Widespread anticoagulant poison exposure is linked with immune dysregulation and severe notoedric mange in urban bobcats

peer reviewe

Data from: Genome-wide expression reveals multiple systemic effects associated with detection of anticoagulant poisons in bobcats (Lynx rufus)

Anticoagulant rodenticides (ARs) are indiscriminate toxicants that threaten non-target predatory and scavenger species through secondary poisoning. Accumulating evidence suggests that AR exposure may have disruptive sublethal consequences on individuals that can affect fitness. We evaluated AR-related effects on genome wide expression patterns in a population of bobcats in southern California. We identify differential expression of genes involved in xenobiotic metabolism, endoplasmic reticulum stress response, epithelial integrity, and both adaptive and innate immune function. Further, we find that differential expression of immune related genes may be attributable to AR-related effects on leukocyte differentiation. Collectively, our results provide an unprecedented understanding of the sublethal effects of AR exposure on a wild carnivore. These findings highlight potential detrimental effects of ARs on a wide variety of species worldwide that may consume poisoned rodents and indicate the need to investigate gene expression effects of other toxicants added to natural environments by humans

Data from: Disease and freeways drive genetic change in urban bobcat populations

Urbanization profoundly impacts animal populations by causing isolation, increased susceptibility to disease, and exposure to toxicants. Genetic effects include reduced effective population size, increased population substructure, and decreased adaptive potential. We investigated the influence that urbanization and a disease epizootic had on the population genetics of bobcats (Lynx rufus) distributed across a highly fragmented urban landscape. We genotyped more than 300 bobcats, sampled from 1996-2012, for variation at nine neutral and seven immune gene-linked microsatellite loci. We found that two freeways are significant barriers to gene flow. Further, a 3-year disease epizootic, associated with secondary anticoagulant rodenticide exposure, caused a population bottleneck that led to significant genetic differentiation between pre- and post-disease populations that was greater than that between populations separated by major freeways for > 60 years. However, balancing selection acted on immune-linked loci during the epizootic, maintaining variation at functional regions. Conservation assessments need to assay loci that are potentially under selection in order to better preserve the adaptive potential of populations at the urban-wildland interface. Further, inter-connected regions that contain appropriate habitat for wildlife will be critical to the long-term viability of animal populations in urban landscapes

Serieys_et_al_2014_EvolutionaryApplications_AccessibleDataSheet

Data for nine neutral and seven immune-linked microsatellite markers for bobcats sampled in Los Angeles and Ventura Counties of Southern California from 1996-2012. File contains three excel sheets: 1) data for neutral markers, 2) data for immune-linked markers, and 3) an information sheet assist in interpretation of sample data. Sample type, region sampled, year sampled and exact locations included for each sample

Data from: Urbanization and anticoagulant poisons promote immune dysfunction in bobcats

Understanding how human activities influence immune response to environmental stressors can support biodiversity conservation across increasingly urbanizing landscapes. We studied a bobcat (Lynx rufus) population in urban southern California that experienced a rapid population decline from 2002–2005 due to notoedric mange. Because anticoagulant rodenticide (AR) exposure was an underlying complication in mange deaths, we aimed to understand sublethal contributions of urbanization and ARs on 65 biochemical markers of immune and organ function. Variance in immunological variables was primarily associated with AR exposure and secondarily with urbanization. Use of urban habitat and AR exposure has pervasive, complex and predictable effects on biochemical markers of immune and organ function in free-ranging bobcats that include impacts on neutrophil, lymphocyte and cytokine populations, total bilirubin and phosphorus. We find evidence of both inflammatory response and immune suppression associated with urban land use and rat poison exposure that could influence susceptibility to opportunistic infections. Consequently, AR exposure may influence mortality and has population-level effects, as previous work in the focal population has revealed substantial mortality caused by mange infection. The secondary effects of anticoagulant exposure may be a worldwide, largely unrecognized problem affecting a variety of vertebrate species in human-dominated environments

Genome-wide expression reveals multiple systemic effects associated with detection of anticoagulant poisons in bobcats (Lynx rufus).

Anticoagulant rodenticides (ARs) are indiscriminate toxicants that threaten nontarget predatory and scavenger species through secondary poisoning. Accumulating evidence suggests that AR exposure may have disruptive sublethal consequences on individuals that can affect fitness. We evaluated AR-related effects on genome-wide expression patterns in a population of bobcats in southern California. We identify differential expression of genes involved in xenobiotic metabolism, endoplasmic reticulum stress response, epithelial integrity and both adaptive and innate immune function. Further, we find that differential expression of immune-related genes may be attributable to AR-related effects on leucocyte differentiation. Collectively, our results provide an unprecedented understanding of the sublethal effects of AR exposure on a wild carnivore. These findings highlight potential detrimental effects of ARs on a wide variety of species worldwide that may consume poisoned rodents and indicate the need to investigate gene expression effects of other toxicants added to natural environments by humans

Molecular detection of tick-borne pathogens in caracals (Caracal caracal) living in human-modified landscapes of South Africa

Background: Wild carnivores living alongside humans and domestic animals are vulnerable to changes in the infectious disease dynamics in their populations. The aims of this study were to determine the prevalence and diversity of selected tick-borne pathogens (TBPs) of veterinary and/or zoonotic concern in wild populations of caracals (Caracal caracal) occurring in human-modified landscapes in South Africa. Using molecular techniques, we screened 57 caracal blood samples for infection by rickettsial bacteria and piroplasms in three regions of South Africa: rangeland in the Central Karoo (n = 27) and Namaqualand (n = 14) as well as the urban edge of the Cape Peninsula (n = 16) of South Africa. To characterise pathogen identity, we sequenced the 18S rRNA and 16S rRNA genes from positive samples and analysed sequences within a phylogenetic framework. We also examine the diversity of potential tick vectors. Results: All individuals tested were infected with at least one tick-borne pathogen. Pathogens included Hepatozoon felis, Babesia felis, Babesia leo and a potentially novel Babesia species. An Anaplasma species previously described in South African domestic dogs was also found in 88% of urban edge caracals. Higher rates of co-infection characterised urban edge caracals (81% vs 15% and 0% in the two rangeland populations), as well as a greater incidence of mixed infections. Host attached tick species include Haemaphysalis elliptica, an important pathogen vector among carnivore hosts. Conclusions: This study confirms the occurrence of previously undocumented tick-borne pathogens infecting free-ranging caracals in human-modified landscapes. We identify clear differences in the pathogen profiles among our study populations and discuss the likely health costs to caracals living adjacent to urban areas.Arts and Sciences, Irving K. Barber School of (Okanagan)Non UBCBiology, Department of (Okanagan)ReviewedFacult

Widespread Anticoagulant Poison Exposure is Linked with Immune Dysregulation and Severe Notoedric Mange in Urban Bobcats

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