Missouri Deer Owners Win Preliminary Legal Challenge from Judge Robert D. Schollmeyer blocking enforcement of new state regulations to help stop CWD in cervid from spreading
Missouri Deer Owners Win Preliminary Legal Challenge from Judge Robert D. Schollmeyer blocking enforcement of new state regulations to help stop CWD in cervid from spreading
POLITICS THREATENING YET ANOTHER STATE WITH CHRONIC WASTING DISEASE CWD TSE PRION AKA MAD COW DISEASE IN CERVIDS
Missouri Deer Owners Win Preliminary Legal Challenge
August 14, 2015
Missouri Deer Owners Win Preliminary Legal Challenge Against Restrictive
New State Rules
Contact: Jean Paul Bradshaw at Lathrop & Gage LLP
(816-460-5507/jpbradshaw@lathropgage.com)
(Aug. 13, 2015) – A Missouri state court has entered a ruling blocking
enforcement of new state regulations that threaten the existence of the state’s
growing farmed-deer industry by preventing the importation of privately owned
cervids into the state. In a 33-page ruling entered today, Judge Robert D.
Schollmeyer of the 20th Judicial Circuit Court of Missouri granted Plaintiff’s
Motion for a Preliminary Injunction in the matter of Donald Hill, et al. v.
Missouri Conservation Commission, et al. The Court held that Plaintiffs are
likely to prevail in their argument that the privately owned animals they raise
and import for breeding and hunting (including white-tailed deer and other
cervids, or hoofed animals) are not subject to regulation by the Missouri
Department of Conservation (MDC) as communally owned “wildlife resources of the
state.”
As a result, importation of privately owned cervids will be allowed under
rules administered by the Missouri Department of Agriculture (MDA). Prior to the
adoption of the new rules by the MDC, the MDA had regulated the importation of
cervids as livestock. Those rules include, among other requirements, that the
animal being imported come from a herd that is certified as having no positive
test results for Chronic Wasting Disease (CWD), as well as a number of other
diseases, for at least five years. This program was designed by the United
States Department of Agriculture.
The order prohibits the MDC from enforcing a controversial series of new
regulations that went into effect earlier this year—including a complete ban on
importing cervids into Missouri—until the legality of the regulations can be
finally resolved. The Court found not only that Plaintiffs had shown that the
MDC likely was without the authority to issue the new regulations, but that the
potential harm to Plaintiffs outweighed any threat posed by Chronic Wasting
Disease, the stated reason for the regulations. “Without question, Plaintiffs
will suffer irreparable harm… up to and including the loss of their businesses
should the regulations remain in effect throughout the upcoming hunting season,”
the Court’s order stated. “By contrast, Defendants cannot show an imminent
threat to Missouri’s cervid population or other public interests that would
justify the regulations remaining in effect while their Constitutionality is
finally resolved.” Contrary to Defendants’ argument that farmed cervids are
communally owned “wildlife resources of the state,” the ruling noted that the
Missouri Court of Appeals has already ruled that breeder deer owned by Plaintiff
Don Hill were “domestic animals” under Missouri law. The ruling also noted that
the MDC’s own regulations require all “hoofed wildlife of the state” to be
excluded from private hunting preserves, and that the department has said in
other cases that deer on private hunting preserves are “the sole property” of
the preserve owner.
Despite the claimed risks of spreading Chronic Wasting Disease through
interstate cervid movement, the Court noted that the MDC itself has imported
free-ranging elk from Kentucky in recent years from herds using CWD
certifications very similar to that required by the Missouri Department of
Agriculture. Defendants’ expert witness admitted that free-ranging cervids pose
a greater risk of spreading disease-causing agents compared with animals in
fenced-in preserves. The ruling follows a two-day hearing last month in
Gasconade County Circuit Court. The next step in the litigation will be a final
hearing on a request that the Court enter a judgment declaring the regulations
invalid. No date for that final hearing has been set. The named Plaintiffs in
the action are Donald Hill; Oak Creek Whitetail Ranch, LLC; Travis Broadway;
Winter Quarters Wildlife Ranch, LLC; Troy Popielarz; Kevin Grace; and Whitetail
Sales and Service, LLC. Plaintiffs are being represented by Jean Paul Bradshaw,
Jay Felton, Rachel Stephens and Eric Weslander of Lathrop & Gage LLP. Mr.
Bradshaw and Ms. Stephens represented Plaintiffs at the hearing.
while it appears that the deer owners (lol, only God owns deer and elk) to have won a battle, they have not won the war. however, with great sadness, the state of Missouri lost big time for now. ...
Friday, August 14, 2015
Carcass Management During a Mass Animal Health Emergency Draft Programmatic
Environmental Impact Statement—August 2015
Friday, August 14, 2015
Susceptibility of cattle to the agent of chronic wasting disease from elk
after intracranial inoculation
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD $$$
Tuesday, January 06, 2015
APHIS Provides Additional Information on Chronic Wasting Disease (CWD)
Indemnity Requests January 5, 2015 05:26 PM EST
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
Chronic wasting disease (CWD) is a widespread and expanding prion disease
in free-ranging and captive cervid species in North America. The zoonotic
potential of CWD prions is a serious public health concern. Current literature
generated with in vitro methods and in vivo animal models (transgenic mice,
macaques and squirrel monkeys) reports conflicting results. The susceptibility
of human CNS and peripheral organs to CWD prions remains largely unresolved. In
our earlier bioassay experiments using several humanized transgenic mouse lines,
we detected protease-resistant PrPSc in the spleen of two out of 140 mice that
were intracerebrally inoculated with natural CWD isolates, but PrPSc was not
detected in the brain of the same mice. Secondary passages with such
PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient
prion transmission with clear clinical and pathological signs in both humanized
and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD
isolates in a new humanized transgenic mouse line led to clinical prion
infection in 2 out of 20 mice. These results indicate that the CWD prion has the
potential to infect human CNS and peripheral lymphoid tissues and that there
might be asymptomatic human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
The propensity for trans-species prion transmission is related to the
structural characteristics of the enciphering and heterologous PrP, but the
exact mechanism remains mostly mysterious. Studies of the effects of primary or
tertiary prion protein structures on trans-species prion transmission have
relied primarily upon animal bioassays, making the influence of prion protein
structure vs. host co-factors (e.g. cellular constituents, trafficking, and
innate immune interactions) difficult to dissect. As an alternative strategy, we
used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species
prion conversion.
To assess trans-species conversion in the RT-QuIC system, we compared
chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions,
as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each
prion was seeded into each host recombinant PrP (full-length rPrP of
white-tailed deer, bovine or feline). We demonstrated that fCWD is a more
efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests
adaptation to the new host.
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD. ***This insinuates that, at the level
of protein:protein interactions, the barrier preventing transmission of CWD to
humans is less robust than previously estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
Transmission of scrapie prions to primate after an extended silent
incubation period
Emmanuel E. Comoy1 , Jacqueline Mikol1 , Sophie Luccantoni-Freire1 ,
Evelyne Correia1 , Nathalie Lescoutra-Etchegaray1 , Valérie Durand1 , Capucine
Dehen1 , Olivier Andreoletti2 , Cristina Casalone3 , Juergen A. Richt4 n1 ,
Justin J. Greenlee4 , Thierry Baron5 , Sylvie L. Benestad6 , Paul Brown1 […]
& Jean-Philippe Deslys1 - Show fewer authors Scientific Reports 5, Article
number: 11573 (2015) doi:10.1038/srep11573 Download Citation
Epidemiology | Neurological manifestations | Prion diseases Received: 16
February 2015 Accepted: 28 May 2015 Published online: 30 June 2015 ABSTRACT
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion
disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD)
in humans and having guided protective measures for animal and human health
against animal prion diseases. Recently, partial transmissions to humanized mice
showed that the zoonotic potential of scrapie might be similar to c-BSE. We here
report the direct transmission of a natural classical scrapie isolate to
cynomolgus macaque, a highly relevant model for human prion diseases, after a
10-year silent incubation period, with features similar to those reported for
human cases of sporadic CJD. Scrapie is thus actually transmissible to primates
with incubation periods compatible with their life expectancy, although fourfold
longer than BSE. Long-term experimental transmission studies are necessary to
better assess the zoonotic potential of other prion diseases with high
prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98
scrapie.
snip...
Discussion
We describe the transmission of spongiform encephalopathy in a non-human
primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of
this extended incubation period in a facility in which other prion diseases are
under study, we are obliged to consider two alternative possibilities that might
explain its occurrence. We first considered the possibility of a sporadic origin
(like CJD in humans). Such an event is extremely improbable because the
inoculated animal was 14 years old when the clinical signs appeared, i.e. about
40% through the expected natural lifetime of this species, compared to a peak
age incidence of 60–65 years in human sporadic CJD, or about 80% through their
expected lifetimes. Moreover, sporadic disease has never been observed in
breeding colonies or primate research laboratories, most notably among hundreds
of animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own
facility.
The second possibility is a laboratory cross-contamination. Three facts
make this possibility equally unlikely. First, handling of specimens in our
laboratory is performed with fastidious attention to the avoidance of any such
cross-contamination. Second, no laboratory cross-contamination has ever been
documented in other primate laboratories, including the NIH, even between
infected and uninfected animals housed in the same or adjacent cages with daily
intimate contact (P. Brown, personal communication). Third, the cerebral lesion
profile is different from all the other prion diseases we have studied in this
model19, with a correlation between cerebellar lesions (massive spongiform
change of Purkinje cells, intense PrPres staining and reactive gliosis26) and
ataxia. The iron deposits present in the globus pallidus are a non specific
finding that have been reported previously in neurodegenerative diseases and
aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease
due to thiamine deficiency28 but blood thiamine levels were within normal limits
(data not shown). The preferential distribution of spongiform change in cortex
associated with a limited distribution in the brainstem is reminiscent of the
lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of
lesion profiles should be interpreted with caution. It is of note that the same
classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation
periods and lesional profiles as a sample derived from a MM1 sCJD
patient30.
We are therefore confident that the illness in this cynomolgus macaque
represents a true transmission of a sheep c-scrapie isolate directly to an
old-world monkey, which taxonomically resides in the primate subdivision
(parvorder of catarrhini) that includes humans. With an homology of its PrP
protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant
model for assessing zoonotic risk of prion diseases. Since our initial aim was
to show the absence of transmission of scrapie to macaques in the worst-case
scenario, we obtained materials from a flock of naturally-infected sheep,
affecting animals with different genotypes32. This c-scrapie isolate exhibited
complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice
expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal
communication). From the standpoint of zoonotic risk, it is important to note
that sheep with c-scrapie (including the isolate used in our study) have
demonstrable infectivity throughout their lymphoreticular system early in the
incubation period of the disease (3 months-old for all the lymphoid organs, and
as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie
infectivity has been identified in blood34, milk35 and skeletal muscle36 from
asymptomatic but scrapie infected small ruminants which implies a potential
dietary exposure for consumers.
Two earlier studies have reported the occurrence of clinical TSE in
cynomolgus macaques after exposures to scrapie isolates. In the first study, the
“Compton” scrapie isolate (derived from an English sheep) and serially
propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque,
rhesus macaque or chimpanzee within 7 years following intracerebral challenge1;
conversely, after 8 supplementary passages in conventional mice, this “Compton”
isolate induced TSE in a cynomolgus macaque 5 years after intracerebral
challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years
post-exposure8. However, multiple successive passages that are classically used
to select laboratory-adapted prion strains can significantly modify the initial
properties of a scrapie isolate, thus questioning the relevance of zoonotic
potential for the initial sheep-derived isolate. The same isolate had also
induced disease into squirrel monkeys (new-world monkey)9. A second historical
observation reported that a cynomolgus macaque developed TSE 6 years
post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe
(derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the
same inoculum remained healthy 9 years post-exposure1. This inoculum also
induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie
transmission attempts in macaque failed but had more shorter periods of
observation in comparison to the current study. Further, it is possible that
there are differences in the zoonotic potential of different scrapie
strains.
The most striking observation in our study is the extended incubation
period of scrapie in the macaque model, which has several implications. Firstly,
our observations constitute experimental evidence in favor of the zoonotic
potential of c-scrapie, at least for this isolate that has been extensively
studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should
be confirmed by performing duplicate intracerebral exposures and assessing the
transmissibility by the oral route (a successful transmission of prion strains
through the intracerebral route may not necessarily indicate the potential for
oral transmission37). However, such confirmatory experiments may require more
than one decade, which is hardly compatible with current general management and
support of scientific projects; thus this study should be rather considered as a
case report.
Secondly, transmission of c-BSE to primates occurred within 8 years post
exposure for the lowest doses able to transmit the disease (the survival period
after inoculation is inversely proportional to the initial amount of infectious
inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25
mg) of scrapie-infected sheep brain suggests that the macaque has a higher
species barrier for sheep c-scrapie than c-BSE, although it is notable that
previous studies based on in vitro conversion of PrP suggested that BSE and
scrapie prions would have a similar conversion potential for human PrP38.
Thirdly, prion diseases typically have longer incubation periods after oral
exposure than after intracerebral inoculations: since humans can develop Kuru 47
years after oral exposure39, an incubation time of several decades after oral
exposure to scrapie would therefore be expected, leading the disease to occur in
older adults, i.e. the peak age for cases considered to be sporadic disease, and
making a distinction between scrapie-associated and truly sporadic disease
extremely difficult to appreciate.
Fourthly, epidemiologic evidence is necessary to confirm the zoonotic
potential of an animal disease suggested by experimental studies. A relatively
short incubation period and a peculiar epidemiological situation (e.g., all the
first vCJD cases occurring in the country with the most important ongoing c-BSE
epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD.
Sporadic CJD are considered spontaneous diseases with an almost stable and
constant worldwide prevalence (0.5–2 cases per million inhabitants per year),
and previous epidemiological studies were unable to draw a link between sCJD and
classical scrapie6,7,40,41, even though external causes were hypothesized to
explain the occurrence of some sCJD clusters42,43,44. However, extended
incubation periods exceeding several decades would impair the predictive values
of epidemiological surveillance for prion diseases, already weakened by a
limited prevalence of prion diseases and the multiplicity of isolates gathered
under the phenotypes of “scrapie” and “sporadic CJD”.
Fifthly, considering this 10 year-long incubation period, together with
both laboratory and epidemiological evidence of decade or longer intervals
between infection and clinical onset of disease, no premature conclusions should
be drawn from negative transmission studies in cynomolgus macaques with less
than a decade of observation, as in the aforementioned historical transmission
studies of scrapie to primates1,8,9. Our observations and those of others45,46
to date are unable to provide definitive evidence regarding the zoonotic
potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation
period of the scrapie-affected macaque in the current study also underscores the
limitations of rodent models expressing human PrP for assessing the zoonotic
potential of some prion diseases since their lifespan remains limited to
approximately two years21,47,48. This point is illustrated by the fact that the
recently reported transmission of scrapie to humanized mice was not associated
with clinical signs for up to 750 days and occurred in an extreme minority of
mice with only a marginal increase in attack rate upon second passage13. The low
attack rate in these studies is certainly linked to the limited lifespan of mice
compared to the very long periods of observation necessary to demonstrate the
development of scrapie. Alternatively, one could estimate that a successful
second passage is the result of strain adaptation to the species barrier, thus
poorly relevant of the real zoonotic potential of the original scrapie isolate
of sheep origin49. The development of scrapie in this primate after an
incubation period compatible with its lifespan complements the study conducted
in transgenic (humanized) mice; taken together these studies suggest that some
isolates of sheep scrapie can promote misfolding of the human prion protein and
that scrapie can develop within the lifespan of some primate species.
In addition to previous studies on scrapie transmission to primate1,8,9 and
the recently published study on transgenic humanized mice13, our results
constitute new evidence for recommending that the potential risk of scrapie for
human health should not be dismissed. Indeed, human PrP transgenic mice and
primates are the most relevant models for investigating the human transmission
barrier. To what extent such models are informative for measuring the zoonotic
potential of an animal TSE under field exposure conditions is unknown. During
the past decades, many protective measures have been successfully implemented to
protect cattle from the spread of c-BSE, and some of these measures have been
extended to sheep and goats to protect from scrapie according to the principle
of precaution. Since cases of c-BSE have greatly reduced in number, those
protective measures are currently being challenged and relaxed in the absence of
other known zoonotic animal prion disease. We recommend that risk managers
should be aware of the long term potential risk to human health of at least
certain scrapie isolates, notably for lymphotropic strains like the classical
scrapie strain used in the current study. Relatively high amounts of infectivity
in peripheral lymphoid organs in animals infected with these strains could lead
to contamination of food products produced for human consumption. Efforts should
also be maintained to further assess the zoonotic potential of other animal
prion strains in long-term studies, notably lymphotropic strains with high
prevalence like CWD, which is spreading across North America, and atypical/Nor98
scrapie (Nor98)50 that was first detected in the past two decades and now
represents approximately half of all reported cases of prion diseases in small
ruminants worldwide, including territories previously considered as scrapie
free. Even if the prevailing view is that sporadic CJD is due to the spontaneous
formation of CJD prions, it remains possible that its apparent sporadic nature
may, at least in part, result from our limited capacity to identify an
environmental origin.
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
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
PPo3-22:
Detection of Environmentally Associated PrPSc on a Farm with Endemic
Scrapie
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh
Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of
Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories
Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University
of Nottingham; Sutton Bonington, Loughborough UK
Key words: scrapie, evironmental persistence, sPMCA
Ovine scrapie shows considerable horizontal transmission, yet the routes of
transmission and specifically the role of fomites in transmission remain poorly
defined. Here we present biochemical data demonstrating that on a
scrapie-affected sheep farm, scrapie prion contamination is widespread. It was
anticipated at the outset that if prions contaminate the environment that they
would be there at extremely low levels, as such the most sensitive method
available for the detection of PrPSc, serial Protein Misfolding Cyclic
Amplification (sPMCA), was used in this study. We investigated the distribution
of environmental scrapie prions by applying ovine sPMCA to samples taken from a
range of surfaces that were accessible to animals and could be collected by use
of a wetted foam swab. Prion was amplified by sPMCA from a number of these
environmental swab samples including those taken from metal, plastic and wooden
surfaces, both in the indoor and outdoor environment. At the time of sampling
there had been no sheep contact with these areas for at least 20 days prior to
sampling indicating that prions persist for at least this duration in the
environment. These data implicate inanimate objects as environmental reservoirs
of prion infectivity which are likely to contribute to disease transmission.
*** 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".
Tuesday, July 21, 2015
Texas CWD Medina County Herd Investigation Update July 16, 2015
• 66 Texas sites, 2 Mexico sites
Wednesday, July 22, 2015
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf
Guarding the Henhouse
Thursday, July 23, 2015
*** Chronic Wasting Disease (CWD) 101 Drs. Walter Cook & Donald S.
Davis
Sunday, July 26, 2015
*** TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK
ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE ***
Tuesday, July 28, 2015
TEXAS Kills 35 Deer at Medina County Ranch (Texas Captive CWD)
Tuesday, August 11, 2015
Why Has the Federal Government Cut Funding for Chronic Wasting Disease
Research?
http://chronic-wasting-disease.blogspot.com/2015/08/why-has-federal-government-cut-funding.html
Tuesday, August 11, 2015
Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
IF the state of Texas does not get serious real fast with CWD, and test all
those deer, that 5 year plan is a ticking time bomb waiting to happen.
all cervid tested after slaughter, and test results must be released to the
public.
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a
mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the
environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of
protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple
autoclave will not kill this TSE prion agent.
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
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Longitudinal Detection of Prion Shedding in Saliva and Urine by
CWD-Infected Deer by RT-QuIC
Davin M. Henderson1, Nathaniel D. Denkers1, Clare E. Hoover1, Nina
Garbino1, Candace K. Mathiason1 and Edward A. Hoover1# + Author Affiliations
1Prion Research Center, Department of Microbiology, Immunology, and
Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado
State University, Fort Collins, CO 80523
ABSTRACT Chronic Wasting Disease (CWD) is an emergent, rapidly spreading
prion disease of cervids. Shedding of infectious prions in saliva and urine is
thought to be an important factor in CWD transmission. To help elucidate this
issue, we applied an in vitro amplification assay to determine the onset,
duration, and magnitude of prion shedding in longitudinally collected saliva and
urine samples from CWD-exposed white-tailed deer. We detected prion shedding as
early as 3 months after CWD exposure and sustained shedding throughout the
disease course. We estimated that a 50% lethal dose (LD50) for cervidized
transgenic mice would be contained in 1 ml of infected deer saliva or 10 ml or
urine. Given the average course of infection and daily production of these body
fluids, an infected deer would shed thousands of prion infectious doses over the
course of CWD infection. The direct and indirect environmental impact of this
magnitude of prion shedding for cervid and non-cervid species is surely
significant.
Importance: Chronic wasting disease (CWD) is an emerging and uniformly
fatal prion disease affecting free ranging deer and elk and now recognized in 22
United States and 2 C anadian Provinces. It is unique among prion diseases in
that it is transmitted naturally though wild populations. A major hypothesis for
CWD's florid spread is that prions are shed in excreta and transmitted via
direct or indirect environmental contact. Here we use a rapid in vitro assay to
show that infectious doses of CWD prions are in fact shed throughout the
multi-year disease course in deer. This finding is an important advance in
assessing the risks posed by shed CWD prions to animals as well as humans.
FOOTNOTES
↵#To whom correspondence should be addressed: Edward A. Hoover, Prion
Research Center, Department of Microbiology, Immunology and Pathology, Colorado
State University, Fort Collins, Colorado, US Email: edward.hoover@colostate.edu
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
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). The clinical signs
of CWD in affected adults are weight loss and behavioural changes that can span
weeks or months (Williams, 2005). In addition, signs might include excessive
salivation, behavioural alterations including a fixed stare and changes in
interaction with other animals in the herd, and an altered stance (Williams,
2005). These signs are indistinguishable from cervids experimentally infected
with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be
introduced into countries with BSE such as GB, for example, infected deer
populations would need to be tested to differentiate if they were infected with
CWD or BSE to minimise the risk of BSE entering the human food-chain via
affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
*** Singeltary reply ;
ruminant feed ban for cervids in the United States ?
31 Jan 2015 at 20:14 GMT
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
CWD, spreading it around...
for the game farm industry, and their constituents, to continue to believe
that they are _NOT_, and or insinuate that they have _NEVER_ been part of the
problem, will only continue to help spread cwd. the game farming industry, from
the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet
mills, shooting pens, to large ranches, are not the only problem, but it is
painfully obvious that they have been part of the problem for decades and
decades, just spreading it around, as with transportation and or exportation and
or importation of cervids from game farming industry, and have been proven to
spread cwd. no one need to look any further than South Korea blunder ;
===========================================
spreading cwd around...
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...
Friday, May 13, 2011
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.
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
HAVE YOU BEEN THUNDERSTRUCK ?
Saturday, July 18, 2015
CHARLES "SAM" JAMES, Columbia, Missouri, was charged in a one-count federal
indictment for violations of the Lacey Act involved the sale of white-tailed
deer transported in violation of Missouri and Florida law
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or
Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE
RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today
announced that the test results from the depopulation of a quarantined captive
deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the
herd, tested positive for Chronic Wasting Disease (CWD).
*** see history of this CWD blunder here ;
On June 5, 2013, DNR conducted a fence inspection, after gaining approval
from surrounding landowners, and confirmed that the fenced had been cut or
removed in at least four separate locations; that the fence had degraded and was
failing to maintain the enclosure around the Quarantined Premises in at least
one area; that at least three gates had been opened;and that deer tracks were
visible in and around one of the open areas in the sand on both sides of the
fence, evidencing movement of deer into the Quarantined Premises.
The overall incidence of clinical CWD in white-tailed deer was 82%
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death
(mo)
*** 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.
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
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, June 25, 2015
Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm
Tuesday, July 14, 2015
TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD
postive farm Yellow ear tag
Friday, June 01, 2012
*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
Tuesday, November 27, 2012
Pennsylvania ‘Pink 23’ Adams County exposed CWD Escaped Deer shot, but
where are the other escapees ?
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
Earl Ray Tomblin, Governor Frank Jezioro, Director
News Release: November 4, 2011
Facebook: WV Commerce - State Parks
Hoy Murphy, Public Information Officer (304) 957-9365 hoy.r.murphy@wv.gov
Contact: Curtis Taylor, Wildlife Resources Section Chief 304-558-2771
DNR.Wildlife@wv.gov
Elk escape from captive cervid facility in Pennsylvania near West Virginia
border
SOUTH CHARLESTON, W.Va. – The West Virginia Division of Natural Resources
(WVDNR) has confirmed with officials from the Pennsylvania Department of
Agriculture (PDA) that at least two elk, including one adult bull and one cow,
have escaped from a captive cervid facility (deer and elk farms) in Greene
County, Pa. Greene County shares a common border with Marshall, Wetzel and
Monongalia counties in West Virginia. The elk escaped from a captive cervid
facility located approximately three miles from the West Virginia-Pennsylvania
border.
The PDA regulates captive cervid facilities in Pennsylvania. A
representative of the agency was unaware if the recent escaped elk were tagged.
The WVDNR regulates captive cervid facilities in West Virginia. In West
Virginia, all captive cervids in breeding facilities must be ear-tagged, and
there are currently no reported elk escapes from any facility in West Virginia.
A bull elk has been seen recently in Wetzel County, W.Va., according to
WVDNR officials. There have been no reports of cow elk sightings in either
Wetzel County, W.Va., or Greene County, Pa. No free-ranging wild elk live within
150 miles of Wetzel County. The elk sighted in Wetzel County is likely the
escaped animal from the captive facility in Pennsylvania.
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Monday, June 11, 2012
*** OHIO Captive deer escapees and non-reporting ***
Thursday, October 23, 2014
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
Thursday, April 02, 2015
OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's
properties near Millersburg
Wednesday, February 11, 2015
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with
two counts of tampering with evidence
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
Tuesday, December 09, 2014
Missouri MDC reports one new case of CWD, found in Adair County
Friday, October 17, 2014 Missouri Final action on Orders of Rule making
Breeders and Big Game Hunting Preserves http://chronic-wasting-disease.blogspot.com/2014/10/missouri-final-action-on-orders-of-rule.html
Thursday, September 11, 2014 Missouri Nixon's Veto Stands Overide Fails on
Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the House http://chronic-wasting-disease.blogspot.com/2014/09/missouri-nixons-veto-stands-overide.html
Thursday, May 01, 2014 Missouri DNR CWD prevention and captive cervid farming
Update
Tuesday, March 26, 2013 CWD Missouri remains confined to Linn-Macon-County
Core Area with four new cases http://chronic-wasting-disease.blogspot.com/2013/03/cwd-missouri-remains-confined-to-linn.html
Wednesday, January 23, 2013
Missouri sixth case CWD documented northwest Macon County http://chronic-wasting-disease.blogspot.com/2013/01/missouri-sixth-case-cwd-documented.html
Tuesday, January 24, 2012 CWD found in two free-ranging deer from Macon County
Missouri http://chronic-wasting-disease.blogspot.com/2012/01/cwd-found-in-two-free-ranging-deer-from.html
Friday, February 26, 2010 Chronic wasting disease found in Missouri deer http://chronic-wasting-disease.blogspot.com/2010/02/chronic-wasting-disease-found-in.html
Sunday, March 25, 2012 Three more cases of CWD found in free-ranging deer in
Macon County http://chronic-wasting-disease.blogspot.com/2012/03/three-more-cases-of-cwd-found-in-free.html
From: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2012 6:26 PM
To: warhovert@missouri.edu
Cc: abbottjm@missouri.edu ; waltermr@missouri.edu ;
John.McLaughlin@missouri.edu ; connerek@missouri.edu ; contact@dnr.mo.gov ;
Shelly.Witt@mda.mo.gov ; Animal.Health@mda.mo.gov ; acfa@mda.mo.gov ;
animalid@mda.mo.gov ; Linda.Hickam@mda.mo.gov
Subject: re-Missouri officials seek states' advice on chronic wasting
disease in deer
Thursday, May 31, 2012
Missouri MDC staff will provide information on five recently found cases of
CWD in free-ranging deer in northwest Macon County June 2, 2012
Wednesday, September 05, 2012
Missouri MDC seeks hunters’ help when processing harvested deer and
preventing CWD
Thursday, December 20, 2012
MISSOURI Initial CWD sampling test results available online from MDC so far
one adult buck has tested positive for the disease
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri October 20, 2011
Chronic Wasting Disease Found in Captive Deer
The Missouri departments of Agriculture, Conservation and Health and Senior
Services and the U.S. Department of Agriculture announced that a captive
white-tailed deer in Macon County, Missouri has tested positive for Chronic
Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and
moose.
snip...
The animal that tested positive for CWD was a captive white-tailed deer
inspected as part of the State's CWD surveillance and testing program.
Preliminary tests were conducted by the USDA National Veterinary Services
Laboratory in Ames, Iowa.
snip...
In February 2010 a case of CWD was confirmed in Linn County on a captive
hunting preserve operated by the same entity, Heartland Wildlife Ranches, LLC.
The Linn County facility was depopulated and no further infection was identified
at that facility. The current case was identified through increased surveillance
required by the management plan implemented from the previous CWD incident.
snip...
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
The Missouri Department of Agriculture discovers the state's first case of
CWD in a captive white-tailed deer.
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer February 25, 2010
Chronic Wasting Disease Found in Captive Deer
The Missouri Departments of Agriculture, Conservation and Health and Senior
Services and the U.S. Department of Agriculture announced today that a captive
white-tailed deer in Linn County, Missouri has tested positive for Chronic
Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and
moose.
"There is no evidence that CWD poses a risk to domestic animals or humans,"
said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly
and effectively handle these situations."
The animal that tested positive for CWD was a white-tailed deer inspected
as part of the State's CWD surveillance and testing program. Preliminary tests
were conducted by the USDA National Veterinary Services Laboratory in Ames,
Iowa.
Upon receiving the confirmed CWD positive, Missouri's departments of
Agriculture, Conservation and Health and Senior Services initiated their CWD
Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee,
a task force comprised of veterinarians, animal health officers and conservation
officers from USDA, MDA, MDC and DHSS working together to mitigate challenges
associated with CWD.
CWD is transmitted by live animal to animal contact or soil to animal
contact. The disease was first recognized in 1967 in captive mule deer in the
Colorado Division of Wildlife captive wildlife research facility in Fort
Collins, Colorado. CWD has been documented in deer and/or elk in Colorado,
Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York,
Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the
Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that
the disease can be transmitted to humans.
"Missouri's proactive steps to put a testing protocol in place and create a
contingency plan years ago is proving beneficial. We are in a solid position to
follow pre-established steps to ensure Missouri's valuable whitetail deer
resource remains healthy and strong," said Jason Sumners Missouri's Deer
Biologist.
For more information regarding CWD, please contact Dr. Taylor Woods at
(573) 751-3377.
see video;
Danger of Canned Hunting Indiana Wildlife
Sunday, December 28, 2014
CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA
USAHA INC DECEMBER 28, 2014
Friday, August 07, 2015
Texas CWD Captive, and then there were 4 ?
Thursday, August 06, 2015
WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
Tuesday, July 21, 2015
Texas CWD Medina County Herd Investigation Update July 16, 2015
• 66 Texas sites, 2 Mexico sites
TSS
posted by Terry S. Singeltary Sr. at
9:54 AM
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