Biology subjects

DuRant, S. E.

Publications and source records attributed to DuRant, S. E..

5 recordsLinked to original sources

bioRxiv2025

The nutritional content of anthropogenic resources affects wildlife disease dynamics

Wildlife have become increasingly reliant on human-supplemented food, affecting interactions between individuals and subsequently disease transmission. Much of the research investigating the impact of human-supplemented food has focused on host behavioral changes and food availability. However, the nutritional quality of food can significantly impact disease transmission depending on whether it boosts or hinders immunity. Few studies have investigated links between nutrition, immunity, and pathogen transmission, which weakens efforts to guide and manage infectious disease at the wildlife-human interface. We investigate these interactions using a data-driven transmission model that explicitly incorporates feedback between nutrition, immunity, and pathogen transmission in the bacterial pathogen, Mycoplasma gallisepticum and its avian hosts which are heavily dependent on supplemental food sources. We also examine the nutritional content and sales frequency of one of, if not the, most common source of anthropogenic food supplementation, bird feeder food. We find that food with lower nutritional quality is purchased for wild bird supplementation far more frequently than food with high nutritional quality. Further, our transmission model demonstrates that these lower quality food sources result in large epidemics that cause destabilizing population declines. Our results suggest that nutritional quality plays an important role in disease transmission and provide insight into the ecological and immunological consequences of human behavior on infectious disease in wildlife.

ecology↗

bioRxiv2025

Prior infection induces long-lasting partial immunity to reduce transmission within flocks in an avian host-pathogen system.

Population-level differences in the ability to maintain immunity can lead to contrasting survival outcomes between groups and determine how future outbreaks will spread. Pathology and infectiousness during subsequent infections can be influenced by immunity and an increase in resistance or tolerance of individuals. However, determining the longevity and effectiveness of immunity in wildlife population is challenging due to lack of infrastructure for long term monitoring of populations and individuals and host-pathogen specific tests. Further, predicting wildlife disease dynamics requires an understanding of individual-level heterogeneity in pathology and behavior as well as a knowledge of how populations with differing partial immunity will transmit disease, which is currently limited. Using an avian host-pathogen system, we ran two experiments to determine if previously exposed birds had immunity to MG after three years and if Mycoplasma gallisepticum (MG) transmission differed between first and second infection index birds. Birds retained partial immunity to MG for three years after their original infection and showed signs of being resistant to infection. The transmission experiment revealed that although first and second-infection index birds experienced pathology and pathogen growth, only first infection birds transmitted MG. Three years could represent lifetime protection for individuals who survive their first infection and a reduction in risk for other members of their flock. Our research has important implications for understanding MG epidemics in wild populations of birds as well as disease in wildlife more broadly.

ecology↗

bioRxiv2024

Diet driven differences in host tolerance are linked to shifts in global gene expression in a common avian host-pathogen system

As humans alter the landscape, wildlife have become increasingly dependent on anthropogenic resources, altering interactions between individuals and subsequently disease transmission dynamics. Further, nutritional quantity and quality greatly impact an individual hosts immune capacity and ability to mitigate damage caused by infectious disease. Thus, understanding the impact of dietary nutrition on immune function is critical for predicting disease severity and transmission as human activity both facilitates the dispersal of pathogens and alters dietary options for wildlife. Here, we use transcriptomics to explore the previously unstudied molecular mechanisms underpinning diet-driven differences in pathogen tolerance using a widespread avian bacterial pathogen, Mycoplasma gallisepticum (MG). MG is an ideal model for understanding the dietary drivers of disease as the human supplementation that wild birds commonly rely on, bird feeders, are also an important source for MG transmission. Significant diet-driven differences in the expression of many genes encoding immune response and translational machinery proteins are seen both in the absence of MG and during the recovery period. Prior to infection, protein-fed birds are more transcriptionally primed for infection than lipid-fed birds which translates to greater tolerance in protein-fed birds during the recovery period. Given the significant importance of human supplemented food in wildlife disease systems, the molecular mechanisms by which interactions between diet and infection emerge provide insight into the ecological and immunological consequences of human behavior and wildlife disease.

ecology↗

bioRxiv2023

Male pathology regardless of behaviour drives transmission in an avian host-pathogen system

Host sex is an important source of heterogeneity in the severity of epidemics. Pinpointing the mechanisms causing this heterogeneity can be difficult because differences in behaviour among sexes (e.g. greater territorial aggression in males) can bias exposure risk, obfuscating the role of immune function, which can lead to differences in pathology, in driving differential susceptibility between sexes. Thus, sex-biased transmission driven by differences in immune function independent of behaviour is poorly understood, especially in non-mammalian systems. Here we examine the previously unexplored potential for male-biased pathology to affect transmission using an avian host-pathogen system. We employ a sex-dependent multistate transmission model parameterized with isolated, individual-based experimental exposures of domestic canaries and experimental transmission data of house finches. The experiment revealed that male birds have shorter incubation periods, longer recovery periods, higher pathogen burdens, and greater disease pathology, than females. Our model revealed that male-biased pathology led to epidemic size rapidly increasing with the proportion of male birds, with a nearly 16-fold increase in total epidemic size from an all-female to an all-male simulation. Our results demonstrate that female-biased resistance, independent of male behaviour, can drive sex-dependent transmission in wildlife, indicating that sex-based differences in immune function, not just differences in exposure risk, can shape epidemic dynamics.

ecology↗

bioRxiv2022

Deepwater Horizon crude oil reduces aerobic capacity of birds

Crude oil spills can have catastrophic effects on marine and inland ecosystems, yet it is difficult to accurately quantify the extent of ecological damage caused by oil spills. For instance, avian population damage assessments conducted after large oil spills (e.g., Deepwater Horizon spill) often focus on the number of visibly oiled birds. However, birds without visible oiling can exhibit hematological damage from oil ingestion. If such hematological responses limit oxygen deliver to tissues and impair aerobic performance, then energy-mediated effects from oil ingestion may ultimately affect endpoints of demographic significance (e.g., survival and reproduction). We investigated whether oil ingestion affects aerobic performance in birds by orally dosing zebra finches (Taeniopygia guttata) with 2 or 6 mL/kg of weathered MC252 crude oil for 28 days. After 14 and 28 days of dosing, we measured hematological indices (oxidative damage, packed cell volume [PCV], hemoglobin, reticulocytes), maximum metabolic rate (MMR), resting metabolic rate (RMR), and short-distance flight performance. Finches exposed to oil exhibited lower hemoglobin and PCV, higher reticulocyte counts, and greater oxidative damage. Shifts in these hematological indices appeared to alter organismal energetics, resulting in reduced MMR, RMR, and aerobic scope. Short-distance burst-flight was not negatively impacted by oil ingestion. Collectively, these results suggest oil ingestion impairs metabolic performance, which may negatively impact a birds ability to perform sustained energetically expensive activities (e.g., migration). SignificanceThe 2010 Deepwater Horizon oil spill released an unprecedented volume of crude oil (MC252) into the northern Gulf of Mexico and contaminated 2100 km of shoreline habitat that serves as critical breeding grounds and migratory stop-over sites for birds. Here we describe the impact of oil ingestion on the aerobic capacity of zebra finches, a model songbird. Oil ingestion reduced maximum metabolic rate and aerobic scope, which may be caused in part by hematological damage. These data suggest oil ingestion limits the ability of birds to perform essential energetically demanding activities (e.g., migration, nest incubation), thus quantification of avian injury based on external oiling alone may underestimate the true impact of oil spills on avian populations.

pharmacology and toxicology↗