TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for Spreading Cattle Tick Fever, and what about CWD TSE Prion Disease ?
TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for
Spreading Cattle Tick Fever, and what about CWD TSE Prion Disease ?
I think prudent actions should be taken to prevent this, before it is
documented. once documented, by then it’s way too late to do something about
it...just saying...TSS
Once-exotic antelope blamed for spread of cattle fever tick Imported
antelope, deer are spreading the parasite By Lynn Brezosky, SAN ANTONIO
EXPRESS-NEWS
April 22, 2016 Updated: April 22, 2016 11:20pm
SAN ANTONIO - The nilgai, a once-exotic antelope imported from Asia for
zoos and let loose for trophy hunts on Texas ranches, are now being blamed for
spreading the potentially devastating cattle fever tick the farthest into the
U.S. interior in decades, possibly since it was declared eradicated in
1943.
The Laguna Atascosa National Wildlife Refuge in lower Cameron County, about
2 miles north of the Mexican border at the southernmost tip of Texas, is being
called ground zero for infested nilgai and white-tailed deer, which also are
hosts. The park came under quarantine after the tick was found on the carcasses
of hunted game in 2014.
While the U.S. has strict rules requiring infected animals to be
quarantined and treated to keep the ticks from spreading, Mexico does not. And
the nilgai, cattle and other hosts for the nefarious fever tick roam unchecked
across the border. The situation is especially grave because the animals are
free-ranging and compromise ongoing eradication efforts such as systematic
treatment or moving cattle out of infested pastures. According to the U.S.
Department of Agriculture, an extended tick outbreak could cost U.S. ranchers
and the broader economy more than $1.2 billion in extermination expenses and
lost revenue from diseased animals.
It's estimated that 70 percent of white-tailed deer and nearly 70 percent
of nilgai on the refuge are infested, prompting officials to require that
animals killed by hunters be tested and skinned on site, freezing the heads that
are kept for mounting for 24 hours to kill the ticks. In the last year, the U.S.
Department of Agriculture has contracted with helicopters and sharp shooters for
aerial attacks that have so far killed about 200 of the nilgai.
snip...
> TEXAS Nilgai Exotic Antelope Let Loose for Trophy Hunts Blamed for
Spreading Cattle Tick Fever
If I were a cattle rancher, I would also be extremely concerned with CWD in
cervid in Texas, and other states, and the eventual possibility that the exact
same thing happening therefrom, if it has not happened already, imo...tss
>>>These results suggest that cattle experimentally inoculated
with CWD may have some limited amount of prion infectivity outside of the brain
and spinal cord that may represent a previously unrecognized risk for
transmission. This information could have an impact on regulatory officials
developing plans to reduce or eliminate TSEs and farmers with concerns about
ranging cattle on areas where CWD may be present<<<
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Limited amplification of chronic wasting disease prions in the
peripheral tissues of intracerebrally inoculated cattle
Authors
item Haley, Nicholas - item Siepker, Christopher - item Greenlee, Justin
item Richt, Jürgen -
Submitted to: Journal of General Virology Publication
Type: Peer Reviewed Journal Publication Acceptance
Date: March 30, 2016
Publication Date: N/A
Interpretive Summary: Chronic Wasting Disease (CWD), a fatal
neurodegenerative disease that occurs in farmed and wild cervids (deer and elk)
of North America, is a transmissible spongiform encephalopathy (TSE). TSEs are
caused by infectious proteins called prions that are resistant to various
methods of decontamination and environmental degradation. Cattle could be
exposed to chronic wasting disease (CWD) by contact with infected farmed or
free-ranging cervids. The purpose of this study was to use an in vitro
amplification method called real time quaking induced conversion (RT-QuIC) to
assess tissues from cattle inoculated with CWD for low levels of prions not
detected by traditional diagnostic methods such as western blot and
immunohistochemistry. This study reports that prions were identified by RT-QuIC
only in cattle that were confirmed positive by traditional methods. However,
prions were rarely identified in some peripheral tissues such as mesenteric
lymph node, tonsil, or nasal turbinate that were not considered positive by
traditional methods. These results suggest that cattle experimentally inoculated
with CWD may have some limited amount of prion infectivity outside of the brain
and spinal cord that may represent a previously unrecognized risk for
transmission. This information could have an impact on regulatory officials
developing plans to reduce or eliminate TSEs and farmers with concerns about
ranging cattle on areas where CWD may be present.
Technical Abstract: Chronic wasting disease (CWD) is a fatal
neurodegenerative disease, classified as a prion disease or transmissible
spongiform encephalopathy (TSE) similar to bovine spongiform encephalopathy
(BSE). Cervids affected by CWD accumulate an abnormal protease resistant prion
protein throughout the central nervous system (CNS), as well as in both
lymphatic and excretory tissues – an aspect of prion disease pathogenesis not
observed in cattle with BSE. Using seeded amplification through real time
quaking induced conversion (RT-QuIC), we investigated whether the bovine host or
prion agent was responsible for this aspect of TSE pathogenesis. We blindly
examined numerous central and peripheral tissues from cattle inoculated with CWD
for prion seeding activity. Seeded amplification was readily detected in the
CNS, though rarely observed in peripheral tissues, with a limited distribution
similar to that of BSE prions in cattle. This seems to indicate that prion
peripheralization in cattle is a host-driven characteristic of TSE infection.
These results suggest that cattle experimentally inoculated with CWD may
have some limited amount of prion infectivity outside of the brain and spinal
cord that may represent a previously unrecognized risk for transmission. This
information could have an impact on regulatory officials developing plans to
reduce or eliminate TSEs and farmers with concerns about ranging cattle on areas
where CWD may be present.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease - (Abstract Only) -
(12-Aug-15) Transmission of chronic wasting disease to sentinel reindeer
(Rangifer tarandus tarandus) - (Abstract Only) - (12-Aug-15) Transmission of
scrapie prions to primate after an extended silent incubation period - (Peer
Reviewed Journal) Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573. Transmission of the agent of
sheep scrapie to deer results in PrPSc with two distinct molecular profiles -
(Abstract Only) Greenlee, J., Moore, S.J., Smith, J.., West Greenlee, M.H.,
Kunkle, R. 2015. Scrapie transmits to white-tailed deer by the oral route and
has a molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62.
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral
tissues of intracerebrally inoculated cattle
STANLEY PRUSINER AND THE DINOSAUR END OF TIME SCENARIO WITH TSE PRION aka
mad cow type disease
The BSE Inquiry
Dr. Stanley Prusiner (scheduled to give oral evidence 06/06/98)
TRANSCRIPT OF A LECTURE BY DR STANLEY PRUSINER
GIVEN AT COLUMBIA UNIVERSITY, NEW YORK CITY
(OCTOBER 1997)
{2 MONTHS BEFORE MY MOM DIED FROM HVCJD confirmed...tss}
snip...
111. So we are very enthusiastic about that line of approach, to get at the
structure of PrP Scrapie.
112. Let me summarize. What I have told you today is that sporadic and
infectious forms of the disease have PrPc being converted into PrP Scrapie. This
is wild type PrPc being converted into wild type PrP Scrapie. The inherited
forms of the disease: it is mutant PrPc which is converted into mutant PrP
Scrapie.
113. Now, that is me many years later.
What I have told you today is that prions contain only protein called PrP
Scrapie and no nucleic acid has been found.
114. A chromosomal gene encodes PrP Scrapie and its precursor PrPc.
115. Mutations in the PrP gene cause inherited prion diseases. PrP Scrapie
is formed from PrPc as the protein changes its conformation.
116. Prion strain specific properties are encripted in the conformation of
PrP Scrapie and in caveoiae-like domains PrP Scrapie acts as a template
directing the conversion of PrPc into nascent PrP Scrapie. I think there are
many implications for the future from these studies. First of all, I think that
we will, in the future, learn about profound effects of conformational changes
regulating metabolism. We will learn much more about the dynamic plasticity of
protein structure as better technologies become available to study this. We will
learn about transient metabolic regulation through conformational changes.
117. In some fascinating work started by Reid Wickner, and then carried on
by many other people now, it appears that there are some prion like phenomena in
yeast, and also in fungi that regulates stable metabolic states. I would not be
surprised if protein polymerization might not be partially under the control of
these kinds of conformational shifts.
118. The prion diseases are clearly disorders of protein conformation; and
they share many features with the common neurodegenerative illnesses: age
dependence, progressive fatal course, the majority are sporadic, about 15 per
cent of these are familial diseases that are autosomal dominant; the pathologic
protein deposits are found. These diseases progress in the absence of any
recognition by the immune system.
119. If you take all of the descriptors they equally well apply to
Alzheimer’s disease, Parkinson's disease, and ALS. What is different, of course,
is that attempts to transmit these diseases to experimental animals have failed
in the past. I do not think that is an important aspect of what I am talking
about.
120. How do we treat these diseases? I think we can use what we have been
learning about protein X to develop transgenic animals that will be resistant to
prions, where we take advantage of the dominant negative experiments that nature
has already done both in sheep and in humans. But for humans, of course, we need
peptidomimetic drugs that will attach either to PrPc at the protein X binding
site or attach to protein X at the PrPc binding site; and I think such drugs
will be highly effective.
121. I am hopeful that this work will progress relatively rapidly in the
near future. Both Fred Cohen and I are putting a large amount of effort into
such studies.
122. Now, do not look at the bottom of the slide, only look at the top.
This is from the Chicago Tribune, October 12th 1997. This is a quiz to see
whether you guys have been alert. So what was this Nobel Prize awarded for, a
new type of germ that was described as being like which of the following?
Dracula, Jekyll and Hyde, Wolfman, Xena: The Warrior Princess.
123. Okay. How many people vote for A? How many for 8? So the answer, this
is great, Jekyll and Hyde. When shaped one way the germ is benign, but if it is
folded differently it causes disease.
124. I thought I would end with this. Many of you probably have children
who have seen 'The Lost World', and some of you have even gone to see this.
125. What you did not learn in 'The Lost World' was that the dinosaurs were
dying of a disease called "OX". The reason is that the scriptwriters left out
the whole story of prions from Michael Crichton's book; and I tried, with the
producers, to get it reinstated, but I failed.
126. But at the end of the book, just like in 'Jurassic Park' where the
good guys survive, the bad guys are eaten by the dinosaurs. This all takes place
on an island off the coast of Costa Rica, where the Germans have produced a big
plant to make dinosaurs all based on technology from Menlow Parke?), California.
127. The good guys are now leaving. The boat left the jungle river behind,
and they moved into darkness ‘Sarah Harding’ - she is a wonderful character in
the book; you have to read about her - stared at him ... "They made a mistake on
that island many years ago ... They were manufacturing infant dinosaurs ... And
as the carnivores grew they fed them a special animal protein extract. And the
extract was made of ground up sheep."
128. Now Levine -- you must understand that Levine is a Harvard professor
--: "So, What's wrong with that?" "In a zoo, they never use sheep extract", she
said, "because of the danger of infection",
129. "Infection", Levine repeated .. .'What kind of infection?" (Harvard).
"Prions," Malcom said, from the other side of the boat .... "Prions •• , Harding
said, "are the simplest disease causing entities known, even simpler than
viruses. They're just protein fragments. They're so simple they can't even
invade a body - they have to be passively ingested. But once eaten, they cause
disease; Scrapie, in sheep; mad cow disease, and Kuru, a brain disease of human
beings. And the dinosaurs developed a prion disease called ‘DX’ - that is a
medical student question in San Francisco -- "from a bad batch of sheep protein
extract. The lab battled it for years, trying to get rid of it." "You're saying
they didn't?" "For a while it seemed they did. The dinosaurs were flourishing.
But then something happened. The disease began to spread."
130. And with that I will end.
Media enquiries for Dr Prusiner: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Telephone number 001 4154764482 Fascimile number 001 4154768386 Issued on behalf
of the witness by: The SSE Inquiry Press Office 6th Floor Hercules House
Hercules Road London SE1 7DU Tel: 0171 261 8377/8383 Fax: 0171 8030893 Website:
http://www.bse.org.uk email:
inquiry@bse.org.uk
bseinquiry.gov.uk/
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
22
Visits to Colorado State University, College of Veterinary Medicine and the
Wyoming Game and Fish Department, Sybille Wildlife Research and Conservation
Education Unit.
The main objective here was to obtain some understanding of CWD. A visit
was made to the University of wyoming Game and Fish Department, Sybille wildlife
Research and Conservation Education Unit where most of the cases of CWD have
occurred. The Sybille Wildlife facility is situated some 50 miles northeast of
Laramie, Wyoming through the Laramie Mountains. Here most of the hoofed big game
species of North America; Hule Deer (odocoileus hemionus), Whitetail Deer
(Odocoileus virginianus), Elk (Cervis canadensis) Mountain Goat (Oreamnos
americana), Bighorn Sheep (0vis canadensis} and Pronghorn (Antilocapra
americana) and some other wildlife species are kept in small numbers for
experimental use in the investigation of wildlife diseases.
A colony of the blackfooted ferret (Hustela nigripes) has been established
because of its imminent extinction. At present there are only 35 but it is
proposed to breed up to 200 and then, probably in 1991, re-introduce them into
the wild in a nation wide operation. Blackfooted ferret diet is mainly Prairie
Dog (Cynoms spp.) and it is thought that the elimination of this species from
large areas by poisoning campaigns in the past has been responsible for the
precipitous ferret decline.
The buildings and pens at the facility are entirely of wooden/log
construction with heavy duty wire mesh fences. Pen floors are bare earth. A long
race connecting many different areas within the facility enables movement of
deer and antelope between pens when necessary. There is provision for holding
deer of different sizes in a custom built crush for bleeding and
treatments.
23
The educational role of the unit includes school visits to provide
instruction in the work of the department and to promote conservation. I was
accompanied on this visit by Stuart Young and Beth Williams. on arrival I was
introduced to Hughie Dawson who has managed the facility for some 20
years.
CWD occurred principally in two locations, this one at Sybille and in a
similar facility at Fort Collins, Colorado, some 120 miles southwest. It was
estimated that in total probably 60-10 cases of CWD have occurred.
It was difficult to gain a clear account of incidence and temporal sequence
of events ( - this presumably is data awaiting publication - see below) but
during the period 1981-84, 10-15 cases occurred at the Sybille facility.
Recollections as to the relative total numbers of cases at each facility were
confusing. Beth Williams recalled that more cases had occurred in the Colorado
facility.
The morbidity amongst mule deer in the facilities ie. those of the natural
potentially exposed group has been about 90% with 100% mortality. the age
distribution of affected deer was very similar to that in ESE. The clinical
duration of cases was 6-8 weeks. Mortality in CWD cases was greatest in winter
months which can be very cold.
When the problem was fully appreciated both the Sybille and the Colorado
facilities were depopulated. All cervids were culled but Pronghorn, Bighorn
Sheep and Mountain goat, where present simultaneously in the facility, were
retained. There have been no cases of CWD in these non cervid species.
A few cases continue to occur at Sybille, the last was 4 months ago.
24
An account of the occurrence of CWD at the Colorado facility was obtained
from Terry spraker, Diagnostic Laboratory, CSU College of Veterinary Medicine,
Fort Collins. He examined tissues from cases of CWD at the Colorado facility
some time prior to Beth Williams's involvement and examination of brains which
resulted in the initial diagnosis. The deer holding facilities in Colorado
comprise the Colorado Division of Wildlife Research Pen, established 10 years
ago and some older deer pens at the Foot Hills Campus of CSU, close to Fort
Collins. Originally there were just 1-2 cases CWD/year and a total of 24 over
several years. In contrast to Beth Williams recollection Terry Spraker thought
more cases had‘ occurred at Sybille than in Colorado. The cull at the Colorado
facility involved 20-30 clinically normal deer. Early lesions in dorsal nucleus
of the vagus and olfactory cortex were found in (some) of these deer. At the
time of the cull here Pronghorn was the only other hoofed species present.
Bighorn sheep and Mountain Goat were introduced only one year after the cull and
occupied ground where CWD had occurred. Immediately after depopulation the
ground was ploughed and disinfection was carried out using ?1% NaOH. The
buildings/pens were not changed. There has been no recurrence of disease at the
Colorado facility since the cull.
25
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and
compared with natural cases (‘’first passage by this route’’ MARKED OUT...TSS)
resulted in a more rapidly progressive clinical disease with repeated episodes
of synocopy ending in coma. one control animal became affected, it is J believed
through contamination of inoculum (?saline). Further CWD transmissions were
carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission
occurred in all of these species with the shortest incubation period in the
ferret.
Mouse and hamster transmissions were attempted at Wyoming State Diagnostic
Laboratory, Laramie and at CSU Fort Collins but were unsuccessful.
Also at the Wyoming State Diagnostic Laboratory, Laramie, transmission to
goats was attempted. In 1984 three goats were inoculated intracerebrally with a
10% CWD brain suspension. one goat, untreated, was placed in contact with the
CWD inoculated goats and three controls, housed separately, received saline
intracerebrally. To date these animals remain healthy.
Epidemiology of CWD
Descriptive epidemiological data has been collected from the two wildlife
facilities and a publication is in preparation.
The occurrence of CWD must be viewed against the context of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite its subsequent recognition as a
new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA viewed it as a wildlife problem and
consequently not their province! Thus
26
there have been no specific epidemiological studies, other than information
gained from noting the occurrence of cases. Because of the relatively short term
nature of the programmed research at the facilities it has not been possible to
keep Mule Deer under the appropriate experimental circumstances or for
sufficient periods to establish horizontal or maternal transmission. Beth
Williams is of the view that the occurrence of CWD at Sybille is entirely
related to propagative spread by contagion. Investigations have failed to
identify any common source of infection and the incident has presented a
protracted time course with sporadic cases throughout. There is no evidence that
wild born deer were responsible for introduction of the disease to the
facility.
I asked Hughie Dawson about the nutritional aspects of the deer kept at
Sybille. Mule Deer calves are reared on condensed milk and homogenised or
pasteurised domestic cow's milk from birth to 1 month or to 6 months. some would
be given "Lamb milk replacer" which has a higher butter fat content than either
of the former products, but is derived also from domestic cow's milk. It was
thought that at the Colorado facility calves would receive only "evaporated
milk". Calves are weaned on to a pelletted feed containing corn, wheat bran and
linseed meal with no crude mineral suppliment. Salt licks ("sulphur blocks")
which have a specific mineral composition are supplied.
CWD has occurred or is suspected to have occurred in establishments
supplied with Mule Deer from the Colorado facility. In some cases evidence for
this is tenuous. For example, it is understood that Denver zoo state that "they
have not had cases of CWD" and yet they have had cases of Mule Deer succumbing
to a chronic wasting disorder which was not diagnosed. A case of CWD occurred in
a Mule Deer in Toronto zoo in 1976. The animal in
27
question came from Denver zoo but was originally from the Colorado wildlife
facility.
Pathology of CWD
A paper (Williams et al) is in preparation on the distribution of brain
lesions in CWD. Vacuolar changes occur predominantly in the dorsal nucleus of
the vagus nerve (this nucleus is invariably affected), the hypothalamus and the
olfactory cortex with occasional vacuolation of the olfactory tract white
matter.
Cerebellar lesions are sometimes present but there are very few changes in
the spinal cord which probably accounts for the rarity of ataxia clinically. As
in sheep scrapie the hypothalamic lesions correlate with the common clinical
occurrence of polydipsia. Beth Williams is aware of occasional neuronal vacuoles
occurring in the red nucleus of clinically normal deer! Spraker has added that
he has experienced vacuoles in neurons of Gasserian ganglia and at the level of
the obex in normal deer.
It has never been reported but Pat Merz carried out SAF detection on CWD
brain material. Work may be undertaken with NIH on the immunohistological
demonstration of PrP in sections but to date there has been no PrP work.
Does CWD occur in free-living cervids?
There is some, mostly circumstantial, evidence that CWD occurs in
free-living cervids but to what extent, if at all, this represents an
established reservoir of infection in the wild is not known.
At Sybille two Mule Deer orphans (wild caught) and a White—tail Deer
(Odocoileus virginianus) hybrid developed clinical signs when only 2 1/2 years
of age.
28
An Elk (Cervus canadensis) wild caught as an adult, presumed 2 years old,
developed signs when 3-4 years old.
Another group of elk, wild caught 400 miles from the facility, with an age
range 2-8 years, old subsequently developed the disease in the facility (?period
of captivity). The location of capture relative to the facility did not
apparently rule out that they may have at some time had fence-line nose contact
with animals in the facility!
Cases have also occurred in Mule Deer that were obtained from the wild
within one hour of birth but these were never kept completely isolated through
to maturity.
Also at Sybille there has been one case of CWD diagnosed in a free ranging
Elk. It was killed in Sybille Canyon 3 miles from the facility. It could have
had fence-line contact with captive Mule Deer in the facility.
Similar incidents had occurred in Colorado. In 1985 a free-ranging affected
Elk was caught in the Rocky Mountain National Park within a 2 mile radius of the
Colorado Division of Wildlife Research Pen. In 1986 and again in 1987 a single
affected Mule Deer on each occasion was caught within a 5 mile radius of the
Pen. These latter cases occurred within 2 years of the -cervid cull at the Pen
(?1985). Brain tissue from the free—ranging Elk brain was inoculated into mice
but for some reason these were kept for only 6 months and then the experiment
was abandoned.
A specific exercise has been carried out by Beth Williams with the Wyoming
State Diagnostic Laboratory and Fish Department to sample the brains of healthy
wild Mule Deer for histological examination. On two separate occasions the first
in 1985 and again in 1987 a total of 150 Mule Deer
29
brains were collected from areas of, and ajacent to, Sybille Canyon. These
deer would have been shot under a game permit by local hunters. As they were
brought down from the hills to the Game station for the mandatory registration
of the kill the heads were removed and ages estimated. Most were 2-5 year old
with a few 6 year old. For obvious reasons hunters were reluctant to give up
stag heads. Thus, but for 15-20 brains from stags, examinations were on brains
from females. No evidence of CWD lesions was found in any of these brains.
However, it was considered that sporadic cases of CWD, should they occur in the
wild population, would soon become separated from the herd and fall prey to
coyotes (Canis latrans).
The possibility of any reservoir of infection in wild cervids originating
from scrapie in domestic sheep flocks seems remote. Scrapie has been recorded in
only three flocks in Wyoming since 1947 and Beth Williams could recall only one
previous occurrence in 1966. This had involved a Suffolk flock close to the
border with Nebraska. However, there has been one new confirmed and a suspected
affected flock this year in Wyoming. In the latter a ewe bought—in from an
Illinois flock is incriminated.
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 about 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. Whether they were scrapie infected sheep or
not is unclear. There were domestic sheep and goats present in the facility also
in the 1960's but there is no evidence that these animals developed scrapie.
During the 60's hybridization studies between the Bighorn and domestic sheep
were carried
30
out, again, without evidence of scrapie. Domestic goats were also kept at
Sybille in the 1960's.
Spraker considers that the nasal route is responsible for transmission of
CWD through nose to nose contact, which may well occur also between captive and
free—living individuals.
In domestic cattle of which about 15-20 adults were necropsied per year at
the Diagnostic Laboratory, CSU., Spraker had not encountered any lesions
suggesting BSE. Polioencephalomalacia (PEM) and Encephalic Listeriosis were the
most common morphologic neuropathological diagnoses. No bovine rabies was
seen.
31
Appendix I
VISIT TO USA - OR A E WRATHALL — INFO ON BSE AND SCRAPIE
Dr Clark lately of the Scrapie Research Unit, Mission Texas has I
successfully transmitted ovine and caprine Scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-
Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:- i/c 1ml; i/m, 5ml; s/c 5ml; oral 30ml.
1/6 went down after 48 months with a scrapie/BS2-like disease.
Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.
Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason given for
not publishing.
Diagnosis in A, B, C was by histopath. No reports on SAF were given.
2. Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally— (and naturally) infected sheep by ET. He had
found difficulty in obtaining embryos from naturally infected sheep (cf
SPA).
3. Prof. A Robertson gave a brief accout of BSE. The us approach was
to
32
accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in
USA.
4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.
5. Scrapie agent was reported to have been isolated from a solitary fetus.
6. A western blotting diagnostic technique (? on PrP) shows some
promise.
7. Results of a questionnaire sent to 33 states on" the subject of the
national sheep scrapie programme survey indicated
17/33 wished to drop it
6/33 wished to develop it
8/33 had few sheep and were neutral
Information obtained from Dr Wrathall‘s notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.
33
snip...see full text ;
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
and the rest is history ;
US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''
Senator Michael Machado from California
''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''
Stanley Prusiner
''nobody has ever ask us to comment''
''they don't want us to comment''
''they never ask''
i tried to see Venemon, after Candian cow was discovered with BSE. went to
see lyle. after talking with him... absolute ignorance... then thought I should
see Venemon... it was clear his entire policy was to get cattle bonless beef
prods across the border... nothing else mattered...
his aids confirmed this... 5 times i tried to see Venemon, never worked...
eventually met with carl rove the political... he is the one that arranged
meeting with Venemon... just trying to give you a sense of the distance... healh
public safety...
was never contacted...
yes i believe that prions are bad to eat and you can die from them...
END
Dr. Stan bashing Ann Veneman - 3 minutes
Recall Authority and Mad Cow Disease: Is the Current System Good for
Californians?
Tuesday, February 24, 2004
JOINT HEARING
AGRICULTURE AND WATER RESOURCES HEALTH AND HUMAN SERVICES AND SELECT
COMMITTEE ON GOVERNMENT OVERSIGHT - MACHADO, ORTIZ, and SPEIER, Chairs
ALL VIDEOS OF THIS HEARING HAVE BEEN REMOVED FROM THE WWW, LIKE IT NEVER
HAPPENED...but we know different...TSS
Saturday, April 16, 2016
APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal
Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
2015 Report of the Committee on Wildlife Diseases Chronic Wasting Disease
CWD TSE Prion
Chair: Colin Gillin, OR
Vice Chair: Peregrine Wolff, NV
Chronic Wasting Disease Research and Updates in Colorado
Michael Miller, Colorado Division of Parks and Wildlife
Dr. Michael Miller, Colorado Division of Parks and Wildlife, led a brief
discussion on the implications of a recent study on chronic wasting disease
(CWD) host range. The Case Western study results, presented at an international
prion conference in May 2015, complement other efforts to assess human
susceptibility to chronic wasting disease that have been ongoing since the
mid-1990s. Findings from a variety of experimental & epidemiological studies
support messaging since the mid-1990s that human illness resulting from CWD
exposure appears unlikely. The new study’s results are consistent with other
previous & contemporary data suggesting a low probability of human prion
disease resulting from CWD exposure. Dr. Miller noted that even though human
illness seems unlikely, minimizing the occurrence of CWD and encouraging other
precautions for minimizing human exposure to CWD may be prudent. Trends observed
in Colorado since 2002 suggest increasing infection rates in affected mule deer
and elk herds, with the exception of one population unit intensively managed
through harvest in the early 2000s. Controlling CWD will likely need to rely on
hunting in order to remain politically, socially, and fiscally sustainable.
Consequently, early intervention -- while infection rates are still low -- may
offer the best opportunity to both suppress epidemics and minimize the
likelihood of hunters harvesting infected animals. Dr. Miller suggested that the
timing and approaches to CWD control may deserve more attention and
reconsideration than given in recent years.
Summary of Recent Chronic Wasting Disease events in Texas Mitch Lockwood,
Texas Parks and Wildlife Department
Bob Ditmar (TPWD), Andy Schwartz, Texas Animal Health Commission
Introduction:
• 3.9 million free-ranging white-tailed deer
• 700K white-tailed deer hunters
• 600K white-tailed deer harvested annually
• $3.6 billion economic output for all hunting
• $2.1 billion for deer hunting
• 1,300 deer breeding facilities
• > 110,000 deer in breeding facilities
• > 2,200 free-ranging deer moved annually through various permits
Texas Parks and Wildlife Department (TPWD) has been conducting CWD
surveillance throughout the state since 2002. Biologists have collected more
than 26,000 samples from hunter-harvested deer, and others have collected more
than 21,000 samples in order to meet TPWD permitting requirements, totaling
almost 48,000 samples. Additionally, Texas Animal Health Commission (TAHC) has
maintained a Voluntary CWD Herd Certification Program since 1995. In 2012, CWD
was discovered in 2 mule deer samples from far West Texas (Hueco Mountains) as a
result of a targeted surveillance effort. This area is directly adjacent to a
region in New Mexico with documented CWD occurrence. To date, five more positive
samples have been obtained from this population through hunter harvested mule
deer, indicating a disease prevalence of 10%.
Mule deer and white-tailed deer are regulated by TPWD, while other
susceptible species (including elk) are regulated by the TAHC. This has
generated the need for enhanced coordination and communication between these two
agencies. The TPWD/TAHC CWD Management Plan was developed by both agencies in
consultation with the state’s CWD Task Force. The Task Force is comprised of
wildlife biologists, deer and elk breeders, veterinarians and other
animal-health experts from TPWD, TAHC, Texas Veterinary Medical Diagnostic
Laboratory, Texas Department of State Health Services, Texas A&M College of
Veterinary Medicine, and USDA. The plan includes mandatory check stations for
susceptible species taken inside the CWD Containment Zone, which covers portions
of Hudspeth, Culberson, and El Paso counties. Artificial movement of deer is
prohibited in the CWD Containment Zone.
On June 30, 2015 a sample from a Medina County (area on border of southern
Edwards Plateau and northern South Texas Plains ecoregions) deer breeding
facility was confirmed positive for CWD. The index breeding facility
participated in TAHC’s voluntary CWD Herd Certification Program, and had tested
62 of 65 mortalities prior to June 2015 (60 not detected, 2 location results)
since permitted in 2006. There were a total of 136 adult deer in the inventory
on June 30, 2015, and the herd was considered to be relatively young.
During the previous 5 years, 107 deer were transferred from 30 deer
breeding facilities into the index facility. During that same period, 835 were
transferred from the index facility to 147 different facilities including 96
deer breeding facilities, 46 release sites, 3 DMP sites, and 2 sites in
Mexico.
TPWD and TAHC immediately placed a temporary moratorium on movements of all
captive deer in the state, and TAHC placed a Hold Order on the 177 “Tier 1”
facilities. Since then, TPWD and TAHC worked with the CWD Task Force and
industry stakeholders to develop a plan to lift the moratorium on deer
transfers, which includes additional CWD testing requirements in deer breeding
facilities or on registered release sites. Additionally, TAHC has removed the
Hold Order for 120 facilities, leaving a total 57 facilities remaining under a
Hold Order as of October 16, 2015. Most deer breeding facilities were authorized
to transfer deer by August 24, 2015. Depopulation at the index facility was
initiated in July 28 and completed on September 30, 2015. CWD was detected in a
total of 4 (out of 136 adults) white-tailed deer in the index facility, all of
which were 2-year-old bucks that were natural additions.
On September 15, 2015, CWD was confirmed in one of the trace-forward
facilities, from which 84 deer had transferred out to 9 different facilities (5
deer breeding facilities, 3 release sites, and 1 nursing facility) since it
received deer from the index herd. This resulted in 7 additional Hold Orders
being issued by TAHC, 4 of which have since been released. The CWD-positive at
the trace-forward facility was also a 2-year-old buck that was born in the index
facility. In summary, CWD has been detected in a total of 5 captive white-tailed
deer in Texas, 4 of which were located in the index facility, and 1 was located
in a trace-forward facility. There are 36 deer from the 2-year-old cohort
originating in the index facility that are reported to be alive in 7 deer
breeding facilities, and possibly as many as 6 deer from that cohort still alive
on release sites. Additionally, there are 33 deer that traced through the index
facility that are still alive in 15 deer breeding facilities, and possibly as
many as 51 trace-through deer are still alive on 24 different release sites, and
2 trace-through deer may still be alive in Mexico.
TPWD has intensified the statewide CWD surveillance efforts, with a goal to
collect samples from more than 8,000 hunter-harvested deer, including 300
samples within a 5-mile radius of the index facility. TAHC will continue to
pursue indemnity on exposed deer located in trace-forward facilities in an
attempt to conduct a more thorough epidemiological investigation. TPWD and TAHC
have committed to reevaluate movement qualification standards that apply to deer
breeding facilities and release sites following the 2015-16 hunting season. Both
agencies are exploring ante-mortem testing protocols, and will continue to seek
guidance from experts in the field.
Epidemiology of Recent CWD Cases in Ohio
Susan Skorupski, Assistant Director, USDA-APHIS-VS
Background
Ohio has had a voluntary Chronic Wasting Disease (CWD) Herd Certification
Program for all cervidae for at least 12 years. Ohio has 331 cervidae herds in
the CWD monitoring program with 256 at Certified level. In October 2012, Ohio
White Tail Deer rule became effective. It includes several categories of white
tail deer operations. Monitored Herds cannot sell or give away animals and
includes hunting preserves. Under this rule, hunting preserves cannot move live
animals from the premises and must annually sample 30 animals or 30% of
harvested deer, based on the number of deer harvested during the previous year.
Herds with Status are herds enrolled in the CWD Certification Program but not
yet at certified level. Certified Status Herds are enrolled in the CWD
monitoring program and have reached certified status. Ohio has 135 Monitored
Herds, including 24 hunting preserves, 75 Herds with Status, and 256 Certified
Status herds. Ohio’s approach to infected animals and associated animals and
herds
Infected herd – herd where a CWD infected animal resided when the test
positive sample was collected. Herd quarantined.
Exposed herd – any herd where an animal that tested CWD positive has
resided within the 5 years before the CWD diagnosis. Whole herd quarantined Herd
that contains an exposed animal – whole herd quarantined unless epidemiology
information suggests the animal is of lower risk of spreading CWD.
Exposed animal – animal that was exposed to the CWD infected animal any
time during the five years prior to when the animal died or was euthanized and
sampled/tested positive for CWD.
Recent CWD history in Ohio
a.Pennsylvania traces
In the spring of 2014, Ohio received information on traces associated with
CWD positive cases in Pennsylvania. Three Ohio herds were designated as Exposed
herds because positive deer from infected herds in PA had been in the Ohio herd
s during the previous 5 years. Fifty Ohio herds received 256 exposed deer from
the 5 PA herds and 3 Ohio exposed herds. 85 of those animals were tested with
Not Detected results in Ohio herds. 66 animals were traced to Out of State
herds. That leaves 101 animals either standing in quarantined herds or not
tested when they died or were harvested. 18 herds/preserves remain under
quarantine.
b. First CWD positive found in Ohio
On October 22, 2014, National Veterinary Services Laboratory (NVSL)
confirmed a CWD positive result for a 2.5 year old buck killed at a hunting
preserve in Holmes County Ohio on October 2, 2014. The hunting preserve had been
under quarantine since April 1, 2014 because of PA traces and was required to do
100% sampling of harvested deer. The positive animal had official identification
tracing the animal to a CWD certified Pennsylvania herd. Records including a
Certificate of Veterinary Inspection indicate the animal moved to Ohio March 13,
2013. Genetic testing was conducted to support the accuracy of the trace to the
Pennsylvania herd. This herd was depopulated without indemnity April 27-29,
2015. 224 animals were depopulated at owner expense and sampled for CWD. All
tests had Not Detected results for CWD. The premises was evaluated as a
minimally contaminated facility. No cervidae have been added to the premises at
this time.
The owner of the hunting preserve business also owns or is associated with
breeding herds at other locations in Holmes County.
c. Second positive premises in Ohio
A white tail deer breeding herd owned by the same person who owned the CWD
positive hunting preserve was designated as a positive herd in the spring of
2015. A CWD positive animal was sampled on 3/12/2015 and reported on March 25,
2015. The animal was a 5 year old whitetail doe purchased from a Wisconsin herd
in February 2013. A second CWD positive animal was reported from this herd on
May 22, 2015. This animal was a 1.5 year old natural addition doe. This herd was
initially established in the fall of 2012 with the purchase of a CWD certified
herd from the estate of a deceased owner. In the spring and fall of 2013,
additional animals were added from at least 9 OH herds , 1 WI herd, 17 PA herds,
and 3 IN herds. This herd had been quarantined since April 1,2014 because of
traces from several CWD exposed or positive herds in Pennsylvania, including the
herd that was the source of the CWD positive deer in the Ohio hunting preserve.
It had received over 120 animals from these herds.
On June 15 and 16, this herd was depopulated with federal indemnity.
Samples were collected for research purposes. 241 animals including 44 fawns
were euthanized, sampled and tested. Sixteen additional positive were
identified. They originated from 5 Ohio CWD certified herds and 4 Pennsylvania
CWD certified herds. One of the Ohio herds was the herd that was used to
initially establish this herd. One positive animal was over 60 months of age so
that Ohio herd was not designated as an exposed herd. The other three Ohio herds
were quarantined as exposed herds.
Records reviews identified 334 exposed animals associated with Ohio exposed
herds. 42 Ohio herds containing these animals were quarantined. They have
remained under quarantine until the quarantined animal(s) are euthanized and
tested Not Detected for CWD or 60 months have passed since animals entered the
herd. From Ohio Exposed Herd 1, 56 animals moved to 21 Ohio herds and 83 animals
moved out of state. 27 animals were either already dead and tested with CWD Not
Detected results or have since been tested with CWD Not Detected results. From
Ohio Exposed Herd 2, 76 animals moved to 16 Ohio herds and 94 animals moved out
of state. 25 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. From Oho
Exposed Herd 3, 21 animals moved to 5 Ohio herds and 4 animals moved out of
state. 7 animals were either already dead and tested with CWD Not Detected
results or have since been tested with CWD Not Detected results. Ohio received 2
exposed animals from the exposed herd in Pennsylvania associated with this case.
In summary, 334 exposed animals were identified and traced to 40 Ohio herds. 59
of those in Ohio have been tested with Not Detected CWD results. 181 have been
traced out of state and 94 are still standing in 26 quarantined herds/hunting
preserves.
Ohio Exposed Herd 1 has been in the CWD Certification Program since
September 2003 and has an inventory as of 48 head over 1 year old. Ohio Exposed
Herd 2 has been in the CWD Certification Program since October 2003 and has an
inventory of 93 animals. Ohio Exposed Herd 3 has been in the CWD Certification
Program since February 2009 but started with a status date of May, 2001 and has
an inventory of 17 deer.
In addition Ohio received reports of 72 exposed deer form OOS Exposed herds
traced to 18 Ohio herds. 18 of those animals had moved to out of state herds. 30
animals were tested in Ohio with Not Detected results. 12 animals remain in 7
quarantined herds.
The summary of all traces associated with positive cases in Ohio and
Pennsylvania in 2014 – 2015 are:
Total exposed animals traced to Ohio:661
Total tested Not Detected: 176
Total animals traced to Out of State Premises: 265
Total premises initially quarantined 87
Total premises remaining quarantined: 40
Total Hunting Preserves quarantined: 10
USDA Cervid Health Program Updates
Randy Pritchard, USDA, APHIS, Veterinary Services
Voluntary Chronic Wasting Disease (CWD) Herd Certification Program
The APHIS National CWD Herd Certification Program (HCP) was implemented in
2014. It is a voluntary Federal-State-industry cooperative program administered
by APHIS and implemented by participating States. The program provides uniform
national herd certification standards that minimize the risk of spreading CWD in
farmed cervid populations. Participating States and herd owners must comply with
requirements for animal identification, fencing, recordkeeping,
inspections/inventories, as well as animal mortality testing and response to any
CWD-exposed, suspect, and positive herds. APHIS monitors the Approved State HCPs
to ensure consistency with Federal standards through annual reporting by the
States. With each year of successful surveillance, participating herds will
advance in status until reaching five years with no evidence of CWD, at which
time herds are certified as being low-risk for CWD. Only captive cervids from
enrolled herds certified as low risk for CWD may move interstate. Currently, 30
States participate in the voluntary CWD Herd Certification Program; 29 have
Approved HCPs and one has Provisional Approved status. VS is working with the
remaining State to transition it to Approved status. FY2015 marks the second
year that Approved States have submitted their CWD HCP annual reports to APHIS.
APHIS is currently reviewing these reports.
Review of CWD Program Standards
The CWD Program Standards provide clarification and guidance on how to meet
CWD Herd Certification Program and interstate movement requirements. VS
committed to an annual review of the Program Standards by representatives of the
cervid industry and appropriate State and Federal agencies. VS planned to
perform a review in FY2015; however, this did not occur due to the response to
highly pathogenic avian influenza (HPAI). VS expects to conduct a review in
FY2016.
CWD in Farmed and Wild Cervids
Retrospective Epidemiology of CWD in Farmed Cervids: In response to a 2014
USAHA Resolution, VS asked States to include a retrospective summary of the
epidemiology of all positive herds with their annual HCP reports for FY2015.
Unfortunately, the response to HPAI delayed completion of this summary. Five
States reported information to date. A few States indicated that they did not
have the resources to devote to this request. VS will continue to gather this
data and to collect more comprehensive data in the future.
Summary of CWD detections. As of September 30, 2015, CWD has been confirmed
in wild deer and elk in 21 U.S. States, and in farmed cervids in 16 States. In
total, 23 States have identified CWD in wild and/or farmed cervids. CWD has been
reported in 70 farmed cervid herds in the United States. Confirmation of the
disease in 3 free-ranging, wild white-tailed deer in Michigan in 2015 marked the
first report of CWD in the wild cervid population in this State. FY2015 CWD
Detections in Farmed Cervids: In FY2015, CWD was identified in eight farmed
cervid herds: one white-tailed deer breeding herd in Pennsylvania, one elk
breeding herd in Utah (traced back from a hunting facility in Utah), one
white-tailed deer (WTD) breeding herd and one WTD hunting preserve in Ohio
(owned by the same producer), two WTD breeding herds in Wisconsin, one WTD and
elk herd in Texas, and a second WTD herd in Texas (traced from the first
positive herd in Texas). The positive animals in Utah, Ohio, and Texas
represented the first reported cases of CWD in captive cervids in all three of
these States.
White-Tailed Deer Breeding Herd, Pennsylvania: On October 6, 2014, the
National Veterinary Services Laboratories (NVSL) confirmed CWD in a 6-year-old
doe from a captive WTD breeding facility in Reynoldsville, Pennsylvania. The doe
was euthanized and tested because she was classified as a CWD- exposed animal
that had previously resided in two trace back exposed herds. This herd was
assembled in 2013 through the purchase of 16 animals from other HCP-certified
herds in Pennsylvania, and had been under quarantine for receiving exposed
animals from a trace back exposed herd. The remaining herd of eight WTD was
depopulated with Federal indemnity on February 18, 2015, and no additional
positive animals were detected. USDA collected samples for research
purposes.
Elk Breeding Herd, Utah: On December 23, 2014, NVSL confirmed CWD in
3-year-old captive elk. The elk had been at a hunting park located in northern
Utah, where he had resided for approximately 3 weeks prior to being hunter
killed. All hunter-killed animals at the hunt park are required to be tested for
CWD, and this animal was sampled through routine surveillance. The elk was
traced back to its herd of origin, and that facility was quarantined. The herd
was assembled in 1999 with bulls, and later elk cows, that originated from
Colorado. Historical testing records for the herd were unavailable. The
remaining 70 elk were depopulated using Federal indemnity funds on March 3,
2015, and an additional 25 elk were confirmed as CWD-positive. USDA collected
samples for research purposes.
White-Tailed Deer Hunting Preserve, Ohio: On October 22, 2014, NVSL
confirmed CWD in a buck taken from a captive WTD deer hunting preserve in Ohio.
This was the first time that CWD had been detected in Ohio. The preserve was
tested as part of Ohio’s CWD monitoring program. The herd had been under
quarantine since April 2014 because it was a trace-forward herd associated with
a CWD-exposed herd in Pennsylvania. The positive animal was traced to its herd
of origin, a captive WTD breeding herd in Pennsylvania, through DNA identity
testing. On November 26, 2014, the Ohio State Veterinarian issued an Order of
Destruction for animals on the hunting preserve. The State executed this Order
on April 27-30, 2015. The herd of 224 WTD was depopulated and no other positives
were detected. USDA did not provide Federal indemnity.
White-Tailed Deer Breeding Herd, Ohio: On March 31, 2015, NVSL confirmed
CWD infection in a 5-year-old WTD doe from a captive breeding herd in
Holmesville, Ohio. The index animal was received from a Wisconsin WTD farm in
January 2013. The CWD-positive herd was owned by the same individual as the Ohio
hunt preserve that was found to be CWD positive in October 2014. On May 22,
2015, NVSL confirmed a second positive case in the same herd -- a yearling WTD
doe that was a natural addition in the same breeding herd. The herd had been
under quarantine since April 1, 2014 due to epidemiological linkages with two
WTD herds in Pennsylvania – one a positive herd and the other a traceback
exposed herd. USDA provided Federal indemnity and depopulated this herd on June
15 and 16, 2015. USDA collected samples for research purposes. NVSL confirmed
CWD in 16 additional animals in the herd. Of the 16 positives, one was natural
addition and the rest were purchased additions. The positive animals were
purchased from February 26, 2013 through September 24, 2013, except for one
purchased in 2012. Eleven purchased additions traced-back to 3 herds in
Pennsylvania and four purchased additions traced to three other herds in
Ohio.
White-Tailed Deer Breeding Herd, Wisconsin: On October 6, 2014, NVSL
confirmed CWD in a 2-year-old doe born in June of 2012 that died on a Richland
County farm. The facility is within the CWD management zone in Wisconsin. The
remaining 51 deer were euthanized on November 20, 2014, and seven additional
positives (all males born in 2012) were found. Two of these 7 were purchased
additions with the last added to the herd in January 2013. All sales from this
herd were to shooting preserves. This premises was double fenced and had been
compliant in a herd certification program for over 10 years.
White-Tailed Deer Breeding Herd, Wisconsin: On June 19, 2015, NVSL
confirmed CWD in a 7-year-old female WTD from a breeding facility in Eau Claire
County. The doe was a natural addition to this breeding herd. This is the first
positive CWD case, captive or wild, in this county. The doe was found dead and
was showing no clinical signs of CWD at the time of death. Since 2003, this herd
has tested 391 animals for CWD and all had “not detected” results. In addition,
317 animals have tested “not detected” from the associated hunting preserve over
the same time period. A second positive natural addition doe from this herd was
confirmed positive by NVSL on September 10, 2015. Several escape episodes have
occurred from this herd. The herd is currently under quarantine and plans are
underway for depopulation with State indemnity.
White-Tailed Deer and Elk Breeding Herd, Texas: On June 30, 2015, NVSL
confirmed CWD in a 2-year-old WTD buck from a captive WTD and elk breeding herd
in Medina County, Texas, approximately 500 miles from previously reported
positive free-ranging mule deer in far West Texas. This was the first time that
the disease had been detected in farmed cervids in the State. The index buck was
born on the premises and found dead on June 18, 2015. Over 40 high-risk deer
(i.e., pen mates, dam, others) were euthanized and tested after the index case
was found. The NVSL confirmed CWD infection in two of those deer. Interestingly,
all three of the positive deer identified to date on this premises have the same
AI sire. However, the significance of this finding is unclear. In the past 5
years, records indicate that 130 WTD from 33 facilities moved into the positive
herd and 838 WTD moved out of the positive herd to 147 different herds. One
positive WTD was found in one of these trace-out herds (see herd description
below). Additionally, 23 elk were also moved from this herd to another herd in
TX in 2014. All trace-outs have been intrastate except for movements to two
premises in Mexico. Premises that have received deer from the index herd are
under movement restrictions. VS is collaborating with animal health authorities
in Mexico. VS paid indemnity and depopulated this herd on September 30, 2015,
and no additional positive animals were detected. USDA collected samples for
research purposes.
White-Tailed Deer Herd, Texas: On September 14, 2015 NVSL confirmed CWD
from tissues from a WTD in Lavaca County, Texas. This animal was a traceout from
the first CWD positive herd from June 30, 2015. Additional epidemiology is
ongoing.
Friday, February 05, 2016
*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION
Detections in Farmed Cervids and Wild ***
Friday, April 22, 2016
Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in
a Mule Deer
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Friday, February 05, 2016
TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER
RELEASE SITE
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Wednesday, April 20, 2016
UTAH CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM
70 mule deer and two elk have tested positive
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA 2016 ***
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
12:04 PM
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