Life histories of animals tend to vary along a slow to fast continuum. Those with fast life histories have shorter life spans, faster development, and higher reproductive rates relative to animals with slower life histories. These differences in life histories have been linked to differences in investment in immunological defenses. Animals with faster life histories are predicted to invest relatively more in innate immune responses, which include rapidly‐deployed, non‐specific defenses against a broad spectrum of invaders. On the other hand, animals with slower life histories are predicted to invest relatively more in adaptive immune responses, which are more slowly‐deployed and are highly pathogen‐specific. These predictions have been confirmed in some taxa, but other studies have not found this association. We tested this prediction by measuring innate and adaptive immunity of white‐footed mice Peromyscus leucopus, chipmunks Tamias striatus, and gray squirrels Sciurus carolinensis, three species of rodents that inhabit deciduous forests in the northeastern US. These species exhibit a range of life histories, with mice having a relatively fast life history, squirrels a relatively slow one, and chipmunks an intermediate one. We found mice to have the greatest ‘bacterial killing capacity’, a common measure of innate immunity, and squirrels the lowest, consistent with the pace‐of‐life immune‐defense hypothesis. We also found squirrels to mount the most pronounced antibody response when challenged with lipopolysaccharide (LPS), an immunogenic component of bacteria, while mice had the lowest, again consistent with predictions based on their life histories. These results have implications beyond ecoimmunology because the probability that a host species will transmit an infection – its ‘reservoir competence’ – has been linked to its immune strategy. Understanding the relationship between immunology and reservoir competence is a critical frontier in the ecology of infectious diseases.

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The kori bustard (Ardeotis kori) is a popular avian resident of zoos and wild animal parks throughout North America and Europe. As this species' numbers continue to decline throughout its native African range, the need for its successful captive management becomes increasingly apparent. To this end, an understanding of the factors causing morbidity and mortality in the captive kori bustard population is critical. Here, the demographics, husbandry practices, and causes of morbidity and mortality of 94% of captive kori bustards (198 individuals) housed in zoos throughout the United States between 1988 and 2008 are described, and suggestions for captive management targets in this species are presented. The most common clinical and pathologic findings observed were lameness (48 cases), gastrointestinal parasitism (45 cases), and wing integumentary trauma (32 cases). Trauma was a very common cause of morbidity (135 cases) and was the most common cause of mortality (53 individuals, 40% of deceased animals). Considering the high prevalence of traumatic injury and death observed in this population, captive management of kori bustards should focus on developing strategies that minimize opportunity for injury. Priorities include preventing exposure to potentially hostile exhibit mates, decreasing stress associated with human interactions, and researching the effects of diet on skeletal development of young birds.

The kori bustard ( Ardeotis kori) is one of the largest extant flighted birds and is displayed in zoos primarily in North America and Europe. In captivity, kori bustard diets are primarily based on animal proteins, whereas in the wild these birds eat a wide variety of plants, insects, and small vertebrate prey. The purpose of this study was to compare circulating iron, total iron binding capacity, and percent transferrin saturation levels in apparently healthy wild and captive kori bustards. Adult captive kori bustards had slightly higher percent transferrin saturation levels than juvenile captive birds, although this finding was not statistically significant. This information can be referenced as a guide for the assessment of nutrition and health in captive birds.

Feline upper respiratory tract disease (FURTD), often caused by infections etiologies, is a multifactorial syndrome affecting feline populations worldwide. Because of its highly transmissible nature, infectious FURTD is most prevalent anywhere cats are housed in groups such as animal shelters, and is associated with negative consequences such as decreasing adoption rates, intensifying care costs, and increasing euthanasia rates. Understanding the etiology and pathophysiology of FURTD is thus essential to best mitigate the negative consequences of this disease. Clinical signs of FURTD include acute respiratory disease, with a small fraction of cats developing chronic sequelae. It is thought that nasal mucosal microbiome changes play an active role in the development of acute clinical signs, but it remains unknown if the microbiome may play a role in the development and progression of chronic clinical disease. To address the knowledge gap surrounding how microbiomes link to chronic FURTD, we asked if microbial community structure of upper respiratory and gut microbiomes differed between cats with chronic FURTD signs and clinically normal cats. We selected 8 households with at least one cat exhibiting chronic clinical FURTD, and simultaneously collected samples from cohabitating clinically normal cats. Microbial community structure was assessed via 16S rDNA sequencing of both gut and nasal microbiome communities. Using a previously described ecophylogenetic method, we identified 136 and 89 microbial features within gut and nasal microbiomes respectively that significantly associated with presence of active FURTD clinical signs in cats with a history of chronic signs. Overall, we find that nasal and gut microbial community members associate with the presence of chronic clinical course, but more research is needed to confirm our observations.