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Veterinary Research 2012
The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis)Abstract: Host exposure to stressors can have ramifications for the spread, persistence or emergence of pathogens [1]. In this paper, we consider a stressor to be any external factor that elicits a stress response that is characterized by impairment of an organism's ability to function normally, including their capacity to mount an immune response [2]. When an organism is exposed to a stressor, its resistance to infection may be reduced through this suppression of the immune system [3-5]. Lowered resistance may increase the chance of infection upon exposure to a parasite/pathogen and/or lead to greater amplification of the pathogen in the host. These effects might lead to higher morbidity of the infected animal, enabling vectors to obtain blood meals more effectively and become infected themselves, thus spreading the infection more easily. Whereas stress is well-associated with increased susceptibility to disease [6], links among stressors, their physiological mediators, and resistance to pathogens are not well established, especially in free-living animals. Stressors might take many forms in natural systems including inclement weather, food shortages, territorial conflicts, or threat of predation [2]. In human-modified landscapes, stressors may be even more common including such factors as noise, air, and water pollution, greater abundance of predators, and low-quality habitat and food availability [7-9].In the US, a particularly important zoonotic pathogen is West Nile virus, or WNV. WNV causes morbidity and mortality in birds, mammals, domestic livestock and humans [10]. WNV has worldwide distribution; it has been found in North America, Australia, Europe, Asia and Africa [11]. For North American birds, WNV can cause substantial morbidity and mortality, particularly for some species of passerines [12-14], owls [15] and sage grouse (Centrocercus urophasianus) [16]. The enzootic cycle of WNV occurs between the vector mosquitoes, primarily Culex spp., and Passeriform birds [1
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