmission. Unfortunately, the effects of behavior can be very hard to quantify. Even in systems in which behavior and parasite transmission can be linked, demonstrating causality becomes incredibly difficult. For example, in my earlier post on boldness and parasite transmission, Dizney and Dearing (2013) could not determine whether infection caused the boldness, or whether boldness determined infection. It seemed likely that boldness was influencing infection given the biology of the system, but this inference was by no means proven beyond all doubt. Thankfully, such hindrances are not universal.

Daly and Johnson (2011), for instance, performed simple, yet elegant experiments with tadpoles. By comparing the number of infections anesthetized tadpoles and regular tadpoles received, the authors elucidated the effect of tadpole behavior on parasite infection (the authors had shown previously that anesthesia does not affect tadpole physiology or immunity). Anesthetized tadpoles had a much greater number of parasites (in this case trematodes) than the control tadpoles, demonstrating that tadpole behavior protected the tadpoles from infection. Expanding upon these results, another group determined that tadpole behavior also influenced the location of the parasite infections (Sears et al. 2013). Anesthetized tadpoles sustained the majority of their infections in the head, while untreated tadpoles suffered them in the tail. As one might imagine, parasites in the brain are a much more serious infection than in the tail, especially because these tadpoles lose their tails in the course of their development. Thus, tadpole behavior not only reduced the number of infections the tadpoles suffered, but also shunted the infections that they did receive to less critical areas.

If these examples seem a tad different from any human disease (who has heard of someone being able to control whether a cold causes headaches or congestion), house finches may provide a more relevant example. Recent work with house finches has demonstrated a number of interesting correlations among behavior, infection status, and the immune system. For example, in a study testing house finch preference to associate with a sick or healthy bird, house finch males chose to associate with a healthy male more than a sick one, and males that were closer to the sick bird invested more in immune defense than finches that chose to be farther away (Zylberberg et al. 2013). In another house finch study, similarly, male birds that invested more in surveillance behaviors (which are thought to reduce parasite exposure because the finch would not be blindly entering a novel area or eating a novel food) invested less in immune defense. Furthermore, as male avoidance of novelty decreased, investment in immunity increased (Zylberberg et al. 2014). Thus, house finch males appear to balance investment in anti-parasite immunity and behavior – as investment in behavioral defenses increase, immunity declines, and vice versa. These results may be more applicable to humans in that while we cannot control where a parasite infects us (as far as I know), we can perform behaviors akin to the house finches: We can control whether we choose to go to work when we are sick, or how much we wash our hands, or whether we eat food off the floor (e.g., “the 10 second rule”). It remains unknown whether such behaviors, or lack thereof, correlate with the immune system in humans as they do in house finches. If they do, the next question becomes “why?” Why should some individuals invest in behavior and others the immune system? Do individuals differ at birth or during childhood in some way that set them on a behavior or immune system course? Are these differences selectively favored? Perhaps a population with mixed defense strategies survives better through time than one in which all individuals use the same parasite defense strategy? Perhaps things to think about the next time you are debating whether the 10 or 30 second rule applies.


Daly, E. W., and P. T. J. Johnson. 2011. Beyond immunity: quantifying the effects of host anti-parasite behavior on parasite transmission. Oecologia 165:1043-1050.

Dizney, L., and M. D. Dearing. 2013. The role of behavioural heterogeneity on infection patterns: implications for pathogen transmission. Anim Behav 86.

Sears, B. F., P. W. Snyder, and J. R. Rohr. 2013. Infection deflection: hosts control parasite location with behaviour to improve tolerance. Proceedings of the Royal Society B-Biological Sciences 280:5.

Zylberberg, M., K. C. Klasing, and T. P. Hahn. 2013. House finches (Carpodacus mexicanus) balance investment in behavioral and immunological defenses against pathogens. Integrative and Comparative Biology 53:E400.

Zylberberg, M., K. C. Klasing, and T. P. Hahn. 2014. In house finches, Haemorhous mexicanus, risk takers invest more in innate immune function. Animal Behaviour 89:115-122.