A Look to the Future: New and Innovative Invasive Wildlife Management and Eradication Technologies

Certain wildlife tools and discoveries have been true “game changers” for invasive species management and eradications on islands. This article provides an overview of 3 cutting-edge technologies that are being eagerly pursued, but are not yet operational, for invasive wildlife management to build efficiency, reduce environmental impacts, and/or improve animal welfare practices

Environmental Contaminant Concentrations in Canada Goose (\u3ci\u3eBranta canadensis\u3c/i\u3e) Muscle: Probabilistic Risk Assessment for Human Consumers

The issue of food insecurity affects millions of people in the United States every year. Often these people rely on soup kitchens, food banks, and shelters for proper meals, and these organizations often depend on donations to meet needs. One of the most limited food resources is meat. To help alleviate this problem, the U.S. Department of Agriculture Wildlife Services donates more than 60 tons of wild game (deer, moose, feral hogs, goats, geese, and ducks) to a variety of charitable organizations each year. Although commercially produced meat routinely undergoes screening for contaminants, potential exposure to environmental contaminants from eating wild game is not well characterized. In this study, the concentration of 17 contaminants of concern in the breast meat of wild geese was examined. These concentrations were then used in a probabilistic model to estimate potential risk associated with consumption of this meat. Based on model predictions, more than 99% of all adults were below exposure limits for all of the compounds tested. For all consumer age classes modeled, consumption of wild goose meat may expose a small fraction of these populations to levels of lead higher than the recommended exposure limits. Similarly, mercury exposure was predicted to be higher than the recommended limits when the meat was served as steaks. This information about concentrations of contaminants of concern in goose meat and potential exposures associated with meat consumption based on probabilistic models will enable others to make informed decisions about the risks associated with the consumption of wild meat

Environmental Contaminant Concentrations in Canada Goose (\u3ci\u3eBranta canadensis\u3c/i\u3e) Muscle: Probabilistic Risk Assessment for Human Consumers

The issue of food insecurity affects millions of people in the United States every year. Often these people rely on soup kitchens, food banks, and shelters for proper meals, and these organizations often depend on donations to meet needs. One of the most limited food resources is meat. To help alleviate this problem, the U.S. Department of Agriculture Wildlife Services donates more than 60 tons of wild game (deer, moose, feral hogs, goats, geese, and ducks) to a variety of charitable organizations each year. Although commercially produced meat routinely undergoes screening for contaminants, potential exposure to environmental contaminants from eating wild game is not well characterized. In this study, the concentration of 17 contaminants of concern in the breast meat of wild geese was examined. These concentrations were then used in a probabilistic model to estimate potential risk associated with consumption of this meat. Based on model predictions, more than 99% of all adults were below exposure limits for all of the compounds tested. For all consumer age classes modeled, consumption of wild goose meat may expose a small fraction of these populations to levels of lead higher than the recommended exposure limits. Similarly, mercury exposure was predicted to be higher than the recommended limits when the meat was served as steaks. This information about concentrations of contaminants of concern in goose meat and potential exposures associated with meat consumption based on probabilistic models will enable others to make informed decisions about the risks associated with the consumption of wild meat

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

Effects of Repeated Sublethal External Exposure to Deep Water Horizon Oil on the Avian Metabolome

We assessed adverse effects of external sublethal exposure of Deepwater Horizon, Mississippi Canyon 252 oil on plasma and liver metabolome profiles of the double-crested cormorant (Phalacrocorax auritus), a large (1.5 to 3.0 kg) diving waterbird common in the Gulf of Mexico. Metabolomics analysis of avian plasma showed significant negative effects on avian metabolic profiles, in some cases after only two external exposures (26 g cumulative) to oil. We observed significant (p \u3c 0.05) changes in intermediate metabolites of energy metabolism and fatty acid and amino acid metabolic pathways in cormorants after repeated exposure to oil. Exposure to oil increased several metabolites (glycine, betaine, serine and methionine) that are essential to the one-carbon metabolism pathway. Lipid metabolism was affected, causing an increase in production of ketone bodies, suggesting lipids were used as an alternative energy source for energy production in oil exposed birds. In addition, metabolites associated with hepatic bile acid metabolism were affected by oil exposure which was correlated with changes observed in bile acids in exposed birds. These changes at the most basic level of phenotypic expression caused by sublethal exposure to oil can have effects that would be detrimental to reproduction, migration, and survival in avian species

Is Sensitivity to Anticoagulant Rodenticides Affected by Repeated Exposure in Hawks?

A seminal question in wildlife toxicology is whether exposure to an environmental contaminant, in particular a secondgeneration anticoagulant rodenticide, can evoke subtle long lasting effects on body condition, physiological function and survival. Many reports indicate that non-target predators often carry residues of several rodenticides, which is indicative of multiple exposures. An often-cited study in laboratory rats demonstrated that exposure to the second-generation anticoagulant rodenticide brodifacoum prolongs blood clotting time for a few days, but weeks later when rats were re-exposed to the first-generation anticoagulant rodenticide warfarin, coagulopathy was more pronounced in brodifacoum-treated rats than naïve rats exposed to warfarin. To further investigate this phenomenon, American kestrels were fed environmentally realistic doses of chlorophacinone or brodifacoum for a week, and following a week-long recovery period, birds were then challenged with a low-level dietary dose of chlorophacinone. In the present study, neither hematocrit nor clotting time (prothrombin time, Russell’s viper venom time) were differentially affected in sequentially exposed kestrels compared to naïve birds fed low-level dietary dose of chlorophacinone. While the present findings do not reveal lasting effects of anticoagulant exposure on blood clotting ability, findings in laboratory rats and other species have demonstrated such effects on blood clotting, and even other molecular pathways associated with immune function and xenobiotic metabolism. Additional studies using an environmentally realistic route of exposure and dose are underway to further test this hypothesis

Development of Dietary-Based Toxicity Reference Values to Assess the Risk of Chlorophacinone to Non-Target Raptorial Birds

Regulatory changes in the use of some second-generation anticoagulant rodenticides in parts of North America may result in expanded use of first-generation anticoagulant rodenticides (FGARs). Recent toxicological studies with captive raptors have demonstrated that these species are considerably more sensitive to the FGAR diphacinone than traditional avian wildlife test species (mallard, bobwhite). We have now examined the toxicity of the FGAR chlorophacinone (CPN) to American kestrels fed rat tissue mechanically amended with CPN, or rat tissue containing biologically-incorporated CPN, for 7 days. Nominal CPN concentrations in these diets were 0.15, 0.75, and 1.5 μg/g food wet weight, and actual CPN concentration in diets were analytically verified as being close to target values. Food intake was consistent among groups, body weight fluctuated by less than 6%, exposure and adverse effects were generally dose-dependent, and there were no dramatic differences in toxicity between mechanically-amended and biologically-incorporated CPN diets. Using benchmark dose statistical methods, toxicity reference values at which clotting times were prolonged in 50% of the kestrels was estimated to be about 80 μg CPN consumed/kg body weight-day for prothrombin time and 40 μg CPN/kg body weight-day for Russell’s viper venom time. Based upon carcass CPN residues reported in rodents from field baiting studies, empirical measures of food consumption in kestrels, and dietary-based toxicity reference values derived from the 7-day exposure scenario, some free-ranging raptors consuming CPN-exposed prey might exhibit coagulopathy and hemorrhage. These sublethal responses associated with exposure to environmentally realistic concentrations of CPN could compromise survival of exposed birds

Low Secondary Risks for Captive Coyotes from a Sodium Nitrite Toxic Bait for Invasive Wild Pigs

An acute toxic bait is being developed to deliver micro‐encapsulated sodium nitrite (SN) to stimulate severe methemoglobinemia and humane death for invasive wild pigs (Sus scrofa), thereby providing a new tool for reducing their populations. During April 2016, we evaluated sensitivity to SN and outcomes of secondary consumption in the ubiquitous mammalian scavenger, coyote (Canis latrans), to determine secondary risks of consuming carcasses of wild pigs that died from consuming the SN toxic bait. At the National Wildlife Research Center in Fort Collins, Colorado, USA, we first evaluated whether coyotes fed carcasses of domestic pigs killed by consumption of SN bait showed signs of SN intoxication. Second, we conducted chemical analysis of residual SN in the coyotes for evidence of SN passing from pigs to coyotes. Last, we conducted an acute oral toxicity test (LD50) with SN for coyotes by feeding them meatballs containing capsules of SN. We found no evidence that captive coyotes experienced SN intoxication from consuming on carcasses that had been freshly poisoned with SN, despite consuming ¯ x = 1.6 kg of tissues/coyote within 24 hours. None of the captive coyotes consumed digestive tracts or stomach contents from poisoned carcasses, which contained the highest levels of residual SN. Chemical analysis indicated that only ≤34.14 mg/kg of residual SN were passed from the tissues of the pigs into the coyotes, confirming that SN does not bioaccumulate. All coyotes quickly vomited various doses of SN during the LD50 test and fully recovered, suggesting a natural defense against secondary poisoning from SN. Testing with captive coyotes indicates that the risks of secondary poisoning for free‐ranging coyotes are likely low, although field‐testing should be used to confirm

Toxicity reference values for chlorophacinone and their application for assessing anticoagulant rodenticide risk to raptors

Despite widespread use and benefit, there are growing concerns regarding hazards of second-generation anticoagulant rodenticides to non-target wildlife which may result in expanded use of first-generation compounds, including chlorophacinone (CPN). The toxicity of CPN over a 7-day exposure period was investigated in American kestrels (Falco sparverius) fed either rat tissue mechanically- amended with CPN, tissue from rats fed Rozol bait (biologically-incorporated CPN), or control diets (tissue from untreated rats or commercial bird of prey diet) ad libitum. Nominal CPN concentrations in the formulated diets were 0.15, 0.75 and 1.5 µg/g food wet weight, and measured concentrations averaged 94 % of target values. Kestrel food consumption was similar among groups and body weight varied by less than 6 %. Overt signs of intoxication, liver CPN residues, and changes in prothrombin time (PT), Russell’s viper venom time (RVVT) and hematocrit, were generally dose-dependent. Histological evidence of hemorrhage was present at all CPN dose levels, and most frequently observed in pectoral muscle and heart. There were no apparent differences in toxicity between mechanically-amended and biologically-incorporated CPN diet formulations. Dietary-based toxicity reference values at which clotting times were prolonged in 50 % of the kestrels were 79.2 µg CPN consumed/kg body weight-day for PT and 39.1 µg/kg body weight-day for RVVT. Based upon daily food consumption of kestrels and previously reported CPN concentrations found in small mammals following field baiting trials, these toxicity reference values might be exceeded by free-ranging raptors consuming such exposed prey. Tissue-based toxicity reference values for coagulopathy in 50 % of exposed birds were 0.107 µg CPN/g liver wet weight for PT and 0.076 µg/g liver for RVVT, and are below the range of residue levels reported in raptor mortality incidents attributed to CPN exposure. Sublethal responses associated with exposure to environmentally realistic concentrations of CPN could compromise survival of free-ranging raptors, and should be considered in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs