Critical disease windows shaped by stress exposure alter allocation trade-offs between development and immunity

Area of Science:

• Ecology and Evolutionary Biology
• Environmental Toxicology
• Immunology

Background:

• Environmental stressors can alter host susceptibility to pathogens, influencing disease emergence.
• Stress effects on hosts are duration-dependent: chronic stress is often immunosuppressive, while acute stress can temporarily boost immunity.
• Host susceptibility to stress and disease varies with developmental stage (ontogeny), particularly during critical windows.

Purpose of the Study:

• To investigate how stressor duration and timing interact to shape critical windows and influence disease processes in vertebrates.
• To test how physiological stress and pathogenic infection interact to shape development and disease dynamics using ranavirus and larval amphibians as a model.
• To examine resource trade-offs induced by stressors, mediated by the neuroendocrine stress axis, impacting development, immune function, and energy allocation.

Main Methods:

• Wood frog larvae (Lithobates sylvaticus) were exposed to chronic or acute corticosterone (glucocorticoid hormone) treatments.
• Splenocyte immunohistochemistry was used to analyze immune function in association with ranavirus infection.
• Effects on time to metamorphosis, survival rates, and viral replication were assessed.

Main Results:

• Both chronic and acute corticosterone exposure suppressed splenocyte proliferation.
• Viral replication increased only under chronic corticosterone treatment.
• Ranavirus infection decreased survival and delayed metamorphosis in control and chronic stress groups, but chronic stress accelerated metamorphosis in uninfected larvae; acute stress accelerated metamorphosis and increased survival in infected larvae.

Conclusions:

• Interactions between stress exposure and infection create resource trade-offs, influencing the allocation between development and somatic functions.
• Critical disease windows are shaped by stress exposure, as altered differentiation rates impact organismal susceptibility.
• Understanding these stress-disease dynamics is crucial for predicting disease emergence in changing environments.