Human-induced landscape change associated with habitat loss and fragmentation places wildlife populations at risk. One issue in these landscapes is a change in the prevalence of disease which may result in increased mortality and reduced fecundity. Our understanding of the influence of habitat loss and fragmentation on the prevalence of wildlife diseases is still in its infancy. What is evident is that changes in disease prevalence as a result of human-induced landscape modification are highly variable. The importance of infectious diseases for the conservation of wildlife will increase as the amount and quality of suitable habitat decreases due to human land-use pressures. We review the experimental and observational literature of the influence of human-induced landscape change on wildlife disease prevalence, and discuss disease transmission types and host responses as mechanisms that are likely to determine the extent of change in disease prevalence. It is likely that transmission dynamics will be the key process in determining a pathogen's impact on a host population, while the host response may ultimately determine the extent of disease prevalence. Finally, we conceptualize mechanisms and identify future research directions to increase our understanding of the relationship between human-modified landscapes and wildlife disease prevalence. This review highlights that there are rarely consistent relationships between wildlife diseases and human-modified landscapes. In addition, variation is evident between transmission types and landscape types, with the greatest positive influence on disease prevalence being in urban landscapes and directly transmitted disease systems. While we have a limited understanding of the potential influence of habitat loss and fragmentation on wildlife disease, there are a number of important areas to address in future research, particularly to account for the variability in increased and decreased disease prevalence. Previous studies have been based on a one-dimensional comparison between unmodified and modified sites. What is lacking are spatially and temporally explicit quantitative approaches which are required to enable an understanding of the range of key causal mechanisms and the reasons for variability. This is particularly important for replicated studies across different host-pathogen systems. Furthermore, there are few studies that have attempted to separate the independent effects of habitat loss and fragmentation on wildlife disease, which are the major determinants of wildlife population dynamics in human-modified landscapes. There is an urgent need to understand better the potential causal links between the processes of human-induced landscape change and the associated influences of habitat fragmentation, matrix hostility and loss of connectivity on an animal's physiological stress, immune response and disease susceptibility. This review identified no study that had assessed the influence of human-induced landscape change on the prevalence of a wildlife sexually transmitted disease. A better understanding of the various mechanisms linking human-induced landscape change and the prevalence of wildlife disease will lead to more successful conservation management outcomes.

Wildlife disease prevalence in human-modified landscapes.

Decades of research demonstrate that roads impact wildlife and suggest traffic noise as a primary cause of population declines near roads. We created a “phantom road” using an array of speakers to apply traffic noise to a roadless landscape, directly testing the effect of noise alone on an entire songbird community during autumn migration. Thirty-one percent of the bird community avoided the phantom road. For individuals that stayed despite the noise, overall body condition decreased by a full SD and some species showed a change in ability to gain body condition when exposed to traffic noise during migratory stopover. We conducted complementary laboratory experiments that implicate foraging-vigilance behavior as one mechanism driving this pattern. Our results suggest that noise degrades habitat that is otherwise suitable, and that the presence of a species does not indicate the absence of an impact.

/pdf/a-phantom-road-experiment-reveals-traffic-noise-is-an-3aaeomv8x8.pdf

A phantom road experiment reveals traffic noise is an invisible source of habitat degradation.

Anthropogenic noise is a pervasive pollutant that decreases environmental quality by disrupting a suite of behaviors vital to perception and communication. However, even within populations of noise-sensitive species, individuals still select breeding sites located within areas exposed to high noise levels, with largely unknown physiological and fitness consequences. We use a study system in the natural gas fields of northern New Mexico to test the prediction that exposure to noise causes glucocorticoid-signaling dysfunction and decreases fitness in a community of secondary cavity-nesting birds. In accordance with these predictions, and across all species, we find strong support for noise exposure decreasing baseline corticosterone in adults and nestlings and, conversely, increasing acute stressor-induced corticosterone in nestlings. We also document fitness consequences with increased noise in the form of reduced hatching success in the western bluebird (Sialia mexicana), the species most likely to nest in noisiest environments. Nestlings of all three species exhibited accelerated growth of both feathers and body size at intermediate noise amplitudes compared with lower or higher amplitudes. Our results are consistent with recent experimental laboratory studies and show that noise functions as a chronic, inescapable stressor. Anthropogenic noise likely impairs environmental risk perception by species relying on acoustic cues and ultimately leads to impacts on fitness. Our work, when taken together with recent efforts to document noise across the landscape, implies potential widespread, noise-induced chronic stress coupled with reduced fitness for many species reliant on acoustic cues.

https://www.pnas.org/content/pnas/115/4/E648.full.pdf

Chronic anthropogenic noise disrupts glucocorticoid signaling and has multiple effects on fitness in an avian community.

Hormones in the city: endocrine ecology of urban birds.

SUMMARY Roads have been associated with behavioral and physiological changes in wildlife. In birds, roads decrease reproductive success and biodiversity and increase physiological stress. Although the consequences of roads on individuals and communities have been well described, the mechanisms through which roads affect birds remain largely unexplored. Here, we examine one mechanism through which roads could affect birds: traffic noise. We exposed nestling mountain white-crowned sparrows ( Zonotrichia leucophrys oriantha ) to experimentally elevated traffic noise for 5 days during the nestling period. Following exposure to traffic noise we measured nestling stress physiology, immune function, body size, condition and survival. Based on prior studies, we expected the traffic noise treatment to result in elevated stress hormones (glucocorticoids), and declines in immune function, body size, condition and survival. Surprisingly, nestlings exposed to traffic noise had lower glucocorticoid levels and improved condition relative to control nests. These results indicate that traffic noise does affect physiology and development in white-crowned sparrows, but not at all as predicted. Therefore, when evaluating the mechanisms through which roads affect avian populations, other factors (e.g. edge effects, pollution and mechanical vibration) may be more important than traffic noise in explaining elevated nestling stress responses in this species.

/pdf/effects-of-experimentally-elevated-traffic-noise-on-nestling-1xh3j5y7u0.pdf

Effects of Experimentally Elevated Traffic Noise on Nestling White-Crowned Sparrow Stress Physiology, Immune Function and Life History

http://ondicrino.com/wp-content/uploads/2014/10/10.1016j.ygen_.2011.06.001.pdf

Proximity to a high traffic road: glucocorticoid and life history consequences for nestling white-crowned sparrows.

Acute stress decreases corticosterone-binding globulin for 24 hours and a second stressor during this time increases sleep disruptions in Mountain White-crowned Sparrows

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Proximity to a high traffic road: glucocorticoid and life history consequences for nestling white-crowned sparrows.

Acute stress decreases corticosterone-binding globulin for 24 hours and a second stressor during this time increases sleep disruptions in Mountain White-crowned Sparrows