Mountain lions prey selectively on prion-infected mule deer
Caroline E. Krumm1,2, Mary M. Conner3, N. Thompson Hobbs4, Don O. Hunter5 and Michael W. Miller1,* 1Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526-2097, USA 2Graduate Degree Program in Ecology, and 4Natural Resource Ecology Laboratory, Colorado State University, Fort Collins, CO 80523, USA 3Department of Wildland Resources, Utah State University, Logan, UT 84322-5230, USA 5United States Fish and Wildlife Service, Fort Collins, CO 80526, USA *Author for correspondence (firstname.lastname@example.org).
The possibility that predators choose prey selectively based on age or condition has been suggested but rarely tested. We examined whether mountain lions (Puma concolor) selectively prey upon mule deer (Odocoileus hemionus) infected with chronic wasting disease, a prion disease. We located kill sites of mountain lions in the northern Front Range of Colorado, USA, and compared disease prevalence among lion-killed adult (2 years old) deer with prevalence among sympatric deer taken by hunters in the vicinity of kill sites. Hunter-killed female deer were less likely to be infected than males (odds ratios (OR) 5 0.2, 95% confidence intervals (CI) 5 0.1–0.6; p 5 0.015). However, both female (OR 5 8.5, 95% CI 5 2.3–30.9) and male deer (OR 5 3.2, 95% CI 5 1–10) killed by a mountain lion were more likely to be infected than samesex deer killed in the vicinity by a hunter (p < 0.001), suggesting that mountain lions in this area actively selected prion-infected individuals when targeting adult mule deer as prey items.
Keywords: chronic wasting disease; predation; prion; Puma concolor; selection; vulnerability
Intuitively, we expect predators to be more successful in capturing animals that are slow or less alert. The ‘sanitation effect’ of predators selecting weak individuals over prime, healthy specimens (Leopold 1933; Mech 1970) has been documented in several studies (Mech 1966; Kolenosky 1972; Schaller 1972). Although theory suggests that removing infected animals could ‘sanitize’ and slow the rate of prion transmission (Gross & Miller 2001), prevalence can be remarkably high in mule deer populations preyed upon by mountain lions (Miller et al. 2008). Prion transmission among deer can occur via several mechanisms, including indirect transmission from exposure to prions in the environment (Miller et al. 2004). We observed that mountain lions typically consumed greater than 85 percent of a deer carcass, often including brain tissue, and this may be beneficial in decreasing prion contamination at kill sites. However, the extent to which selective predation by mountain lions alters the dynamics of prion disease epidemics in natural mule deer populations remains unclear (Miller et al. 2008).
Seems prudent now, to do studies of prion disease of mountain lions in CWD zones. But that probably makes to much sense.
ALSO, what about mountain lion feces after consuming a CWD infected mule deer. a good healthy dump of prions I suppose, for the environment. ...TSS
Thursday, December 25, 2008 Lions and Prions and Deer Demise
HOWEVER, why ignore the old science and transmission studies to date ??
Species Born Onset/Died
Ocelot May 1987 Mar 1994 Ocelot Jul 1980 Oct 1995 Puma 1986 May 1991 Puma 1980 May 1995 Puma 1978 May 1995 Lion Nov 1986 Dec 1998 Tiger 1981 Dec 1995 Tiger Feb 1983 Oct 1998 Ankole 1987 May 1995 Ankole 1986 Feb 1991 Bison 1989/90 Oct 1996
Maff data on 15 May 99
kudu 6 gemsbok 1 nyala 1 oryx 2 eland 6 cheetah 9 puma 3 tiger 2 ocelot 2 bison 1 ankole 2 lion 1
Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.
Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.
The chemical and biological properties of the infectious agent are identical to those of the BSE and vCJD agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent.
The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.
References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588
Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320
Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.
Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.
Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.
Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.
Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.
Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444
Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271
Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.
Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441
Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.
TSEs in Exotic Ruminants TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.
References: Jeffrey, M. and Wells, G.A.H, (1988) Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet.Path. 25. 398-399
Kirkwood, J.K. et al (1990) Spongiform encephalopathy in an Arabian oryx (Oryx leucoryx) and a Greater kudu (Tragelaphus strepsiceros) Veterinary Record 127. 418-429.
Kirkwood, J.K. (1993) Spongiform encephalopathy in a herd of Greater kudu (Tragelaphus strepsiceros): epidemiological observations. Veterinary Record 133. 360-364
Kirkwood, J. K. and Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.
Food and Agriculture Organisation (1998) Manual on Bovine Spongiform Encephalopathy.
Subject: FSE: FIRST CONFIRMED CASE REPORTED IN PORTUGAL AND POTENTIAL MAD CAT ESCAPES LAB IN USA Date: August 9, 2007 at 2:27 pm PST
DIA-45 FELINE SPONGIFORM ENCEPHALOPATHY: FIRST CONFIRMED CASE REPORTED IN PORTUGAL
J.F. Silva1, J.J. Correia, 1 J. Ribeiro2, S. Carmo2 and L.Orge3
1 Faculdade de Medicina Veterinária (UTL), Lisbon, Portugal 2 Clínica Veterinária Ani+, Queluz, Portugal 3 Laboratório Nacional de Investigação Veterinária, Unidade de BSE, Lisbon, Portugal
Feline spongiform encephalopathy (FSE), affecting domestic and captive feline species, is a prion disease considered to be related to bovine spongiform encephalopathy (BSE). Here we report the first case diagnosed in Portugal, highlighting the neuroapthological findings. In 2004 a 9-year old intact female Siamese cat was referred with chronic progressive behavioural changes, polydipsia, gait abnormalities and episodes of hypersalivation. Clinical signs progressed to tetraparesis and dementia and euthanasia was performed. At necropsy, brain and spinal cord had no significative changes. Tissue samples from brain, cerebellum, brainstem and spinal cord were collected for histopathology and immunohistochemistry for detection of PrPres. Histology revealed neuropil and neuronal perikarion vacuolation in several areas of the central nervous system together with gliosis and cell rarefaction at the granular layer of the cerebellum. Immunohistochemical detection of PrPres showed a strong and widespread PrPres accumulation as granular and linear deposits as well as associated with some neurons. These findings are supportive of FSE. To the authors knowledge this is the first confirmed case of FSE reported in Portugal.
SNIP...SEE FULL TEXT ;
AS THE CROW FLIES, SO DO TSE'S
Sunday, November 01, 2009
American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases