Research Projects

Our research examines patterns and drivers of host-pathogen interactions across multiple scales, from within-host processes to community-level dynamics. We apply field, experimental, molecular, modeling, and database approaches to diverse study systems, including insect pathogens, avian diseases, bat viruses and mammal parasites. Specific themes we address include: (1) The role of host behavior in infectious disease ecology and evolution, (2) Environmental and genetic determinants of host resistance and pathogen virulence, (3) Anthropogenic processes affecting disease dynamics, and (4) Global drivers of pathogen richness across wildlife communities. We also study insect ecology, evolution and conservation, especially through our work with monarch butterflies. Major projects underway by lab members are summarized below:

Seasonal animal migration and infectious disease dynamics

Seasonal long-distance migration occurs in many animal systems, from birds to marine species, terrestrial mammal and insects. Our work linking migrations to infectious disease dynamics has emphasized that even though animal migration is often assumed to enhance the spread of infectious disease, there are several ways that migration can have the opposite effect and actually lower pathogen risk. This can occur through periodic host escape from pathogens that accumulate in the environment over time, and when infected animals migrate less successfully (processes we refer to as migratory escape and migratory culling). We have explored these processes empirically using monarch butterflies and their interactions with a protozoan parasite as a model system, and this work was supported in part by an Early Career Development Award from the National Science Foundation from 2007-2013. Monarchs have a global distribution and are best known for undertaking a spectacular annual migration in N. America, but non-migratory populations also occur throughout the tropics and subtropics. Our work showed that the remarkable geographic variation in parasite prevalence among wild populations likely arises from variation in host migratory propensity, and further provided support for migratory escape and culling in driving down prevalence in the North American migratory populations. More recent work indicated that the energetic demands of migration can generate tradeoffs between lipid reserves (necessary for long-distance journeys) and costly immune defense.

An important part of this work has been the creation and expansion of a citizen science program, now in its 8th year, to monitor infections in wild monarch populations: Project Monarch Health,

Monarch Butterfly Parasites Website

Current and former lab members who contributed to this work include: Alexa Fritzsche, Dara Satterfield, Barbara Han, Becky Bartel, Jaap de Roode

Throughout their breeding range, monarch butterflies (Danaus plexippus) are infected with a protozoan parasite, Ophryocystis elektroscirrha. Monarchs are best known for a spectacular long-distance migration that they undertake yearly in both eastern and western North America. Non-migratory populations also occur in Florida, Hawaii, and other tropical locations. Parasite prevalence differs dramatically among populations, with fewer than 8% of monarchs infected in the eastern US, and over 80% infected in S. Florida. Through long-term studies of monarchs and their parasites, we are investigating the effects of parasitism on monarch fitness, the effect of monarch migration on the dynamics of this host-parasite interaction, the evolution of virulence of the parasite, and environmental and genetic determinants of host resistance.


Global variation in the ecology of mammalian parasites

We continue to examine global-scale patterns of parasitism in wild mammals in collaboration with a larger group of scientists from UGA and 7other institutions. Our comparative studies, funded by the National Science Foundation, NCEAS and Conservation International, have examined how host behavior and environmental variation affect parasite biodiversity, how parasites influence extinction risk and vice versa, and ecological forces and evolutionary constraints that affect traits of the parasites themselves. We have more recent analyses underway to examine the role of host phylogeny and geography in explaining overlap in parasite communities in wild carnivores and ungulates, and just received a Research Coordination Network grant from the NSF EEID panel (2013-2018) to bridge our data with similar records of infectious diseases from other host groups, to develop methods that address issues such as incomplete sampling for parasites and taxonomic and geographic biases, and to test hypotheses about the distribution and diversity of infectious diseases at a global scale. A major goal of this work has been to connect hypotheses that explain pathogen transmission in single-host-single-parasite interactions to understand pathogen diversity at much larger spatial and taxonomic scales.

Global Mammal Parasites Project Website

Current and former lab members who contributed to this work include: Amy Pedersen, Barbara Han, Jamie Winternitz , Shan Huang

A major accomplishment of our work has been to create a comprehensive database of parasites and pathogens reported from primates, carnivores, and ungulates based on reports in the published literature. This now represents over 20,000 lines of data, with a searchable interface published online (see link at right) . We recently updated this information using records published through 2010, and our database represents an important resource for the scientific community and for wildlife managers and public health workers.

Social and mating behavior and infectious disease dynamics

In exploring another type of animal behavior, we have examined the roles of social and mating behavior in infectious disease spread in birds, primates and other mammal species. Earlier comparative work tested whether group size and mating systems predicted variation in primate infectious diseases, including STDs. We also examine the association between seasonal flocking behavior of House Finches and annual outbreaks of a bacterial eye disease (mycoplasmal conjunctivitis). More recently, we've used social network approaches to empirically quantify social contacts in wild apes, and merged these contact networks with epidemic models to predict outbreak size and the efficacy of control strategies. A key result was that control strategies targeted towards animals that are central to the network could avoid outbreaks with a third fewer vaccines than random vaccination. Another recent project took a comparative approach in mammals to show that interspecific variation in the strength of sexual selection explains more immunogenetic variation at the MHC across large numbers of wild mammals than does variation in parasite risk.

Current and former lab members who contributed to this work include: Julie Rushmore, Jamie Winternitz, Andy Davis

Former PhD student Julie Rushmore studied social dynamics in chimpanzees from Kibale National Park, Uganda, for 10 months in 2010.

Anthropogenic change and host-pathogen interactions

A major interest of lab members examines how anthropogenic change affects infectious disease dynamics in wildlife populations. Past work included synthetic reviews that examined mechanisms by which global climate change can alter pathogen dynamics. A major theme from this work was that climate signals on disease are more apparent in natural systems not subject to the socioeconomic forces and pathogen control measures that can mask climate signals in human-disease interactions. Other work examined how urbanization affects wildlife-pathogen interactions, focusing on West Nile virus and salmonellosis in wild songbirds. More recently, we've worked with collaborators at the CDC and University of Michigan to examine how two human activities, resource provisioning and wildlife culling, influence the ecology of rabies in vampire bats, which are the prime reservoir for rabies virus in Latin America. This study grew from a PhD thesis by Daniel Streicker into a much larger project that is now funded by the NSF. Recent findings showed that rabies persists endemically at low prevalence across a network of > 18 sites spanning much of Peru, a pattern that is best explained by high movements of bats among colonies and a high frequency of immunizing non-lethal exposures. Other findings showed that culling of bats by humans was linked to higher exposure to rabies in the bats, meaning that this activity likely results in the opposite of its intended effect. Another project is now examining more directly how resource provisioning (in the form of livestock rearing) affects vampire bat feeding and movement behavior, stress levels and immune function, and whether stable isotopes and microbiota can signal subtle variations in diet, habitat use and intraspecific contact. In other work, we are asking how human planting of exotic milkweeds in North America might change the migration ecology of monarch butterflies, with consequences for parasite spread and evolution.

Current and former lab members who contributed to this work include: Daniel Streicker, Cat Bradley, Dan Becker, Dara Satterfield

Former PhD student and now postdoc Daniel Streicker launched a project focused on anthropogenic change and the dynamics of rabies virus in vampire bats in Peru.

Former PhD student Cat Bradley studied urbanization and West Nile virus in cardinals and other songbirds around metro-Atlanta from 2003-2009.

Evolution of host defenses and pathogen virulence

Several lab members are interested in the evolution of host resistance and pathogen virulence in natural populations. Much of this work has focused on the monarch-protozan interaction, and combined field collections of wild host and pathogen genotypes with laboratory experiments. Work in collaboration with students and postdocs showed high levels of variation in parasite virulence within and among populations and provided some of the first solid empirical evidence that optimal intermediate pathogen virulence can be driven by tradeoffs between within-host replication increasing transmission on the one hand, but cutting short the infectious period on the other hand. Our work also provided support for genetic variation in host resistance and underlying effects of environmental stressors and for effects of age, sex and parasite infection on host immune defense. We found strong evidence for genotype-specific interactions between monarchs and parasites that could ultimately impede selection on host resistance or pathogen virulence in wild populations. More recent work examines how resource limitation and long-distance migratory behavior affect immune defense and pathogen resistance in monarchs, take an ecoimmunological perspective.

Current and former lab members who contributed to this work include: Jaap de Roode, Elizabeth Lindsey, Dara Satterfield, Alexa Fritzsche

A captive monarch ecloses in a laboratory experiment to characterize genetic variation in host resistance and pathogen virulence.

Geographic variation in monarch butterflies

Monarch butterflies populate islands and continents worldwide, including North America, South and Central America, Caribbean and Pacific Islands, and Australia. Monarchs in these populations are exposed to different climates, host plant species, and natural enemies, and experience different levels of geographic isolation and migratory strategies. Divergent selective forces may have affected traits associated with monarch flight ability, including wing size and shape, and monarch responses to different host plant species and performance in different thermal regimes. We have examined geographic variation in phenotypic traits of monarch butterflies from different populations, and have collaborated with other researchers who are using molecular markers to examine monarch evolutionary genetics.

Current and former lab members who contributed to this work include: Andy Davis, Jaap de Roode


Posters from some past projects in the lab - click here