Context-dependent immunity in Gopher Tortoises, Gopherus polyphemus
Type of DegreeDissertation
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Infectious diseases in wildlife are a significant threat to biological diversity, especially In light of recent anthropogenic alterations to the environment. North American tortoises (genus Gopherus) have experienced declines as a result of an upper respiratory tract disease (URTD) which can be caused by Mycoplasma agassizii and Mycoplasma testudineum infection. Recent evidence suggests that URTD is a result of multiple environmental contexts, beyond simply pathogen presence. The objective of this dissertation was to examine contexts in which the environment directly affects immunity in Gopher Tortoises, Gopherus polyphemus. Herein, I tested four hypotheses related to the environmental contexts of disease resistance in G. polyphemus: (1) population-level differences in URTD exist across G. polyphemus populations and disease state is positively related to diagnostic markers of mycoplasmosis; (2) natural seasonal acclimation causes seasonally-altered disease resistance; (3) rapid temperature change causes a lag of optimal baseline immune function, during which disease resistance is increased; (4) G. polyphemus alters thermoregulatory set-point and immune function as a response to acute bacterial infection. Across seven populations of G. polyphemus, I found that the frequency of external symptoms of disease varied considerably, and that this variation is directly related to the year in which a population is sampled. However, traditional diagnostic markers of mycoplasmosis failed to positively identify individuals with external symptoms of URTD. Antibody titers to M. agassizii were positively related to the presence of nasal scarring consistent with chronic URTD. Experimental manipulations of G. polyphemus seasonal acclimation state demonstrated that winter causes a significant reduction in immune function. Moreover, rapid temperature increase during winter does not cause an increase in immune function, suggesting that acclimation states constrain immunity. Furthermore, rapid temperature decreases during the summer significantly reduced immune function, suggesting a direct mechanism by which aberrant weather may increase disease frequency. While immunity was strongly temperature dependent in G. polyphemus, I failed to find support for a predicted seasonal lag of immunity. Lastly, I found that when acutely stimulated with lipopolysaccharide, a bacterial endotoxin, G. polyphemus has an immunological response consistent with fever. This fever response included an increase in body temperature, a reduction in plasma iron, and an increase in innate immunity. The fever response was not directly related to acclimation state, as both winter-acclimated and summer-acclimate tortoises consistently displayed fevers. As a whole, this dissertation provides a strong link between the environmental context of thermoregulatory potential and disease resistance in G. polyphemus. Increased environmental change, especially as a result of a changing climate, will likely exacerbate the negative effects of disease in this taxon.