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.

Citations

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.

Advertisements

Should you steal your (sick) co-worker’s food?

Do you have a co-worker, friend, or roommate? If you do, have you ever been in a position to “borrow” that person’s food? Did you? Ethical dilemmas aside, did you consider whether said person was sick?

Let’s say I have a co-worker named Gunter. If I take Gunter’s lunch, I will benefit from acquiring a “free lunch.” However, I might suffer costs if Gunter discovers who took his lunch. When I decide whether to purloin Gunter’s food, therefore, I am conducting a cost-benefit analysis. An additional factor I might include in this analysis could be whether Gunter is sick. If Gunter is sick, for example, I might risk acquiring his infection by eating his food. Such infection would likely more than negate the benefits I obtained from eating Gunter’s food. Gunter’s sickness would consequently dissuade me from “borrowing” his food. But, what if from past experience I know that Gunter gets incredibly angry when anyone borrows his food – except when he is sick. Naturally, he is more displeased about losing his lunch when he is sick than when he is healthy, but when he is sick he doesn’t have the energy to confront anyone about the loss. And now I have a conundrum. I am likely to suffer negative consequences from a healthy Gunter if I am discovered with his lunch. I may also acquire an infection from Gunter if I take his lunch when he is sick. But I am less likely to suffer negative consequences from Gunter at that time, even if I am discovered. So should I steal Gunter’s lunch, and when?

Unfortunately, no simple answer exists for this situation. The answer all depends on the cost:benefit ratio – the benefits I get from Gunter’s food relative to the costs I may suffer from stealing. If benefits are high enough, it would be optimal for me to steal all the time, regardless of Gunter’s state. If benefits are high, but costs due to Gunter’s behavioral response are high, it might only be optimal for me to steal when Gunter is sick.

If you think this example is a little contrived, well, you’re right. But not so much as you might think. For instance, Bouwman and Hawley (2010) discovered that male house finches preferentially fed near males who were infected with a bacterial parasite (mycoplasma), even though feeding sites enabled high transmission rates of the parasite. Bouwman and Hawley also noted that infected males were less aggressive than uninfected males. The authors therefore concluded that males who fed near an infected male benefited from encountering less aggressive males (meaning the former males were more likely to be able to feed without incident). This benefit might or might not outweigh the costs of infection for the population as a whole, but at least at the individual level, benefits appeared to override the consequences.

This house finch result has interesting implications for the evolution of host-parasite interactions. We often think of hosts evolving to maximize fitness, which means reducing parasite costs to an absolute minimum, but this does not have to come from reducing parasite infection to a minimum. If you engage in behaviors that lead to infection, but you get more benefits from those behaviors than the costs of infection, selection will favor that behavior, even though it increases infection.

 

Citations

Bouwman, K. M., and D. M. Hawley. 2010. Sickness behaviour acting as an evolutionary trap? Male house finches preferentially feed near diseased conspecifics. Biology Letters 6:462-465.

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.

Citations

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.