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.