Parasites and pathogens function as a necessary and critical part of ecosystems, creating evolutionary pressure on hosts and influencing host genetics, social dynamics and behavior, and ultimately, fitness. And, while much work has been done examining the ecological effects of infectious disease, much less is known about how human activities influence the ecology and evolutionary trajectory of host and parasite. Questions that remain unanswered include how do urban landscapes alter the social and genetic structure of wildlife populations? How do these alterations result in selective pressure on the host’s immune response to pathogens? And, how do human activities and host population dynamics interact to change parasite transmission patterns and evolutionary trajectory? To address these research questions, we use lab and field tools from molecular genetics, disease ecology, parasitology and microbiology, and transmission and dispersal modeling. Urban wildlife populations make an ideal study system for answering these questions due to their co-occurrence with human populations, the wealth of parasites and pathogens carried by these species, and the residential nature of both macaque populations throughout Southeast Asia and raccoon and opossum populations in the St. Louis region.

Our work focuses on mammalian host populations; specifically, we study the effects of human actions on the population and landscape genetics and infectious diseases of wildlife populations, examining how both direct and indirect human actions alter the evolution of host-parasite interactions in urban communities. Pathogen-mediated selection is most likely to act in loci significant in immune function, and building on my past research, work in my lab continues to examine the effects of human activities, including urban land use development and conservation and disease management, on selection of host immune responses. In the wild, rarely is an individual infected with only one parasite; thus, we also examine pathogen-driven selection in the context of co-infection, both between micro- and macro- parasites and within a community of parasites, including through measuring immune responses directly and by parasite-removal experiments. More specifically, our work addresses questions of spatial, temporal, and resource competition within parasites and questions related to how immune systems – primed by one parasite – can effectively respond to co-infections, i.e. by limiting parasite species richness and focus on investigating the evolution of susceptibility and resistance in urban populations by testing for signatures of selection across relevant immune loci in response to significant macro- and micro-parasite burdens.

Future research aims to address the interplay between wildlife endocrinology, parasitism and infection, population genetics, and animal behavior in urban and suburban wildlife communities. This will facilitate an understanding of how human activities impact the ecology and evolution of wildlife populations, including changes in stress levels and shifting dispersal patterns, which can alter the risk of pathogen transmission in unexpected ways.

Past Research:

How do urban landscapes alter the social and genetic structure of wildlife populations?

Understanding the role of human activities in shaping the genetic structure of host populations is critical in light of increasing human-wildlife-pathogen interactions. My research examined direct and indirect effects of anthropogenic activities on host populations, individuals, and genes. On the island of Bali, Indonesia, long-tailed macaques (Macaca fascicularis) exist in close contact with human populations, benefiting from the religious protection afforded them when in residence at one of 42 large temples across the island. My work found that despite the ubiquity of macaques throughout Southeast Asia, the highly urbanized populations on Bali have significant levels of genetic differentiation. Recent land use alterations, from large scale rice agriculture to increased urbanization, have resulted in changes to macaque social dynamics (Lane et al. 2010), with landscape and management practices reducing overall dispersal and gene flow (Lane-deGraaf et al. 2012). Management practices developing from increases in local tourism have resulted in regions of extremely low macaque dispersal, and this unexpected pattern of gene flow, linked directly to shifting land use, was also reflected in an increase in gastrointestinal parasitism in populations with high tourist contact rates (Lane et al. 2011).

How do human activities result in selective pressure on the host’s immune response to pathogens?

Unlike the macaque system, African buffalo (Syncerus caffer) populations thrive in large South African national parks. These populations are actively managed for bTB, with some parks actively culling bTB+ individuals as a disease management strategy. In my work comparing the genetic diversity of buffalo populations in two parks with differing disease management strategies, we found evidence of disease-driven selection at IFNG, the locus which codes for IFNγ, a cytokine critical in the immune response to bTB, occurring in populations with observation-only management strategies. However, in populations where bTB+ animals are culled as a management strategy, genetic diversity has been reduced across loci and rare alleles have been selectively eliminated, potentially reducing the ability of that population to respond to novel pathogens (Lane-deGraaf et al. 2015). Determining the signature of selection of bTB and/or culling as a management practice in wild buffalo populations may have important implications for future management approaches to bTB throughout its range.