Proceedings of the Vertebrate Pest Conference

Human activities threaten wildlife with a variety of novel stressors such as exposure to toxicants. Anticoagulant rodenticides (ARs) are toxicants applied worldwide and through bioaccumulation, threaten species that prey on poisoned rodents or their predators. We studied a population of urban bobcats in southern California that declined rapidly from 2002-2005 due to notoedric mange. We first assessed prevalence of AR exposure using blood and liver samples across the population and found widespread exposure (>90%). Death associated with mange was strongly correlated with cumulative first- and second-generation AR exposure. These findings suggested that exposure to both first- and second-generation ARs were an underlying cause of the disease. We next aimed to understand the sublethal immunological and physiological effects of AR exposure in this natural population. We used two approaches: 1) we used a comprehensive suite of health assays (complete blood counts, blood chemistry assessment, and immunological profiling), and 2) we quantified AR-induced differential gene expression in blood for a subset of individuals. We found that sublethal AR exposure, primarily measured as exposure to diphacinone, is associated with hallmark indicators of generalized systemic inflammation that in persistence could promote immune dysfunction. Further, differential gene expression findings supported the results of immunological profiling. Further, a decrease in the expression of genes associated with epithelial maintenance simultaneous to a decrease in gene expression linked with ectoparasitic immune response may explain the link between AR exposure and mange vulnerability. Such indirect effects of sublethal exposure exemplify the challenge of protecting wild populations from common toxicants in human-dominated environments.