Apparent stability masks underlying change in a mule deer herd with unmanaged chronic wasting disease
Apparent stability masks underlying change in a mule deer herd with unmanaged chronic wasting disease
Commun Biol. 2022; 5: 15. Published online 2022 Jan 11. doi: 10.1038/s42003-021-02951-z PMCID: PMC8752592 PMID: 35017638
Apparent stability masks underlying change in a mule deer herd with unmanaged chronic wasting disease
Mark C. Fisher,#1 Ryan A. Prioreschi,#2 Lisa L. Wolfe,1 Jonathan P. Runge,1 Karen A. Griffin,1 Heather M. Swanson,2 and Michael W. Millercorresponding author1
Abstract
The contagious prion disease “chronic wasting disease” (CWD) infects mule deer (Odocoileus hemionus) and related species. Unchecked epidemics raise ecological, socioeconomic, and public health concerns. Prion infection shortens a deer’s lifespan, and when prevalence (proportion of adults infected) becomes sufficiently high CWD can affect herd dynamics. Understanding population responses over time is key to forecasting long-term impacts. Here we describe unexpected stability in prevalence and abundance in a mule deer herd where CWD has been left unmanaged. High apparent prevalence (~30%) since at least 2005 likely drove observed changes in the proportion and age distribution of wild-type native prion protein (PRNP) gene homozygotes among deer sampled. Predation by mountain lions (Puma concolor) may be helping keep CWD in check. Despite stable appearances, prion disease nonetheless impairs adult survival and likely resilience in this deer herd, limiting its potential for growth despite refuge from hunter harvest and favorable habitat and winter conditions.
Conclusions
Reassessing the Table Mesa herd after more than a decade revealed unexpected superficial stability in apparent CWD prevalence and deer abundance in the time since our original study ended. Some combination of predation by mountain lions and perhaps subtle genetic shifting in the mule deer host or unidentified environmental factors may have contributed to the net absence of measurable change, at least on the surface. Despite the appearance of stability, the Table Mesa deer herd seems far from healthy. High disease incidence appears to be truncating the age distribution of the otherwise dominant wild-type individuals. Moreover, low adult survival sustained for over a decade likely impairs the resilience of this herd and limits its potential for growth despite an abundance of available habitat and relatively mild winter conditions. Periodic reassessment of this and other infected cervid herds will inform on long-term implications of CWD outbreaks to help better frame the policy choices surrounding intervention alternatives.
NATURAL RESOURCES
Scientists to study walking-dead deer in Wyo’s most CWD-infected herd
The vast majority of mule deer in a herd north of Riverton are testing positive for the deadly disease. Causes remain mysterious, though signs suggest environmental transmission.
Mike Koshmrl by Mike Koshmrl January 4, 2022
It’s become a foregone conclusion for Riverton outfitter Ken Metzler that when one of his mule deer hunters shoots a buck, the animal is afflicted with chronic wasting disease, he said.
“We had 98% last year and this year,” Metzler said of the positivity rate. “And we had every one of them tested but a couple.”
Generally, the lethal disease’s sky-high prevalence isn’t a deterrent for the out-of-state hunters eager to target a muley on the Fremont County ranchland where Wyoming Trophy Hunts leads its clients, he said. Applications to hunt with Metzler’s guides are still pouring in, especially since the pandemic began, even though the likelihood of taking home a trophy-class deer has declined. As the population has fallen, hunting licenses have also been cut.
“I’ve dropped from 100 hunters to probably, oh, 20,” said Metzler. Of the clients who do get out to hunt, Metzler said, “we’re not killing big bucks.” Meat from younger, fatter bucks typically goes in the freezer, even though public health experts caution against consuming CWD-positive animals. But when the hunters walk up to a downed animal and find a sickly looking, “flat ass skinny” deer, Metzler calls up the warden and gets the OK to pitch the remains, he said.
Given the condition deer are in, Metzler would support a larger reduction in licenses if it would help the herd bounce back.
The Wyoming Game and Fish Department and U.S. Geological Survey researchers share concern and curiosity over what to make of the mule deer herd that Metzler’s business depends on. The Project Herd — as Game and Fish knows it — is easily Wyoming’s big game herd most ravaged by the degenerative prion disease. In fact, the data show the herd is also among the most CWD-infected wild cervid populations known to exist in North America.
“We have a proposal for a study for this herd because of the extraordinarily high rates of CWD,” Game and Fish Dubois Wildlife Biologist Zach Gregory said.
Plans are still in the rough, initial phases, Gregory told WyoFile, but researchers intend to find funding for 40 GPS collars that will be fitted to a random sample of deer in the Project Herd as soon as next winter. Some — likely a good portion — will be CWD-positive animals and therefore destined for death, but they’ll be tested while alive using rectal biopsies and then let loose.
The hope is to glean some clarity about the factors contributing to the alarming disease prevalence.
“Are these positive deer in different places than these negative deer?” Gregory asked. “That’s going to potentially help us identify the hotspots.”
Just how much CWD?
Only time will tell whether those collared, sickened deer point Gregory and his USGS counterparts toward locations like the ranches where Wyoming Trophy Hunts guides — where, according to Metzler, virtually all buck mule deer are CWD-positive.
What’s already understood is that the Project Herd is an anomaly in the region and is itself a hotspot. The herd roams Wyoming’s deer hunt units 171 and 157, in west-central Wyoming, which are both within the borders of the Wind River Indian Reservation, although non-native hunting is confined to non-tribal lands within.
The herd is considered a priority for CWD surveillance, and between 2016 and 2020 Game and Fish staff gathered tissue samples from 139 of its bucks. Of those, 85 came up positive, for a prevalence rate of 61%.
Preliminary test results for 2021’s tissue samples showed a higher rate of CWD: 78%, according to Game and Fish Regional Wildlife Coordinator Daryl Lutz.
“It’s the highest that’s been recorded, maybe anywhere in the world in wildlife,” Lutz told attendees at a public meeting last month.
The Wildlife Health Laboratory supervisor for the state of Wyoming, Hank Edwards, wouldn’t go that far, instead emphasizing the multi-year positivity rate. There are agricultural parts in southwest Saskatchewan, he noted, where prevalence has been documented in the 60-70% range. Annual reports from the provincial government confirm it, and say that in over a dozen Saskatchewan wildlife management zones, more than 50% of mule deer bucks are testing positive for the degenerative disease.
Edwards did label CWD’s prevalence in the Project Herd “alarmingly high,” and he pointed out it’s Wyoming’s most CWD-infected deer herd by a nearly 20% margin. Statewide, 12.5% of the nearly 6,500 CWD samples processed during 2020 tested positive, statistics that span species, sex and cause of death, according to Game and Fish’s most recent CWD surveillance report.
“Every herd responds differently,” Edwards said, “for a number of reasons.”
In the Sublette Herd, which roams the Green and Snake river basins, CWD is just now arriving, and 0.8% of 375 samples tested to date have hit for the prion disease. There’s also significant variation in herds that for decades have suffered from CWD’s inexorable effects, like listlessness, physical wasting and inevitable death. In southeastern Wyoming’s Laramie Mountains, one of the first places where CWD was found in wild deer, 22% of hunter-killed bucks have been positive in the last five years. But in the Black Hills, the long-term prevalence in mule deer bucks is just 5.9%, though Edwards said that rate may have been dragged down by other diseases, like epizootic hemorrhagic disease (often called blue tongue).
Ahead of the study, wildlife managers hesitate to hazard a guess for why the Project Herd’s disease rates are a whole order of magnitude greater.
An enigma
One reason is that the Project Herd today is poorly understood. It’s a rare mule deer herd where the population isn’t monitored, although Gregory and others are trying to change that. There are several explanations for why the Project Herd is shrouded in so much unknown. It’s a smaller, low-density herd, Gregory said, that generally occupies riparian areas, private agricultural ground and the reservation, where it’s difficult, or impossible, for agency staff to regularly count deer.
Rather than counting deer, Game and Fish has used two metrics to monitor the herd: hunter satisfaction and landowner surveys to gauge perception of the population. Satisfaction has fallen off, and landowners are also noticing downward changes.
As recently as 2018 and ‘19, nobody surveyed thought the mule deer population was too low. But in the last two years, nearly half of respondents felt there were too few deer.
“This dramatic shift in landowner sentiment supports hunter and department personnel observations indicating a substantial population decline in the herd,” wildlife managers wrote in Game and Fish’s most recent “job completion report” for Lander-area big game herds.
To help the herd hold up, Game and Fish slashed doe-fawn hunting licenses by half ahead of the 2020 hunting season, though that’s still not enough in the eyes of an outfitter like Metzler.
Mike Miller, a longtime CWD researcher and wildlife veterinarian for the Colorado Division of Wildlife, was not surprised outfitters like Metzler are observing so few older bucks in an area where prevalence is so high. He’s seen it before, while studying Colorado’s Table Mesa Herd, where prevalence in bucks was approaching 50%.
“We didn’t catch older male deer,” Miller said. “You just didn’t.”
The captures he referred to outside of Boulder, Colorado, occurred 14 years ago. But he returned to capture mule deer more recently and it was the same outcome: “I don’t think we caught any bucks that were aged over 5 or 6 years,” Miller said. “They’re just not there.”
Chronic wasting disease is killing them before they can reach those middle ages, he said, and that’s even true in Boulder County, where hunting is prohibited.
Causes and solutions
Miller declined to theorize what’s going on with the Project Herd directly. But he said common themes tend to emerge among deer herds in the few cases where CWD prevalence rates have been so off the charts. The herds are usually non-migratory, and consistently gather at concentrated food sources. Clay-type soils that effectively bond with the transmissible prions and even enhance infectivity can also be contributing factors, he said.
“I’m not implying that these deer are captive, but where you do see these really, really high infection rates commonly, is in deer and elk that are in captivity,” Miller said. “They’re living in a very small area and feeding and watering in the same places, day in and day out.”
When those kinds of conditions exist without a fence, he said, there can be the same effect. There are management methods to encourage these types of deer herds to move around more to reduce transmission, but easy solutions are unlikely, he said.
“It’s hard when infection rates get this high,” Miller said. “You’ve probably got a lot of contamination in the environment, and in the wild that’s just really hard to do anything about.”
Still, Edwards hopes that the coming GPS data on the Project Herd mule deer points his agency toward next steps that could create a healthier population. Once the sources of CWD’s spread are identified, be it a silage pile or some other hypothetical factor, he said, then more concrete steps could follow.
“It all depends on what’s going on,” Edwards said. “You have to know the sources to try to change the transmission factors. Maybe at the end of this research, it’s not such a gray picture.”
''The herd is considered a priority for CWD surveillance, and between 2016 and 2020 Game and Fish staff gathered tissue samples from 139 of its bucks. Of those, 85 came up positive, for a prevalence rate of 61%.''
''Preliminary test results for 2021’s tissue samples showed a higher rate of CWD: 78%, according to Game and Fish Regional Wildlife Coordinator Daryl Lutz.''
“It’s the highest that’s been recorded, maybe anywhere in the world in wildlife,” Lutz told attendees at a public meeting last month.''
''The Wildlife Health Laboratory supervisor for the state of Wyoming, Hank Edwards, wouldn’t go that far, instead emphasizing the multi-year positivity rate. There are agricultural parts in southwest Saskatchewan, he noted, where prevalence has been documented in the 60-70% range. Annual reports from the provincial government confirm it, and say that in over a dozen Saskatchewan wildlife management zones, more than 50% of mule deer bucks are testing positive for the degenerative disease.''
''Edwards did label CWD’s prevalence in the Project Herd “alarmingly high,” and he pointed out it’s Wyoming’s most CWD-infected deer herd by a nearly 20% margin. Statewide, 12.5% of the nearly 6,500 CWD samples processed during 2020 tested positive, statistics that span species, sex and cause of death, according to Game and Fish’s most recent CWD surveillance report.''
wow...incredibly alarming...terry
How many deer die from cwd?
that dog don't hunt no more...
15 minute mark video shows sick deer with cwd, and this deer DIED FROM CWD, IT'S DOCUMENTED, commentator says ''so if anyone every tells you, that a deer has never died from CWD, think of this picture, because the Wisconsin Veterinary Lab told us, what when they looked at her sample under a microscope, she was the hottest animal they had ever seen, and that's in terms of the fluorescents that comes off the slide when the look at it, so, a lot of Prion in her system.''
see much more about 2 hours long...
If CWD is always fatal, where are all of the dead cervids?
Infected cervids appear healthy for a vast majority of their infection, only showing clinical symptoms for a brief period of time before death occurs. Cervids with clinically evident CWD eventually become emaciated and can die from starvation if they avoid other causes of death. Ongoing studies have found that CWD infected cervids have died from starvation despite an abundance of available row crops available for consumption (WI DNR, 2019). Additionally, some infected cervids that die directly from CWD show evidence of aspiration pneumonia, which may be caused by preceding symptoms like difficulty swallowing and excessive salivation (CWD Alliance).
However, CWD is a neurodegenerative disease and infected cervids seem to be more prone to other causes of mortality, including vehicular collisions and predation, compared to healthy cervids (Haley & Hoover, 2015). Additionally, cervids infected with CWD appear to be more susceptible to hunter harvest due to potential behavioral changes (Edmunds et al., 2016). The role of predators, scavengers, and natural decomposition make observations of intact dead cervids a relatively rare occurrence regardless of disease status. In combination with the limited number of infected cervids that die directly from CWD, these factors contribute to the infrequent observation of cervids that suffer acute deaths from CWD in the wild.
There are documented observations of cervids infected with CWD courtesy of the CWD Alliance, the Wisconsin Department of Natural Resources, the Wyoming Game and Fish Department, and the University of Wyoming. Additionally, there is the story of a hunter witnessing a CWD-infected cervid’s death directly from the disease, courtesy of the Quality Deer Management Association.
The second year of results span January 2018 to January 2019.
The higher mortality of CWD-positive deer was attributed directly and indirectly to the disease, according to DNR researchers. "The disease was determined to be the cause of death in several animals, but CWD-positive deer die from lots of causes, and the disease seems to make the animal more vulnerable to those," Storm said.
Sickened animals are less aware of their surroundings, less responsive to stimuli and less physically coordinated, according to researchers. Hunting was the leading cause (four times higher than any other) of death for all deer in the study.
Studies in the western USA have found that CWD negatively impacts elk and mule deer survival and population size, but no field research has documented the impact of CWD on white-tailed deer survival or population growth in Wisconsin. Furthermore, there is not any ongoing work in the Midwest that specifically addresses the direct impact of CWD on deer survival.
We show that a chronic disease that becomes endemic in wildlife populations has the potential to be population-limiting and the strong population-level effects of CWD suggest affected populations are not sustainable at high disease prevalence under current harvest levels.
it's not rocket science...
CWD POPULATION DECLINE
In the endemic area of Wyoming, for example, the prevalence of CWD in mule deer has increased from approximately 11% in 1997 to 36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011).
In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.'' ''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
Wyoming has a problem...
Colorado Chronic Wasting Disease Response Plan December 2018
I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.
Impact on Rural Landowners CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections.
As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
____________________
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
MONDAY, NOVEMBER 29, 2021
HOW MANY DEER DIE FROM CWD TSE PRION?
FRIDAY, JANUARY 28, 2022
Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
NEVER SAY NEVER, with the TSE Prion disease...
***> AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
snip...
Volume 16: Reference Material
3. Statistics
Other spongiform encephalopathies
3.24 Feline Spongiform Encephalopathy (FSE), in domestic cats, was first recognised in 1990. At the time, domestic cats were the sixth species in which a scrapie-like spongiform encephalopathy had been diagnosed. Commercially produced cat food including MBM was the most likely source of the disease. 1 By December 1998, when the outbreak appeared to be tailing off, there had been 85 cases, including one each in Northern Ireland, Norway and Liechtenstein.
Figure 3.36 below shows the course of the disease from 1989 to 1997: by the end of June 1997, the number of cases had reached 80.
Figure 3.36: Distribution of Feline Spongiform Encephalopathy cases by month and year, by date of onset of clinical signs, Great Britain, 1989-97
3.25 In contrast to FSE, which had a similar clinical duration and mean age at clinical onset as BSE, spongiform encephalopathies in exotic ungulates in Great Britain occurred at an earlier age, and had a much shorter duration. In cases involving big cats, it is supposed that the animals became infected from being fed raw bovine tissues, including the spinal cord and brain. 2 The ungulates were infected through MBM in their feed.
Figure 3.37: Spongiform encephalopathies in exotic species in Great Britain, as at 31 December 1999
Puma (Felis concolor) *3 early 92
* One of the puma cases did not exhibit clinical signs but had minimal histological lesions and was positive for scrapie associated fibrils and and prion protein
snip...see image;
IN CONFIDENCE CJD TO CATS...
It should be noted that under experimental conditions cats succumb to an encephalopathy after intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease.
http://web.archive.org/web/20090506055329/http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf
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.
TSE and Surveillance Statistics Exotic species and domestic cats November 2018
Contents Number of confirmed cases of FSE in domestic cats by year
Number of confirmed cases of FSE in domestic cats by year of birth
Number of TSEs in exotic species by year reported
Transmissible Spongiform Encephalopathies in exotic species
Number of confirmed cases of FSE in domestic cats by year Data valid to 30 November 2018 Includes one case from Guernsey Year Reported No. of cases 1988 0 1989 0 1990 12 1991 12 1992 10 1993 11 1994 16 1995 8 1996 6 1997 6 1998 4 1999 2 2000 1 2001 1 2002 0 2003 0 2004 0 2005 0 2006 0 2007 0 2008 0 2009 0 2010 0 2011 0 2012 0 2013 0 2014 0 2015 0 2016 0 2017 0 2018 0 Total 89 Year of Onset No. of cases 1988 0 1989 1 1990 16 1991 11 1992 14 1993 10 1994 14 1995 4 1996 7 1997 8 1998 1 1999 1 2000 1 2001 1 2002 0 2003 0 2004 0 2005 0 2006 0 2007 0 2008 0 2009 0 2010 0 2011 0 2012 0 2013 0 2014 0 2015 0 2016 0 2017 0 2018 0 Total 89
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.
Bovine spongiform encephalopathy Update
Ray Bradley
Veterinary Laboratories Agency, New Haw, Addlestone, KT15 3NB, United Kingdom, Email: raybradley@btinternet.com
Received 8 July 2002, accepted 24 July 2002
snip...
TSE IN CAPTIVE WILD ANIMALS
TSE almost certainly related to BSE (but as yet not proven by experimental challenge) has been reported in five species of captive wild Felidae in Great Britain (GB) (Bradley 1997). These are: cheetah 5 cases (with five further cases in cheetah exported from the UK to Ireland (1), Australia (1) and France (2+1unknown)), lions 3, ocelots 3, pumas 3 and tigers 3. All of these are assumed to have been exposed following consumption of uncooked cattle carcasses containing infected central nervous tissue. This might have been present in heads, necks or other parts of the vertebral column. Protection was secured by the 1990 SBO ban and there have been very few cases that were born thereafter. TSE has also been reported in captive wild Bovidae in GB (Bradley 1997), but not elsewhere or in any natural environment inhabited by these animals. Eight species have been affected. In two, a nyala and a greater kudu, brain tissue has been inoculated into in-bred strains of mice. This shows the disease is experimentally transmissible and that the agent responsible is biologically indistinguishable from the BSE agent, i.e. it is of the same strain type (Bruce et al. 1994). The number of confirmed TSE by species is: Arabian oryx, bison, gemsbok, nyala and scimitar-horned oryx, one each; ankole, two; eland and greater kudu, six. All these species have presumably been exposed to infected MBM in concentrate diets that had similar formulations to those used in cattle feed before 1988. The reason for the cases occurring after 1988 (BAB cases) is, as in cattle, presumably cross contamination of diets with MBM intended for use in non-ruminant species. So far as records permit, no cases have been reported in animals born after January 1993.
BSE is considered to occur in 16 species: cattle, domestic cats, nyala and greater kudu (types of antelopes), gemsbok, eland, Arabian oryx, scimitar-horned oryx, ankole, bison, cheetah, lion, tiger, puma, ocelot and humans (brains from Variant Creutzfeldt-Jakob Disease (vCJD) patients). Other than feline spongiform encephalopathy (FSE) in domestic cats, all these are rare diseases in captive wild animals in the UK. Cases of FSE have also been found in cheetah in Ireland, France and Australia, but only in captive animals exported from the UK. There have not been any reports of naturally occurring cases of TSE in pigs or poultry. The spread of BSE is associated with concentrate feeding and the vehicle of infectivity was meat and bonemeal (MBM). There is continuing controversy on the origin of BSE. There were changes in rendering practices and evidence suggest this may have changed the evolution of the epidemic.
It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption. snip...
10. The case of SE in a cheetah that occurred during the period, involved a 7 year-old female which had been born and lived all her life at Whipsnade (except for the final stages when she was moved to the Animal Hospital at Regent’s Park for diagnosis and treatment). This animal, which died in December 1993, had been fed on cuts of meat and bone from carcases of cattle unfit for human consumption and it was thought likely that she had been exposed to spinal cord (Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species. Journal of Zoo and Wildlife Medicine 26, 577-582: J/ZWM/26/577).
11. During the period we also collated information on cases of SE that occurred in wild animals at or from other zoos in the British Isles. The total number of cases of which I was aware in June 1996, when I presented a review on occurrence of spongiform encephalopathies in zoo animals (at the Royal College of Pathologists’ Symposium on Transmitting prions: BSE, CJD, and other TSEs, The Royal Society, London, 4th July 1996), was 25, involving 10 species. The animals involved were all from the families Bovidae and Felidae, and comprised: 1 Nyala Tragelaphus angasi, 5 Eland Taurotragus oryx, 6 greater kudu Tragelaphus strepsiceros, 1 Gemsbok Oryx gazella, 1 Arabian oryx Oryx leucoryx, 1 Scimitar-horned oryx Oryx dammah, 4 Cheetah Acinonyx jubatus, 3 Puma Felis concolor 2 Ocelot Felis pardalis, and 1 Tiger Panthera tigris. (A spongiform encephalopathy, which was thought probably to have a different aetiology, had also been reported in 3 ostriches Struthio camelus in Germany). This list did not include cases of BSE in domesticated species in zoos (ie BSE in Ankole or other cattle, or SEs, assumed to be scrapie, in mouflon sheep Ovis musimon).
The BSE Inquiry / Statement No 324
Dr James Kirkwood (not scheduled to give oral evidence)
Statement to the BSE Inquiry
James K Kirkwood BVSc PhD FIBiol MRCVS
[This witness has not been asked to give oral evidence in Phase 1 of the Inquiry]
1. I became involved in the field of TSEs through my work as Head of the Veterinary Science Group at the Zoological Society of London’s Institute of Zoology. I held this post from November 1984 until June 1996, when I took up my present post at UFAW. During this time, concurrent with the BSE epidemic, cases of scrapie-like spongiform encephalopathies occurred in animals at the Zoological Society of London’s collections at Regent’s Park and Whipsnade and in other zoos. It was appropriate to investigate the epidemiology of these cases in order to try to determine the possible impact on zoo animals and breeding programmes, and to consider how the disease in zoo animals might be controlled.
2. Throughout the period from 1985 to March 1996, I worked at the Institute of Zoology (IoZ). I was Head of the Veterinary Science Group of the IoZ and Senior Veterinary Officer of the Zoological Society of London (ZSL). I was responsible for the provision of the veterinary service for the ZSL collections.
3. During the period from 1985 to March 1996, scrapie-like spongiform encephalopathies were diagnosed in the following animals which died, or were euthanased, at London Zoo and Whipsnade:
Animal Sex Date of Death Age (mos)
Arabian Oryx Oryx leucoryx F 24.3.89 38
Greater kudu Tragelaphus strepsiceros (Linda) F 18.8.89 30
Greater kudu (Karla) F 13.11.90 19 Greater kudu (Kaz) M 6.6.91 37
Greater kudu (Bambi) M 24.10.91 36
Greater kudu (346/90) M 26.2.92 18
Greater kudu (324/90) F 22.11.92 38
Cheetah Acinonyx jubatus (Michelle) F 22.12.93 91
All these cases were described in papers published in the scientific literature (as cited below).
TSE surveillance statistics: exotic species and domestic cats
September 2019
Contents
Number of confirmed cases of FSE in domestic cats by year..............................................1
Number of confirmed cases of FSE in domestic cats by year of birth..................................1
Number of TSEs in exotic species by year reported ............................................................2
Transmissible Spongiform Encephalopathies in exotic species...........................................3
1
Number of confirmed cases of FSE in domestic cats by year
Year Reported No. of cases
ZOO ANIMALS AND TSE PRION DISEASE
The 82 zoo animals with BSE:
never say never with TSE Prion disease...
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:25 PM
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