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Avian immune systems are multifaceted and vary widely among individuals, populations, and species, all of which will affect the dynamics of infectious diseases in the wild. Historically, ecoimmunology sought to uncover the proximate and ultimate drivers of heterogeneity in immune defenses. More recently, the field has begun to interface with disease ecology, asking not only about the causes of immune variation but also about its links to within- and between-host disease processes. This chapter briefly reviews the complexity of avian immune systems, outlines theories of how and why these defenses vary, and provides an overview of both common and novel techniques in ecoimmunology. Subsequent sections highlight two research questions as critical to the synergy between ecoimmunology and disease ecology: (1) How do immune phenotypes predict individual infection outcomes? and (2) How do within-host measures of immunity inform population-level transmission dynamics?

The dynamics of infectious disease are driven by the fundamental processes that mediate host–pathogen interactions. A basic understanding of the mechanisms underlying these interactions is essential for disease ecologists regardless of their scale of inquiry. This chapter covers the terms and concepts commonly used in ecological studies of infectious disease across levels of organization and scales of inquiry, from the individual host organism to host populations and multispecies communities. When applicable, aspects that are unique to birds and their biology are highlighted. The between-host processes discussed in the beginning of the chapter arise from the within-host processes between the pathogen and the host’s immune system. These processes are then used as a framework to introduce the basics of epidemiological modeling and the population-level disease dynamics. The chapter is not meant to be exhaustive but, instead, to provide a common foundation for readers approaching this topic from unique backgrounds. Given the transdisciplinary nature of avian infectious disease ecology, many of the terms used have multiple meanings assigned to them that are taxon- or discipline-specific. Such variation in key terminology is, in large part, a consequence of the transdisciplinary and multiscaled approaches inherent in studying host–pathogen–vector–environment interactions.

The Hamilton-Zuk hypothesis predicts that ornament expression is a signal of the ability of individuals to resist parasite infection. Thus, across a population (i.e., between-individuals) more ornamented individuals should have lower levels of parasitism. Numerous studies have tested this prediction and the results are mixed. One reason for these conflicting results may be that many studies have examined this relationship at the between-individual level, which may be affected by confounding factors such as selective mortality. Using within-subject centering we examined the relationship between male ornamentation and avian blood parasites at both the between- and the within-individual level. These relationships focus on differences in genetically-based resistance to parasites and the trade-off in resource allocation between parasite resistance and ornament expression within an individual, respectively. We studied male common yellowthroats (Geothlypis trichas), which have two plumage ornaments, a yellow, carotenoid-based bib (throat and chest) and a black, melanin-based facial mask. Surprisingly, within-individuals, an increase in parasitism between years was associated with an increase in mask size and, potentially, greater concentration of carotenoids in the yellow feathers. This suggests that males may be able to tolerate an increase in parasitism and still increase ornament expression. In contrast, ornamentation was not related to parasitism at the between-individual level. Thus, our study revealed relationships between ornaments and parasitism at the within-individual level that were not present at the between-individual level. Our results highlight the importance of examining both within- and between-individual relationships as correlations between variables, such as ornaments and parasites, may depend on the level of analysis (i.e., within- or between- individuals). This article is protected by copyright. All rights reserved.

Host competence, or how well an individual transmits pathogens, varies substantially within and among animal populations. As this variation can alter the course of epidemics and epizootics, revealing its underlying causes will help predict and control the spread of disease. One host trait that could drive heterogeneity in competence is host tolerance, which minimizes fitness losses during infection without decreasing pathogen load. In many cases, tolerance should increase competence by extending infectious periods and enabling behaviors that facilitate contact among hosts. However, we argue that the links between tolerance and competence are more varied. Specifically, the different physiological and behavioral mechanisms by which hosts achieve tolerance should have a range of effects on competence, enhancing the ability to transmit pathogens in some circumstances and impeding it in others. Because tissue-based pathology (damage) that reduces host fitness is often critical for pathogen transmission, we focus on two mechanisms that can underlie tolerance at the tissue level: damage-avoidance and damage-repair. As damage-avoidance reduces transmission-enhancing pathology, this mechanism is likely to decrease host competence and pathogen transmission. In contrast, damage-repair does not prevent transmission-relevant pathology from occurring. Rather, damage-repair provides new, healthy tissues that pathogens can exploit, likely extending the infectious period and increasing host competence. We explore these concepts through graphical models and present three disease systems in which damage-avoidance and damage-repair alter host competence in the predicted directions. Finally, we suggest that by incorporating these links, future theoretical studies could provide new insights into infectious disease dynamics and host–pathogen coevolution.

Summary Male ornaments are hypothesized to signal the ability of males to produce an effective immune response without extensive oxidative stress and damage to DNA. We examined this hypothesis in male common yellowthroats (Geothlypis trichas), which have two ornaments, a black (eumelanin-based) facial mask and a yellow (carotenoid-based) bib. In our study population, only the black mask is sexually selected. As predicted by the oxidative stress hypothesis, males with larger black masks were more resistant to oxidative stress, as measured by an in vitro assay of the resistance of erythrocytes to haemolysis by free radicals. Furthermore, males with larger masks also tended to have lower levels of glutathione, which was predicted because glutathione inhibits eumelanin production. In contrast, mask size was not related to absolute levels of oxidative stress measured in the plasma. Although the yellow bib is not under sexual selection in our population, males with larger bibs and feathers with greater carotenoid chroma had lower levels of oxidative stress. The oxidative stress hypothesis was first proposed for carotenoid-based ornaments. However, our results suggest that, even in the same individuals, carotenoid and eumelanin-based plumage ornaments may both signal the ability of males to resist or manage oxidative stress.

Supplemental translocations to small, isolated populations can be a valuable strategy to counteract the effects of genetic drift by increasing genetic diversity. We studied the genetic consequences of a translocation of greater prairie-chickens (Tympanuchus cupido pinnatus) to Wisconsin, which has a small population (