Savannah River Site, South Carolina
Does thermal variability drive parental nesting behaviors and offspring phenotype in birds?
The overarching goal of this research is to better understand the interactions among environmental temperature, parental behavior, and offspring outcomes. Our previous research indicated that temperatures experienced early in development are a major driver of phenotype in birds and can even affect secondary sex ratios. In addition, temperature affects parental care behaviors and costs of reproduction in parents. With predicted rapid shifts in the thermal climate we must understand how parents mitigate exposure of offspring to extreme temperatures, and how embryonic exposure to high temperatures will shape offspring traits. We are currently using a newly established nest box system in Fayetteville, AR to study these relationships in Eastern Bluebirds. Our lab also developed a program that uses machine learning to identify on and off-bouts in nest thermal data, which can be downloaded here.
Does maternal behavior elicit bidirectional interactions between infectious diseases and offspring immune phenotype?
Pathogens are forceful drivers of ecological interactions and host evolution, shaping host behavioral patterns and reproductive decisions, which can ultimately alter the developmental environment to generate an important source of nongenomic inheritance. When these transgenerational effects influence offspring immune phenotype, disease-induced parental effects exert selection on the pathogen, creating a bidirectional link between host and pathogen evolutionary processes. This link can be mediated by changes in parental care behaviors. Using domestic canaries we are exploring the role of parental incubation behavior in shaping host-pathogen interactions.
Do macronutrients shape host immune defenses to affect host disease recovery and the evolution of virulence
Physiological interactions within hosts govern the ability of pathogens to develop, reproduce, and spread among hosts. Nutritional resources fundamentally shape host physiology and therefore, disease dynamics. Consider that pathogens steal resources from their hosts but also elicit energetically costly immune responses. These increased energetic costs leave few resources available for basic maintenance needs or reproductive efforts. Yet, how these within-host processes scale-up to shape ecological, epidemiological, and evolutionary dynamics remains largely overlooked and poorly resolved. To address these knowledge gaps, we are experimentally testing (1) how resources affect multiple mechanisms of host resistance and tolerance and (2) the functional consequences for ecological (host dynamics), epidemiological (disease invasion), and evolutionary (virulence evolution) dynamics. This research is in collaboration with Dr. Jessica Hite, UW Madison.
Does sublethal exposure to crude oil have consequences for fitness-related traits in an avian model organism?
Historically, avian population damage estimates following a crude oil spill focus exclusively on surveys of birds with oiled feathers; however, birds without oiled feathers may ingest crude oil by consuming contaminated food. We developed a metric to use as a potential indicator of oxidative damage in avian red blood cells: the formation of heme degradation products (HDPs). We characterized the formation of HDPs in avian red blood cells and posited that HDPs may be a molecular initiating event that could affect aerobic metabolic scope, and thus energetically taxing behaviors (e.g., flight and thermoregulation). Zebra finches exposed to crude oil exhibited elevated HDPs, altered hematological indices, reduced metabolic performance, and suppressed immune function; however, we did not detect a decline in flight performance. These results suggest that crude oil ingestion may cause birds to reallocate energy away from non-essential biological processes and towards detoxification and repair. Taken as a whole, these data suggest that avian population damage estimates that focus exclusively on surveys of birds with oiled feathers may underestimate the impact of oil spills on bird populations. Picture credit: Louisiana Governors Office
Stress and Immune interactions
Chronic stress, potentially through its influence on glucocorticoids like corticosterone, is thought to have negative consequences for immune function. While corticosterone may directly inhibit immune cells, chronic stress may also influence allocation of energy, ultimately shifting resources away from the immune system. If so, then the effects of chronic stress on immune responses may be greater during costly life history stages. We are investigating how chronic stress influences healing after a small biopsy , the ernegetic cost of healing, and whether healing and energy expenditure differ with life history stage. By monitoring corticosterone concentrations we will also determine whether glucocorticoids, in part, mediate effects of stress on immune processes.
Physiology of an imperiled amphibian, the eastern hellbender
The decline of the hellbender in North America embodies many of the characteristics surrounding the plight of amphibians around the world. Hellbenders are exposed to disease, parasites, habitat modification, altered climate, and contaminants. Unfortunately, hellbenders are also persecuted by humans for various reasons. Because hellbenders flourish in well-oxygenated mountain streams with low levels of siltation, we shouldn't view hellbenders as a nuisance, but as indicators of stream health. We can be proud of the quality of our streams when healthy hellbender populations are present! Despite the dramatic declines of eastern hellbenders and the listing of the Ozark subspecies, we know little about the basic physiology of hellbenders. However, to best conserve healthy hellbender populations and rehabilitate threatened populations it is imperative that we understand how hellbenders respond physiologically to changes in their environment. To this end, our research has focused on how ecto- and endo-parasites influence hellbender physiology.