Parasitic infections are ubiquitous, but the consequences to hosts can vary substantially. Variation in the consequences of infection can be related to individual differences in the use of two parasite defense strategies, resistance and tolerance. Resistance entails reducing parasite burden by removing parasites or restricting parasite reproduction. Tolerance involves minimizing the costs associated with a given parasite burden. Genetic variation, environmental conditions, and life history stage can contribute to variation in resistance and tolerance, but the physiological mechanisms that underlie investment in each strategy are not well understood. I proposed that glucocorticoid hormones, which mediate responses to challenges in the physical and social environment in vertebrates, might alter host investment in resistance and tolerance (Chapter I). Glucocorticoids influence a suite of physiological processes including immune function, resource allocation, and tissue growth, all which could alter resistance and tolerance. Using a combination of observational and experimental studies, I test the hypothesis that glucocorticoids mediate resistance and tolerance to infection in red-winged blackbirds (Agelaius phoeniceus) infected with Haemosporidians, including malaria (Plasmodium) and malaria-like (Haemoproteus and Leucocytozoon) parasites. I performed a medication experiment (Chapter II) to identify the physiological consequences of Haemosporidian infection and explored the relationships between glucocorticoids and parasite resistance and tolerance in both an observational field study and a hormone manipulation experiment (Chapters III and IV). Medication treatment effectively reduced Plasmodium burden, increased hematocrit and hemoglobin, and reduced the rate of red blood cell production (Chapter II). In an observational field study (Chapter III), red-winged blackbirds with higher plasma glucocorticoid concentrations maintained higher hematocrit than expected for their parasite burdens, suggesting a positive association between glucocorticoids and tolerance. In this study, I found no support for a relationship between glucocorticoids and resistance. However, experimental elevation of glucocorticoids (Chapter IV) yielded nearly opposite results: the higher of two doses of glucocorticoids increased Plasmodium burdens and caused a decrease in body mass with increasing parasite burden, indicative of a decrease in tolerance. I discuss possible causes of the differences in our observational and experimental studies and the implications of my work for future studies of individual variation in parasite tolerance (Chapter V). / Ph. D. / Why does a cold leave some people bed-ridden, while others can go about their day with only a few sniffles? We can easily see that people react differently when they encounter an infection, but it is not clear why. When faced with an infection, there are two main defense strategies: resistance and tolerance. Resisting infection means reducing the number of parasites or pathogens in the body. Tolerance, on the other hand, refers to reducing the damage or costs that occur during infection. For example, an individual could resist a cold by using the immune system to kill off viruses. If someone tolerates a cold, they might not feel very sick, despite the presence of viruses. Individuals that are more tolerant could be suppressing their own immune response, which can cause the inflammation that leads to a stuffy nose, or these individuals might be repairing damage caused by the virus. Individuals can vary in the extent to which they resist or tolerate infection, but we do not know why this variation exists. In this dissertation, I investigate how the hormones associated with physiological stress might influence resistance and tolerance to malaria and malaria-like parasite infections in red-winged blackbirds. First, I performed a study in which I treated birds infected with a blood-borne parasite with anti-malarial medication to identify the costs of chronic infection. Then I observed the relationships between glucocorticoids (the hormones associated with physiological stress) and estimates of resistance and tolerance in wild red-winged blackbirds. Finally, I used hormone implants to increase stress hormone concentrations in birds held in aviaries, and assessed whether the implants caused changes in resistance and/or tolerance. My results suggest that chronic malaria infection can 5 damage or destroy red blood cells and birds compensate by increasing the rate of blood cell production. In wild red-winged blackbirds, birds with higher concentrations of stress hormones were able to maintain a higher proportion of red blood cells in the blood for a given parasite burden, suggesting they were more tolerant. Stress hormone levels were not associated with the total number of parasites, and thus, we have no evidence for a relationship between the hormones and resistance. When we increased the hormone levels in the aviary experiment, we found nearly opposite results. A high dose of stress hormones caused an increase in the number of parasites and increased the cost of infection. In this dissertation, I discuss possible explanations for the different results in the observational study and the experiment and suggest avenues for future studies.
| Identifer | oai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/86535 |
| Date | 10 July 2017 |
| Creators | Schoenle, Laura A. |
| Contributors | Biological Sciences, Moore, Ignacio T., Bonier, Frances, Hawley, Dana M., Walters, Jeffrey R., Hopkins, William A. |
| Publisher | Virginia Tech |
| Source Sets | Virginia Tech Theses and Dissertation |
| Detected Language | English |
| Type | Dissertation |
| Format | ETD, application/pdf, application/pdf |
| Rights | In Copyright, http://rightsstatements.org/vocab/InC/1.0/ |
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