*** Persistence of ovine scrapie infectivity in a farm environment
following cleaning and decontamination ***
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc
MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C.
Maddison, BSc, PhD3 + Author Affiliations 1Animal and Plant Health Agency,
Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary
Medicine and Science, The University of Nottingham, Sutton Bonington,
Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary
Medicine and Science, The University of Nottingham, Sutton Bonington,
Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence:
ben.maddison@adas.co.uk
Abstract
Scrapie of sheep/goats and chronic wasting disease of deer/elk are
contagious prion diseases where environmental reservoirs are directly implicated
in the transmission of disease. In this study, the effectiveness of recommended
scrapie farm decontamination regimens was evaluated by a sheep bioassay using
buildings naturally contaminated with scrapie. Pens within a farm building were
treated with either 20,000 parts per million free chorine solution for one hour
or were treated with the same but were followed by painting and full
re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible
lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their
scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue.
All animals became infected over an 18-month period, even in the pen that had
been subject to the most stringent decontamination process. These data suggest
that recommended current guidelines for the decontamination of farm buildings
following outbreaks of scrapie do little to reduce the titre of infectious
scrapie material and that environmental recontamination could also be an issue
associated with these premises.
SNIP...
Discussion Thorough pressure washing of a pen had no effect on the amount
of bioavailable scrapie infectivity (pen B). The routine removal of prions from
surfaces within a laboratory setting is treatment for a minimum of one hour with
20,000 ppm free chlorine, a method originally based on the use of brain
macerates from infected rodents to evaluate the effectiveness of decontamination
(Kimberlin and others 1983). Further studies have also investigated the
effectiveness of hypochlorite disinfection of metal surfaces to simulate the
decontamination of surgical devices within a hospital setting. Such treatments
with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower
than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous
treatment of the pen surfaces did not effectively remove the levels of scrapie
infectivity over that of the control pens, indicating that this method of
decontamination is not effective within a farm setting. This may be due to the
high level of biological matrix that is present upon surfaces within the farm
environment, which may reduce the amount of free chlorine available to
inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had
also became scrapie positive within nine months, with all animals in this pen
being RAMALT positive by 18 months of age. Pen D was no further away from the
control pen (pen A) than any of the other pens within this barn. Localised hot
spots of infectivity may be present within scrapie-contaminated environments,
but it is unlikely that pen D area had an amount of scrapie contamination that
was significantly different than the other areas within this building.
Similarly, there were no differences in how the biosecurity of pen D was
maintained, or how this pen was ventilated compared with the other pens. This
observation, perhaps, indicates the slower kinetics of disease uptake within
this pen and is consistent with a more thorough prion removal and
recontamination. These observations may also account for the presence of
inadvertent scrapie cases within other studies, where despite stringent
biosecurity, control animals have become scrapie positive during challenge
studies using barns that also housed scrapie-affected animals (Ryder and others
2009). The bioassay data indicate that the exposure of the sheep to a farm
environment after decontamination efforts thought to be effective in removing
scrapie is sufficient for the animals to become infected with scrapie. The main
exposure routes within this scenario are likely to be via the oral route, during
feeding and drinking, and respiratory and conjunctival routes. It has been
demonstrated that scrapie infectivity can be efficiently transmitted via the
nasal route in sheep (Hamir and others 2008), as is the case for CWD in both
murine models and in white-tailed deer (Denkers and others 2010, 2013).
Recently, it has also been demonstrated that CWD prions presented as dust when
bound to the soil mineral montmorillonite can be infectious via the nasal route
(Nichols and others 2013). When considering pens C and D, the actual source of
the infectious agent in the pens is not known, it is possible that biologically
relevant levels of prion survive on surfaces during the decontamination regimen
(pen C). With the use of galvanising and painting (pen D) covering and sealing
the surface of the pen, it is possible that scrapie material recontaminated the
pens by the movement of infectious prions contained within dusts originating
from other parts of the barn that were not decontaminated or from other areas of
the farm.
Given that scrapie prions are widespread on the surfaces of affected farms
(Maddison and others 2010a), irrespective of the source of the infectious prions
in the pens, this study clearly highlights the difficulties that are faced with
the effective removal of environmentally associated scrapie infectivity. This is
likely to be paralleled in CWD which shows strong similarities to scrapie in
terms of both the dissemination of prions into the environment and the facile
mode of disease transmission. These data further contribute to the understanding
that prion diseases can be highly transmissible between susceptible individuals
not just by direct contact but through highly stable environmental reservoirs
that are refractory to decontamination. The presence of these environmentally
associated prions in farm buildings make the control of these diseases a
considerable challenge, especially in animal species such as goats where there
is lack of genetic resistance to scrapie and, therefore, no scope to re-stock
farms with animals that are resistant to scrapie.
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE)
Accepted October 12, 2014. Published Online First 31 October 2014
***raising the possibility that deer may be susceptible to multiple scrapie
strains. ***
Saturday, August 02, 2014
Structural effects of PrP polymorphisms on intra- and inter-species prion
transmission
*** Finally, our findings showing that Tg(DeerPrP), but not Tg(ElkPrP) are
sensitive to infection with SSBP/1 belie previously published results showing
that SSBP/1 of the same provenance caused disease in two lines of Tg mice
expressing elk PrP (13). However, our results appear to be consistent with the
reported susceptibilities of elk and deer to sheep prions. In previous studies,
of six elk inoculated with scrapie, three presented with neurological signs and
neuropathology, but only after long and variable times to disease onset ranging
from 25 to 46 months (29). In contrast, our results with SSBP/1 demonstrate
relatively facile transmission of scrapie to deer, with all inoculated animals
developing within 19 to 20 months, which is in accordance with susceptibility of
deer to a US scrapie isolate with a similar time to disease onset (24).
Polymorphisms ovine PrP add a further level of complexity, since they control
the propagation scrapie strains. Occupancy of residue 136 by A or V is of
particular importance. Our previous results indicated that SSBP/1 is comprised
of a dominant strain that is preferentially propagated by sheep PrP encoding V
at 136 (12). In contrast, the scrapie prions used in the deer transmission
studies of Greenlee and colleagues were isolated from a sheep encoding A136,
***raising the possibility that deer may be susceptible to multiple scrapie
strains. ***
Significance
The unpredictable recurrences of prion epidemics, their incurable
lethality, and the capacity of animal prions to infect humans, provide
significant motivation to ascertain the parameters governing disease
transmission. The unprecedented spread, and uncertain zoonotic potential of
chronic wasting disease (CWD), a contagious epidemic among deer, elk, and other
cervids, is of particular concern. Here we demonstrate that naturally occurring
primary structural differences in cervid PrPs differentially impact the
efficiency of intra- and interspecies prion transmission. Our results not only
deliver new information about the role of primary structural variation on prion
susceptibility, but also provide functional support to a mechanism in which
plasticity of a tertiary structural epitope governs prion protein conversion and
intra- and inter-species susceptibility to prions.-
snip...
Saturday, August 02, 2014
Structural effects of PrP polymorphisms on intra- and inter-species prion
transmission
now, decades later ;
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. ...To our knowledge, this is the first established
experimental model of CWD in TgSB3985. We found evidence for co-existence or
divergence of two CWD strains adapted to Tga20 mice and their replication in
TgSB3985 mice. Finally, we observed phenotypic differences between
cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice.
Further studies are underway to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. ... CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. ... CWD prions (as inferred by prion seeding activity by
RT-QuIC) are shed in urine of infected deer as early as 6 months post
inoculation and throughout the subsequent disease course. Further studies are in
progress refining the real-time urinary prion assay sensitivity and we are
examining more closely the excretion time frame, magnitude, and sample variables
in relationship to inoculation route and prionemia in naturally and
experimentally CWD-infected cervids.
Conclusions. ... Our results suggested that the odds of infection for CWD
is likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. ... During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
see full text and more ;
PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
spreading cwd around...tss
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of
farmed elk in Saskatchewan in a single epidemic. All of these herds were
depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease
eradication program. Animals, primarily over 12 mo of age, were tested for the
presence CWD prions following euthanasia. Twenty-one of the herds were linked
through movements of live animals with latent CWD from a single infected source
herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily
infected herds.
***The source herd is believed to have become infected via importation of
animals from a game farm in South Dakota where CWD was subsequently diagnosed
(7,4). A wide range in herd prevalence of CWD at the time of herd depopulation
of these herds was observed. Within-herd transmission was observed on some
farms, while the disease remained confined to the introduced animals on other
farms.
spreading cwd around...tss
Friday, May 13, 2011
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the
Republic of Korea Chronic Wasting Disease (CWD) outbreaks and surveillance
program in the Republic of Korea
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim,
Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research
Division, National Veterinary Research and Quarantine Service, Republic of Korea
Chronic wasting disease (CWD) has been recognized as an important prion
disease in native North America deer and Rocky mountain elks. The disease is a
unique member of the transmissible spongiform encephalopathies (TSEs), which
naturally affects only a few species. CWD had been limited to USA and Canada
until 2000.
On 28 December 2000, information from the Canadian government showed that a
total of 95 elk had been exported from farms with CWD to Korea. These consisted
of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72
elk in 1997, which had been held in pre export quarantine at the “source
farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD
surveillance program was initiated by the Ministry of Agriculture and Forestry
(MAF) in 2001.
All elks imported in 1997 were traced back, however elks imported in 1994
were impossible to identify. CWD control measures included stamping out of all
animals in the affected farm, and thorough cleaning and disinfection of the
premises. In addition, nationwide clinical surveillance of Korean native
cervids, and improved measures to ensure reporting of CWD suspect cases were
implemented.
Total of 9 elks were found to be affected. CWD was designated as a
notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and
2005.
Since February of 2005, when slaughtered elks were found to be positive,
all slaughtered cervid for human consumption at abattoirs were designated as
target of the CWD surveillance program. Currently, CWD laboratory testing is
only conducted by National Reference Laboratory on CWD, which is the Foreign
Animal Disease Division (FADD) of National Veterinary Research and Quarantine
Service (NVRQS).
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the
human consumption was confirmed as positive. Consequently, all cervid – 54 elks,
41 Sika deer and 5 Albino deer – were culled and one elk was found to be
positive. Epidemiological investigations were conducted by Veterinary
Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary
services.
Epidemiologically related farms were found as 3 farms and all cervid at
these farms were culled and subjected to CWD diagnosis. Three elks and 5
crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and
confirmed as negative.
Further epidemiological investigations showed that these CWD outbreaks were
linked to the importation of elks from Canada in 1994 based on circumstantial
evidences.
In December 2010, one elk was confirmed as positive at Farm 5.
Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer –
were culled and one Manchurian Sika deer and seven Sika deer were found to be
positive. This is the first report of CWD in these sub-species of deer.
Epidemiological investigations found that the owner of the Farm 2 in CWD
outbreaks in July 2010 had co-owned the Farm 5.
In addition, it was newly revealed that one positive elk was introduced
from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed
(species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as
negative.
: Corresponding author: Dr. Hyun-Joo Sohn (+82-31-467-1867, E-mail:
shonhj@korea.kr) 2011 Pre-congress Workshop: TSEs in animals and their
environment 5
Research Article
Demographic Patterns and Harvest Vulnerability of Chronic Wasting Disease
Infected White-Tailed Deer in Wisconsin
DANIEL A. GREAR,1 Department of Wildlife Ecology, University of Wisconsin,
Madison, WI 53706, USA MICHAEL D. SAMUEL, U.S. Geological Survey—Wisconsin
Cooperative Wildlife Research Unit, University of Wisconsin, Madison, WI 53706,
USA JULIE A. LANGENBERG, Wisconsin Department of Natural Resources, Madison, WI
53707, USA DELWYN KEANE, Wisconsin Veterinary Diagnostic Laboratory, Madison, WI
53705, USA
Abstract
Chronic wasting disease (CWD) is a fatal disease of white-tailed deer
(Odocoileus virginianus) caused by transmissible protease-resistant prions.
Since the discovery of CWD in southern Wisconsin in 2001, more than 20,000 deer
have been removed from a .2,500-km2 disease eradication zone surrounding the
three initial cases. Nearly all deer removed were tested for CWD infection and
sex, age, and harvest location were recorded. Our analysis used data from a
310-km2 core study area where disease prevalence was higher than surrounding
areas. We found no difference in harvest rates between CWD infected and
noninfected deer. Our results show that the probability of infection increased
with age and that adult males were more likely to be infected than adult
females. Six fawns tested positive for CWD, five fawns from the core study area,
including the youngest (5 months) free-ranging cervid to test positive. The
increase in male prevalence with age is nearly twice the increase found in
females. We concluded that CWD is not randomly distributed among deer and that
differential transmission among sex and age classes is likely driving the
observed patterns in disease prevalence. We discuss alternative hypotheses for
CWD transmission and spread and, in addition, discuss several possible nonlinear
relationships between prevalence and age. Understanding CWD transmission in
free-ranging cervid populations will be essential to the development of
strategies to manage this disease in areas where CWD is found, as well as for
surveillance strategies in areas where CWD threatens to spread. (JOURNAL OF
WILDLIFE MANAGEMENT 70(2):546–553; 2006)
Key words
Chronic wasting disease (CWD), disease prevalence, epidemiology, harvest
vulnerability, Odocoileus virginianus, prion, transmissible spongiform
encephalopathy (TSE), white-tailed deer, Wisconsin.
> > > Six fawns tested positive for CWD, five fawns from the core
study area, including the youngest (5 months) free-ranging cervid to test
positive. < < <
Wisconsin : Six White-Tailed Deer Fawns Test Positive for CWD
Date: May 13, 2003 Source: Wisconsin Department of Natural Resources
Contacts: Julie Langenberg Wildlife Veterinarian 608-266-3143 Tom Hauge
Director, Bureau of Wildlife Management 608-266-2193
MADISON -- Six fawns in the area of south central Wisconsin where chronic
wasting disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health officials.
These are the youngest wild white-tailed deer detected with chronic wasting
disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were
sampled from the eradication zone over the last year. The majority of fawns
sampled were between the ages of 5 to 9 months, though some were as young as 1
month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of
the positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified.
"This is the first intensive sampling for CWD in fawns anywhere," said Dr.
Julie Langenberg, Department of Natural Resources wildlife veterinarian, "and we
are trying to learn as much as we can from these data".
"One noteworthy finding is simply the fact that we found positive fawns,"
Dr. Langenberg said. "These results do show us that CWD transmission can happen
at a very young age in wild white-tailed deer populations. However, we found
that the percentage of fawns infected with CWD is very low, in the area of 0.14
percent. If there was a higher rate of infection in fawns, then fawns dispersing
in the spring could be much more worrisome for disease spread."
Dr. Langenberg noted that while the youngest CWD-positive fawns had
evidence of disease-causing prions only in lymph node tissue, several of the
older CWD-positive fawns had evidence of CWD prions in both lymph node and brain
tissues -- suggesting further progression of the disease.
"Finding CWD prions in both lymph and brain tissues of deer this young is
slightly surprising," said Langenberg, "and provides information that CWD
infection and illness may progress more rapidly in a white-tailed deer than
previously suspected. Published literature suggests that CWD doesn't cause
illness in a deer until approximately 16 months of age. Our fawn data shows that
a few wild white-tailed deer may become sick from CWD or may transmit the
disease before they reach that age of 16 months."
One of the positive fawns was shot with a doe that was also CWD positive.
Information about these fawn cases combined with will help researchers who are
studying the age and routes of CWD transmission in wild deer populations. "More
data analysis and ongoing deer movement studies should give us an even better
understanding of how this disease moves across the landscape", said Langenberg.
"Thanks to eradication zone hunters who submitted deer of all ages for
sampling, we have a valuable set of fawn data that is contributing to our
state's and the nation's understanding about CWD," Langenberg said.
> > > Two of the six fawns with CWD detected were 5 to 6 months
old. < < <
Why doesn't the Wisconsin DNR want to routinely test fawns ?
The DNR highly discourages the testing of any fawns regardless of where
they were harvested. Of the more than 15,000 fawns from the CWD-MZ that have
been tested, only 23 were test positive, and most of those were nearly one year
old. It is exceedingly unlikely that a deer less than one year old would test
positive for CWD, even in the higher CWD prevalence areas of southern Wisconsin.
Few fawns will have been exposed to CWD, and because this disease spreads
through the deer's body very slowly, it is very rare in a fawn that the disease
has progressed to a level that is detectable. This means that testing a fawn
provides almost no information valuable to understanding CWD in Wisconsin's deer
herd and does not provide information of great value to the hunter in making a
decision about venison consumption.
> > > It is exceedingly unlikely that a deer less than one year
old would test positive for CWD < < < ???
Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm
and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.
specific susceptibility? 194. It is probable, based on age-class specific
prevalence data from wild cervids and epidemiological evidence from captive
cervids in affected research centres, that both adults and fawns may become
infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000).
198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed
deer which had become enclosed by an elk farm fence, in Sioux County,
northwestern Nebraska, four fawns only eight months old were among the 50% of
CWD-positive animals; these fawns were not showing any clinical signs of CWD
(Davidson, 2002).
SCWDS BRIEFS
Volume 17 January 2002 Number 4
CWD News from Nebraska and Kansas
Infection with the chronic wasting disease (CWD) agent recently was found
in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent
to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.
Four of the positive deer were fawns approximately 8 months old, which is
unusually young for animals testing positive for CWD.
A January survey of 39 free-ranging deer collected within 15 miles of the
positive elk and deer pens detected 8 (20%) infected animals. Test results are
pending for additional deer collected inside and outside of the enclosure, and
additional surveillance is planned for free-ranging deer in northwestern
Nebraska. Previously, CWD had been documented in Nebraska in only two wild mule
deer, both of which came from Kimball County in the southwestern panhandle
adjacent to the endemic area of northeastern Colorado and southwestern Wyoming.
CWD in adult deer and fawns
A hundred and thirty-three white-tailed deer in the study were killed after
CWD was diagnosed in the deer within the fenced area. Paired samples of
formalin-fixed tissue for CWD diagnosis and frozen tissue for DNA sequence
analysis were collected. Fifty per cent (67/133) of deer were diagnosed with CWD
(Table 2) using an immunohistochemical assay for PrPd in formalin-fixed,
paraffinembedded brain and lymphoid tissues.
Five of the CWD-positive deer were fawns, less than 1 year of age.
Early CWD (PrPd detected in the tonsil or retropharyngeal node but not
brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years
of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid
tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years
of age and three fawns). None of the CWD-positive deer showed clinical signs of
the disease (weight loss, hypersalivation, disorientation) or gross changes
consistent with CWD (serous atrophy of fat) at necropsy.
Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had
CWD i.e. 1 positive out of 51 samples.
2003
Boone-Winnebago Unit Fawn 51 1 2.0%
2011 FAWN CWD POSITIVE ILLINOIS
1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING
2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING
3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTING
For example, in 2008 a fawn tested positive and in 2010 an infected
yearling buck was detected in Smith County
PPo3-40:
Mother to Offspring Transmission of Chronic Wasting Disease
Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug,
Nicholas Haley and Edward A. Hoover Colorado State University, Department of
Microbiology, Immunology and Pathology, Fort Collins, CO USA
Key words: Chronic wasting disease, vertical transmission, muntjac deer
We have developed a new cervid model in small Asian muntjac deer (Muntiacus
reevesi) to study potential modes of vertical transmission of chronic wasting
disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally
infected with CWD tested PrPCWD lymphoid positive by 4 months post infection.
Six fawns were born to these CWD-infected doe. Six fawns were born to 6
CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been
monitored for CWD infection by immunohistochemistry and sPMCA performed on
serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in
one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal
lymphoid tissue has yield positive results on another fawn at 10 days of age. In
addition, sPMCA assays have also demonstrated amplifiable prions in maternal
placental (caruncule) and mammary tissue of the dam. Additional pregnancy
related fluids and tissues from the doe as well as tissue from the nonviable
fawns are currently being probed for the presence of CWD. In summary, we have
employed the muntjac deer model, to demonstrate for the first time the
transmission of CWD from mother to offspring. These studies provide the
foundation to investigate the mechanisms and pathways of maternal prion
transfer.
> > > PrPCWD has been detected in one fawn as early as 40 days of
age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive
results on another fawn at 10 days of age < < <
Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus)
The rapid infection of deer fawns following exposure by the most plausible
natural route is consistent with the efficient horizontal transmission of CWD in
nature and enables accelerated studies of transmission and pathogenesis in the
native species. Introduction
never say never as far as cwd transmission to humans, and second hand
friendly fire there from i.e. iatrogenic. see ;
as I said, what if ?
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
===========================================
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT IF ?
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in
vitro approaches
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier ro conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
>>> There is no evidence that humans or livestock can get the
disease, according to the Centers for Disease Control and Prevention.
hang on now, what do you call this ;
> First transmission of CWD to transgenic mice over-expressing bovine
prion protein gene (TgSB3985)
PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping
up the future of prion research
Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First
transmission of CWD to transgenic mice over-expressing bovine prion protein gene
(TgSB3985)
FORGOT TO ADD THIS ONE...
P.126: Successful transmission of chronic wasting disease (CWD) into mice
over-expressing bovine prion protein (TgSB3985)
Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana
Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1
1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of
California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA
Keywords: chronic wasting disease, transmission, transgenic mouse, bovine
prion protein
Background. CWD is a disease affecting wild and farmraised cervids in North
America. Epidemiological studies provide no evidence of CWD transmission to
humans. Multiple attempts have failed to infect transgenic mice expressing human
PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal
human PrPC in vitro provides additional evidence that transmission of CWD to
humans cannot be easily achieved. However, a concern about the risk of CWD
transmission to humans still exists. This study aimed to establish and
characterize an experimental model of CWD in TgSB3985 mice with the following
attempt of transmission to TgHu mice.
Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were
intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse
(CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly
injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD)
or elk (CWD/Elk). Animals were observed for clinical signs of neurological
disease and were euthanized when moribund. Brains and spleens were removed from
all mice for PrPCWD detection by Western blotting (WB). A histological analysis
of brains from selected animals was performed: brains were scored for the
severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain
regions.
Results. Clinical presentation was consistent with TSE. More than 90% of
TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres
in the brain but only mice in the latter group carried PrPCWD in their spleens.
We found evidence for co-existence or divergence of two CWD/ Tga20 strains based
on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk
or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen
by WB. However, on neuropathological examination we found presence of amyloid
plaques that stained positive for PrPCWD in three CWD/WTD- and two
CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and
CWD/Elkinfected mice were similar but unique as compared to profiles of BSE,
BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM
mice tested positive for PrPCWD by WB or by immunohistochemical detection.
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
TSS
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor
Department of Chemical Engineering University of Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION
CONGRESS SEPTEMBER 8-11 2010
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independent outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independently of the the
Department.
The statistical results regarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
Tuesday, October 21, 2014
Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer
Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE
The deer from an infected Reynoldsville, Jefferson County farm tested
positive for Chronic Wasting Disease. Two other white-tailed deer died in April
on the farm and tested positive for the disease. This marks the 14th
white-tailed deer in the state to test positive for the disease since 2012.
snip
“This is an unprecedented level of infection in a captive deer herd,” said
Greig. “The department and deer farmers worked together to accommodate the
requests of these researchers. The more we know, the greater the chance we can
eradicate the disease.”
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD
index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the
loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana,
quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO
LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Monday, June 23, 2014
PRION 2014 CHRONIC WASTING DISEASE CWD
Thursday, July 03, 2014
*** How Chronic Wasting Disease is affecting deer population and what’s the
risk to humans and pets?
Tuesday, July 01, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND
POTENTIAL RISK FACTORS THERE FROM
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Tuesday, October 07, 2014
Wisconsin white-tailed deer tested positive for CWD on a Richland County
breeding farm, and a case of CWD has been discovered on a Marathon County
hunting preserve
Thursday, October 02, 2014
IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game
Hunting Preserves
Saturday, October 18, 2014
Chronic wasting disease threatens Canadian agriculture, Alberta MLA
says
Saturday, October 25, 2014
118th USAHA Annual Meeting CWD and Captive Cerivds
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper
(Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE PRION
disease in cervids
***SINGELTARY SUBMISSION
The Scottish Parliament’s Rural Affairs, Climate Change and Environment
Committee has been looking into deer management, as you can see from the
following press release,
***and your email has been forwarded to the committee for information:
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population
Sunday, July 21, 2013
Welsh Government and Food Standards Agency Wales Joint Public Consultation
on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations
2013
*** Singeltary Submission WG18417
Saturday, September 20, 2014
North Carolina Captive cervid licenses and permits Senate Bill 744
Singeltary Submission
