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Emily M Hall

The crossroads of stress and disease

Emerging infectious diseases associated with wildlife population declines are rising at an alarming rate. This looming threat to biodiversity has been hypothesized to result from immunosuppressive stressors generated by ecological change. Based on physiological theory, the stress-induced susceptibility hypothesis posits that environmental change increases energetic demands which cause organisms to divert resources away from resisting infections. However, twenty years after this hypothesis was proposed, we still have neither a clear understanding of how environmental stressors affect disease outcomes in natural populations, nor causal links between environmental change and disease-associated population declines.

I study the stress-induced susceptibility hypothesis in the context of roads, which pose many challenges to amphibian populations such as direct road-kill, dispersal impairment, and contamination from run-off. Through a combination of field, mesocosm, and laboratory experiments we have revealed strong evidence that roads are decreasing larval performance via salinity from de-icing salts increasing osmoregulatory maintenance costs. Our results suggest that this osmotic stressor is increasing heterogeneity in disease susceptibility and thus the likelihood of disease-associated die-offs. My research explores the following questions:

  1. Are there parental environmental effects or plastic responses to the roadside environment?

We combined a reciprocal transplant with physiological assays to evaluate the plastic responses at different life-stages of wood frogs to the roadside habitat. We inferred from results that tadpoles respond to the roadside environment with an energetic trade-off between osmoregulation and body growth, which is an important investment for tadpoles as their fitness is highly correlated with size at metamorphosis. We also found indications that adults breeding in these ponds are in poor health and have high allostatic load, a sign of chronic stress. Read the full paper here.


  1. Do roads affect disease susceptibility and the likelihood of a die-off in wood frog tadpoles?

Because we observed ranavirus-associated (a group of virulent pathogens of vertebrate ectortherms) die-offs of >90% of tadpoles in some ponds, we monitored the occurrence of these events. Although the presence of the pathogen was ubiquitous (measured by environmental DNA; highly correlated with infection levels in tadpoles: full paper here), die-offs were more likely to occur near heavily salted state highways. We then examined how disease susceptibility varied in tadpoles from ponds across a gradient of proximity to roads.

  1. What are the seasonal drivers of ranavirus related die-offs?

Ranavirus epidemics in larval wood frog populations display striking seasonality. Understanding the drivers of these sudden, massive die-offs can help predict and mitigate populations at high disease risk. While there are several types of explanations for this seasonality—from seasonal introductions of virus to environmental stressors to windows of susceptibility during larval development—most studies have focused on single factors in laboratory settings. Here we used environmental DNA (eDNA) and larval samples to characterize the time course of epidemics in a set of ephemeral wetlands in the Northeast USA and evaluated multiple hypotheses for seasonal die-offs.


  1. Are epidemiological factors that increase transmission efficiency altered by road salt stress?

In the laboratory we explored how exposure to relevant concentrations of road salt affects several factors that influence ranavirus transmission efficiency. We found the stress of salt affected viral shedding rates, mortality rates, and the physiological response to infection in wood frog larvae. This approach combining physiological assays with exposure studies offers the ability to infer how stress-induced susceptibility could increase probability of an epidemic.


Conservation biologists and wildlife management alike need mechanistic studies to understand the factors that influence infectious disease dynamics in wildlife to inform policy. As such, strengthening the causal links to anthropogenic disturbances is key to advancing conservation efforts. Furthermore, this research will provide better estimates of epidemiological parameters with the added effects of stressors on susceptibility. We have also advanced the surveillance techniques for this disease system, which will greatly improve our ability to study this threat to amphibian populations. Our approach contributes to the growing knowledge of emerging infectious diseases that are a threat to biodiversity and wildlife health, and demonstrates the stress-induced susceptibility hypothesis in a natural population.

Career Goals

To understand how environmental change can cause disease-associated population declines, I aim to integrate the mechanistic framework of physiology, which allows us to predict responses to change, into the phenomenological framework of disease ecology. With my strengths in environmental physiology and conducting ecological experiments examining disease susceptibility, I aim to contribute to the growth of the new field of conservation physiology. Building on my dissertation research, I want to advance the field by developing tools to assist wildlife biologists in assaying population health and monitoring disease. Furthermore, I aim to invoke the use of predictive, theoretical models in management decisions regarding conservation efforts.