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Journal articles on the topic 'Feral ferrets'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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1

Caley, Peter, L. M. McElrea, and Jim Hone. "Mortality rates of feral ferrets (Mustela furo) in New Zealand." Wildlife Research 29, no. 4 (2002): 323. http://dx.doi.org/10.1071/wr02004.

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Life-table data from feral ferret populations in New Zealand were analysed to estimate their mortality rates, and to test for any additive effect of Mycobacterium bovis infection on observed mortality rates. The observed instantaneous mortality rate was best estimated by modelling mortality as a 2-phase step model with different rates for juveniles (μ1 = 1.45 year–1, 95% C.I. 1.2–1.7 year–1) and adults (μ2 = 0.55 year–1, 95% C.I. 0.4–0.9 year–1). This corresponds to a survival probability of 0.25 during the first year of life, rising to 0.55 year–1 thereafter, and a life expectancy of 0.95 years. At a population level, no additional mortality due to M. bovis infection was observed, suggesting either that the rate of disease-induced mortality was negligible, or that it was compensatory with natural mortality.

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2

Medina‐Vogel, G., G. J. Hickling, and B. K. Clapperton. "Assessing spatial activity in captive feral ferrets,Mustela furoL. (Camivora: Mustelidae)." New Zealand Journal of Zoology 27, no. 2 (January 2000): 75–83. http://dx.doi.org/10.1080/03014223.2000.9518213.

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3

Byrom, Andrea E. "Dispersal and survival of juvenile feral ferrets Mustela furo in New Zealand." Journal of Applied Ecology 39, no. 1 (February 2002): 67–78. http://dx.doi.org/10.1046/j.1365-2664.2002.00689.x.

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4

Caley, P., J. Hone, and PE Cowan. "The relationship between prevalence ofMycobacterium bovisinfection in feral ferrets and possum abundance." New Zealand Veterinary Journal 49, no. 5 (October 2001): 195–200. http://dx.doi.org/10.1080/00480169.2001.36232.

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5

Henning, J., P. R. Davies, and J. Meers. "Seropositivity to rabbit haemorrhagic disease virus in non-target mammals during periods of viral activity in a population of wild rabbits in New Zealand." Wildlife Research 33, no. 4 (2006): 305. http://dx.doi.org/10.1071/wr03061.

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As part of a longitudinal study of the epidemiology of rabbit haemorrhagic disease virus (RHDV) in New Zealand, serum samples were obtained from trapped feral animals that may have consumed European rabbit (Oryctolagus cuniculus) carcasses (non-target species). During a 21-month period when RHDV infection was monitored in a defined wild rabbit population, 16 feral house cats (Felis catus), 11 stoats (Mustela erminea), four ferrets (Mustela furo) and 126 hedgehogs (Erinaceus europaeus) were incidentally captured in the rabbit traps. The proportions of samples that were seropositive to RHDV were 38% for cats, 18% for stoats, 25% for ferrets and 4% for hedgehogs. Seropositive non-target species were trapped in April 2000, in the absence of an overt epidemic of rabbit haemorrhagic disease (RHD) in the rabbit population, but evidence of recent infection in rabbits was shown. Seropositive non-target species were found up to 2.5 months before and 1 month after this RHDV activity in wild rabbits was detected. Seropositive predators were also trapped on the site between 1 and 4.5 months after a dramatic RHD epidemic in February 2001. This study has shown that high antibody titres can be found in non-target species when there is no overt evidence of RHDV infection in the rabbit population, although a temporal relationship could not be assessed statistically owning to the small sample sizes. Predators and scavengers might be able to contribute to localised spread of RHDV through their movements.

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6

Ogilvie, Shaun C., and Charles T. Eason. "Evaluation of iophenoxic acid and rhodamine B for marking feral ferrets(Mustela furo)." New Zealand Journal of Zoology 25, no. 2 (January 1998): 105–8. http://dx.doi.org/10.1080/03014223.1998.9518142.

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7

Gillies, Craig, and Matthew Brady. "Trialling monitoring methods for feral cats, ferrets and rodents in the Whangamarino wetland." New Zealand Journal of Zoology 45, no. 3 (July 3, 2018): 192–212. http://dx.doi.org/10.1080/03014223.2017.1418756.

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8

Byrom, AE, P. Caley, BM Paterson, and G. Nugent. "Feral ferrets (Mustela furo) as hosts and sentinels of tuberculosis in New Zealand." New Zealand Veterinary Journal 63, sup1 (March 10, 2015): 42–53. http://dx.doi.org/10.1080/00480169.2014.981314.

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9

Alterio, Nic. "Secondary poisoning of stoats (Mustela erminea), feral ferrets (Mustela furo),and feral house cats (Felis catus) by the anticoagulant poison, brodifacoum." New Zealand Journal of Zoology 23, no. 4 (January 1996): 331–38. http://dx.doi.org/10.1080/03014223.1996.9518092.

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10

Smith, G. P., J. R. Ragg, H. Moller, and K. A. Waldrup. "Diet of feral ferrets (Mustela furo) from pastoral habitats in Otago and Southland, New Zealand." New Zealand Journal of Zoology 22, no. 4 (January 1995): 363–69. http://dx.doi.org/10.1080/03014223.1995.9518054.

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11

Lugton, I. W., G. Wobeser, R. S. Morris, and P. Caley. "Epidemiology ofMycobacterium bovisinfection in feral ferrets (Mustela furo) in New Zealand: I. Pathology and diagnosis." New Zealand Veterinary Journal 45, no. 4 (January 8, 1997): 140–50. http://dx.doi.org/10.1080/00480169.1997.36014.

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12

STUART, PETER, ANNETTA ZINTL, THEO DE WAAL, GRACE MULCAHY, CONALL HAWKINS, and COLIN LAWTON. "Investigating the role of wild carnivores in the epidemiology of bovine neosporosis." Parasitology 140, no. 3 (October 15, 2012): 296–302. http://dx.doi.org/10.1017/s0031182012001588.

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SUMMARYNeospora caninumis a protozoan parasite, primarily associated with bovine abortion. The only definitive hosts discovered to date are carnivores. This study aimed to identify the role of mammalian carnivores in the epidemiology of bovine neosporosis. A sample bank of serum, fecal and brain samples was established: American mink (Mustela vison), red foxes (Vulpes vulpes), pine martens (Martes martes), badgers (Meles meles), stoats (Mustela erminea), otters (Lutra lutra) and feral ferrets (Mustela putorius). Approximately 1% of mink and 1% of fox samples were positive by IFAT. According to PCR analysis of DNA extracted from brain tissue, 3% of the mink, 4% of the otters and 6% of the foxes examined were infected withN. caninum.All fecal samples tested negative forN. caninumDNA (n = 311), suggesting that the species that tested positive were intermediate not definitive hosts. This is the first time that tissues from mustelids have tested positive forN. caninum. The need to test 2 relatively large (∼200 mg) targeted parts of the brain to avoid false negatives was also identified. The relatively low prevalence ofN. caninumin Irish carnivores suggests that the local ecology of a species has an important influence on its epidemiological role.

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13

YOCKNEY, I. J., G. NUGENT, M. C. LATHAM, M. PERRY, M. L. CROSS, and A. E. BYROM. "Comparison of ranging behaviour in a multi-species complex of free-ranging hosts of bovine tuberculosis in relation to their use as disease sentinels." Epidemiology and Infection 141, no. 7 (February 22, 2013): 1407–16. http://dx.doi.org/10.1017/s0950268813000289.

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SUMMARYSentinel species are increasingly used by disease managers to detect and monitor the prevalence of zoonotic diseases in wildlife populations. Characterizing home-range movements of sentinel hosts is thus important for developing improved disease surveillance methods, especially in systems where multiple host species co-exist. We studied ranging activity of major hosts of bovine tuberculosis (TB) in an upland habitat of New Zealand: we compared home-range coverage by ferrets (Mustela furo), wild deer (Cervus elaphus), feral pigs (Sus scrofa), brushtail possums (Trichosurus vulpecula) and free-ranging farmed cattle (Bos taurus). We also report in detail the proportional utilization of a seasonal (4-monthly) range area for the latter four species. Possums covered the smallest home range (<30 ha), ferrets covered ∼100 ha, pigs ∼4 km2, deer and cattle both >30 km2. For any given weekly period, cattle, deer and pigs were shown to utilize 37–45% of their estimated 4-month range, while possums utilized 62% during any weekly period and 85% during any monthly period of their estimated 4-month range. We suggest that present means for estimating TB detection kernels, based on long-term range size estimates for possums and sentinel species, probably overstate the true local surveillance coverage per individual.

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14

Ragg, J. R. "The denning behaviour of feral ferrets (Mustela furo) in a pastoral habitat, South Island, New Zealand." Journal of Zoology 246, no. 4 (December 1998): 443–86. http://dx.doi.org/10.1017/s0952836998301211.

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15

Caley, Peter, and Jim Hone. "Estimating the force of infection; Mycobacterium bovis infection in feral ferrets Mustela furo in New Zealand." Journal of Animal Ecology 71, no. 1 (January 2002): 44–54. http://dx.doi.org/10.1046/j.0021-8790.2001.00573.x.

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16

Ragg, J. R. "The denning behaviour of feral ferrets (Mustela furo) in a pastoral habitat, South Island, New Zealand." Journal of Zoology 246, no. 4 (December 1998): 471–77. http://dx.doi.org/10.1111/j.1469-7998.1998.tb00185.x.

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17

Lugton, I. W., G. Wobeser, R. S. Morris, and P. Caley. "Epidemiology ofMycobacterium bovisinfection in feral ferrets (Mustela furo) in New Zealand: II. Routes of infection and excretion." New Zealand Veterinary Journal 45, no. 4 (January 8, 1997): 151–57. http://dx.doi.org/10.1080/00480169.1997.36015.

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18

Ragg, J. R., K. A. Waldrup, and H. Moller. "The distribution of gross lesions of tuberculosis caused byMycobacterium bovisin feral ferrets (Mustela furo) from Otago, New Zealand." New Zealand Veterinary Journal 43, no. 7 (December 1995): 338–41. http://dx.doi.org/10.1080/00480169./1995.35916.

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19

CALEY, PETER, and JIM HONE. "Assessing the host disease status of wildlife and the implications for disease control: Mycobacterium bovis infection in feral ferrets." Journal of Applied Ecology 42, no. 4 (June 1, 2005): 708–19. http://dx.doi.org/10.1111/j.1365-2664.2005.01053.x.

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20

Costa, M., C. Fernandes, J. D. S. Birks, A. C. Kitchener, M. Santos-Reis, and M. W. Bruford. "The genetic legacy of the 19th-century decline of the British polecat: evidence for extensive introgression from feral ferrets." Molecular Ecology 22, no. 20 (September 17, 2013): 5130–47. http://dx.doi.org/10.1111/mec.12456.

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21

Gao, Jinghui, Sophia Petraki, Xingshen Sun, Leonard A. Brooks, Thomas J. Lynch, Chih-Lin Hsieh, Reem Elteriefi, et al. "Derivation of induced pluripotent stem cells from ferret somatic cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 4 (April 1, 2020): L671—L683. http://dx.doi.org/10.1152/ajplung.00456.2019.

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Ferrets are an attractive mammalian model for several diseases, especially those affecting the lungs, liver, brain, and kidneys. Many chronic human diseases have been difficult to model in rodents due to differences in size and cellular anatomy. This is particularly the case for the lung, where ferrets provide an attractive mammalian model of both acute and chronic lung diseases, such as influenza, cystic fibrosis, A1A emphysema, and obliterative bronchiolitis, closely recapitulating disease pathogenesis, as it occurs in humans. As such, ferrets have the potential to be a valuable preclinical model for the evaluation of cell-based therapies for lung regeneration and, likely, for other tissues. Induced pluripotent stem cells (iPSCs) provide a great option for provision of enough autologous cells to make patient-specific cell therapies a reality. Unfortunately, they have not been successfully created from ferrets. In this study, we demonstrate the generation of ferret iPSCs that reflect the primed pluripotent state of human iPSCs. Ferret fetal fibroblasts were reprogrammed and acquired core features of pluripotency, having the capacity for self-renewal, multilineage differentiation, and a high-level expression of the core pluripotency genes and pathways at both the transcriptional and protein level. In conclusion, we have generated ferret pluripotent stem cells that provide an opportunity for advancing our capacity to evaluate autologous cell engraftment in ferrets.

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22

Garcí, A., S. E. Erdman, S. Xu, Y. Feng, A. B. Rogers, M. D. Schrenzel, J. C. Murphy, and J. G. Fox. "Hepatobiliary Inflammation, Neoplasia, and Argyrophilic Bacteria in a Ferret Colony." Veterinary Pathology 39, no. 2 (March 2002): 173–79. http://dx.doi.org/10.1354/vp.39-2-173.

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Hepatobiliary disease was diagnosed in eight of 34 genetically unrelated cohabitating pet ferrets ( Mustela putorios furo) during a 7-year period. The eight ferrets ranged in age from 5 to 8 years and exhibited chronic cholangiohepatitis coupled with cellular proliferation ranging from hyperplasia to frank neoplasia. Spiral- shaped argyrophilic bacteria were demonstrated in livers of three ferrets, including two with carcinoma. Sequence analysis of a 400-base pair polymerase chain reaction product amplified from DNA derived from fecal bacteria from one ferret demonstrated 98% and 97% similarity to Helicobacter cholecystus and Helicobacter sp. strain 266-11, respectively. The clustering of severe hepatic disease in these cohabitating ferrets suggests a possible infectious etiology. The role of Helicobacter species and other bacteria in hepatitis and/or neoplasia in ferrets requires further study.

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23

Sauter, C. M., and R. S. Morris. "Behavioural studies on the potential for direct transmission of tuberculosis from feral ferrets (Mustela furo) and possums (Trichosurus vulpecula) to farmed livestock." New Zealand Veterinary Journal 43, no. 7 (December 1995): 294–300. http://dx.doi.org/10.1080/00480169./1995.35909.

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24

Lipiec, Marek, Lukasz Radulski, and Wojciech Iwaniak. "Case of mycobacteriosis in a pet ferret in Poland." Veterinary Record Case Reports 6, no. 3 (August 2018): e000542. http://dx.doi.org/10.1136/vetreccr-2017-000542.

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A seven-year-old dead pet ferret (Mustela putorius furo) was brought to the National Veterinary Research Institute, Department of Microbiology, to have the disease diagnosed and cause of death determined. Significant loss of fur and various numerous skin lesions—such as nodules, bruises and small scabs— were found. A prominent subcutaneous cyst filled with semiliquid mass was observed on the right hindlimb, and the left eyelid was slightly swollen left eyelid with symptoms of conjunctivitis. On the basis of combined findings, the authors concluded that the ferret’s death was caused by a generalized Mycobacterium aviumsubspecies avium infection. Some immunodeficiency resulting from ferret’s age could be a predisposing factor. A feral cat, which was the only animal the ferret had contacted several weeks before the appearance of the first clinical symptoms, was a possible source of infection.

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25

Ratz, Hiltrun, and Brian Murphy. "Effects of habitat and introduced mammalian predators on the breeding success of Yellow-eyed Penguins Megadyptes antipodes, South Island, New Zealand." Pacific Conservation Biology 5, no. 1 (1999): 16. http://dx.doi.org/10.1071/pc990016.

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The endemic Yellow-eyed Penguin Megadyptes antipodes is threatened by habitat loss and introduced predators on mainland New Zealand. Nine colonies in the Catlins (south-east coast of South Island) were studied to measure breeding success, penguin abundance, and predator abundance in three successive breeding seasons (1991/92 to 1993/94). Nest numbers increased in all nine colonies in the three years despite predation (probably by Stoats Mustefa erminea) being the most important cause of breeding failure. Larger colonies with higher breeding success were in small gullies with limited shrubs and bushes rather than in the most intact mature forest colonies hitherto assumed to be optimal habitat for the birds. Penguin nests were concentrated near the forest edge, but predators were not, so the predation risk was not elevated near the forest edge. Fragmentation of the original forest habitat had no observable adverse effect on breeding success. Stoats dominated the predator guild, while Ferrets M. furo and Feral Cats Felis catus were rare. Trapping to kill predators early in the season had no marked effect on subsequent predation losses, but trapping intervention when a predation outbreak occurred curtailed further chick deaths. A simple population model predicts that Yellow-eyed Penguins populations will grow provided the average total chicks loss is less than 43% per season, or at least 0.85 chick per nest fledges each year. This requires predation losses to be less than 34%.

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26

Ford, GE. "Role of the dog, fox, cat and human as carnivore vectors in the transmission of the Sarcosporidia that affect sheep meat production." Australian Journal of Agricultural Research 37, no. 1 (1986): 79. http://dx.doi.org/10.1071/ar9860079.

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The roles of six carnivores as potential sources to sheep of the sarcosporidial parasites causing cysts in meat were compared in a series of experiments carried out between 1973 and 1980. The research was concomitant with other studies that confirmed the prey-predator-prey-predator cycle of transmission. Infected carnivores act as vectors, excreting in their faeces coccidial sporocysts infective to the meat animal. For 60 experimental infections, sheep meat containing sarcocysts or sarcocysts removed from sheep meat were fed to experimental carnivores. Faecal samples were examined for sporocysts over 60 days post infection. Neither macroscopic (visible) sarcocysts nor microscopic sarcocysts from sheep carcasses were transmissible by humans or by ferrets (domestic polecats). Microscopic sarcocysts were readily infective to dogs, both domestic and dingo, as well as to foxes, but not to cats. Large numbers of sporocysts that could contaminate the environment were excreted. Both fat and thin visible sarcocysts were transmitted exclusively to cats. Although cats responded with relatively low levels of sporocysts, these were considered adequate to provide sufficient pasture contamination for the life cycle to be perpetuated. It is concluded that, while domestic dogs may be the greatest source of infection for sheep with microscopic sarcocysts, foxes as vectors also pose a threat to sheep production. Similarly, due to their widespread presence, feral cats play a role as well as domestic or semi-domestic cats in the spread of sarcocysts causing visible carcass lesions.

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27

Norbury, Grant, Richard Heyward, and John Parkes. "Short-term ecological effects of rabbit haemorrhagic disease in the short-tussock grasslands of the South Island, New Zealand." Wildlife Research 29, no. 6 (2002): 599. http://dx.doi.org/10.1071/wr00085.

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Rabbit haemorrhagic disease (RHD) has reduced populations of rabbits (Oryctolagus cuniculus) across most rabbit-prone short-tussock grasslands of New Zealand, at scales rarely seen there before. Flow-on effects to other parts of these ecosystems will be inevitable. We report evidence for increases in pasture biomass, increases in abundance of other exotic herbivores, declines in abundance of rabbit-specialist predators, and short-term increases in predation rates of some native birds by these predators. At one site in Central Otago, RHD reduced an index of rabbit abundance by 88%, and an index of their grazing impacts by 77%. Recovered biomass consisted mostly of fast-growing exotic pasture species of moderate palatability to livestock. Spotlight counts and hunters' returns suggest increases in possum (Trichosurus vulpecula) and hare (Lepus europeaus) abundance, but their grazing pressure is unlikely to replace that originally imposed by rabbits. The apparent increase in possum numbers poses an increased risk from the spread and maintenance of bovine tuberculosis (Tb), although this risk may be offset by declines in the counts of ferrets (Mustela furo), which also carry Tb. Declines in predator numbers (including feral cats, Felis catus) may also, in the longer term, benefit some native fauna that are secondary prey of these predators. There is evidence for increased predation of some native birds' eggs since RHD arrived. It is not possible at this stage to generalise the effects of RHD-induced declines in rabbit abundance on New Zealand ecosystems. Effects are highly variable, and their implications for pastoral production, management of bovine Tb, and conservation of native species are likely to vary locally according to the suite of plant and animal species originally present.

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28

Ragg, J. R., H. Moller, and K. A. Waldrup. "The prevalence of bovine tuberculosis (Mycobacterium bovis) infections in feral populations of cats (Felis cutus), ferrets (Mustela furo) and stoats (Mustela erminea) in Otago and Southland, New Zealand." New Zealand Veterinary Journal 43, no. 7 (December 1995): 333–37. http://dx.doi.org/10.1080/00480169./1995.35915.

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29

Alterio, N., H. Moller, and H. Ratz. "Movements and habitat use of feral house cats Felis catus, stoats Mustela erminea and ferrets Mustela furo, in grassland surrounding Yellow-eyed penguin Megadyptes antipodes breeding areas in spring." Biological Conservation 83, no. 2 (February 1998): 187–94. http://dx.doi.org/10.1016/s0006-3207(97)00052-9.

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30

Moller, Henrik, and Nic Alterio. "Home range and spatial organisation of stoats (Mustela erminea), ferrets (Mustela furo) and feral house cats (Felis catus) on coastal grasslands, Otago Peninsula, New Zealand: Implications for yellow‐eyed penguin (Megadyptes antipodes) conservation." New Zealand Journal of Zoology 26, no. 3 (January 1999): 165–74. http://dx.doi.org/10.1080/03014223.1999.9518186.

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31

Ragg, J. R., C. G. Mackintosh, and H. Moller. "The scavenging behaviour of ferrets (Mustela furo), feral cats (Felis domesticus), possums (Trichosurus vulpecula), hedgehogs (Erinaceus europaeus) and harrier hawks (Circus approximans) on pastoral farmland in New Zealand: Implications for bovine tuberculosis transmission." New Zealand Veterinary Journal 48, no. 6 (December 2000): 166–75. http://dx.doi.org/10.1080/00480169.2000.36188.

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32

Caley, P. "Broad-scale possum and ferret correlates of macroscopicMycobacterium bovisinfection in feral ferret populations." New Zealand Veterinary Journal 46, no. 4 (August 1998): 157–62. http://dx.doi.org/10.1080/00480169.1998.36080.

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33

Medina, Alexandre E., Thomas E. Krahe, and Ary S. Ramoa. "Early Alcohol Exposure Induces Persistent Alteration of Cortical Columnar Organization and Reduced Orientation Selectivity in the Visual Cortex." Journal of Neurophysiology 93, no. 3 (March 2005): 1317–25. http://dx.doi.org/10.1152/jn.00714.2004.

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Fetal alcohol syndrome (FAS) is a major cause of learning and sensory deficits in children. The visual system in particular is markedly affected, with an elevated prevalence of poor visual perceptual skills. Developmental problems involving the neocortex are likely to make a major contribution to some of these abnormalities. Neuronal selectivity to stimulus orientation, a functional property thought to be crucial for normal vision, may be especially vulnerable to alcohol exposure because it starts developing even before eye opening. To address this issue, we examined the effects of early alcohol exposure on development of cortical neuron orientation selectivity and organization of cortical orientation columns. Ferrets were exposed to ethanol starting at postnatal day (P) 10, when the functional properties and connectivity of neocortical neurons start to develop. Alcohol exposure ended at P30, just before eye opening at P32. Following a prolonged alcohol-free period (15–35 days), long-term effects of early alcohol exposure on cortical orientation selectivity were examined at P48–P65, when orientation selectivity in normal ferret cortex has reached a mature state. Optical imaging of intrinsic signals revealed decreased contrast of orientation maps in alcohol- but not saline-treated animals. Moreover, single-unit recordings revealed that early alcohol treatment weakened neuronal orientation selectivity while preserving robust visual responses. These findings indicate that alcohol exposure during a brief period of development disrupts cortical processing of sensory information at a later age and suggest a neurobiological substrate for some types of sensory deficits in FAS.

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34

Diak, James, and Banu Örmeci. "Ferrrate(VI) and freeze-thaw treatment for oxidation of hormones and inactivation of fecal coliforms in sludge." Water Science and Technology 75, no. 7 (January 23, 2017): 1625–32. http://dx.doi.org/10.2166/wst.2017.021.

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This study examined the individual and combined effects of potassium ferrate(VI) additions and freeze-thaw conditioning for the treatment and dewatering of wastewater sludge in cold climates, with particular focus on the inactivation of fecal coliforms and oxidation of estrogens, androgens, and progestogens. The first phase of the study evaluated the effects of potassium ferrate(VI) pre-treatment followed by freeze-thaw at −20 °C using a low (0.5 g/L) and high (5.0 g/L) dose of potassium ferrate(VI). The results showed that pre-treatment of anaerobically digested sludge with 5 g/L of potassium ferrate(VI) reduced the concentration of fecal coliforms in the sludge cake to below 100 MPN/g DS. The second phase evaluated the ability of ferrate(VI) to oxidise selected hormones in sludge. Anaerobically digested sludge samples were spiked with 10 different hormones: estrone (E1), 17α-estradiol, 17β-estradiol (E2), estriol (E3), 17α-ethinylestradiol (EE2), equilin, mestranol, testosterone, norethindrone and norgestrel in two groups of low (3–75 ng/mL) and high (12–300 ng/L) concentration ranges of hormones. The samples were treated with either 0.5 or 1.0 g/L of potassium ferrate(VI), and hormone concentrations were measured again after treatment. Potassium ferrate(VI) additions as low as 1.0 g/L reduced the concentration of estrogens in sludge. Potassium ferrate(VI) additions of 0.5 and 1.0 g/L were less effective at reducing the concentrations of androgens and progestogens. Increasing ferrate(VI) dose would likely result in more substantial decreases in the concentrations of fecal coliforms and hormones. The results of this study indicate that the combined use of freeze-thaw and ferrate(VI) has the potential to provide a complete sludge treatment solution in cold regions.

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35

Clapperton, B. K. "Advances in New Zealand mammalogy 1990–2000: Feral ferret." Journal of the Royal Society of New Zealand 31, no. 1 (March 2001): 185–203. http://dx.doi.org/10.1080/03014223.2001.9517647.

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36

Brown, Janine L. "Fecal Steroid Profiles in Black-Footed Ferrets Exposed to Natural Photoperiod." Journal of Wildlife Management 61, no. 4 (October 1997): 1428. http://dx.doi.org/10.2307/3802147.

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37

Smits, Saskia L., V. Stalin Raj, Minoushka D. Oduber, Claudia M. E. Schapendonk, Rogier Bodewes, Lisette Provacia, Koert J. Stittelaar, Albert D. M. E. Osterhaus, and Bart L. Haagmans. "Metagenomic Analysis of the Ferret Fecal Viral Flora." PLoS ONE 8, no. 8 (August 20, 2013): e71595. http://dx.doi.org/10.1371/journal.pone.0071595.

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38

Golden, Glen J., Meredith J. Grady, Hailey E. McLean, Susan A. Shriner, Airn Hartwig, Richard A. Bowen, and Bruce A. Kimball. "Biodetection of a specific odor signature in mallard feces associated with infection by low pathogenic avian influenza A virus." PLOS ONE 16, no. 5 (May 26, 2021): e0251841. http://dx.doi.org/10.1371/journal.pone.0251841.

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Outbreaks of avian influenza virus (AIV) infection included the spread of highly pathogenic AIV in commercial poultry and backyard flocks in the spring of 2015. This resulted in estimated losses of more than $8.5 million from federal government expenditures, $1.6 billion from direct losses to produces arising from destroyed turkey and chicken egg production, and economy-wide indirect costs of $3.3 billion from impacts on retailers and the food service industries. Additionally, these outbreaks resulted in the death or depopulation of nearly 50 million domestic birds. Domesticated male ferrets (Mustela putorius furo) were trained to display a specific conditioned behavior (i.e. active scratch alert) in response to feces from AIV-infected mallards in comparison to feces from healthy ducks. In order to establish that ferrets were identifying samples based on odors associated with infection, additional experiments controlled for potentially confounding effects, such as: individual duck identity, housing and feed, inoculation concentration, and day of sample collection (post-infection). A final experiment revealed that trained ferrets could detect AIV infection status even in the presence of samples from mallards inoculated with Newcastle disease virus or infectious laryngotracheitis virus. These results indicate that mammalian biodetectors are capable of discriminating the specific odors emitted from the feces of non-infected versus AIV infected mallards, suggesting that the health status of waterfowl can be evaluated non-invasively for AIV infection via monitoring of volatile fecal metabolites. Furthermore, in situ monitoring using trained biodetectors may be an effective tool for assessing population health.

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WEAVER, C. E., and M. J. BAUM. "Differential Regulation of Brain Aromatase by Androgen in Adult and Fetal Ferrets*." Endocrinology 128, no. 3 (March 1991): 1247–54. http://dx.doi.org/10.1210/endo-128-3-1247.

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Tobet, S. A., M. E. Basham, and M. J. Baum. "Estrogen receptor immunoreactive neurons in the fetal ferret forebrain." Developmental Brain Research 72, no. 2 (April 1993): 167–80. http://dx.doi.org/10.1016/0165-3806(93)90182-a.

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Fitzgibbon, T., and B. E. Reese. "Position of growth cones within the retinal nerve fibre layer of fetal ferrets." Journal of Comparative Neurology 323, no. 2 (September 8, 1992): 153–66. http://dx.doi.org/10.1002/cne.903230203.

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Fitzgibbon, T., and B. E. Reese. "Organization of retinal ganglion cell axons in the optic fiber layer and nerve of fetal ferrets." Visual Neuroscience 13, no. 5 (September 1996): 847–61. http://dx.doi.org/10.1017/s095252380000910x.

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AbstractPrevious authors have hypothesized that retinotopic projections may be influenced by ‘preordering’ of the axons as they grow towards their targets. In some nonmammalian species, axons are reorganized at or near the optic nerve head to establish a retinotopic order. Data are ambiguous concerning the retinotopy of the mammalian retinal nerve fiber layer and whether fibers become reorganized at the optic nerve head. We have examined this question in fetal and newborn ferrets (Mustela putorius furo) by comparing the arrangement of axons in the retinal nerve fiber layer with that in the optic nerve. Dil or DiA crystals were implanted into fixed tissue in the innermost layers of the retinal periphery, or at a location midway between the periphery and the optic nerve head. Fluorescence labelling was examined in 100–200 μm Vibratome sections, or the eyecup and nerve were photooxidized and 1–2 μm longitudinal or transverse sections were examined. Regardless of fetal age, eccentricity or quadrant of the implant site, a segregation of labelled peripheral axons from unlabelled central ones was not detected within the nerve fiber layer. Axons coursed into the nerve head along the margin of their retinal quadrant of origin, often entering the optic nerve as a radial wedge, thus preserving a rough map of retinal circumference. However, peripheral axons were in no way restricted to the peripheral (nor central) portions of the nerve head or nerve, indicating that the optic axons do not establish a map of retinal eccentricity. Our results demonstrate that (1) the nerve fiber layer is retinotopic only with respect to circumferential position and (2) optic axons are not actively reorganized to establish a retinotopic ordering at the nerve head. The present results suggest that any degree of order present within the optic nerve is a passive consequence of combining the fascicles of the retinal nerve fiber layer; optic axons are not instructed to establish, nor constrained to maintain, a retinotopic order within the optic nerve.

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Fehér, Enikő, Péter Pazár, Eszter Kovács, Szilvia L. Farkas, György Lengyel, Ferenc Jakab, Vito Martella, and Krisztián Bányai. "Molecular detection and characterization of human gyroviruses identified in the ferret fecal virome." Archives of Virology 159, no. 12 (August 14, 2014): 3401–6. http://dx.doi.org/10.1007/s00705-014-2203-3.

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Heide, Michael, Christiane Haffner, Ayako Murayama, Yoko Kurotaki, Haruka Shinohara, Hideyuki Okano, Erika Sasaki, and Wieland B. Huttner. "Human-specific ARHGAP11B increases size and folding of primate neocortex in the fetal marmoset." Science 369, no. 6503 (June 18, 2020): 546–50. http://dx.doi.org/10.1126/science.abb2401.

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The neocortex has expanded during mammalian evolution. Overexpression studies in developing mouse and ferret neocortex have implicated the human-specific gene ARHGAP11B in neocortical expansion, but the relevance for primate evolution has been unclear. Here, we provide functional evidence that ARHGAP11B causes expansion of the primate neocortex. ARHGAP11B expressed in fetal neocortex of the common marmoset under control of the gene’s own (human) promoter increased the numbers of basal radial glia progenitors in the marmoset outer subventricular zone, increased the numbers of upper-layer neurons, enlarged the neocortex, and induced its folding. Thus, the human-specific ARHGAP11B drives changes in development in the nonhuman primate marmoset that reflect the changes in evolution that characterize human neocortical development.

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Nizza, Sandra, Francesca Rando, Filomena Fiorito, Ugo Pagnini, Giuseppe Iovane, and Luisa De Martino. "Fecal microbiota and antibiotic resistance in ferrets (Mustela putorius furo) from two captive breeding facilities in Italy." Research in Veterinary Science 96, no. 3 (June 2014): 426–28. http://dx.doi.org/10.1016/j.rvsc.2014.03.015.

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Fox, J. G., B. J. Paster, F. E. Dewhirst, N. S. Taylor, L. L. Yan, P. J. Macuch, and L. M. Chmura. "Helicobacter mustelae isolation from feces of ferrets: evidence to support fecal-oral transmission of a gastric Helicobacter." Infection and Immunity 60, no. 2 (1992): 606–11. http://dx.doi.org/10.1128/iai.60.2.606-611.1992.

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Thomas, Maciej, Violetta Kozik, Krzysztof Barbusiński, Aleksander Sochanik, Josef Jampilek, and Andrzej Bąk. "Potassium Ferrate (VI) as the Multifunctional Agent in the Treatment of Landfill Leachate." Materials 13, no. 21 (November 6, 2020): 5017. http://dx.doi.org/10.3390/ma13215017.

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Possible use of potassium ferrate (VI) (K2FeO4) for the treatment of landfill leachate (pH = 8.9, Chemical Oxygen Demand (COD) 770 mg O2/L, Total Organic Carbon (TOC) 230 mg/L, Total Nitrogen (Total N) 120 mg/L, Total Phosphorus (Total P) 12 mg/L, Total Coli Count (TCC) 6.8 log CFU/mL (Colony-Forming Unit/mL), Most Probable Number (MPN) of fecal enterococci 4.0 log/100 mL, Total Proteolytic Count (TPC) 4.4 log CFU/mL) to remove COD was investigated. Central Composite Design (CCD) and Response Surface Methodology (RSM) were applied for modelling and optimizing the purification process. Conformity of experimental and predicted data (R2 = 0.8477, Radj2 = 0.7462) were verified using Analysis of Variance (ANOVA). Application of K2FeO4 using CCD/RSM allowed to decrease COD, TOC, Total N, Total P, TCC, MPN of fecal enterococci and TPC by 76.2%, 82.6%, 68.3%, 91.6%, 99.0%, 95.8% and 99.3%, respectively, by using K2FeO4 0.390 g/L, at pH = 2.3 within 25 min. Application of equivalent amount of iron (as FeSO4 × 7H2O and FeCl3 × 6H2O) under the same conditions allowed to diminish COD, TOC, Total N, Total P, TCC, MPN of fecal enterococci and TPC only by 38.1%, 37.0%, 20.8%, 95.8%, 94.4%, 58.2%, 90.8% and 41.6%, 45.7%, 29.2%, 95.8%, 92.1%, 58.2%, 90.0%, respectively. Thus, K2FeO4 could be applied as an environmentally friendly reagent for landfill leachate treatment.

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Lipsitz, Lee, David T. Ramsey, James A. Render, Steven J. Bursian, and Richard J. Auelrich. "Persistent fetal intraocular vasculature in the European ferret (Mustela putorius ): clinical and histological aspects." Veterinary Ophthalmology 4, no. 1 (March 2001): 29–33. http://dx.doi.org/10.1046/j.1463-5224.2001.00115.x.

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Li, Ziyi, Maryam Rezaei Sabet, Qi Zhou, Xiaoming Liu, Wei Ding, Yulong Zhang, Jean-Paul Renard, and John F. Engelhardt. "Developmental Capacity of Ferret Embryos by Nuclear Transfer Using G0/G1-Phase Fetal Fibroblasts1." Biology of Reproduction 68, no. 6 (June 1, 2003): 2297–303. http://dx.doi.org/10.1095/biolreprod.102.012369.

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Buckley, Daniel J., and Mathieu Lundy. "The current distribution and potential for future range expansion of feral ferret Mustela putorius furo in Ireland." European Journal of Wildlife Research 59, no. 3 (November 29, 2012): 323–30. http://dx.doi.org/10.1007/s10344-012-0677-4.

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