Cultivation of marijuana and the associated use of toxicants have been recently documented in occupied fisher habitat. In addition to the four fisher mortalities attributed to anticoagulant rodenticides by Gabriel et al. , we documented nine additional pesticide toxicosis cases in the present study. The average incidence of toxicosis cases per year for the five year Gabriel et al. study spanning 2007–2011 was 5.6% . However, in the final three years of our study, we detected an increase in incidence per year to 18.7% . Exposure also increased from 79% to 85% for the same two time periods. This increase in cases and exposure could signify either an increase in the number of cultivation sites or area impacted or that cultivators are increasing the level of toxicants being dispersed within occupied fisher home ranges. In either case, this anthropogenic threat is of increasing concern. Previous reports of cholecalciferol poisonings have not been reported in a remote forest dwelling carnivore. This type of toxicant has been promoted as an alternative to anticoagulant rodenticides due to the minimized risk for secondary poisonings. Nevertheless, plant and animal based food flavorizers are often incorporated into rodenticides to enhance palatability to omnivorous rodents. Because fishers are omnivorous, they could be susceptible to primary poisoning if they are attracted to these compounds when they are impregnated with flavorizers. In addition, the massive amount of rodenticide dispersed at some cultivation sites e.g>40 kg in some sites, rolling grow table which have cultivation footprints of typically less than 0.2ha likely pose a secondary risk of poisoning to fishers. Fishers may consume numerous prey that may have recently ingested these rodenticides, with the likely exception of cholecalciferol.
As was noted previously for a subset of cases, toxicosis deaths occurred primarily in the spring. Additionally, males were more likely than females to die of poisoning relative to predation and other causes. This finding may be due to fewer predation events involving males than females or the higher prevalence of poison-related mortality in males. These trends could also be due to behavioral factors. Female fishers in California increase their crepuscular and diurnal activity in spring to saThisfy the additional energy requirements of lactation and care of weaned kits but typically within the confines of their established home-ranges. Male fishers may make extensive forays outside their normal home ranges in spring to search out females for mating opportunities. Marijuana cultivation coincides with the increased activity of fishers in early spring and frequently involves dispersal of large amounts of toxicants near occupied fisher home ranges. Furthermore, survival of female fishers in one population was found to be influenced by the number of marijuana cultivation sites in the 95% fixed kernel home range. The relationship between the number of ARs to which a fisher has been exposed and the increasing probability of death due to poisoning suggests that these pesticides may be acting additively or synergistically. However, little experimental data are available demonstrating exposure to multiple ARs increasing the risk of coagulopathy. Our data suggest that coagulopathy risk increases significantly with each additional new AR compound exposure, though it’s possible this pattern is reflecting an additive relationship between AR number and cumulative level of exposure. However, potential synergistic mechanisms need to be addressed due to the significant amount of other pesticides, herbicides, molluscicides and fungicides documented at marijuana cultivation sites. Because fishers are exposed to > 1.7 different ARs on average, our concerns on the potential unknown mechanisms of deleterious effects of multiple ARs warrants further investigation.
Human-related mortalities were relatively rare, and although a small number were associated with research activities, such mortalities represented < 1% of the captured fishers. This figure is comparable to other studies. Vehicle-related mortalities were also relatively rare with only three marked fishers suffering vehicle strikes, which represented < 2% of all mortalities. The higher number of uncollared fishers found killed in roadways suggests that roadkill may be a more local concern, associated with individual high-traffic corridors. Field biologists did not always accurately identify general causes of disease. We found only a moderate correspondence between biologist-determined and necropsy-confirmed causes of death except for the detection of disease-related mortalities, which were significantly underestimated by initial field assessments. For example, the three fisher deaths attributed to CDV and many of the toxicosis cases were preliminarily attributed to other causes in the field. The underestimation of disease has been observed in other wildlife studies because gross observations in the field are inadequate to detect subtle signs of disease. These findings fortify the need for full necropsies when studying causes of mortality, especially when knowledge of the frequencies of cause-specific mortality is required in managing or reducing the most significant limiting factors for fishers. Although predation was often correctly identified by both field biologists and the pathologists, the incorporation of molecular forensic approaches coupled with traditional pathology allowed us to more definitively identify both predation events and predator species. Predation is often implicated as the cause of mortality when field evidence such as tracks near or adjacent to the carcass, bite wounds, wound patterns or feces and/or hair near the carcass are found. However in our study, field observations misclassified 5 fishers as predation due to circumstantial predator evidence found near the carcass .
Field observations can be misleading, for example, bite wounds in soft Thissue often change shape and size due to environmental factors and visual artifacts that resemble ante-mortem hemorrhaging can occur due to autolysis, scavengers consuming Thissue and releasing non-clotted blood, or freezing and defrosting of a carcass. Finally, we present mainly the proximate causes of mortality for fishers though there were a few cases where ultimate causes could be ascertained e.g. anesthesia related death but clinically infected with CDV. However, it would be difficult, if not impossible, to determine whether some of the predation mortalities were ultimately going to result in toxicosis. Many of the predation cases exhibited ante-mortem hemorrhaging that could have been due directly to predation or alternatively, AR exposure. Anticoagulant rodenticides have previously been shown to cause lethargy and weakness in exposed animals, but teasing these two causes of death apart was not possible. This study presents the first large assessment of cause-specific mortality frequencies in California fishers. We have identified predation and natural disease as the top two mortality factors. In addition, mortality from and exposure to toxicants appears to be on the rise and we have found exposure to multiple ARs increases probability of death from these compounds. Increases of additive mortality of only 10% can prevent fisher population expansion even in the presence of suitable habitat with no dispersal barriers. Therefore, the high proportion of fisher mortality consisting of predation and disease may help explain the lack of growth and expansion of these populations to nearby suitable habitat. However, the growing number of toxicosis cases in fishers and the correlation of contributing mechanisms such as marijuana cultivation within fisher habitat suggest an emerging threat. Beyond direct poisoning, rodenticides have the potential to limit fitness through prey depletion and heightened competition between fishers and other carnivores. Future research should focus on the relationship between marijuana cultivation and associated rodenticide use and prey population cycles because carnivore population dynamics are often heavily influenced by fluctuations in prey base. Managing these threats should focus not only on the impacts on current fisher populations but also the reduction of threats that may be limiting expansion for future population growth. One recommendation is the complete removal of toxicants left at current and historicaltrespass marijuana grow sites. Most sites are not remediated, indoor plant table thus toxicants associated with these sites are a continuing threat. Furthermore, as female adult survival is notably important for population size and persistence in the southern Sierra Nevada population, forest managers should consider managing against habitat features that are conducive to interactions between fishers and their predators. Investigating these and other mechanisms for reducing mortality in California fishers within West coast DPS can be of assistance in effectively implementing policy or management options to potentially curb mortality rates in order to promote population recovery within California in addition to other fisher populations throughout the West Coast DPS.We would like to acknowledge the contributions of the following people and organizations. University of California at Davis Veterinary Medical Teaching Hospital, the graduate group of Comparative Pathology, Drs. Jonna Mazet, the field biologists at all the projects sites. Integral Ecology Research Center, California Animal Health and Food Safety Laboratory System, Hoopa Valley Tribal Forestry, United States Forest Service, National Park Service, United States Fish and Wildlife Service, California Department of Water Resources, California Department of Fish and Wildlife, California Department of Forestry and Fire Protection, and the Sierra Nevada Conservancy, and the Bureau of Indian Affairs provided logistical support.
We would like to thank two anonymous reviewers for making notable suggestions that improved the manuscript. Most of all we would like to thank the late Dr. Linda Munson forinitially taking the fisher health project under her wing. Her mentorship and contributions to wildlife conservation will be remembered and appreciated.Cannabis is one of the most frequently used psychoactive substances in the world and is the subject of major debates between proponents of the gateway hypothesis and advocates of legalization. Proponents of the gateway hypothesis have argued that epidemiological studies indicate that the early use of cannabis is an important risk factor for initiating cocaine use, that cannabis dependence predicts cocaine dependence , that cannabis use may be associated with poor cognitive and psychiatric outcomes in adulthood , and that major changes in legalization of the possession, sale, and cultivation of cannabis in the United States may exacerbate these poor outcomes by increasing the level of cannabis use in adolescents and young adults. Currently, its use exceeds that of tobacco smoking among adolescents in the United States, in which 37.1% of high school seniors in 2017 reported using cannabis within the past year. Advocates of legalization and medicinal use argue that it is unclear whether the relationship between prior cannabis use and later cocaine use or cocaine use disorder is caused by cannabis use per se or other drug-associated factors, such as concomitant psychiatric disorders and socioeconomic status. However, epidemiological studies cannot establish causal relationships between the pharmacological effects of exposure to cannabis and the development of cocaine use. Preclinical studies provide a controlled way to study causal relationships between early-life cannabinoid exposure and cocaine use, including compulsive-like use, later in life. Previous studies reported that exposure to the cannabinoid receptor agonist WIN55,212-2 during adolescence decreased the reactivity of dopaminergic neurons to WIN , produced cross-tolerance to cocaine in adolescence, and produced cross-sensitization to the psychomotor effects of cocaine in adolescence but not in adulthood. This effect appears to be mediated by the modulation of eukaryotic initiation factors in the brain. Such modifications of key neural substrates may reprogram the adolescent brain and make it more susceptible to the later use of other illicit drugs, such as cocaine. However, other groups found that prior treatment with either the main psychoactive constituent of cannabis or WIN had no effect on behavioral responses to amphetamine in either adolescence or adulthood. However, in the study by Ellgren et al. , cannabinoid exposure lasted only 5 days, the doses of cannabinoid were low, and the animals were injected only once per day. A major limitation of these preclinical studies is the use of an animal model of cocaine exposure that reflects neither the direct acquisition of cocaine use nor the compulsive nature of cocaine use disorder . To address this issue, we tested the effect of adolescent exposure to the cannabinoid receptor agonist WIN on key addiction-related behaviors using a more complex animal model of drug addiction. The model included measures of irritability-like behavior, which has recently been used as a measure of the negative emotional state in animal models of addiction. We also assessed cocaine-induced locomotion in adolescence and adulthood and the acquisition of cocaine self-administration under conditions of short access and long access in adulthood. The long-access model represents a comprehensive model of human addiction because it produces the escalation of cocaine intake that is associated with the emergence of negative emotional states and compulsive-like responding despite adverse consequence.All behavioral testing was conducted during the dark phase.