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Researchers have long sought to understand and predict an animal’s response to stressful stimuli. Since the introduction of the concept of homeostasis, a variety of model frameworks have been proposed to describe what is necessary for an animal to remain within this stable physiological state and the ramifications of leaving it. Romero et al. (Horm Behav 55(3):375–389, 2009) introduced the reactive scope model to provide a novel conceptual framework for the stress response that assumes an animal’s ability to tolerate a stressful stimulus may degrade over time in response to the stimulus. We provide a mathematical formulation for the reactive scope model using a system of ordinary differential equations and show that this model is capable of recreating existing experimental data. We also provide an experimental method that may be used to verify the model as well as several potential additions to the model. If future experimentation provides the necessary data to estimate the model’s parameters, the model presented here may be used to make quantitative predictions about physiological mediator levels during a stress response and predict the onset of homeostatic overload.

 

One of the biggest unanswered questions in the field of stress physiology is whether variation in chronic stress intensity will produce proportional (a gradient or graded) physiological response. We were specifically interested in the timing of the entrance into homeostatic overload, or the start of chronic stress symptoms. To attempt to fill this knowledge gap we split 40 captive house sparrows (Passer domesticus) into four groups (high stress, medium stress, low stress, and a captivity-only control) and subjected them to six bouts of chronic stress over a 6-month period. We varied the number of stressors/day and the length of each individual bout with the goal of producing groups that would experience different magnitudes of wear-and-tear. To evaluate the impact of chronic stress, at the start and end of each stress bout we measured body weight and three plasma metabolites (glucose, ketones, and uric acid) in both a fasted and fed state. All metrics showed significant differences across treatment groups, with the high stress group most frequently showing the greatest changes. However, the changes did not produce a consistent profile that matched the different chronic stress intensities. We also took samples after a prolonged recovery period of 6 weeks after the chronic stressors ended. The only group difference that persisted after 6 weeks was weight—all differences across groups in metabolites recovered. The results indicate that common blood metabolites are sensitive to stressors and may show signs of wear-and-tear, but are not reliable indicators of the intensity of long-term chronic stress. Furthermore, regulatory mechanisms are robust enough to recover within 6 weeks post-stress.

 

To further elucidate the role that wear‐and‐tear plays in the transition from acute to chronic stress, we manipulated the intensity and duration of applied chronic stress to determine if behavior would respond proportionately. We brought wild house sparrows into captivity and subjected them to high‐stress, medium‐stress, low‐stress, or captivity‐only. We varied the number of stressors per day and the duration of stress periods to vary wear‐and‐tear, and thus the potential to exhibit chronic stress symptoms. The behaviors we assessed were neophobia (the fear of the new; assessed via food approach latency) and perch hopping (activity). We predicted that our birds would show proportionate decreases in neophobia and activity throughout a long‐term chronic stress paradigm. Our results indicate that neophobia is sensitive to the intensity of chronic stress, however, the birds became more neophobic, which was the opposite of what we expected. Conversely, perch hopping did not differ across treatment groups and is thus not sensitive to the intensity of chronic stress. Together, these data show that different behavioral measurements are impacted differently by chronic stress.

 

Preparing for pandemics requires a degree of interdisciplinary work that is challenging under the current paradigm. This review summarizes the challenges faced by the field of pandemic science and proposes how to address them.

The structure of current siloed systems of research organizations hinders effective interdisciplinary pandemic research. Moreover, effective pandemic preparedness requires stakeholders in public policy and health to interact and integrate new findings rapidly, relying on a robust, responsive, and productive research domain. Neither of these requirements are well supported under the current system.

We propose a new paradigm for pandemic preparedness wherein interdisciplinary research and close collaboration with public policy and health practitioners can improve our ability to prevent, detect, and treat pandemics through tighter integration among domains, rapid and accurate integration, and translation of science to public policy, outreach and education, and improved venues and incentives for sustainable and robust interdisciplinary work.

 

Abstract Background Individual behavioural decisions are responses to a person’s perceived social norms that could be shaped by both their physical and social environment. In the context of the COVID-19 pandemic, these environments correspond to epidemiological risk from contacts and the social construction of risk by communication within networks of friends. Understanding the circumstances under which the influence of these different social networks can promote the acceptance of non-pharmaceutical interventions and consequently the adoption of protective behaviours is critical for guiding useful, practical public health messaging. Methods We explore how information from both physical contact and social communication layers of a multiplex network can contribute to flattening the epidemic curve in a community. Connections in the physical contact layer represent opportunities for transmission, while connections in the communication layer represent social interactions through which individuals may gain information, e.g. messaging friends. Results We show that maintaining focus on awareness of risk among each individual’s physical contacts promotes the greatest reduction in disease spread, but only when an individual is aware of the symptoms of a non-trivial proportion of their physical contacts (~ ≥ 20%). Information from the social communication layer without was less useful when these connections matched less well with physical contacts and contributed little in combination with accurate information from physical contacts. Conclusions We conclude that maintaining social focus on local outbreak status will allow individuals to structure their perceived social norms appropriately and respond more rapidly when risk increases. Finding ways to relay accurate local information from trusted community leaders could improve mitigation even where more intrusive/costly strategies, such as contact-tracing, are not possible. 

The modern world involves both increasingly frequent introduction of novel invasive animals into new habitat ranges and novel epidemic-causing pathogens into new host populations. Both of these phenomena have been well studied. Less well explored, however, is how the success of species invasions may themselves be affected by the pathogens they bring with them. In this paper, we construct a simple, modified Susceptible-Infected-Recovered model for a vector-borne pathogen affecting two annually reproducing hosts. We consider an invasion scenario in which a susceptible native host species is invaded by a disease-resistant species carrying a vector-borne infection. We assume the presence of abundant, but previously disease-free, competent vectors. We find that the success of invasion is critically sensitive to the infectivity of the pathogen. The more the pathogen is able to spread, the more fit the invasive host is in competition with the more vulnerable native species; the pathogen acts as a ‘wingman pathogen,’ enhancing the probability of invader establishment. While not surprising, we provide a quantitative predictive framework for the long-term outcomes from these important coupled dynamics in a world in which compound invasions of hosts and pathogens are increasingly likely.

 

Abstract When a novel disease strikes a naïve host population, there is evidence that the most immediate response can involve host evolution while the pathogen remains relatively unchanged. When hosts also live in metapopulations, there may be critical differences in the dynamics that emerge from the synergy among evolutionary, ecological, and epidemiological factors. Here we used a Susceptible-Infected-Recovery model to explore how spatial and temporal ecological factors may drive the epidemiological and rapid-evolutionary dynamics of host metapopulations. For simplicity, we assumed two host genotypes: wild type, which has a positive intrinsic growth rate in the absence of disease, and robust type, which is less likely to catch the infection given exposure but has a lower intrinsic growth rate in the absence of infection. We found that the robust-type host would be strongly selected for in the presence of disease when transmission differences between the two types is large. The growth rate of the wild type had dual but opposite effects on host composition: a smaller increase in wild-type growth increased wild-type competition and lead to periodical disease outbreaks over the first generations after pathogen introduction, while larger growth increased disease by providing more susceptibles, which increased robust host density but decreased periodical outbreaks. Increased migration had a similar impact as the increased differential susceptibility, both of which led to an increase in robust hosts and a decrease in periodical outbreaks. Our study provided a comprehensive understanding of the combined effects among migration, disease epidemiology, and host demography on host evolution with an unchanging pathogen. The findings have important implications for wildlife conservation and zoonotic disease control.