Symbiotic microbes that inhabit animal scent glands can produce volatile compounds used as chemical signals by the host animal. Though several studies have demonstrated correlations between scent gland bacterial community structure and host animal odour profiles, none have systematically demonstrated a causal relationship. In birds, volatile compounds in preen oil secreted by the uropygial gland serve as chemical cues and signals. Here, we tested whether manipulating the uropygial gland microbial community affects chemical profiles in the dark-eyed junco (Junco hyemalis). We found an effect of antibiotic treatment targeting the uropygial gland on both bacterial and volatile profiles. In a second experiment, we cultured bacteria from junco preen oil, and found that all of the cultivars produced at least one volatile compound common in junco preen oil, and that most cultivars produced multiple preen oil volatiles. In both experiments, we identified experimentally generated patterns in specific volatile compounds previously shown to predict junco reproductive success. Together, our data provide experimental support for the hypothesis that symbiotic bacteria produce behaviourally relevant volatile compounds within avian chemical cues and signals.

Urban habitats can shape interactions between hosts and parasites by altering not only exposure rates but also within-host processes. Artificial light at night (ALAN) is common in urban environments, and chronic exposure can impair host immunity in ways that may increase infection. However, studies of causal links between this stressor, immunity, and infection dynamics are rare, particularly in migratory animals. Here, we experimentally tested how ALAN affects cellular immunity and haemosporidian parasite intensity across the annual cycle of migrant and resident subspecies of the dark-eyed junco ( Junco hyemalis ). We monitored an experimental group exposed to light at night and a control group under natural light/dark cycles as they passed through short days simulating early spring to longer days simulating the breeding season, followed by autumn migration. Using generalized additive mixed models, we show that ALAN increased inflammation, and leucocyte counts were greatest in early spring and autumn. At the start of the experiment, few birds had active infections based on microscopy, but PCR revealed many birds had chronic infections. ALAN increased parasitaemia across the annual cycle, with strong peaks in spring and autumn that were largely absent in control birds. As birds were kept in indoor aviaries to prevent vector exposure, this increased parasitaemia indicates relapse of chronic infection during costly life-history stages (i.e. reproduction). Although the immunological and parasitological time series were in phase for control birds, cross-correlation analyses also revealed ALAN desynchronized leucocyte profiles and parasitaemia, which could suggest a general exaggerated inflammatory response. Our study shows how a common anthropogenic influence can shape within-host processes to affect infection dynamics.

Annual migration is common across animal taxa and can dramatically shape the spatial and temporal patterns of infectious disease. Although migration can decrease infection prevalence in some contexts, these energetically costly long-distance movements can also have immunosuppressive effects that may interact with transmission processes in complex ways. Here, we develop a mechanistic model for the reactivation of latent infections driven by physiological changes or energetic costs associated with migration (i.e. ‘migratory relapse’) and its effects on disease dynamics. We determine conditions under which migratory relapse can amplify or reduce infection prevalence across pathogen and host traits (e.g. infectious periods, virulence, overwinter survival, timing of relapse) and transmission phenologies. We show that relapse at either the start or end of migration can dramatically increase prevalence across the annual cycle and may be crucial for maintaining pathogens with low transmissibility and short infectious periods in migratory populations. Conversely, relapse at the start of migration can reduce the prevalence of highly virulent pathogens by amplifying culling of infected hosts during costly migration, especially for highly transmissible pathogens and those transmitted during migration or the breeding season. Our study provides a mechanistic foundation for understanding the spatio-temporal patterns of relapsing infections in migratory hosts, with implications for zoonotic surveillance and understanding how infection patterns will respond to shifts in migratory propensity associated with environmental change. Further, our work suggests incorporating within-host processes into population-level models of pathogen transmission may be crucial for reconciling the range of migration–infection relationships observed across migratory species.

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Organisms are expected to invest less in reproduction in response to a stressor, but theory predicts that this effect should depend on the frequency and duration of stressors in the environment. Here, we investigated how an acute stressor affected testes function in a songbird, and how chronic stressors influenced the acute stress response. We exposed male dark-eyed juncos () either to chronic or minimal (control) disturbance during testicular recrudescence, after which we measured baseline testosterone, testosterone after an acute handling stressor, and capacity to produce testosterone after hormonal stimulation. In a 2×2 design, we then killed males from the two chronic treatment groups either immediately or after an acute stressor to investigate the effect of long- and short-term stressors on the testicular transcriptome. We found that chronically disturbed birds had marginally lower baseline testosterone. The acute stressor suppressed testosterone in control birds, but not in the chronic disturbance group. The ability to elevate testosterone did not differ between the chronic treatments. Surprisingly, chronic disturbance had a weak effect on the testicular transcriptome, and did not affect the transcriptomic response to the acute stressor. The acute stressor, on the other hand, upregulated the cellular stress response and affected expression of genes associated with hormonal stress response. Overall, we show that testicular function is sensitive to acute stressors but surprisingly robust to long-term stressors, and that chronic disturbance attenuates the decrease in testosterone in response to an acute stressor.