We used a multinomial logistic regression model to assess the effects of several variables on the relative frequencies of cause-specific mortality which consisted of “natural disease,” “poisoning,” “predation,” and “human-caused,” however, we excluded unknown causes. We pooled human-caused mortalities with those from vehicular strike as “vehicular/ human” for modeling due to small sample sizes and the common anthropogenic source of mortality. We used two different data sets for modeling. The first included 136 radio-collared and uncollared fisher mortalities documented between 2007 and 2014 for which cause of mortality was known. We built models using all possible combinations of 1–5 variables which included population, sex, age class, season and year. The second data set included 72 fisher mortalities pulled from the previous group for which exposure status for both anticoagulant rodenticides and the three pathogens was known; no demographic parameters were used for this model. Models were built using all possible combinations of 1–8 variables which included IgG and IgM titers to CDV and T. gondii, IgG titer to CPV, exposure to AR, seedling grow rack and the total number of AR detected. The latter two variables were not used in the same model to avoid multicollinearity among variables.We employed an information-theoretic approach to identify the most parsimonious models relating demographic parameters and disease and toxicant exposure parameters to cause of mortality. We calculated the Akaike Information Criteria score corrected for small sample sizes for each model and compared the scores among competing models.
We considered as final models those with ΔAICc < 2. The model was built using the outcome categories “predation,” “poisoning” and “natural disease” as the reference groups in three separate analyses, resulting in odds ratios for “predation vs. disease,” “predation vs. poisoning,” “predation vs. human-caused,” “poisoning vs. disease,” “poisoning vs. human-caused” and “disease vs. human-caused.” Model coefficients were estimated using the maximum-likelihood method.Of the 21 mortality events for collared fishers attributed to natural disease, 48% were attributed to bacterial infections, 28% to emaciation, 14% to viral infections, 5% to a protozoal infection and 5% to malignant neoplasia . Of the 10 bacterial infections, nine were associated with interstitial pneumonia or bronchopneumonia. Three of the four northern California mortalities due to bacterial infection had a concurrent, nematode parasiThism of the lungs, which was not identified to genera. The nematode parasiThism cases were associated with interstitial pneumonia with bacterial infiltrates, although this wasnot the proximate cause of mortality. Four of the six fisher mortalities due to bacterial infection in the southern Sierra Nevada had bacterial infiltrates associated with interstitial pneumonia, but contamination with mixed bacterial flora prevented identification. Two of these cases also involved an unknown lung nematode. The remaining two cases were septic with mixed bacterial flora, which may have resulted from cutaneous punctures with associated necrosis and bacterial infiltration consistent with predator bite wounds.
All six fishers that died due to starvation were severely emaciated with no pericardial, renal, mesentery or subcutaneous fat. All of these cases showed emaciation with no other detectable concurrent disease processes. For five of the six emaciation cases, the cause for emaciation was unknown. The remaining case was a female fisher with an acute complete fracture of the left mandible coupled with numerous canine, incisor and molar teeth fractures. The source of this acute trauma was unknown however predation, an illegal snare or vehicular strike, though presumptive, may have been the contributing cause due to the force required. In addition, two altricial kits were recovered from abandoned den sites and determined to have died of emaciation.All three fishers that died of a viral etiology were infected with CDV as previously described. We categorized one fisher as predation mortality that had a concurrent systemic CDV infection. The lesions caused by CDV were widespread and severe suggesting that they had a debilitating clinical effect, which facilitated the predation event. The mortality was hence classified as ‘predation’ rather than ‘disease’, though this fisher most likely would have succumbed to distemper due to the systemic infection. The sole mortality attributed to protozoal infection was due to a severe, non-suppurative, menigioencephalomyeliThis caused by T. gondii as determined by immunohistochemistry. The only fisher that died from cancer had systemic lymphoma involving lymph nodes, liver and skin.Thirteen fishers in the two populations died of toxicosis, all of which had trespass marijuana cultivation and associated toxicants within their home ranges.
Anticoagulant rodenticides , which are toxicant compounds that inhibit the recycling of vitamin K1 leading to clotting and coagulation impairment, caused 11 fisher mortalities. In addition to detection of AR in these fishers’ livers, they exhibited coagulopathy and significant hemorrhage. Exposure to ARs alone did not constitute an AR toxicosis case. In addition to ARs, cholecalciferol, another rodenticide which causes hypercalcemia and has been found at several cultivation sites in the northern California project, was assumed to be the contributing cause of death in one male fisher from northern California. This fisher had multifocal mineralization in the aorta, testes and renal medulla. All other causes of hypercalcemia such as chronic renal failure and hyperparathyroidism were ruled out and cholecalciferol rodenticides were discovered near this fisher’s home range. The kidneys for this fisher were submitted for total vitamin D3 assay along with another kidney from a fisher that exhibited no mineralization in any Thissues . Results demonstrated a 7.4 fold difference of total vitamin D3 between the two samples . Unfortunately, sample identifications during laboratory submission were not legible to lab staff, therefore correct assignment of results to the sample could not be completed with confidence. This fisher was also exposed to five different ARs, for a total of six different rodenticides it had consumed. Another collared male fisher from northern California exhibited neurological signs including ataxia, lethargy and seizures before being euthanized . This fisher was near an illegal marijuana cultivation site where bromethalin and carbamate insecticides, as well as numerous organophosphates, were found. However, no carbamates, organophosphates, illicit drugs, greenhouse growing racks metaldehyde or bromethalin were detected in the stomach contents, liver, urine or kidney. In addition, we tested its bile for Anatoxin-a, but did not detect it in the sample. All other potential mechanisms for this fisher’s clinical signs were ruled out leading this case to be classified as suspected toxicosis. Seven of the toxicosis cases were from the northern California population while the remaining 6 were from the southern Sierras . Annual fisher mortality attributed to rodenticides varied with an average of 1.86 toxicosis cases each year . Nine of the 13 toxicosis cases occurred in spring , three in late winter and one in fall . A total of 101 fishers had sufficient liver Thissue to test for anticoagulant rodenticide exposure. Of these fishers, 86 were exposed to one or more ARs and had an average of 1.73 different AR compounds .All 10 fishers killed by vehicular strike were discovered on paved road systems with various speed limits for vehicles. Seven of these were uncollared and opportunistically collected, whereas three road killed fishers from the southern Sierra Nevada population had been radiocollared. Two additional fisher mortalities from the southern Sierras were originally suspected to be vehicular strikes due to the carcasses being discovered near or on a roadway but had no evidence of blunt force trauma, macerated muscles, comminuted fractures, torn viscera or ruptured blood vessels, all of which were observed in all of the 10 confirmed vehicular strike cases. These fishers were finally ruled as AR poisoning due to the significant pleural and abdominal cavity hemorrhaging, in addition to several ARs detected in Thissues.The two cases of human-caused mortalities were due to entrapment in man-made structures.
A radio-collared female adult fisher at HVRFP died of dehydration when she was caught in a live trap that was inadvertently left operational between trapping sessions. The maximum duration over which the fisher could have been left in the live trap was five days. The second fisher was an uncollared, sub-adult male that was discovered in an air quality sampling tube at the KRFP study. This fisher’s Thissues were too autolyzed to perform a necropsy. A third fisher from the southern Sierras was initially suspected to have died from negative reaction from recalled ketamine. However upon necropsy, it was determined that this fisher was infected with CDV exhibiting clinical signs of disease but respiratory depression from anesthesia was the proximate factor which expedited inevitable death due to CDV infection.This study is the first to thoroughly describe necropsy-confirmed, cause-specific mortality of fishers in the West Coast DPS and our findings provide baseline information on the mortality factors potentially limiting fisher populations in other portions of this DPS. The most significant findings of our study were the relative importance of predation and poisoning as mortality factors and the apparent increase of pesticide poisoning frequency in a short span of time. Importantly, our finding that AR poisoning was a more likely cause of death than predation in the northern California population versus the southern Sierra Nevada signifies regional heterogeneity in anthropogenic influences in forest landscapes. Besides differences in likelihood of AR poisoning, we found little heterogeneity in most causes of mortality between the two study populations or among years supporting their generality in California fisher populations. This finding likely reflects similarities in habitat, prey utilization, and predator communities throughout the range of fishers in California. A secondary finding was that field assessment of cause of death significantly underestimated the frequency of natural disease-related mortalities. Our results confirmed earlier findings that predation was a significant mortality factor affecting fishers in California, causing the majority of all fisher deaths. The addition of 28 new predation cases for this study did not change the frequencies of predation events by particular predator species for fishers from both populations determined in an earlier study . Older studies suggested that predation was an insignificant mortality factor, thought primarily to affect vulnerable or reintroduced individuals. In our study, females more frequently died from predation than males, possibly attributable to the smaller mass of females. Female fishers on average were half to two-thirds the mass of males , thus potentially increasing their susceptibility to a greater diversity of predators. Additionally, the importance of predation becomes more clear in light of recent findings suggesting that population size for fisher is heavily influenced by adult female survival . It is unclear why these isolated California populations were subject to such high prevalence of predation relative to other populations, but further investigation of this finding is critical to the conservation of the California populations. Furthermore, we do not know whether the predation rates we observed for fishers are different from predation rates that fisher populations have suffered throughout their evolutionary history. However, recent research into the effects of habitat modification on likelihood of fisher predation does suggest that changes in habitat over the past century may be changing the rate of predation on female fishers by bobcats . Although exposure to the protozoan T. gondii has been shown to predispose individuals to predation or vehicular strikes, we found no significant evidence of this relationship. However, many of the depredated fishers did not have any available blood to sample due to the predator consuming the heart or exposing the thoracic cavity leaving unsuitable samples for testing, resulting in a small sample size with which to detect such a relationship. Then again, all available brain Thissue was tested for gliotic foci due to T. gondii and none were found. Kits died from disease more frequently than any other cause, likely since kits were den-bound and therefore less exposed to predators and humans. Bacterial infections accounted for the largest number of disease-related fisher deaths, and generally manifested as bacterial pneumonia. However, in no instance did we identify a single dominant bacterial pathogen but cultures yielded mixed flora in all cases. These results may be due to post-mortem autolysis and contamination of pathogenic bacteria by opportunistic species. Interestingly, two of the mortalities associated with bacterial infection also had full thickness, circular punctures in the skin suggestive of failed predation attempts resulting in a site for introduction of a bacterial infection. It should be noted that pulmonary viral infections that might have preceded and facilitated bacterial colonization could not be identified but cannot be ruled out. The toxicosis cases discovered in this study signify an increase of this emerging threat for fishers in the West Coast DPS.