Honors Program


Date of this Version


Document Type



Reiman, L. 2020. Infection-Induced Anorexia in the Face of Energetic and Immune Deficiency. Undergraduate Honors Thesis. University of Nebraska-Lincoln.


Copyright Lauren Reiman 2020.


A perplexing quirk of many host-pathogen interactions is that hosts typically reduce their food intake when infected, or merely exposed to, infectious agents. The occurrence of this behavior is widely-documented. Yet, the ecological factors that influence it, how it affects disease outcomes, or why it evolved remains poorly resolved. Addressing this gap carries important implications for both basic and applied biology. Feeding behavior impacts within-host energetics, physiology, and immune functions with downstream consequences for host life history and for the pool of resources available to fuel (or inhibit) parasites and pathogens. The question then becomes, during infection are host and pathogen diets aligned or in conflict? To address this question, I examined how pathogen-mediated anorexia varies across different environmental and genotypic backgrounds using a natural host-pathogen system, the fruit fly Drosophila melanogaster and its bacterial pathogen Providencia rettgeri. First, I examined whether host diet affected pathogen growth using in vitro experiments. Then, I asked whether resource quality affected the feeding choices of infected hosts. In vitro assays indicated that higher resource quality promoted higher growth rates of the bacterial pathogen. Bacteriainfected hosts tended to reduce their overall caloric intake, indicating the occurrence of illnessmediated anorexia. Hosts primarily reduced their intake of high-quality resources which suggests the potential for ‘self-medication ’ by not eating. However, the strength of this response varied among host genotypes that differ in energetics and immune function, with energetically compromised hosts having much higher calorie intake overall. As a first step in understanding links between resources and host immune functions, we examined gene expression in males of this energetically compromised genotype. Infected males had higher expression of the inducible genes, Drosomycin and Diptericin, which code for antimicrobial peptides, indicating that the innate immune response was activated in the host. Future directions will examine how these immune changes in response to diet and energetics jointly alter pathogen growth and transmission potential. Together, these results highlight the importance of examining this ubiquitous, but poorly understood, component of host-pathogen systems across different genetic and environmental contexts.