Reciprocal feedbacks between animal sociality and infection-induced behavioral changes
Pathogens can trigger diverse changes in host social behaviors: Avoidance, enforced exclusion of infected conspecifics, proactive social distancing, active self-isolation, and passive self-isolation. Passive self-isolation (from sickness behaviors like lethargy) is perhaps the most common response; it is triggered by the animal’s inflammatory response (e.g., pro-inflammatory cytokines) and reduces contact between the infected individual and healthy group members. Isolation of an individual from a social group, however, can pose significant fitness costs if it harms social integration, status, or relationships. To persist over evolutionary or even ecologically relevant timescales, these costs should be outweighed by benefits (e.g. physiological benefits such as conserving energy to fight an infection). Our research explores this delicate balance of costs and benefits and broadly asks the question of when it is adaptive to “behave sick”. We use injections of immunostimulants in highly social and cooperative common vampire bats (Desmodus rotundus) to investigate costs and benefits of passive self-isolation. In the future, we plan to extend this research to comparative studies in other bat species that vary in their social structure and life history traits.
Questions: What are social costs of being sick? What are the physiological benefits that counteract these costs? To what extend does the inflammatory response affect social behaviors and vice versa? How has passive-self isolation evolved?
Co-evolution of host social behavior and infectious pathogens
Immunostimulants are widely used to evaluate social costs and physiological benefits of behavioral responses to pathogens. However, far less research has approached this question using actual pathogens that co-evolved with their hosts. The strength and nature of infection-induced behavioral changes is a key element of host-pathogen coevolution. For instance, socially transmitted pathogens can evolve counter-adaptations to a host’s behavioral response that reduces their transmission. Vampire bats are infected with a range of bacterial and viral pathogens that are spread by their many social interactions such as grooming, foodsharing or aggressive encounters. We study the behavioral effects of these naturally occurring and co-evolving pathogens using experimental infections and behavioral observations of individuals, when alone and embedded in their social networks. So far, we have collected behavioral data from rabies infected vampire bats suggesting strain-specific behavioral responses, but we intend to explore this in other vampire bat/pathogen systems as well.
Questions: How do naturally occurring pathogens affect (or even manipulate) host social behaviors? What are the physiological, neurological, and immunological mechanisms underlying these behavioral changes?
Fine-scale behavioral patterns of cross-species transmission
The ability to predict cross-species transmission is often restricted by a knowledge gap. How does contact between reservoir and host species facilitate pathogen transmission across species borders? Answers to this question are often limited because it is difficult to measure contacts of animals in the wild. We combine (1) biologging approaches such as highly efficient and miniaturized proximity sensors to simultaneously track encounters among many individuals with (2) molecular methods to quantify genetic similarity of pathogens in samples. By combining these methods, we aim to improve inferences about transmission between species. Currently, we work on contact networks of neotropical vampire bats, their host species (livestock such as cattle), and co-roosting bat species. In the future, we aim to extend this method to investigate fine-scale behavioral interactions in other systems that involve contact between animals or their use of shared spatial locations.
Questions: What are the small-scale behavioral interactions between reservoir and host animals? How do these contact networks correlate with molecular determinants of transmission? Can we use our data to make pathogen-specific predictions of cross-species transmission?